unique_id,web-scraper-start-url,sub_chapters_x,sub_chapters-href,paragraph,is_paragraph,sub_section_headings,fig_num,sub_chapters_y,images-src,image_caption
02c1e94c-7a22-4289-8700-013c3500e5bb,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,Zika Virus Infection,False,Zika Virus Infection,,,,
48249af6-6f37-4a1c-ba0a-28c61ec34090,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"Zika virus infection is an emerging arboviral disease associated with human illness in Africa, Southeast Asia, and South and Central America; however, its range is expanding as a result of the widespread range of its mosquito vector. The first cases originating in the United States were reported in 2016. The Zika virus was initially described in 1947 from monkeys in the Zika Forest of Uganda through a network that monitored yellow fever. It was not considered a serious human pathogen until the first large-scale outbreaks occurred in Micronesia in 2007;[1] however, the virus has gained notoriety over the past decade, as it has emerged as a cause of symptoms similar to other arboviral infections that include fever, skin rashes, conjunctivitis, muscle and joint pain, malaise, and headache. Mosquitoes of the Aedes genus are the primary vectors, although the virus can also be transmitted sexually, from mother to baby during pregnancy, or through a blood transfusion.",True,Zika Virus Infection,,,,
262e2627-85d4-46d3-92ac-a3d05c4bb5a1,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"Most Zika virus infections result in mild symptoms such as fever, a slight rash, or conjunctivitis. However, infections in pregnant women can adversely affect the developing fetus. Reports in 2015 indicate fetal infections can result in brain damage, including a serious birth defect called microcephaly, in which the infant is born with an abnormally small head (Figure 21.12).[2]",True,Zika Virus Infection,Figure 21.12,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-26.14.png,"Figure 21.12 (a) This colorized electron micrograph shows Zika virus particles (red). (b) Women infected by the Zika virus during pregnancy may give birth to children with microcephaly, a deformity characterized by an abnormally small head and brain. (credit a, b: modifications of work by the Centers for Disease Control and Prevention)"
6beaf8f9-a1d0-4891-9a3d-9f690a5b3774,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"Diagnosis of Zika is primarily based on clinical symptoms. However, the FDA recently authorized the use of a Zika virus RNA assay, to test patient blood and urine to confirm Zika virus disease. There are currently no antiviral treatments or vaccines for Zika virus, and treatment is limited to supportive care.",True,Zika Virus Infection,,,,
309659d3-79a9-4845-b3e5-9c5dc3e9ca15,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,Rabies,False,Rabies,,,,
1e7d6bd7-ef91-4d81-999a-31abd6997453,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"Rabies is a deadly zoonotic disease that has been known since antiquity. The disease is caused by rabies virus (RV), a member of the family Rhabdoviridae, and is primarily transmitted through the bite of an infected mammal. Rhabdoviridae are enveloped RNA viruses that have a distinctive bullet shape (Figure 21.13); they were first studied by Louis Pasteur, who obtained rabies virus from rabid dogs and cultivated the virus in rabbits. He successfully prepared a rabies vaccine using dried nerve tissues from infected animals. This vaccine was used to first treat an infected human in 1885.",True,Rabies,Figure 21.13,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-26.15.png,Figure 21.13 Virions of the rabies virus have a characteristic bullet-like shape. (credit: modification of work by the Centers for Disease Control and Prevention)
6f88cb13-5a89-4ae6-8163-c18214282411,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"The most common reservoirs in the United States are wild animals such as raccoons (30.2% of all animal cases during 2014), bats (29.1%), skunks (26.3%), and foxes (4.1%); collectively, these animals were responsible for a total of 92.6% of animal rabies cases in the United States in 2014. The remaining 7.4% of cases that year were in domesticated animals such as dogs, cats, horses, mules, sheep, goats, and llamas.[3] While there are typically only one or two human cases per year in the United States, rabies still causes tens of thousands of human deaths per year worldwide, primarily in Asia and Africa.",True,Rabies,,,,
adafbcc5-3746-490c-906e-4b25777f98a4,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"The low incidence of rabies in the United States is primarily a result of the widespread vaccination of dogs and cats. An oral vaccine is also used to protect wild animals, such as raccoons and foxes, from infection. Oral vaccine programs tend to focus on geographic areas where rabies is endemic.[4] The oral vaccine is usually delivered in a package of bait that is dropped by airplane, although baiting in urban areas is done by hand to maximize safety.[5] Many countries require a quarantine or proof of rabies vaccination for domestic pets being brought into the country. These procedures are especially strict in island nations where rabies is not yet present, such as Australia.",True,Rabies,,,,
8248e06a-f56c-422f-86f3-f8b559dfcb3a,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"The incubation period for rabies can be lengthy, ranging from several weeks or months to over a year. As the virus replicates, it moves from the site of the bite into motor and sensory axons of peripheral nerves and spreads from nerve to nerve using a process called retrograde transport, eventually making its way to the CNS through the spinal ganglia. Once rabies virus reaches the brain, the infection leads to encephalitis caused by the disruption of normal neurotransmitter function, resulting in the symptoms associated with rabies. The virions act in the synaptic spaces as competitors with a variety of neurotransmitters for acetylcholine, GABA, and glycine receptors. Thus, the action of rabies virus is neurotoxic rather than cytotoxic. After the rabies virus infects the brain, it can continue to spread through other neuronal pathways, traveling out of the CNS to tissues such as the salivary glands, where the virus can be released. As a result, as the disease progresses the virus can be found in many other tissues, including the salivary glands, taste buds, nasal cavity, and tears.",True,Rabies,,,,
f8c6fd93-e09f-4718-bf6e-f36eb278a5e6,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"The early symptoms of rabies include discomfort at the site of the bite, fever, and headache. Once the virus reaches the brain and later symptoms appear, the disease is always fatal. Terminal rabies cases can end in one of two ways: either furious or paralytic rabies. Individuals with furious rabies become very agitated and hyperactive. Hydrophobia (a fear of water) is common in patients with furious rabies, which is caused by muscular spasms in the throat when swallowing or thinking about water. Excess salivation and a desire to bite can lead to foaming of the mouth. These behaviors serve to enhance the likelihood of viral transmission, although contact with infected secretions like saliva or tears alone is sufficient for infection. The disease culminates after just a few days with terror and confusion, followed by cardiovascular and respiratory arrest. In contrast, individuals with paralytic rabies generally follow a longer course of disease. The muscles at the site of infection become paralyzed. Over a period of time, the paralysis slowly spreads throughout the body. This paralytic form of disease culminates in coma and death.",True,Rabies,,,,
b40afdf8-b46b-47c7-ac7b-21b362d7ed87,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"Before present-day diagnostic methods were available, rabies diagnosis was made using a clinical case history and histopathological examination of biopsy or autopsy tissues, looking for the presence of Negri bodies. We now know these histologic changes cannot be used to confirm a rabies diagnosis. There are no tests that can detect rabies virus in humans at the time of the bite or shortly thereafter. Once the virus has begun to replicate (but before clinical symptoms occur), the virus can be detected using an immunofluorescence test on cutaneous nerves found at the base of hair follicles. Saliva can also be tested for viral genetic material by reverse transcription followed by polymerase chain reaction (RT-PCR). Even when these tests are performed, most suspected infections are treated as positive in the absence of contravening evidence. It is better that patients undergo unnecessary therapy because of a false-positive result, rather than die as the result of a false-negative result.",True,Rabies,,,,
e3219dc4-3352-4e05-9eb9-1a8716e9e134,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"Human rabies infections are treated by immunization with multiple doses of an attenuated vaccine to develop active immunity in the patient. Vaccination of an already-infected individual has the potential to work because of the slow progress of the disease, which allows time for the patient’s immune system to develop antibodies against the virus. Patients may also be treated with human rabies immune globulin (antibodies to the rabies virus) to encourage passive immunity. These antibodies will neutralize any free viral particles. Although the rabies infection progresses slowly in peripheral tissues, patients are not normally able to mount a protective immune response on their own.",True,Rabies,,,,
4e9b8c7d-e681-4316-bc30-c924ead6054c,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,Poliomyelitis,False,Poliomyelitis,,,,
8fdf07f1-ad66-4979-b99f-e3912ee41d48,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"Poliomyelitis (polio), caused by poliovirus, is a primarily intestinal disease that, in a small percentage of cases, proceeds to the nervous system, causing paralysis and, potentially, death. Poliovirus is highly contagious, with transmission occurring by the fecal-oral route or by aerosol or droplet transmission. Approximately 72% of all poliovirus infections are asymptomatic; another 25% result only in mild intestinal disease, producing nausea, fever, and headache.[6] However, even in the absence of symptoms, patients infected with the virus can shed it in feces and oral secretions, potentially transmitting the virus to others. In about one case in every 200, the poliovirus affects cells in the CNS.[7]",True,Poliomyelitis,,,,
b661eeaf-0acd-4d0d-96ea-656dfcea7b93,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"After it enters through the mouth, initial replication of poliovirus occurs at the site of implantation in the pharynx and gastrointestinal tract. As the infection progresses, poliovirus is usually present in the throat and in the stool before the onset of symptoms. One week after the onset of symptoms, there is less poliovirus in the throat, but for several weeks, poliovirus continues to be excreted in the stool. Poliovirus invades local lymphoid tissue, enters the bloodstream, and then may infect cells of the CNS. Replication of poliovirus in motor neurons of the anterior horn cells in the spinal cord, brain stem, or motor cortex results in cell destruction and leads to flaccid paralysis. In severe cases, this can involve the respiratory system, leading to death. Patients with impaired respiratory function are treated using positive- pressure ventilation systems. In the past, patients were sometimes confined to Emerson respirators, also known as iron lungs (Figure 21.14).",True,Poliomyelitis,Figure 21.14,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-26.16.png,Figure 21.14 (a) An Emerson respiratory (or iron lung) that was used to help some polio victims to breathe. (b) Polio can also result in impaired motor function. (credit b: modification of work by the Centers for Disease Control and Prevention)
bfb7576e-f0fb-4621-bad9-3228346bc456,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"Direct detection of the poliovirus from the throat or feces can be achieved using reverse transcriptase PCR (RT-PCR) or genomic sequencing to identify the genotype of the poliovirus infecting the patient. Serological tests can be used to determine whether the patient has been previously vaccinated. There are no therapeutic measures for polio; treatment is limited to various supportive measures. These include pain relievers, rest, heat therapy to ease muscle spasms, physical therapy and corrective braces if necessary to help with walking, and mechanical ventilation to assist with breathing if necessary.",True,Poliomyelitis,,,,
d1ac72f7-8c25-4ddb-9240-1fa887086695,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,Two different vaccines were introduced in the 1950s that have led to the dramatic decrease in polio worldwide (Figure 21.15). The Salk vaccine is an inactivated polio virus that was first introduced in 1955. This vaccine is delivered by intramuscular injection. The Sabin vaccine is an oral polio vaccine that contains an attenuated virus; it was licensed for use in 1962. There are three serotypes of poliovirus that cause disease in humans; both the Salk and the Sabin vaccines are effective against all three.,True,Poliomyelitis,Figure 21.15,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-26.17.png,Figure 21.15 (a) Polio is caused by the poliovirus. (b) Two American virologists developed the first polio vaccines: Albert Sabin (left) and Jonas Salk (right). (credit a: modification of work by the Centers for Disease Control and Prevention)
36a60121-42f3-4d20-a73d-da01dd8512cb,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"Attenuated viruses from the Sabin vaccine are shed in the feces of immunized individuals and thus have the potential to infect nonimmunized individuals. By the late 1990s, the few polio cases originating in the United States could be traced back to the Sabin vaccine. In these cases, mutations of the attenuated virus following vaccination likely allowed the microbe to revert to a virulent form. For this reason, the United States switched exclusively to the Salk vaccine in 2000. Because the Salk vaccine contains an inactivated virus, there is no risk of transmission to others. Currently four doses of the vaccine are recommended for children: at 2, 4, and 6–18 months of age, and at 4–6 years of age.",True,Poliomyelitis,,,,
7a924ac2-72ba-456f-9668-0b8f113ff39c,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"In 1988, WHO launched the Global Polio Eradication Initiative with the goal of eradicating polio worldwide through immunization. That goal is now close to being realized. Polio is now endemic in only a few countries, including Afghanistan, Pakistan, and Nigeria, where vaccination efforts have been disrupted by military conflict or political instability.",True,Poliomyelitis,,,,
3173180c-11c4-45d2-8fdd-aa5c6754bd03,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"Yet even the Iron Curtain was no match for polio. The Salk vaccine became widely available in the West in 1955, and by the time the Sabin vaccine was ready for clinical trials, most of the susceptible population in the United States and Canada had already been vaccinated against polio. Sabin needed to look elsewhere for study participants. At the height of the Cold War, Mikhail Chumakov was allowed to come to the United States to study Sabin’s work. Likewise, Sabin, an American microbiologist, was allowed to travel to the Soviet Union to begin clinical trials. Chumakov organized Soviet-based production and managed the experimental trials to test the new vaccine in the Soviet Union. By 1959, over ten million Soviet children had been safely treated with Sabin’s vaccine.",True,Poliomyelitis,,,,
039faa5e-47a3-4624-b3d3-fe59622d2e0d,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"As a result of a global vaccination campaign with the Sabin vaccine, the overall incidence of polio has dropped dramatically. Today, polio has been nearly eliminated around the world and is only rarely seen in the United States. Perhaps one day soon, polio will become the third microbial disease to be eradicated from the general population [small pox and rinderpest (the cause of cattle plague) being the first two].",True,Poliomyelitis,,,,
572c6394-b6c2-4ac5-8218-cb9c6cc18b96,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,Transmissible Spongiform Encephalopathies,False,Transmissible Spongiform Encephalopathies,,,,
7234edbc-c373-4283-bc04-cde301681024,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"Acellular infectious agents called prions are responsible for a group of related diseases known as transmissible spongiform encephalopathies (TSEs) that occurs in humans and other animals. All TSEs are degenerative, fatal neurological diseases that occur when brain tissue becomes infected by prions. These diseases have a slow onset; symptoms may not become apparent until after an incubation period of years and perhaps decades, but death usually occurs within months to a few years after the first symptoms appear.",True,Transmissible Spongiform Encephalopathies,,,,
bee4cee0-aa5d-4388-8c43-14dc39bf7d9a,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"TSEs in animals include scrapie, a disease in sheep that has been known since the 1700s, and chronic wasting disease, a disease of deer and elk in the United States and Canada. Mad cow disease is seen in cattle and can be transmitted to humans through the consumption of infected nerve tissues. Human prion diseases include Creutzfeldt- Jakob disease and kuru, a rare disease endemic to Papua New Guinea.",True,Transmissible Spongiform Encephalopathies,,,,
70976360-b347-4d9e-b099-cb37f6fcab9a,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"Prions are infectious proteinaceous particles that are not viruses and do not contain nucleic acid. They are typically transmitted by exposure to and ingestion of infected nervous system tissues, tissue transplants, blood transfusions, or contaminated fomites. Prion proteins are normally found in a healthy brain tissue in a form called PrPC. However, if this protein is misfolded into a denatured form (PrPSc), it can cause disease. Although the exact function of PrPC is not currently understood, the protein folds into mostly alpha helices and binds copper. The rogue protein, on the other hand, folds predominantly into beta-pleated sheets and is resistant to proteolysis. In addition, PrPSc can induce PrPC to become misfolded and produce more rogue protein (Figure 21.16).",True,Transmissible Spongiform Encephalopathies,Figure 21.16,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-26.18.png,Figure 21.16 The replicative cycle of misfolded prion proteins.
522dc8fd-21de-48ff-9b83-8c3ed26e458f,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"As PrPSc accumulates, it aggregates and forms fibrils within nerve cells. These protein complexes ultimately cause the cells to die. As a consequence, brain tissues of infected individuals form masses of neurofibrillary tangles and amyloid plaques that give the brain a spongy appearance, which is why these diseases are called spongiform encephalopathy. Damage to brain tissue results in a variety of neurological symptoms. Most commonly, affected individuals suffer from memory loss, personality changes, blurred vision, uncoordinated movements, and insomnia. These symptoms gradually worsen over time and culminate in coma and death.",True,Transmissible Spongiform Encephalopathies,,,,
7bfc6094-5b9b-4c3a-816b-fbcae16f47b1,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"The gold standard for diagnosing TSE is the histological examination of brain biopsies for the presence of characteristic amyloid plaques, vacuoles, and prion proteins. Great care must be taken by clinicians when handling suspected prion-infected materials to avoid becoming infected themselves. Other tissue assays search for the presence of the 14-3-3 protein, a marker for prion diseases like Creutzfeldt-Jakob disease. New assays, like RT-QuIC (real- time quaking-induced conversion), offer new hope to effectively detect the abnormal prion proteins in tissues earlier in the course of infection. Prion diseases cannot be cured. However, some medications may help slow their progress. Medical support is focused on keeping patients as comfortable as possible despite progressive and debilitating symptoms.",True,Transmissible Spongiform Encephalopathies,,,,
7e3a00c4-8f7e-4425-8d1a-69d12e7471e1,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"Serious consequences are the common thread among these neurological diseases. Several cause debilitating paralysis, and some, such as Creutzfeldt-Jakob disease and rabies, are always or nearly always fatal. Since few drugs are available to combat these infections, vector control and vaccination are critical for prevention and containment. Figure 20.19 summarizes some important viral and prion infections of the nervous system.",True,Transmissible Spongiform Encephalopathies,Figure 20.19,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.28.png,Figure 20.19 A blood smear (human blood stage) shows an early trophozoite in a delicate ring form (upper left) and an early stage schizont form (center) of Plasmodium falciparum from a patient with malaria. (credit: modification of work by Centers for Disease Control and Prevention)
d3e428f9-8951-418c-8fdd-2fe7eaab55a4,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"Yet even the Iron Curtain was no match for polio. The Salk vaccine became widely available in the West in 1955, and by the time the Sabin vaccine was ready for clinical trials, most of the susceptible population in the United States and Canada had already been vaccinated against polio. Sabin needed to look elsewhere for study participants. At the height of the Cold War, Mikhail Chumakov was allowed to come to the United States to study Sabin’s work. Likewise, Sabin, an American microbiologist, was allowed to travel to the Soviet Union to begin clinical trials. Chumakov organized Soviet-based production and managed the experimental trials to test the new vaccine in the Soviet Union. By 1959, over ten million Soviet children had been safely treated with Sabin’s vaccine.",True,Transmissible Spongiform Encephalopathies,,,,
59e258a1-377b-4acf-9fec-921c6961eb2e,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"As a result of a global vaccination campaign with the Sabin vaccine, the overall incidence of polio has dropped dramatically. Today, polio has been nearly eliminated around the world and is only rarely seen in the United States. Perhaps one day soon, polio will become the third microbial disease to be eradicated from the general population [small pox and rinderpest (the cause of cattle plague) being the first two].",True,Transmissible Spongiform Encephalopathies,,,,
13d5d17d-9ee0-405e-bf80-7ce3ca585f51,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,Transmissible Spongiform Encephalopathies,False,Transmissible Spongiform Encephalopathies,,,,
b1e80149-7a1a-415a-8427-006875eec2bb,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"Acellular infectious agents called prions are responsible for a group of related diseases known as transmissible spongiform encephalopathies (TSEs) that occurs in humans and other animals. All TSEs are degenerative, fatal neurological diseases that occur when brain tissue becomes infected by prions. These diseases have a slow onset; symptoms may not become apparent until after an incubation period of years and perhaps decades, but death usually occurs within months to a few years after the first symptoms appear.",True,Transmissible Spongiform Encephalopathies,,,,
d9606e80-82aa-48c7-ab55-1ff5fcf410cf,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"TSEs in animals include scrapie, a disease in sheep that has been known since the 1700s, and chronic wasting disease, a disease of deer and elk in the United States and Canada. Mad cow disease is seen in cattle and can be transmitted to humans through the consumption of infected nerve tissues. Human prion diseases include Creutzfeldt- Jakob disease and kuru, a rare disease endemic to Papua New Guinea.",True,Transmissible Spongiform Encephalopathies,,,,
9ff448d1-8cdf-4daf-888d-0c58f7569ba8,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"Prions are infectious proteinaceous particles that are not viruses and do not contain nucleic acid. They are typically transmitted by exposure to and ingestion of infected nervous system tissues, tissue transplants, blood transfusions, or contaminated fomites. Prion proteins are normally found in a healthy brain tissue in a form called PrPC. However, if this protein is misfolded into a denatured form (PrPSc), it can cause disease. Although the exact function of PrPC is not currently understood, the protein folds into mostly alpha helices and binds copper. The rogue protein, on the other hand, folds predominantly into beta-pleated sheets and is resistant to proteolysis. In addition, PrPSc can induce PrPC to become misfolded and produce more rogue protein (Figure 21.16).",True,Transmissible Spongiform Encephalopathies,Figure 21.16,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-26.18.png,Figure 21.16 The replicative cycle of misfolded prion proteins.
1c946fb0-961d-4665-907b-bb875f548fe5,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"As PrPSc accumulates, it aggregates and forms fibrils within nerve cells. These protein complexes ultimately cause the cells to die. As a consequence, brain tissues of infected individuals form masses of neurofibrillary tangles and amyloid plaques that give the brain a spongy appearance, which is why these diseases are called spongiform encephalopathy. Damage to brain tissue results in a variety of neurological symptoms. Most commonly, affected individuals suffer from memory loss, personality changes, blurred vision, uncoordinated movements, and insomnia. These symptoms gradually worsen over time and culminate in coma and death.",True,Transmissible Spongiform Encephalopathies,,,,
758ce3fb-923f-47d8-a8e5-06ec92110bc3,https://open.oregonstate.education/microbiology/,21.3	Acellular Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-3acellular-diseases-of-the-nervous-system/,"The gold standard for diagnosing TSE is the histological examination of brain biopsies for the presence of characteristic amyloid plaques, vacuoles, and prion proteins. Great care must be taken by clinicians when handling suspected prion-infected materials to avoid becoming infected themselves. Other tissue assays search for the presence of the 14-3-3 protein, a marker for prion diseases like Creutzfeldt-Jakob disease. New assays, like RT-QuIC (real- time quaking-induced conversion), offer new hope to effectively detect the abnormal prion proteins in tissues earlier in the course of infection. Prion diseases cannot be cured. However, some medications may help slow their progress. Medical support is focused on keeping patients as comfortable as possible despite progressive and debilitating symptoms.",True,Transmissible Spongiform Encephalopathies,,,,
173a5689-1458-4e79-9ea3-1528cd148cae,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,Bacterial Meningitis,False,Bacterial Meningitis,,,,
20fdfc9e-7e60-4079-b889-6a3330fbb377,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Bacterial meningitis is one of the most serious forms of meningitis. Bacteria that cause meningitis often gain access to the CNS through the bloodstream after trauma or as a result of the action of bacterial toxins. Bacteria may also spread from structures in the upper respiratory tract, such as the oropharynx, nasopharynx, sinuses, and middle ear. Patients with head wounds or cochlear implants (an electronic device placed in the inner ear) are also at risk for developing meningitis.",True,Bacterial Meningitis,,,,
ac3f73de-1270-4850-94dc-4a69bcb7d9e4,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Many of the bacteria that can cause meningitis are commonly found in healthy people. The most common causes of non-neonatal bacterial meningitis are Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae. All three of these bacterial pathogens are spread from person to person by respiratory secretions. Each can colonize and cross through the mucous membranes of the oropharynx and nasopharynx, and enter the blood. Once in the blood, these pathogens can disseminate throughout the body and are capable of both establishing an infection and triggering inflammation in any body site, including the meninges (Figure 21.5). Without appropriate systemic antibacterial therapy, the case-fatality rate can be as high as 70%, and 20% of those survivors may be left with irreversible nerve damage or tissue destruction, resulting in hearing loss, neurologic disability, or loss of a limb. Mortality rates are much lower (as low as 15%) in populations where appropriate therapeutic drugs and preventive vaccines are available.[1]",True,Bacterial Meningitis,Figure 21.5,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-26.5.png,Figure 21.5 (a) A normal human brain removed during an autopsy. (b) The brain of a patient who died from bacterial meningitis. Note the pus under the dura mater (being retracted by the forceps) and the red hemorrhagic foci on the meninges. (credit b: modification of work by the Centers for Disease Control and Prevention)
b8b003e8-c594-4d06-ad68-139a9e9e88b9,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"A variety of other bacteria, including Listeria monocytogenes and Escherichia coli, are also capable of causing meningitis. These bacteria cause infections of the arachnoid mater and CSF after spreading through the circulation in blood or by spreading from an infection of the sinuses or nasopharynx. Streptococcus agalactiae, commonly found in the microbiota of the vagina and gastrointestinal tract, can also cause bacterial meningitis in newborns after transmission from the mother either before or during birth.",True,Bacterial Meningitis,,,,
58410786-de50-4c7f-a5b1-e3b17a82f722,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"The profound inflammation caused by these microbes can result in early symptoms that include severe headache, fever, confusion, nausea, vomiting, photophobia, and stiff neck. Systemic inflammatory responses associated with some types of bacterial meningitis can lead to hemorrhaging and purpuric lesions on skin, followed by even more severe conditions that include shock, convulsions, coma, and death—in some cases, in the span of just a few hours.",True,Bacterial Meningitis,,,,
b84e4fa5-532b-46f6-b4fc-a03d3e1929f2,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Diagnosis of bacterial meningitis is best confirmed by analysis of CSF obtained by a lumbar puncture. Abnormal levels of polymorphonuclear neutrophils (PMNs) (> 10 PMNs/mm3), glucose (< 45 mg/dL), and protein (> 45 mg/ dL) in the CSF are suggestive of bacterial meningitis.[2] Characteristics of specific forms of bacterial meningitis are detailed in the subsections that follow.",True,Bacterial Meningitis,,,,
c4768574-f97c-4a19-bbac-88ddc5a2189f,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,Meningococcal Meningitis,False,Meningococcal Meningitis,,,,
0a88835c-aba5-4d08-945b-1b05614cd970,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Meningococcal meningitis is a serious infection caused by the gram-negative coccus N. meningitidis. In some cases, death can occur within a few hours of the onset of symptoms. Nonfatal cases can result in irreversible nerve damage, resulting in hearing loss and brain damage, or amputation of extremities because of tissue necrosis.",True,Meningococcal Meningitis,,,,
8c264b01-ed7d-4c07-9cdb-d09135ab0796,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Meningococcal meningitis can infect people of any age, but its prevalence is highest among infants, adolescents, and young adults.[3] Meningococcal meningitis was once the most common cause of meningitis epidemics in human populations. This is still the case in a swath of sub-Saharan Africa known as the meningitis belt, but meningococcal meningitis epidemics have become rare in most other regions, thanks to meningococcal vaccines. However, outbreaks can still occur in communities, schools, colleges, prisons, and other populations where people are in close direct contact.",True,Meningococcal Meningitis,,,,
821db40d-2e53-40f7-90a6-218db9e0b387,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"N. meningitidis has a high affinity for mucosal membranes in the oropharynx and nasopharynx. Contact with respiratory secretions containing N. meningitidis is an effective mode of transmission. The pathogenicity of N. meningitidis is enhanced by virulence factors that contribute to the rapid progression of the disease. These include lipooligosaccharide (LOS) endotoxin, type IV pili for attachment to host tissues, and polysaccharide capsules that help the cells avoid phagocytosis and complement-mediated killing. Additional virulence factors include IgA protease (which breaks down IgA antibodies), the invasion factors Opa, Opc, and porin (which facilitate transcellular entry through the blood-brain barrier), iron-uptake factors (which strip heme units from hemoglobin in host cells and use them for growth), and stress proteins that protect bacteria from reactive oxygen molecules.",True,Meningococcal Meningitis,,,,
6ea5b43b-5ba2-47bd-aaef-8b0eaae97310,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"A unique sign of meningococcal meningitis is the formation of a petechial rash on the skin or mucous membranes, characterized by tiny, red, flat, hemorrhagic lesions. This rash, which appears soon after disease onset, is a response to LOS endotoxin and adherence virulence factors that disrupt the endothelial cells of capillaries and small veins in the skin. The blood vessel disruption triggers the formation of tiny blood clots, causing blood to leak into the surrounding tissue. As the infection progresses, the levels of virulence factors increase, and the hemorrhagic lesions can increase in size as blood continues to leak into tissues. Lesions larger than 1.0 cm usually occur in patients developing shock, as virulence factors cause increased hemorrhage and clot formation. Sepsis, as a result of systemic damage from meningococcal virulence factors, can lead to rapid multiple organ failure, shock, disseminated intravascular coagulation, and death.",True,Meningococcal Meningitis,,,,
e58abfbb-60ec-444a-82e0-567f1075caab,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Because meningococcoal meningitis progresses so rapidly, a greater variety of clinical specimens are required for the timely detection of N. meningitidis. Required specimens can include blood, CSF, naso- and oropharyngeal swabs, urethral and endocervical swabs, petechial aspirates, and biopsies. Safety protocols for handling and transport of specimens suspected of containing N. meningitidis should always be followed, since cases of fatal meningococcal disease have occurred in healthcare workers exposed to droplets or aerosols from patient specimens. Prompt presumptive diagnosis of meningococcal meningitis can occur when CSF is directly evaluated by Gram stain, revealing extra- and intracellular gram-negative diplococci with a distinctive coffee-bean microscopic morphology associated with PMNs (Figure 21.6).",True,Meningococcal Meningitis,Figure 21.6,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-26.6.png,Figure 21.6 N. meningitidis (arrows) associated with neutrophils (the larger stained cells) in a gram-stained CSF sample. (credit: modification of work by the Centers for Disease Control and Prevention)
b2155ff7-4eb7-4718-bebf-3b2705397440,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Meningococcal infections can be treated with antibiotic therapy, and third-generation cephalosporins are most often employed. However, because outcomes can be negative even with treatment, preventive vaccination is the best form of treatment. In 2010, countries in Africa’s meningitis belt began using a new serogroup A meningococcal conjugate vaccine. This program has dramatically reduced the number of cases of meningococcal meningitis by conferring individual and herd immunity.",True,Meningococcal Meningitis,,,,
316fc27c-efa1-4b23-be9e-a6e878e7b115,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Twelve different capsular serotypes of N. meningitidis are known to exist. Serotypes A, B, C, W, X, and Y are the most prevalent worldwide. The CDC recommends that children between 11–12 years of age be vaccinated with a single dose of a quadrivalent vaccine that protects against serotypes A, C, W, and Y, with a booster at age 16.[4] An additional booster or injections of serogroup B meningococcal vaccine may be given to individuals in high-risk settings (such as epidemic outbreaks on college campuses).",True,Meningococcal Meningitis,,,,
03b8c5c2-29bc-4b53-8005-862261085cee,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Prophylactic vaccination of first-year college students living in dorms is recommended by the CDC, and insurance companies now cover meningococcal vaccination for students in college dorms. Some colleges have mandated vaccination with meningococcal conjugate vaccine for certain students entering college (Figure 21.7).",True,Meningococcal Meningitis,Figure 21.7,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-26.7.png,"Figure 21.7 To prevent campus outbreaks, some colleges now require students to be vaccinated against meningogoccal meningitis. (credit: modification of work by James Gathany, Centers for Disease Control and Prevention)"
e35d383e-2dd3-48da-b74d-1d9e89834b09,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,Pneumococcal Meningitis,False,Pneumococcal Meningitis,,,,
9cefb387-a546-427c-af28-54590cd64424,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Pneumococcal meningitis is caused by the encapsulated gram-positive bacterium S. pneumoniae (pneumococcus, also called strep pneumo). This organism is commonly found in the microbiota of the pharynx of 30–70% of young children, depending on the sampling method, while S. pneumoniae can be found in fewer than 5% of healthy adults. Although it is often present without disease symptoms, this microbe can cross the blood-brain barrier in susceptible individuals. In some cases, it may also result in septicemia. Since the introduction of the Hib vaccine, S. pneumoniae has become the leading cause of meningitis in humans aged 2 months through adulthood.",True,Pneumococcal Meningitis,,,,
a39ad318-afac-4edd-a552-5d5317bbc790,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"With the emergence of drug-resistant strains of S. pneumoniae, pneumococcal meningitis is typically treated with broad-spectrum antibiotics. The two available pneumococcal vaccines are described in Bacterial Infections of the Respiratory Tract.",True,Pneumococcal Meningitis,,,,
ed9af892-bc6d-408d-a287-45d184ef695c,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,Haemophilus influenzae Type b,False,Haemophilus influenzae Type b,,,,
960bee54-cf9c-4563-9b56-3a2521020612,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,Haemophilus influenzae,False,Haemophilus influenzae,,,,
2a4eea33-0fea-4951-8514-8a8ef72df72e,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Meningitis due to H. influenzae serotype b (Hib), an encapsulated pleomorphic gram-negative coccobacilli, is now uncommon in most countries, because of the use of the effective Hib vaccine. Without the use of the Hib vaccine, H. influenzae can be the primary cause of meningitis in children 2 months thru 5 years of age. H. influenzae can be found in the throats of healthy individuals, including infants and young children. By five years of age, most children have developed immunity to this microbe. Infants older than 2 months of age, however, do not produce a sufficient protective antibody response and are susceptible to serious disease. The intracranial pressure caused by this infection leads to a 5% mortality rate and 20% incidence of deafness or brain damage in survivors.[6]",True,Haemophilus influenzae,,,,
c6884d4b-c1d5-45b6-b0bd-a19ade80beed,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Preliminary diagnosis of H. influenzae infections can be made by direct PCR and a smear of CSF. Stained smears will reveal intracellular and extracellular PMNs with small, pleomorphic, gram-negative coccobacilli or filamentous forms that are characteristic of H. influenzae. Initial confirmation of this genus can be based on its fastidious growth on chocolate agar. Identification is confirmed with requirements for exogenous biochemical growth cofactors NAD and heme (by MALDI-TOF), latex agglutination, and RT-PCR.",True,Haemophilus influenzae,,,,
11b3bedf-6f39-4eb5-9438-9ce17101a5b4,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Meningitis caused by H. influenzae is usually treated with doxycycline, fluoroquinolones, second- and third- generation cephalosporins, and carbapenems. The best means of preventing H. influenza infection is with the use of the Hib polysaccharide conjugate vaccine. It is recommended that all children receive this vaccine at 2, 4, and 6 months of age, with a final booster dose at 12 to 15 months of age.[7]",True,Haemophilus influenzae,,,,
563092b4-efa8-46dd-9b3a-e6a1228190bc,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,Clostridium-Associated Diseases,False,Clostridium-Associated Diseases,,,,
da201f88-f3ba-45c8-8c66-569e17f6ecf2,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Species in the genus Clostridium are gram-positive, endospore-forming rods that are obligate anaerobes. Endospores of Clostridium spp. are widespread in nature, commonly found in soil, water, feces, sewage, and marine sediments. Clostridium spp. produce more types of protein exotoxins than any other bacterial genus, including two exotoxins with protease activity that are the most potent known biological toxins: botulinum neurotoxin (BoNT) and tetanusneurotoxin (TeNT). These two toxins have lethal doses of 0.2–10 ng per kg body weight.",True,Clostridium-Associated Diseases,,,,
f62e8ecf-93bf-482e-9a49-23c9a61615c7,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"BoNT can be produced by unique strains of C. butyricum, and C. baratii; however, it is primarily associated with C. botulinum and the condition of botulism. TeNT, which causes tetanus, is only produced by C. tetani. These powerful neural exotoxins are the primary virulence factors for these pathogens.",True,Clostridium-Associated Diseases,,,,
294ea713-60da-47e2-a98f-28e4bd0354bb,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Diagnosis of tetanus or botulism typically involves bioassays that detect the presence of BoNT and TeNT in fecal specimens, blood (serum), or suspect foods. In addition, both C. botulinum and C. tetani can be isolated and cultured using commercially available media for anaerobes. ELISA and RT-PCR tests are also available.",True,Clostridium-Associated Diseases,,,,
2a08e338-a22a-4152-9d25-79cf192e75f1,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,Tetanus,False,Tetanus,,,,
73b99906-b3cc-4653-98b6-c55e1e07084c,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Tetanus is a noncommunicable disease characterized by uncontrollable muscle spasms (contractions) caused by the action of TeNT. It generally occurs when C. tetani infects a wound and produces TeNT, which rapidly binds to neural tissue, resulting in an intoxication (poisoning) of neurons. Depending on the site and extent of infection, cases of tetanus can be described as localized, cephalic, or generalized. Generalized tetanus that occurs in a newborn is called neonatal tetanus.",True,Tetanus,,,,
6ad6f916-aaa5-41e1-80c8-afd406dc3137,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"In generalized tetanus, TeNT enters neurons of the PNS. From there, TeNT travels from the site of the wound, usually on an extremity of the body, retrograde (back up) to inhibitory neurons in the CNS. There, it prevents the release of gamma aminobutyric acid (GABA), the neurotransmitter responsible for muscle relaxation. The resulting muscle spasms often first occur in the jaw muscles, leading to the characteristic symptom of lockjaw (inability to open the mouth). As the toxin progressively continues to block neurotransmitter release, other muscles become involved, resulting in uncontrollable, sudden muscle spasms that are powerful enough to cause tendons to rupture and bones to fracture. Spasms in the muscles in the neck, back, and legs may cause the body to form a rigid, stiff arch, a posture called opisthotonos (Figure 21.9). Spasms in the larynx, diaphragm, and muscles of the chest restrict the patient’s ability to swallow and breathe, eventually leading to death by asphyxiation (insufficient supply of oxygen).",True,Tetanus,Figure 21.9,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-26.9.png,Figure 21.9 A tetanus patient exhibiting the rigid body posture known as opisthotonos. (credit: Centers for Disease Control and Prevention)
562e0848-3e08-49b6-917a-36f4c61eaf84,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Neonatal tetanus typically occurs when the stump of the umbilical cord is contaminated with spores of C. tetani after delivery. Although this condition is rare in the United States, neonatal tetanus is a major cause of infant mortality in countries that lack maternal immunization for tetanus and where birth often occurs in unsanitary conditions. At the end of the first week of life, infected infants become irritable, feed poorly, and develop rigidity with spasms. Neonatal tetanus has a very poor prognosis with a mortality rate of 70%–100%.[8]",True,Tetanus,,,,
8610a703-5539-4833-aa9c-85ce23515742,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Treatment for patients with tetanus includes assisted breathing through the use of a ventilator, wound debridement, fluid balance, and antibiotic therapy with metronidazole or penicillin to halt the growth of C. tetani. In addition, patients are treated with TeNT antitoxin, preferably in the form of human immunoglobulin to neutralize nonfixed toxin and benzodiazepines to enhance the effect of GABA for muscle relaxation and anxiety.",True,Tetanus,,,,
04d097de-86f4-4cea-91ab-958eafe627e5,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"A tetanus toxoid (TT) vaccine is available for protection and prevention of tetanus. It is the T component of vaccines such as DTaP, Tdap, and Td. The CDC recommends children receive doses of the DTaP vaccine at 2, 4, 6, and 15–18 months of age and another at 4–6 years of age. One dose of Td is recommended for adolescents and adults as a TT booster every 10 years.[9]",True,Tetanus,,,,
8f94b1e2-1358-4d0c-840e-975886fe43c2,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,Botulism,False,Botulism,,,,
d6c21c40-2358-42d8-894d-a1809c7e054d,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Botulism is a rare but frequently fatal illness caused by intoxication by BoNT. It can occur either as the result of an infection by C. botulinum, in which case the bacteria produce BoNT in vivo, or as the result of a direct introduction of BoNT into tissues.",True,Botulism,,,,
c7312e32-8ae9-4e62-ac11-e97550f1539e,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Infection and production of BoNT in vivo can result in wound botulism, infant botulism, and adult intestinal toxemia. Wound botulism typically occurs when C. botulinum is introduced directly into a wound after a traumatic injury, deep puncture wound, or injection site. Infant botulism, which occurs in infants younger than 1 year of age, and adult intestinal toxemia, which occurs in immunocompromised adults, results from ingesting C. botulinum endospores in food. The endospores germinate in the body, resulting in the production of BoNT in the intestinal tract.",True,Botulism,,,,
93e09bff-56d1-41da-a7e0-1ab0c80ab252,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Intoxications occur when BoNT is produced outside the body and then introduced directly into the body through food (foodborne botulism), air (inhalation botulism), or a clinical procedure (iatrogenic botulism). Foodborne botulism, the most common of these forms, occurs when BoNT is produced in contaminated food and then ingested along with the food (recall Case in Point: A Streak of Bad Potluck). Inhalation botulism is rare because BoNT is unstable as an aerosol and does not occur in nature; however, it can be produced in the laboratory and was used (unsuccessfully) as a bioweapon by terrorists in Japan in the 1990s. A few cases of accidental inhalation botulism have also occurred. Iatrogenic botulism is also rare; it is associated with injections of BoNT used for cosmetic purposes (see Micro Connections: Medicinal Uses of Botulinum Toxin).",True,Botulism,,,,
00254ab5-0cec-4894-9d16-e30716d9b9a4,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"When BoNT enters the bloodstream in the gastrointestinal tract, wound, or lungs, it is transferred to the neuromuscular junctions of motor neurons where it binds irreversibly to presynaptic membranes and prevents the release of acetylcholine from the presynaptic terminal of motor neurons into the neuromuscular junction. The consequence of preventing acetylcholine release is the loss of muscle activity, leading to muscle relaxation and eventually paralysis.",True,Botulism,,,,
00954c3e-4df2-4a47-86df-d94cff25961a,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"If BoNT is absorbed through the gastrointestinal tract, early symptoms of botulism include blurred vision, drooping eyelids, difficulty swallowing, abdominal cramps, nausea, vomiting, constipation, or possibly diarrhea. This is followed by progressive flaccid paralysis, a gradual weakening and loss of control over the muscles. A patient’s experience can be particularly terrifying, because hearing remains normal, consciousness is not lost, and he or she is fully aware of the progression of his or her condition. In infants, notable signs of botulism include weak cry, decreased ability to suckle, and hypotonia (limpness of head or body). Eventually, botulism ends in death from respiratory failure caused by the progressive paralysis of the muscles of the upper airway, diaphragm, and chest.",True,Botulism,,,,
2a5a7d68-5a03-4c4e-a3e2-ea74df3d4dee,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Botulism is treated with an antitoxin specific for BoNT. If administered in time, the antitoxin stops the progression of paralysis but does not reverse it. Once the antitoxin has been administered, the patient will slowly regain neurological function, but this may take several weeks or months, depending on the severity of the case. During recovery, patients generally must remain hospitalized and receive breathing assistance through a ventilator.",True,Botulism,,,,
aeebe67f-e486-46a8-8595-e1f2af9adf4d,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,Listeriosis,False,Listeriosis,,,,
f6cd5e03-965c-48b0-801f-034abfd1bf7f,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Listeria monocytogenes is a nonencapsulated, nonsporulating, gram-positive rod and a foodborne pathogen that causes listeriosis. At-risk groups include pregnant women, neonates, the elderly, and the immunocompromised. Listeriosis leads to meningitis in about 20% of cases, particularly neonates and patients over the age of 60. The CDC identifies listeriosis as the third leading cause of death due to foodborne illness, with overall mortality rates reaching 16%.[10] In pregnant women, listeriosis can cause also cause spontaneous abortion in pregnant women because of the pathogen’s unique ability to cross the placenta.",True,Listeriosis,,,,
3933556b-4fcd-4f1f-ac07-7e3744a9e91a,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"L. monocytogenes is generally introduced into food items by contamination with soil or animal manure used as fertilizer. Foods commonly associated with listeriosis include fresh fruits and vegetables, frozen vegetables, processed meats, soft cheeses, and raw milk.[11] Unlike most other foodborne pathogens, Listeria is able to grow at temperatures between 0 °C and 50 °C, and can therefore continue to grow, even in refrigerated foods.",True,Listeriosis,,,,
0ea2816e-f0cc-42e1-b439-22602e7565d8,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Ingestion of contaminated food leads initially to infection of the gastrointestinal tract. However, L. monocytogenes produces several unique virulence factors that allow it to cross the intestinal barrier and spread to other body systems. Surface proteins called internalins (InlA and InlB) help L. monocytogenes invade nonphagocytic cells and tissues, penetrating the intestinal wall and becoming disseminating through the circulatory and lymphatic systems. Internalins also enable L. monocytogenes to breach other important barriers, including the blood-brain barrier and the placenta. Within tissues, L. monocytogenes uses other proteins called listeriolysin O and ActA to facilitate intercellular movement, allowing the infection to spread from cell to cell (Figure 21.10).",True,Listeriosis,Figure 21.10,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-26.10.png,"Figure 21.10 (a) An electron micrograph of Listeria monocytogenes infecting a host cell. (b) Listeria is able to use host cell components to cause infection. For example, phagocytosis allows it to enter host cells, and the host’s cytoskeleton provides the materials to help the pathogen move to other cells. (credit a: modification of work by the Centers for Disease Control and Prevention; credit b: modification of work by Keith Ireton)"
995654e2-5483-43a2-a601-dd8f0e8adb15,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"L. monocytogenes is usually identified by cultivation of samples from a normally sterile site (e.g., blood or CSF). Recovery of viable organisms can be enhanced using cold enrichment by incubating samples in a broth at 4 °C for a week or more. Distinguishing types and subtypes of L. monocytogenes—an important step for diagnosis and epidemiology—is typically done using pulsed-field gel electrophoresis. Identification can also be achieved using chemiluminescence DNA probe assays and MALDI-TOF.",True,Listeriosis,,,,
dc43ee21-972c-4e61-af35-adddf5d6ff08,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Treatment for listeriosis involves antibiotic therapy, most commonly with ampicillin and gentamicin. There is no vaccine available.",True,Listeriosis,,,,
8ac0fd2b-76be-4b83-af7a-5ebb5f4610e4,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Prophylactic vaccination of first-year college students living in dorms is recommended by the CDC, and insurance companies now cover meningococcal vaccination for students in college dorms. Some colleges have mandated vaccination with meningococcal conjugate vaccine for certain students entering college (Figure 21.7).",True,Listeriosis,Figure 21.7,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-26.7.png,"Figure 21.7 To prevent campus outbreaks, some colleges now require students to be vaccinated against meningogoccal meningitis. (credit: modification of work by James Gathany, Centers for Disease Control and Prevention)"
861539a7-8ca1-4552-bfc4-4d5dcf42140c,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,Pneumococcal Meningitis,False,Pneumococcal Meningitis,,,,
fd321073-a052-4da2-b40d-2483a4de5329,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"With the emergence of drug-resistant strains of S. pneumoniae, pneumococcal meningitis is typically treated with broad-spectrum antibiotics. The two available pneumococcal vaccines are described in Bacterial Infections of the Respiratory Tract.",True,Pneumococcal Meningitis,,,,
13f18906-5998-43dc-888c-59e6a7b6fb16,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,Haemophilus influenzae Type b,False,Haemophilus influenzae Type b,,,,
0f95dfd0-69c0-4adf-b309-d12724259568,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Preliminary diagnosis of H. influenzae infections can be made by direct PCR and a smear of CSF. Stained smears will reveal intracellular and extracellular PMNs with small, pleomorphic, gram-negative coccobacilli or filamentous forms that are characteristic of H. influenzae. Initial confirmation of this genus can be based on its fastidious growth on chocolate agar. Identification is confirmed with requirements for exogenous biochemical growth cofactors NAD and heme (by MALDI-TOF), latex agglutination, and RT-PCR.",True,Haemophilus influenzae Type b,,,,
c7474776-13ea-4eaa-adf5-48f4c653eeb9,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Meningitis caused by H. influenzae is usually treated with doxycycline, fluoroquinolones, second- and third- generation cephalosporins, and carbapenems. The best means of preventing H. influenza infection is with the use of the Hib polysaccharide conjugate vaccine. It is recommended that all children receive this vaccine at 2, 4, and 6 months of age, with a final booster dose at 12 to 15 months of age.[7]",True,Haemophilus influenzae Type b,,,,
e07290e2-ef6e-4c50-800a-a58119a89ea1,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,Clostridium-Associated Diseases,False,Clostridium-Associated Diseases,,,,
e0683cc9-c0b3-47bc-81d8-e824e5fcf37b,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Species in the genus Clostridium are gram-positive, endospore-forming rods that are obligate anaerobes. Endospores of Clostridium spp. are widespread in nature, commonly found in soil, water, feces, sewage, and marine sediments. Clostridium spp. produce more types of protein exotoxins than any other bacterial genus, including two exotoxins with protease activity that are the most potent known biological toxins: botulinum neurotoxin (BoNT) and tetanusneurotoxin (TeNT). These two toxins have lethal doses of 0.2–10 ng per kg body weight.",True,Clostridium-Associated Diseases,,,,
9441739a-95c4-4d65-8d50-1fa5ad47cf8e,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"BoNT can be produced by unique strains of C. butyricum, and C. baratii; however, it is primarily associated with C. botulinum and the condition of botulism. TeNT, which causes tetanus, is only produced by C. tetani. These powerful neural exotoxins are the primary virulence factors for these pathogens.",True,Clostridium-Associated Diseases,,,,
4fa07bd6-243b-4606-a25b-7ed831c8cc2d,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Diagnosis of tetanus or botulism typically involves bioassays that detect the presence of BoNT and TeNT in fecal specimens, blood (serum), or suspect foods. In addition, both C. botulinum and C. tetani can be isolated and cultured using commercially available media for anaerobes. ELISA and RT-PCR tests are also available.",True,Clostridium-Associated Diseases,,,,
2461158d-1ff1-4145-a09c-56c51d38dea7,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Tetanus is a noncommunicable disease characterized by uncontrollable muscle spasms (contractions) caused by the action of TeNT. It generally occurs when C. tetani infects a wound and produces TeNT, which rapidly binds to neural tissue, resulting in an intoxication (poisoning) of neurons. Depending on the site and extent of infection, cases of tetanus can be described as localized, cephalic, or generalized. Generalized tetanus that occurs in a newborn is called neonatal tetanus.",True,Clostridium-Associated Diseases,,,,
687f1925-2943-4e77-84ef-090cfee106f4,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"In generalized tetanus, TeNT enters neurons of the PNS. From there, TeNT travels from the site of the wound, usually on an extremity of the body, retrograde (back up) to inhibitory neurons in the CNS. There, it prevents the release of gamma aminobutyric acid (GABA), the neurotransmitter responsible for muscle relaxation. The resulting muscle spasms often first occur in the jaw muscles, leading to the characteristic symptom of lockjaw (inability to open the mouth). As the toxin progressively continues to block neurotransmitter release, other muscles become involved, resulting in uncontrollable, sudden muscle spasms that are powerful enough to cause tendons to rupture and bones to fracture. Spasms in the muscles in the neck, back, and legs may cause the body to form a rigid, stiff arch, a posture called opisthotonos (Figure 21.9). Spasms in the larynx, diaphragm, and muscles of the chest restrict the patient’s ability to swallow and breathe, eventually leading to death by asphyxiation (insufficient supply of oxygen).",True,Clostridium-Associated Diseases,Figure 21.9,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-26.9.png,Figure 21.9 A tetanus patient exhibiting the rigid body posture known as opisthotonos. (credit: Centers for Disease Control and Prevention)
d9dfe27a-84d9-44f0-8539-6893d4fa5847,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Neonatal tetanus typically occurs when the stump of the umbilical cord is contaminated with spores of C. tetani after delivery. Although this condition is rare in the United States, neonatal tetanus is a major cause of infant mortality in countries that lack maternal immunization for tetanus and where birth often occurs in unsanitary conditions. At the end of the first week of life, infected infants become irritable, feed poorly, and develop rigidity with spasms. Neonatal tetanus has a very poor prognosis with a mortality rate of 70%–100%.[8]",True,Clostridium-Associated Diseases,,,,
16ec4ee8-dffb-4122-9764-79e49f3b4d1c,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Treatment for patients with tetanus includes assisted breathing through the use of a ventilator, wound debridement, fluid balance, and antibiotic therapy with metronidazole or penicillin to halt the growth of C. tetani. In addition, patients are treated with TeNT antitoxin, preferably in the form of human immunoglobulin to neutralize nonfixed toxin and benzodiazepines to enhance the effect of GABA for muscle relaxation and anxiety.",True,Clostridium-Associated Diseases,,,,
b28d6c80-40ab-4d00-82c6-c9bd833b1873,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"A tetanus toxoid (TT) vaccine is available for protection and prevention of tetanus. It is the T component of vaccines such as DTaP, Tdap, and Td. The CDC recommends children receive doses of the DTaP vaccine at 2, 4, 6, and 15–18 months of age and another at 4–6 years of age. One dose of Td is recommended for adolescents and adults as a TT booster every 10 years.[9]",True,Clostridium-Associated Diseases,,,,
dab40698-1f07-47e3-b034-817b4a7768d4,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Infection and production of BoNT in vivo can result in wound botulism, infant botulism, and adult intestinal toxemia. Wound botulism typically occurs when C. botulinum is introduced directly into a wound after a traumatic injury, deep puncture wound, or injection site. Infant botulism, which occurs in infants younger than 1 year of age, and adult intestinal toxemia, which occurs in immunocompromised adults, results from ingesting C. botulinum endospores in food. The endospores germinate in the body, resulting in the production of BoNT in the intestinal tract.",True,Clostridium-Associated Diseases,,,,
178b9ffc-43c5-4e85-93f7-18ec95614a21,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Intoxications occur when BoNT is produced outside the body and then introduced directly into the body through food (foodborne botulism), air (inhalation botulism), or a clinical procedure (iatrogenic botulism). Foodborne botulism, the most common of these forms, occurs when BoNT is produced in contaminated food and then ingested along with the food (recall Case in Point: A Streak of Bad Potluck). Inhalation botulism is rare because BoNT is unstable as an aerosol and does not occur in nature; however, it can be produced in the laboratory and was used (unsuccessfully) as a bioweapon by terrorists in Japan in the 1990s. A few cases of accidental inhalation botulism have also occurred. Iatrogenic botulism is also rare; it is associated with injections of BoNT used for cosmetic purposes (see Micro Connections: Medicinal Uses of Botulinum Toxin).",True,Clostridium-Associated Diseases,,,,
eb1ddf5c-8fbe-4a5a-a3ec-6537abd94c7f,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"When BoNT enters the bloodstream in the gastrointestinal tract, wound, or lungs, it is transferred to the neuromuscular junctions of motor neurons where it binds irreversibly to presynaptic membranes and prevents the release of acetylcholine from the presynaptic terminal of motor neurons into the neuromuscular junction. The consequence of preventing acetylcholine release is the loss of muscle activity, leading to muscle relaxation and eventually paralysis.",True,Clostridium-Associated Diseases,,,,
1a296d44-ca49-456f-b104-2577ac26d932,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"If BoNT is absorbed through the gastrointestinal tract, early symptoms of botulism include blurred vision, drooping eyelids, difficulty swallowing, abdominal cramps, nausea, vomiting, constipation, or possibly diarrhea. This is followed by progressive flaccid paralysis, a gradual weakening and loss of control over the muscles. A patient’s experience can be particularly terrifying, because hearing remains normal, consciousness is not lost, and he or she is fully aware of the progression of his or her condition. In infants, notable signs of botulism include weak cry, decreased ability to suckle, and hypotonia (limpness of head or body). Eventually, botulism ends in death from respiratory failure caused by the progressive paralysis of the muscles of the upper airway, diaphragm, and chest.",True,Clostridium-Associated Diseases,,,,
ed8bbec2-8538-435f-860a-ae42ed6197a1,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Botulism is treated with an antitoxin specific for BoNT. If administered in time, the antitoxin stops the progression of paralysis but does not reverse it. Once the antitoxin has been administered, the patient will slowly regain neurological function, but this may take several weeks or months, depending on the severity of the case. During recovery, patients generally must remain hospitalized and receive breathing assistance through a ventilator.",True,Clostridium-Associated Diseases,,,,
f129cb05-988f-46e0-a885-e014a5764a20,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"L. monocytogenes is generally introduced into food items by contamination with soil or animal manure used as fertilizer. Foods commonly associated with listeriosis include fresh fruits and vegetables, frozen vegetables, processed meats, soft cheeses, and raw milk.[11] Unlike most other foodborne pathogens, Listeria is able to grow at temperatures between 0 °C and 50 °C, and can therefore continue to grow, even in refrigerated foods.",True,Clostridium-Associated Diseases,,,,
e06cf205-3ae1-4999-9754-b45b1d21c6c7,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Ingestion of contaminated food leads initially to infection of the gastrointestinal tract. However, L. monocytogenes produces several unique virulence factors that allow it to cross the intestinal barrier and spread to other body systems. Surface proteins called internalins (InlA and InlB) help L. monocytogenes invade nonphagocytic cells and tissues, penetrating the intestinal wall and becoming disseminating through the circulatory and lymphatic systems. Internalins also enable L. monocytogenes to breach other important barriers, including the blood-brain barrier and the placenta. Within tissues, L. monocytogenes uses other proteins called listeriolysin O and ActA to facilitate intercellular movement, allowing the infection to spread from cell to cell (Figure 21.10).",True,Clostridium-Associated Diseases,Figure 21.10,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-26.10.png,"Figure 21.10 (a) An electron micrograph of Listeria monocytogenes infecting a host cell. (b) Listeria is able to use host cell components to cause infection. For example, phagocytosis allows it to enter host cells, and the host’s cytoskeleton provides the materials to help the pathogen move to other cells. (credit a: modification of work by the Centers for Disease Control and Prevention; credit b: modification of work by Keith Ireton)"
48177c40-215f-4347-8823-50e71ed50a54,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"L. monocytogenes is usually identified by cultivation of samples from a normally sterile site (e.g., blood or CSF). Recovery of viable organisms can be enhanced using cold enrichment by incubating samples in a broth at 4 °C for a week or more. Distinguishing types and subtypes of L. monocytogenes—an important step for diagnosis and epidemiology—is typically done using pulsed-field gel electrophoresis. Identification can also be achieved using chemiluminescence DNA probe assays and MALDI-TOF.",True,Clostridium-Associated Diseases,,,,
4ed414b2-3fa2-4531-84dd-14a4fc94e98e,https://open.oregonstate.education/microbiology/,21.2	Bacterial Diseases of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-2bacterial-diseases-of-the-nervous-system/,"Treatment for listeriosis involves antibiotic therapy, most commonly with ampicillin and gentamicin. There is no vaccine available.",True,Clostridium-Associated Diseases,,,,
06720fb3-9549-423c-97fd-e82e6b8319db,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,The Central Nervous System,False,The Central Nervous System,,,,
9b82f408-c018-4149-96da-0284517184fd,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,"The brain is the most complex and sensitive organ in the body. It is responsible for all functions of the body, including serving as the coordinating center for all sensations, mobility, emotions, and intellect. Protection for the brain is provided by the bones of the skull, which in turn are covered by the scalp, as shown in Figure 21.3. The scalp is composed of an outer layer of skin, which is loosely attached to the aponeurosis, a flat, broad tendon layer that anchors the superficial layers of the skin. The periosteum, below the aponeurosis, firmly encases the bones of the skull and provides protection, nutrition to the bone, and the capacity for bone repair. Below the boney layer of the skull are three layers of membranes called meninges that surround the brain. The relative positions of these meninges are shown in Figure 21.3. The meningeal layer closest to the bones of the skull is called the dura mater (literally meaning tough mother). Below the dura mater lies the arachnoid mater (literally spider-like mother). The innermost meningeal layer is a delicate membrane called the pia mater (literally tender mother). Unlike the other meningeal layers, the pia mater firmly adheres to the convoluted surface of the brain. Between the arachnoid mater and pia mater is the subarachnoid space. The subarachnoid space within this region is filled with cerebrospinal fluid (CSF). This watery fluid is produced by cells of the choroid plexus—areas in each ventricle of the brain that consist of cuboidal epithelial cells surrounding dense capillary beds. The CSF serves to deliver nutrients and remove waste from neural tissues.",True,The Central Nervous System,Figure 21.3,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-26.3.png,"Figure 21.3 The layers of tissue surrounding the human brain include three meningeal membranes: the dura mater, arachnoid mater, and pia mater. (credit: modification of work by National Institutes of Health)"
f8d841d9-c2ef-4a93-8c78-d22daebc6558,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,"The blood-brain barrier protects the cerebrospinal fluid from contamination, and can be quite effective at excluding potential microbial pathogens. As a consequence of these defenses, there is no normal microbiota in the cerebrospinal fluid. The blood-brain barrier also inhibits the movement of many drugs into the brain, particularly compounds that are not lipid soluble. This has profound ramifications for treatments involving infections of the CNS, because it is difficult for drugs to cross the blood-brain barrier to interact with pathogens that cause infections.",True,The Central Nervous System,,,,
08e8de0b-117c-4474-a895-9f98b344af57,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,"The spinal cord also has protective structures similar to those surrounding the brain. Within the bones of the vertebrae are meninges of dura mater (sometimes called the dural sheath), arachnoid mater, pia mater, and a blood-spinal cord barrier that controls the transfer of blood components from blood vessels associated with the spinal cord.",True,The Central Nervous System,,,,
729a7232-c34c-4128-98da-2e3bc6f2094e,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,"To cause an infection in the CNS, pathogens must successfully breach the blood-brain barrier or blood-spinal cord barrier.",True,The Central Nervous System,,,,
f75374d0-8bb1-44e6-b3f8-15585fec7184,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,The Peripheral Nervous System,False,The Peripheral Nervous System,,,,
7bab42d0-5d07-43ed-922e-221d5d4f93a8,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,"The PNS is formed of the nerves that connect organs, limbs, and other anatomic structures of the body to the brain and spinal cord. Unlike the brain and spinal cord, the PNS is not protected by bone, meninges, or a blood barrier, and, as a consequence, the nerves of the PNS are much more susceptible to injury and infection. Microbial damage to peripheral nerves can lead to tingling or numbness known as neuropathy. These symptoms can also be produced by trauma and noninfectious causes such as drugs or chronic diseases like diabetes.",True,The Peripheral Nervous System,,,,
90577656-0628-439d-869c-a1a8e9340668,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,The Cells of the Nervous System,False,The Cells of the Nervous System,,,,
b5d13990-3f88-413f-bc43-54449f65de09,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,"Tissues of the PNS and CNS are formed of cells called glial cells (neuroglial cells) and neurons (nerve cells). Glial cells assist in the organization of neurons, provide a scaffold for some aspects of neuronal function, and aid in recovery from neural injury.",True,The Cells of the Nervous System,,,,
b6420317-aec2-4cda-b7ef-b8a05210c46f,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,"Neurons are specialized cells found throughout the nervous system that transmit signals through the nervous system using electrochemical processes. The basic structure of a neuron is shown in Figure 21.4. The cell body (or soma) is the metabolic center of the neuron and contains the nucleus and most of the cell’s organelles. The many finely branched extensions from the soma are called dendrites. The soma also produces an elongated extension, called the axon, which is responsible for the transmission of electrochemical signals through elaborate ion transport processes. Axons of some types of neurons can extend up to one meter in length in the human body. To facilitate electrochemical signal transmission, some neurons have a myelin sheath surrounding the axon. Myelin, formed from the cell membranes of glial cells like the Schwann cells in the PNS and oligodendrocytes in the CNS, surrounds and insulates the axon, significantly increasing the speed of electrochemical signal transmission along the axon. The end of an axon forms numerous branches that end in bulbs called synaptic terminals. Neurons form junctions with other cells, such as another neuron, with which they exchange signals. The junctions, which are actually gaps between neurons, are referred to as synapses. At each synapse, there is a presynaptic neuron and a postsynaptic neuron (or other cell). The synaptic terminals of the axon of the presynaptic terminal form the synapse with the dendrites, soma, or sometimes the axon of the postsynaptic neuron, or a part of another type of cell such as a muscle cell. The synaptic terminals contain vesicles filled with chemicals called neurotransmitters. When the electrochemical signal moving down the axon reaches the synapse, the vesicles fuse with the membrane, and neurotransmitters are released, which diffuse across the synapse and bind to receptors on the membrane of the postsynaptic cell, potentially initiating a response in that cell. That response in the postsynaptic cell might include further propagation of an electrochemical signal to transmit information or contraction of a muscle fiber.",True,The Cells of the Nervous System,Figure 21.4,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-26.4.png,Figure 21.4 (a) A myelinated neuron is associated with oligodendrocytes. Oligodendrocytes are a type of glial cell that forms the myelin sheath in the CNS that insulates the axon so that electrochemical nerve impulses are transferred more efficiently. (b) A synapse consists of the axonal end of the presynaptic neuron (top) that releases neurotransmitters that cross the synaptic space (or cleft) and bind to receptors on dendrites of the postsynaptic neuron (bottom).
5dae7588-e094-47d7-b5b2-f05536a4b1e9,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,Meningitis and Encephalitis,False,Meningitis and Encephalitis,,,,
3220be6e-f1c8-41fa-9cda-3b0fd51ebdfd,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,"Although the skull provides the brain with an excellent defense, it can also become problematic during infections. Any swelling of the brain or meninges that results from inflammation can cause intracranial pressure, leading to severe damage of the brain tissues, which have limited space to expand within the inflexible bones of the skull. The term meningitis is used to describe an inflammation of the meninges. Typical symptoms can include severe headache, fever, photophobia (increased sensitivity to light), stiff neck, convulsions, and confusion. An inflammation of brain tissue is called encephalitis, and patients exhibit signs and symptoms similar to those of meningitis in addition to lethargy, seizures, and personality changes. When inflammation affects both the meninges and the brain tissue, the condition is called meningoencephalitis. All three forms of inflammation are serious and can lead to blindness, deafness, coma, and death.",True,Meningitis and Encephalitis,,,,
249017f9-161f-45c6-883c-5b8f09669871,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,"Meningitis and encephalitis can be caused by many different types of microbial pathogens. However, these conditions can also arise from noninfectious causes such as head trauma, some cancers, and certain drugs that trigger inflammation. To determine whether the inflammation is caused by a pathogen, a lumbar puncture is performed to obtain a sample of CSF. If the CSF contains increased levels of white blood cells and abnormal glucose and protein levels, this indicates that the inflammation is a response to an infectioninflinin.",True,Meningitis and Encephalitis,,,,
01bff039-7288-4441-8464-b720d47f9816,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,"Guillain-Barré syndrome (GBS) is a rare condition that can be preceded by a viral or bacterial infection that results in an autoimmune reaction against myelinated nerve cells. The destruction of the myelin sheath around these neurons results in a loss of sensation and function. The first symptoms of this condition are tingling and weakness in the affected tissues. The symptoms intensify over a period of several weeks and can culminate in complete paralysis. Severe cases can be life-threatening. Infections by several different microbial pathogens, including Campylobacter jejuni (the most common risk factor), cytomegalovirus, Epstein-Barr virus, varicella- zoster virus, Mycoplasma pneumoniae,[1] and Zika virus[2] have been identified as triggers for GBS. Anti-myelin antibodies from patients with GBS have been demonstrated to also recognize C. jejuni. It is possible that cross- reactive antibodies, antibodies that react with similar antigenic sites on different proteins, might be formed during an infection and may lead to this autoimmune response. GBS is solely identified by the appearance of clinical symptoms. There are no other diagnostic tests available. Fortunately, most cases spontaneously resolve within a few months with few permanent effects, as there is no available vaccine. GBS can be treated by plasmapheresis. In this procedure, the patient’s plasma is filtered from their blood, removing autoantibodies.",True,Meningitis and Encephalitis,,,,
2ea5d2ad-6698-4441-b284-833599289f7e,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,"The blood-brain barrier protects the cerebrospinal fluid from contamination, and can be quite effective at excluding potential microbial pathogens. As a consequence of these defenses, there is no normal microbiota in the cerebrospinal fluid. The blood-brain barrier also inhibits the movement of many drugs into the brain, particularly compounds that are not lipid soluble. This has profound ramifications for treatments involving infections of the CNS, because it is difficult for drugs to cross the blood-brain barrier to interact with pathogens that cause infections.",True,Meningitis and Encephalitis,,,,
aaf23a97-3c29-4ef3-8232-0f9d155e788c,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,"The spinal cord also has protective structures similar to those surrounding the brain. Within the bones of the vertebrae are meninges of dura mater (sometimes called the dural sheath), arachnoid mater, pia mater, and a blood-spinal cord barrier that controls the transfer of blood components from blood vessels associated with the spinal cord.",True,Meningitis and Encephalitis,,,,
6752b66e-86f6-42c1-939c-df9444b3baf3,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,"To cause an infection in the CNS, pathogens must successfully breach the blood-brain barrier or blood-spinal cord barrier.",True,Meningitis and Encephalitis,,,,
7d0e1d26-d57b-498a-abb6-0f6a68a447cb,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,The Peripheral Nervous System,False,The Peripheral Nervous System,,,,
85d63595-afda-46b1-8e11-7f9e5a1a0720,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,The Cells of the Nervous System,False,The Cells of the Nervous System,,,,
24388f7e-8432-4d0e-aec7-877814f70892,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,"Tissues of the PNS and CNS are formed of cells called glial cells (neuroglial cells) and neurons (nerve cells). Glial cells assist in the organization of neurons, provide a scaffold for some aspects of neuronal function, and aid in recovery from neural injury.",True,The Cells of the Nervous System,,,,
fb4b3f2a-02bb-4a53-bf96-a5308fccb4ee,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,"Neurons are specialized cells found throughout the nervous system that transmit signals through the nervous system using electrochemical processes. The basic structure of a neuron is shown in Figure 21.4. The cell body (or soma) is the metabolic center of the neuron and contains the nucleus and most of the cell’s organelles. The many finely branched extensions from the soma are called dendrites. The soma also produces an elongated extension, called the axon, which is responsible for the transmission of electrochemical signals through elaborate ion transport processes. Axons of some types of neurons can extend up to one meter in length in the human body. To facilitate electrochemical signal transmission, some neurons have a myelin sheath surrounding the axon. Myelin, formed from the cell membranes of glial cells like the Schwann cells in the PNS and oligodendrocytes in the CNS, surrounds and insulates the axon, significantly increasing the speed of electrochemical signal transmission along the axon. The end of an axon forms numerous branches that end in bulbs called synaptic terminals. Neurons form junctions with other cells, such as another neuron, with which they exchange signals. The junctions, which are actually gaps between neurons, are referred to as synapses. At each synapse, there is a presynaptic neuron and a postsynaptic neuron (or other cell). The synaptic terminals of the axon of the presynaptic terminal form the synapse with the dendrites, soma, or sometimes the axon of the postsynaptic neuron, or a part of another type of cell such as a muscle cell. The synaptic terminals contain vesicles filled with chemicals called neurotransmitters. When the electrochemical signal moving down the axon reaches the synapse, the vesicles fuse with the membrane, and neurotransmitters are released, which diffuse across the synapse and bind to receptors on the membrane of the postsynaptic cell, potentially initiating a response in that cell. That response in the postsynaptic cell might include further propagation of an electrochemical signal to transmit information or contraction of a muscle fiber.",True,The Cells of the Nervous System,Figure 21.4,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-26.4.png,Figure 21.4 (a) A myelinated neuron is associated with oligodendrocytes. Oligodendrocytes are a type of glial cell that forms the myelin sheath in the CNS that insulates the axon so that electrochemical nerve impulses are transferred more efficiently. (b) A synapse consists of the axonal end of the presynaptic neuron (top) that releases neurotransmitters that cross the synaptic space (or cleft) and bind to receptors on dendrites of the postsynaptic neuron (bottom).
9ac4942b-fb1b-4b64-8fc4-48d10ad7ee0c,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,Meningitis and Encephalitis,False,Meningitis and Encephalitis,,,,
93b4bb13-e67a-4070-ae4c-08a7c08017b4,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,"Although the skull provides the brain with an excellent defense, it can also become problematic during infections. Any swelling of the brain or meninges that results from inflammation can cause intracranial pressure, leading to severe damage of the brain tissues, which have limited space to expand within the inflexible bones of the skull. The term meningitis is used to describe an inflammation of the meninges. Typical symptoms can include severe headache, fever, photophobia (increased sensitivity to light), stiff neck, convulsions, and confusion. An inflammation of brain tissue is called encephalitis, and patients exhibit signs and symptoms similar to those of meningitis in addition to lethargy, seizures, and personality changes. When inflammation affects both the meninges and the brain tissue, the condition is called meningoencephalitis. All three forms of inflammation are serious and can lead to blindness, deafness, coma, and death.",True,Meningitis and Encephalitis,,,,
f116df4d-d462-479d-8125-2ce36c61a3d0,https://open.oregonstate.education/microbiology/,21.1	Anatomy of the Nervous System,https://open.oregonstate.education/microbiology/chapter/26-1anatomy-of-the-nervous-system/,"Meningitis and encephalitis can be caused by many different types of microbial pathogens. However, these conditions can also arise from noninfectious causes such as head trauma, some cancers, and certain drugs that trigger inflammation. To determine whether the inflammation is caused by a pathogen, a lumbar puncture is performed to obtain a sample of CSF. If the CSF contains increased levels of white blood cells and abnormal glucose and protein levels, this indicates that the inflammation is a response to an infectioninflinin.",True,Meningitis and Encephalitis,,,,
7685eb11-ea74-4b1d-818e-d04119e6681e,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,Malaria,False,Malaria,,,,
2cbeec28-1c9a-4de0-ba42-98e0c87365cb,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"Despite more than a century of intense research and clinical advancements, malaria remains one of the most important infectious diseases in the world today. Its widespread distribution places more than half of the world’s population in jeopardy. In 2015, the WHO estimated there were about 214 million cases of malaria worldwide, resulting in about 438,000 deaths; about 88% of cases and 91% of deaths occurred in Africa.[1] Although malaria is not currently a major threat in the US, the possibility of its reintroduction is a concern. Malaria is caused by several protozoan parasites in the genus Plasmodium: P. falciparum, P. knowlesi, P. malariae, P. ovale, and P. vivax. Plasmodium primarily infect red blood cells and are transmitted through the bite of Anopheles mosquitoes.",True,Malaria,,,,
64e9bd1a-a84a-4d4c-977e-6e94b7eef9c6,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"Currently, P. falciparum is the most common and most lethal cause of malaria, often called falciparum malaria. Falciparum malaria is widespread in highly populated regions of Africa and Asia, putting many people at risk for the most severe form of the disease.",True,Malaria,,,,
5f32f8f4-87a8-4ed0-9c0d-4c82509bbd9a,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"The classic signs and symptoms of malaria are cycles of extreme fever and chills. The sudden, violent symptoms of malaria start with malaise, abrupt chills, and fever (39–41° C [102.2–105.8 °F]), rapid and faint pulse, polyuria, headache, myalgia, nausea, and vomiting. After 2 to 6 hours of these symptoms, the fever falls, and profuse sweating occurs for 2 to 3 hours, followed by extreme fatigue. These symptoms are a result of Plasmodium emerging from red blood cells synchronously, leading to simultaneous rupture of a large number of red blood cells, resulting in damage to the spleen, liver, lymph nodes, and bone marrow. The organ damage resulting from hemolysis causes patients to develop sludge blood (i.e., blood in which the red blood cells agglutinate into clumps) that can lead to lack of oxygen, necrosis of blood vessels, organ failure, and death.",True,Malaria,,,,
81012bb7-463a-4b54-8938-9a2b88b66bca,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"In established infections, malarial cycles of fever and chills typically occur every 2 days in the disease described as tertian malaria, which is caused by P. vivax and P. ovale. The cycles occur every 3 days in the disease described as quartan malaria, which is caused by P. malariae. These intervals may vary among cases.",True,Malaria,,,,
2587dda5-91f0-48ad-a580-2635f5eb3310,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"Plasmodium has a complex life cycle that includes several developmental stages alternately produced in mosquitoes and humans (Figure 20.18). When an infected mosquito takes a blood meal, sporozoites in the mosquito salivary gland are injected into the host’s blood. These parasites circulate to the liver, where they develop into schizonts. The schizonts then undergo schizogony, resulting in the release of many merozoites at once. The merozoites move to the bloodstream and infect red blood cells. Inside red blood cells, merozoites develop into trophozoites that produce more merozoites. The synchronous release of merozoites from red blood cells in the evening leads to the symptoms of malaria.",True,Malaria,Figure 20.18,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.27.png,Figure 20.18 The life cycle of Plasmodium. (credit: modification of work by Centers for Disease Control and Prevention)
a7236bd8-b483-47e3-b58e-6b3c9ef01c6e,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"In addition, some trophozoites alternatively develop into male and female gametocytes. The gametocytes are taken up when the mosquito takes a blood meal from an infected individual. Sexual sporogony occurs in the gut of the mosquito. The gametocytes fuse to form zygotes in the insect gut. The zygotes become motile and elongate into an ookinete. This form penetrates the midgut wall and develops into an oocyst. Finally, the oocyst releases new sporozoites that migrate to the mosquito salivary glands to complete the life cycle.",True,Malaria,,,,
b666347b-e9b0-45c5-93b9-ec27d7ed0bc4,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"Diagnosis of malaria is by microscopic observation of developmental forms of Plasmodium in blood smears and rapid EIA assays that detect Plasmodium antigens or enzymes (Figure 20.19). Drugs such as chloroquine, atovaquone , artemether, and lumefantrine may be prescribed for both acute and prophylactic therapy, although some Plasmodium spp. have shown resistance to antimalarial drugs. Use of insecticides and insecticide-treated bed nets can limit the spread of malaria. Despite efforts to develop a vaccine for malaria, none is currently available.",True,Malaria,Figure 20.19,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.28.png,Figure 20.19 A blood smear (human blood stage) shows an early trophozoite in a delicate ring form (upper left) and an early stage schizont form (center) of Plasmodium falciparum from a patient with malaria. (credit: modification of work by Centers for Disease Control and Prevention)
9401f869-7315-4b62-9e4e-9f55b2647080,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"The Nothing But Nets campaign, an initiative of the United Nations Foundation, has partnered with the Bill and Melinda Gates Foundation to make mosquito bed nets available in developing countries in Africa.",True,Malaria,,,,
ea3230e2-7715-49dc-8f45-552141a9d0c6,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,Visit their website (https://openstax.org/l/22mosquitonet) to learn more about their efforts to prevent malaria.,True,Malaria,,,,
73e83837-84e7-49cc-9a52-18760a653085,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,Toxoplasmosis,False,Toxoplasmosis,,,,
59c2925e-2981-47e0-b2e1-1b2aee615396,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"The disease toxoplasmosis is caused by the protozoan Toxoplasma gondii. T. gondii is found in a wide variety of birds and mammals,[2] and human infections are common. The Centers for Disease Control and Prevention (CDC) estimates that 22.5% of the population 12 years and older has been infected with T. gondii; but immunocompetent individuals are typically asymptomatic, however.[3] Domestic cats are the only known definitive hosts for the sexual stages of T. gondii and, thus, are the main reservoirs of infection. Infected cats shed T. gondii oocysts in their feces, and these oocysts typically spread to humans through contact with fecal matter on cats’ bodies, in litter boxes, or in garden beds where outdoor cats defecate.",True,Toxoplasmosis,,,,
69f3443e-3a92-4eb6-ab33-29f44bce5eef,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"T. gondii has a complex life cycle that involves multiple hosts. The T. gondii life cycle begins when unsporulated oocysts are shed in the cat’s feces. These oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature include birds and rodents, which become infected after ingesting soil, water, or plant material contaminated with the infective oocysts. Once ingested, the oocysts transform into tachyzoites that localize in the bird or rodent neural and muscle tissue, where they develop into tissue cysts. Cats may become infected after consuming birds and rodents harboring tissue cysts. Cats and other animals may also become infected directly by ingestion of sporulated oocysts in the environment. Interestingly, Toxoplasma infection appears to be able to modify the host’s behavior. Mice infected by Toxoplasma lose their fear of cat pheromones. As a result, they become easier prey for cats, facilitating the transmission of the parasite to the cat definitive host[4] (Figure 20.20).",True,Toxoplasmosis,Figure 20.20,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.29.png,Figure 20.20 The infectious cycle of Toxoplasma gondii. (credit: “diagram”: modification of work by Centers for Disease Control and Prevention; credit “cat”: modification of work by “KaCey97078”/Flickr)
a4203d20-c25e-4171-a1fb-0e495ee608a7,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"Toxoplasma infections in humans are extremely common, but most infected people are asymptomatic or have subclinical symptoms. Some studies suggest that the parasite may be able to influence the personality and psychomotor performance of infected humans, similar to the way it modifies behavior in other mammals.[5] When symptoms do occur, they tend to be mild and similar to those of mononucleosis. However, asymptomatic toxoplasmosis can become problematic in certain situations. Cysts can lodge in a variety of human tissues and lie dormant for years. Reactivation of these quiescent infections can occur in immunocompromised patients following transplantation, cancer therapy, or the development of an immune disorder such as AIDS. In patients with AIDS who have toxoplasmosis, the immune system cannot combat the growth of T. gondii in body tissues; as a result, these cysts can cause encephalitis, retinitis, pneumonitis, cognitive disorders, and seizures that can eventually be fatal.",True,Toxoplasmosis,,,,
5a3ec93f-4336-4d93-94ee-0083c27e56a1,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"Toxoplasmosis can also pose a risk during pregnancy because tachyzoites can cross the placenta and cause serious infections in the developing fetus. The extent of fetal damage resulting from toxoplasmosis depends on the severity of maternal disease, the damage to the placenta, the gestational age of the fetus when infected, and the virulence of the organism. Congenital toxoplasmosis often leads to fetal loss or premature birth and can result in damage to the central nervous system, manifesting as mental retardation, deafness, or blindness. Consequently, pregnant women are advised by the CDC to take particular care in preparing meat, gardening, and caring for pet cats.[6] Diagnosis of toxoplasmosis infection during pregnancy is usually achieved by serology including TORCH testing (the “T” in TORCH stands for toxoplasmosis). Diagnosis of congenital infections can also be achieved by detecting T. gondii DNA in amniotic fluid, using molecular methods such as PCR.",True,Toxoplasmosis,,,,
c099d2e8-5614-43bd-a9d3-a56d73a8c1ed,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"In adults, diagnosis of toxoplasmosis can include observation of tissue cysts in tissue specimens. Tissue cysts may be observed in Giemsa- or Wright-stained biopsy specimens, and CT, magnetic resonance imaging, and lumbar puncture can also be used to confirm infection (Figure 20.21).",True,Toxoplasmosis,Figure 20.21,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.30.png,"Figure 20.21 (a) Giemsa-stained Toxoplasma gondii tachyzoites from a smear of peritoneal fluid obtained from a mouse inoculated with T. gondii. Tachyzoites are typically crescent shaped with a prominent, centrally placed nucleus. Microscopic cyst containing T. gondii from mouse brain tissue. Thousands of resting parasites (stained red) are contained in a thin parasite cyst wall. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by USDA)"
fafff4df-4264-4bc1-a5fb-81daa8f8a41f,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"Preventing infection is the best first-line defense against toxoplasmosis. Preventive measures include washing hands thoroughly after handling raw meat, soil, or cat litter, and avoiding consumption of vegetables possibly contaminated with cat feces. All meat should be cooked to an internal temperature of 73.9–76.7 °C (165–170 °F).",True,Toxoplasmosis,,,,
0d694246-7ac2-4934-8aa0-b8e359a02aaf,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"Most immunocompetent patients do not require clinical intervention for Toxoplasma infections. However, neonates, pregnant women, and immunocompromised patients can be treated with pyrimethamine and sulfadiazine—except during the first trimester of pregnancy, because these drugs can cause birth defects. Spiramycin has been used safely to reduce transmission in pregnant women with primary infection during the first trimester because it does not cross the placenta.",True,Toxoplasmosis,,,,
79bccaf7-57b1-4e56-9b25-05943e2baff6,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"The Nothing But Nets campaign, an initiative of the United Nations Foundation, has partnered with the Bill and Melinda Gates Foundation to make mosquito bed nets available in developing countries in Africa.",True,Toxoplasmosis,,,,
0d38fa8b-e7ef-47b5-ab7c-d8a188add139,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,Visit their website (https://openstax.org/l/22mosquitonet) to learn more about their efforts to prevent malaria.,True,Toxoplasmosis,,,,
51f48818-831a-446b-a99b-07f1813b63b3,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,Toxoplasmosis,False,Toxoplasmosis,,,,
ceaf8371-89f7-46b4-a937-6e1f89d70b47,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"The disease toxoplasmosis is caused by the protozoan Toxoplasma gondii. T. gondii is found in a wide variety of birds and mammals,[2] and human infections are common. The Centers for Disease Control and Prevention (CDC) estimates that 22.5% of the population 12 years and older has been infected with T. gondii; but immunocompetent individuals are typically asymptomatic, however.[3] Domestic cats are the only known definitive hosts for the sexual stages of T. gondii and, thus, are the main reservoirs of infection. Infected cats shed T. gondii oocysts in their feces, and these oocysts typically spread to humans through contact with fecal matter on cats’ bodies, in litter boxes, or in garden beds where outdoor cats defecate.",True,Toxoplasmosis,,,,
bc391759-ad60-4126-b9cf-e93f84a2d0dd,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"T. gondii has a complex life cycle that involves multiple hosts. The T. gondii life cycle begins when unsporulated oocysts are shed in the cat’s feces. These oocysts take 1–5 days to sporulate in the environment and become infective. Intermediate hosts in nature include birds and rodents, which become infected after ingesting soil, water, or plant material contaminated with the infective oocysts. Once ingested, the oocysts transform into tachyzoites that localize in the bird or rodent neural and muscle tissue, where they develop into tissue cysts. Cats may become infected after consuming birds and rodents harboring tissue cysts. Cats and other animals may also become infected directly by ingestion of sporulated oocysts in the environment. Interestingly, Toxoplasma infection appears to be able to modify the host’s behavior. Mice infected by Toxoplasma lose their fear of cat pheromones. As a result, they become easier prey for cats, facilitating the transmission of the parasite to the cat definitive host[4] (Figure 20.20).",True,Toxoplasmosis,Figure 20.20,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.29.png,Figure 20.20 The infectious cycle of Toxoplasma gondii. (credit: “diagram”: modification of work by Centers for Disease Control and Prevention; credit “cat”: modification of work by “KaCey97078”/Flickr)
e4ea5227-8fa4-47bb-98a5-6fc27cb8624d,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"Toxoplasma infections in humans are extremely common, but most infected people are asymptomatic or have subclinical symptoms. Some studies suggest that the parasite may be able to influence the personality and psychomotor performance of infected humans, similar to the way it modifies behavior in other mammals.[5] When symptoms do occur, they tend to be mild and similar to those of mononucleosis. However, asymptomatic toxoplasmosis can become problematic in certain situations. Cysts can lodge in a variety of human tissues and lie dormant for years. Reactivation of these quiescent infections can occur in immunocompromised patients following transplantation, cancer therapy, or the development of an immune disorder such as AIDS. In patients with AIDS who have toxoplasmosis, the immune system cannot combat the growth of T. gondii in body tissues; as a result, these cysts can cause encephalitis, retinitis, pneumonitis, cognitive disorders, and seizures that can eventually be fatal.",True,Toxoplasmosis,,,,
8b25ce00-e731-4182-ac41-d20327afdceb,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"Toxoplasmosis can also pose a risk during pregnancy because tachyzoites can cross the placenta and cause serious infections in the developing fetus. The extent of fetal damage resulting from toxoplasmosis depends on the severity of maternal disease, the damage to the placenta, the gestational age of the fetus when infected, and the virulence of the organism. Congenital toxoplasmosis often leads to fetal loss or premature birth and can result in damage to the central nervous system, manifesting as mental retardation, deafness, or blindness. Consequently, pregnant women are advised by the CDC to take particular care in preparing meat, gardening, and caring for pet cats.[6] Diagnosis of toxoplasmosis infection during pregnancy is usually achieved by serology including TORCH testing (the “T” in TORCH stands for toxoplasmosis). Diagnosis of congenital infections can also be achieved by detecting T. gondii DNA in amniotic fluid, using molecular methods such as PCR.",True,Toxoplasmosis,,,,
f54c2bf5-51b4-46be-a5f2-ae146e186d8c,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"In adults, diagnosis of toxoplasmosis can include observation of tissue cysts in tissue specimens. Tissue cysts may be observed in Giemsa- or Wright-stained biopsy specimens, and CT, magnetic resonance imaging, and lumbar puncture can also be used to confirm infection (Figure 20.21).",True,Toxoplasmosis,Figure 20.21,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.30.png,"Figure 20.21 (a) Giemsa-stained Toxoplasma gondii tachyzoites from a smear of peritoneal fluid obtained from a mouse inoculated with T. gondii. Tachyzoites are typically crescent shaped with a prominent, centrally placed nucleus. Microscopic cyst containing T. gondii from mouse brain tissue. Thousands of resting parasites (stained red) are contained in a thin parasite cyst wall. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by USDA)"
0e6b9cf3-0cc1-481f-9792-c502e5e405d6,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"Preventing infection is the best first-line defense against toxoplasmosis. Preventive measures include washing hands thoroughly after handling raw meat, soil, or cat litter, and avoiding consumption of vegetables possibly contaminated with cat feces. All meat should be cooked to an internal temperature of 73.9–76.7 °C (165–170 °F).",True,Toxoplasmosis,,,,
d9abccdd-2bef-4178-a1da-2b8509433125,https://open.oregonstate.education/microbiology/,20.4	Parasitic Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-4parasitic-infections-of-the-circulatory-and-lymphatic-systems/,"Most immunocompetent patients do not require clinical intervention for Toxoplasma infections. However, neonates, pregnant women, and immunocompromised patients can be treated with pyrimethamine and sulfadiazine—except during the first trimester of pregnancy, because these drugs can cause birth defects. Spiramycin has been used safely to reduce transmission in pregnant women with primary infection during the first trimester because it does not cross the placenta.",True,Toxoplasmosis,,,,
a722e31f-faea-48f3-a3bb-5503dbfc50c9,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,Infectious Mononucleosis and Burkitt Lymphoma,False,Infectious Mononucleosis and Burkitt Lymphoma,,,,
d1946a73-29c1-4a79-96cf-fb82ee06b522,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,"Human herpesvirus 4, also known as Epstein-Barr virus (EBV), has been associated with a variety of human diseases, such as mononucleosis and Burkitt lymphoma. Exposure to the human herpesvirus 4 (HHV-4) is widespread and nearly all people have been exposed at some time in their childhood, as evidenced by serological tests on populations. The virus primarily resides within B lymphocytes and, like all herpes viruses, can remain dormant in a latent state for a long time.",True,Infectious Mononucleosis and Burkitt Lymphoma,,,,
93819180-b3b3-4be1-9e9e-d34e38c28eb9,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,"When uninfected young adults are exposed to EBV, they may experience infectious mononucleosis. The virus is mainly spread through contact with body fluids (e.g., saliva, blood, and semen). The main symptoms include pharyngitis, fever, fatigue, and lymph node swelling. Abdominal pain may also occur as a result of spleen and liver enlargement in the second or third week of infection. The disease typically is self-limiting after about a month. The main symptom, extreme fatigue, can continue for several months, however. Complications in immunocompetent patients are rare but can include jaundice, anemia, and possible rupture of the spleen caused by enlargement.",True,Infectious Mononucleosis and Burkitt Lymphoma,,,,
e24bbb31-1d68-4635-9653-ec702f23b599,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,"In patients with malaria or HIV, Epstein-Barr virus can lead to a fast-growing malignant cancer known as Burkitt lymphoma. This condition is a form of non-Hodgkin lymphoma that produces solid tumors chiefly consisting of aberrant B cells. Burkitt lymphoma is more common in Africa, where prevalence of HIV and malaria is high, and it more frequently afflicts children.",True,Infectious Mononucleosis and Burkitt Lymphoma,,,,
ed9febc2-477f-400a-ae4b-093aeb9406d5,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,"Infectious mononucleosis is typically diagnosed based on the initial clinical symptoms and a test for antibodies to EBV-associated antigens. Because the disease is self-limiting, antiviral treatments are rare for mononucleosis. Cases of Burkitt lymphoma are diagnosed from a biopsy specimen from a lymph node or tissue from a suspected tumor.",True,Infectious Mononucleosis and Burkitt Lymphoma,,,,
9a870eb9-c9a6-49aa-a41a-0a3b89cd6f86,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,Ebola Virus Disease,False,Ebola Virus Disease,,,,
dbe2e160-a64d-4e3f-8442-b8050b901609,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,"The Ebola virus disease (EVD) is a highly contagious disease caused by species of Ebolavirus, a BSL-4 filovirus (Figure 20.14). Transmission to humans occurs through direct contact with body fluids (e.g., blood, saliva, sweat, urine, feces, or vomit), and indirect contact by contaminated fomites. Infected patients can easily transmit Ebola virus to others if appropriate containment and use of personal protective equipment is not available or used. Handling and working with patients with EVD is extremely hazardous to the general population and health-care workers. In almost every EVD outbreak there have been Ebola infections among health-care workers. This ease of Ebola virus transmission was recently demonstrated in the Ebola epidemic in Guinea, Liberia, and Sierra Leone in 2014, in which more than 28,000 people in 10 countries were infected and more than 11,000 died.[1]",True,Ebola Virus Disease,Figure 20.14,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.22.png,Figure 20.14 An Ebola virus particle viewed with electron microscopy. These filamentous viruses often exhibit looped or hooked ends. (credit: modification of work by Centers for Disease Control and Prevention)
c08a1cc9-e923-4141-9fa6-3fcc6229e863,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,"After infection, the initial symptoms of Ebola are unremarkable: fever, severe headache, myalgia, cough, chest pain, and pharyngitis. As the disease progresses, patients experience abdominal pain, diarrhea, and vomiting. Hemorrhaging begins after about 3 days, with bleeding occurring in the gastrointestinal tract, skin, and many other sites. This often leads to delirium, stupor, and coma, accompanied by shock, multiple organ failure, and death. The mortality rates of EVD often range from 50% to 90%.",True,Ebola Virus Disease,,,,
4ef823dc-cb3f-4c1b-8655-ca314617c6c2,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,"The initial diagnosis of Ebola is difficult because the early symptoms are so similar to those of many other illnesses. It is possible to directly detect the virus from patient samples within a few days after symptoms begin, using antigen-capture ELISA, immunoglobulin M (IgM) ELISA, PCR, and virus isolation. There are currently no effective, approved treatments for Ebola other than supportive care and proper isolation techniques to contain its spread.",True,Ebola Virus Disease,,,,
af0edf25-0803-4085-bf57-baf5c391bb37,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,Human Immunodeficiency Virus,False,Human Immunodeficiency Virus,,,,
a6332772-6fb4-4f03-a6b4-cf58fba6fabb,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,"Human T-lymphotropic viruses (HTLV), also called human immunodeficiency viruses (HIV) are retroviruses that are the causative agent of acquired immune deficiency syndrome (AIDS). There are two main variants of human immunodeficiency virus (HIV). HIV-1 (Figure 20.15) occurs in human populations worldwide, whereas HIV-2 is concentrated in West Africa. Currently, the most affected region in the world is sub-Saharan Africa, with an estimated 25.6 million people living with HIV in 2015.[2] Sub-Saharan Africa also accounts for two-thirds of the global total of new HIV infections (Figure 20.16).[3]",True,Human Immunodeficiency Virus,Figure 20.15,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.23.png,Figure 20.15 This micrograph shows HIV particles (green) budding from a lymphocyte (top right). (credit: modification of work by Centers for Disease Control and Prevention)
b28f7f68-8038-41c6-aa65-27e28cb2ffa1,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,"HIV is spread through direct contact with body fluids. Casual contact and insect vectors are not sufficient for disease transmission; common modes of transmission include sexual contact and sharing of needles by intravenous (IV) drug users. It generally takes many years before the effects of an HIV infection are detected. HIV infections are not dormant during this period: virions are continually produced, and the immune system continually attempts to clear the viral infection, while the virus persistently infects additional CD4 T cells. Over time, the CD4 T-cell population is devastated, ultimately leading to AIDS.",True,Human Immunodeficiency Virus,,,,
3b6cb327-3d0e-44c9-812c-f13dbf4aa85c,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,"When people are infected with HIV, their disease progresses through three stages based on CD4 T-cell counts and the presence of clinical symptoms (Figure 20.17).",True,Human Immunodeficiency Virus,Figure 20.17,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.25.png,"Figure 20.17 This graph shows the clinical progression of CD4 T cells (blue line), clinical symptoms, and viral RNA (red line) during an HIV infection. (credit: modification of work by Kogan M, and Rappaport J)"
cf35b4cb-d690-41ab-b5bf-d7b422d45241,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,The initial diagnosis of HIV is performed using a serological test for antibody production against the pathogen. Positive test results are confirmed by Western blot or PCR tests. It can take weeks or months for the body to produce antibodies in response to an infection. There are fourth-generation tests that detect HIV antibodies and HIV antigens that are present even before the body begins producing antibodies. Nucleic acid tests (NATs) are a third type of test that is relatively expensive and uncommon; NAT can detect HIV in blood and determine the viral load.,True,Human Immunodeficiency Virus,,,,
6a12f505-3695-46c2-91e0-c1a0f97ddc1e,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,"As a consequence of provirus formation, it is currently not possible to eliminate HIV from an infected patient’s body. Elimination by specific antibodies is ineffective because the virus mutates rapidly—a result of the error-prone reverse transcriptase and the inability to correct errors. Antiviral treatments, however, can greatly extend life expectancy. To combat the problem of drug resistance, combinations of antiretroviral drugs called antiretroviral therapy (ART), sometimes called highly active ART or combined ART, are used. There are several different targets for antiviral drug action (and a growing list of drugs for each of these targets). One class of drugs inhibits HIV entry; other classes inhibit reverse transcriptase by blocking viral RNA-dependent and DNA-dependent DNA polymerase activity; and still others inhibit one of the three HIV enzymes needed to replicate inside human cells.",True,Human Immunodeficiency Virus,,,,
12c86f9a-50ce-42bd-9959-5e2b1ca6a55d,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,"When people are infected with HIV, their disease progresses through three stages based on CD4 T-cell counts and the presence of clinical symptoms (Figure 20.17).",True,Human Immunodeficiency Virus,Figure 20.17,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.25.png,"Figure 20.17 This graph shows the clinical progression of CD4 T cells (blue line), clinical symptoms, and viral RNA (red line) during an HIV infection. (credit: modification of work by Kogan M, and Rappaport J)"
88ba8bb4-0e5c-45cc-a4c1-b9d47e675306,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,The initial diagnosis of HIV is performed using a serological test for antibody production against the pathogen. Positive test results are confirmed by Western blot or PCR tests. It can take weeks or months for the body to produce antibodies in response to an infection. There are fourth-generation tests that detect HIV antibodies and HIV antigens that are present even before the body begins producing antibodies. Nucleic acid tests (NATs) are a third type of test that is relatively expensive and uncommon; NAT can detect HIV in blood and determine the viral load.,True,Human Immunodeficiency Virus,,,,
9e77dadc-cd9f-4fc9-8e1b-24e4fce31e9d,https://open.oregonstate.education/microbiology/,20.3	Viral Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-3viral-infections-of-the-circulatory-and-lymphatic-systems/,"As a consequence of provirus formation, it is currently not possible to eliminate HIV from an infected patient’s body. Elimination by specific antibodies is ineffective because the virus mutates rapidly—a result of the error-prone reverse transcriptase and the inability to correct errors. Antiviral treatments, however, can greatly extend life expectancy. To combat the problem of drug resistance, combinations of antiretroviral drugs called antiretroviral therapy (ART), sometimes called highly active ART or combined ART, are used. There are several different targets for antiviral drug action (and a growing list of drugs for each of these targets). One class of drugs inhibits HIV entry; other classes inhibit reverse transcriptase by blocking viral RNA-dependent and DNA-dependent DNA polymerase activity; and still others inhibit one of the three HIV enzymes needed to replicate inside human cells.",True,Human Immunodeficiency Virus,,,,
72e5229b-fb26-4b0e-9151-6a81517ed652,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,Plague,False,Plague,,,,
e102344d-2b92-4337-8298-76786a35e164,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,"The gram-negative bacillus Yersinia pestis causes the zoonotic infection plague. This bacterium causes acute febrile disease in animals, usually rodents or other small mammals, and humans. The disease is associated with a high mortality rate if left untreated. Historically, Y. pestis has been responsible for several devastating pandemics, resulting in millions of deaths (see Micro Connections: The History of the Plague). There are three forms of plague: bubonic plague (the most common form, accounting for about 80% of cases), pneumonic plague, and septicemic plague. These forms are differentiated by the mode of transmission and the initial site of infection. Figure 20.6 illustrates these various modes of transmission and infection between animals and humans.",True,Plague,Figure 20.6,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.9.png,"Figure 20.6 Yersinia pestis, the causative agent of plague, has numerous modes of transmission. The modes are divided into two ecological classes: urban and sylvatic (i.e., forest or rural). The urban cycle primarily involves transmission from infected urban mammals (rats) to humans by flea vectors (brown arrows). The disease may travel between urban centers (purple arrow) if infected rats find their way onto ships or trains. The sylvatic cycle involves mammals more common in nonurban environments. Sylvatic birds and mammals (including humans) may become infected after eating infected mammals (pink arrows) or by flea vectors. Pneumonic transmission occurs between humans or between humans and infected animals through the inhalation of Y. pestis in aerosols. (credit “diagram”: modification of work by Stenseth NC, Atshabar BB, Begon M, Belmain SR, Bertherat E, Carniel E, Gage KL, Leirs H, and Rahalison L; credit “cat”: modification of work by “KaCey97078”/Flickr)"
9cefacdb-e06c-432a-af6e-309f91f16a3e,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,"In bubonic plague, Y. pestis is transferred by the bite of infected fleas. Since most flea bites occur on the legs and ankles, Y. pestis is often introduced into the tissues and blood circulation in the lower extremities. After a 2- to 6-day incubation period, patients experience an abrupt onset fever (39.5–41 °C [103.1–105.8 °F]), headache, hypotension, and chills. The pathogen localizes in lymph nodes, where it causes inflammation, swelling, and hemorrhaging that results in purple buboes (Figure 20.7). Buboes often form in lymph nodes of the groin first because these are the nodes associated with the lower limbs; eventually, through circulation in the blood and lymph, lymph nodes throughout the body become infected and form buboes. The average mortality rate for bubonic plague is about 55% if untreated and about 10% with antibiotic treatment.",True,Plague,Figure 20.7,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.10.png,"Figure 20.7 (a) Yersinia pestis infection can cause inflamed and swollen lymph nodes (buboes), like these in the groin of an infected patient. (b) Septicemic plague caused necrotic toes in this patient. Vascular damage at the extremities causes ischemia and tissue death. (credit a: modification of work by American Society for Microbiology; credit b: modification of work by Centers for Disease Control and Prevention)"
cac592b6-92e5-4192-9554-6e9174fb1ade,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,"Septicemic plague occurs when Y. pestis is directly introduced into the bloodstream through a cut or wound and circulates through the body. The incubation period for septicemic plague is 1 to 3 days, after which patients develop fever, chills, extreme weakness, abdominal pain, and shock. Disseminated intravascular coagulation (DIC) can also occur, resulting in the formation of thrombi that obstruct blood vessels and promote ischemia and necrosis in surrounding tissues (Figure 20.7). Necrosis occurs most commonly in extremities such as fingers and toes, which become blackened. Septicemic plague can quickly lead to death, with a mortality rate near 100% when it is untreated. Even with antibiotic treatment, the mortality rate is about 50%.",True,Plague,Figure 20.7,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.10.png,"Figure 20.7 (a) Yersinia pestis infection can cause inflamed and swollen lymph nodes (buboes), like these in the groin of an infected patient. (b) Septicemic plague caused necrotic toes in this patient. Vascular damage at the extremities causes ischemia and tissue death. (credit a: modification of work by American Society for Microbiology; credit b: modification of work by Centers for Disease Control and Prevention)"
a23029e9-a411-4c80-aadc-753bbc2f24b6,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,"Pneumonic plague occurs when Y. pestis causes an infection of the lungs. This can occur through inhalation of aerosolized droplets from an infected individual or when the infection spreads to the lungs from elsewhere in the body in patients with bubonic or septicemic plague. After an incubation period of 1 to 3 days, signs and symptoms include fever, headache, weakness, and a rapidly developing pneumonia with shortness of breath, chest pain, and cough producing bloody or watery mucus. The pneumonia may result in rapid respiratory failure and shock. Pneumonic plague is the only form of plague that can be spread from person to person by infectious aerosol droplet. If untreated, the mortality rate is near 100%; with antibiotic treatment, the mortality rate is about 50%.",True,Plague,,,,
75b3b0f2-afc6-403b-857d-dd352e8bc037,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,"Culturing and direct microscopic examination of a sample of fluid from a bubo, blood, or sputum is the best way to identify Y. pestis and confirm a presumptive diagnosis of plague. Specimens may be stained using either a Gram, Giemsa, Wright, or Wayson’s staining technique (Figure 20.8). The bacteria show a characteristic bipolar staining pattern, resembling safety pins, that facilitates presumptive identification. Direct fluorescent antibody tests (rapid test of outer-membrane antigens) and serological tests like ELISA can be used to confirm the diagnosis. The confirmatory method for identifying Y. pestis isolates in the US is bacteriophage lysis.",True,Plague,Figure 20.8,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.11.png,Figure 20.8 This Wright’s stain of a blood sample from a patient with plague shows the characteristic “safety pin” appearance of Yersinia pestis. (credit: modification of work by Centers for Disease Control and Prevention)
fbfa18ab-8faf-4046-b759-dfc684d035ad,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,"Prompt antibiotic therapy can resolve most cases of bubonic plague, but septicemic and pneumonic plague are more difficult to treat because of their shorter incubation stages. Survival often depends on an early and accurate diagnosis and an appropriate choice of antibiotic therapy. In the US, the most common antibiotics used to treat patients with plague are gentamicin, fluoroquinolones, streptomycin, levofloxacin, ciprofloxacin, and doxycycline.",True,Plague,,,,
5cf25cdf-5ecf-4cb1-a7b4-fb4bd99814dc,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,Lyme Disease,False,Lyme Disease,,,,
09d0bde2-beba-4bcb-97d0-091f0d036ac8,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,"Lyme disease is caused by the spirochete Borrelia burgdorferi that is transmitted by the bite of a hard-bodied, black- legged Ixodes tick. I. scapularis is the biological vector transmitting B. burgdorferi in the eastern and north-central US and I. pacificus transmits B. burgdorferi in the western US (Figure 20.9). Different species of Ixodes ticks are responsible for B. burgdorferi transmission in Asia and Europe. In the US, Lyme disease is the most commonly reported vectorborne illness. In 2014, it was the fifth most common Nationally Notifiable disease.[4]",True,Lyme Disease,Figure 20.9,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.14.png,"Figure 20.9 This image shows the 2-year life cycle of the black-legged tick, the biological vector of Lyme disease. (credit “mouse”: modification of work by George Shuklin)"
9539513f-d197-4658-9d22-7622dbaa97b6,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,"Ixodes ticks have complex life cycles and deer, mice, and even birds can act as reservoirs. Over 2 years, the ticks pass through four developmental stages and require a blood meal from a host at each stage. In the spring, tick eggs hatch into six-legged larvae. These larvae do not carry B. burgdorferi initially. They may acquire the spirochete when they take their first blood meal (typically from a mouse). The larvae then overwinter and molt into eight-legged nymphs in the following spring. Nymphs take blood meals primarily from small rodents, but may also feed on humans, burrowing into the skin. The feeding period can last several days to a week, and it typically takes 24 hours for an infected nymph to transmit enough B. burgdorferi to cause infection in a human host. Nymphs ultimately mature into male and female adult ticks, which tend to feed on larger animals like deer or, occasionally, humans. The adults then mate and produce eggs to continue the cycle (Figure 20.9).",True,Lyme Disease,Figure 20.9,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.14.png,"Figure 20.9 This image shows the 2-year life cycle of the black-legged tick, the biological vector of Lyme disease. (credit “mouse”: modification of work by George Shuklin)"
2bb567e5-f2e5-4865-962f-15795b99e07f,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,"The symptoms of Lyme disease follow three stages: early localized, early disseminated, and late stage. During the early-localized stage, approximately 70%–80%[5] of cases may be characterized by a bull’s-eye rash, called erythema migrans, at the site of the initial tick bite. The rash forms 3 to 30 days after the tick bite (7 days is the average) and may also be warm to the touch (Figure 20.10).[6] This diagnostic sign is often overlooked if the tick bite occurs on the scalp or another less visible location. Other early symptoms include flu-like symptoms such as malaise, headache, fever, and muscle stiffness. If the patient goes untreated, the second early-disseminated stage of the disease occurs days to weeks later. The symptoms at this stage may include severe headache, neck stiffness, facial paralysis, arthritis, and carditis. The late-stage manifestations of the disease may occur years after exposure. Chronic inflammation causes damage that can eventually cause severe arthritis, meningitis, encephalitis, and altered mental states. The disease may be fatal if untreated.",True,Lyme Disease,Figure 20.10,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.15.png,"Figure 20.10 (a) A characteristic bull’s eye rash of Lyme disease forms at the site of a tick bite. (b) A darkfield micrograph shows Borrelia burgdorferi, the causative agent of Lyme disease. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by American Society for Microbiology)"
9919f20a-3a97-42a7-8a2f-190a60c5a7c3,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,"A presumptive diagnosis of Lyme disease can be made based solely on the presence of a bull’s-eye rash at the site of infection, if it is present, in addition to other associated symptoms (Figure 20.10). In addition, indirect immunofluorescent antibody (IFA) labeling can be used to visualize bacteria from blood or skin biopsy specimens. Serological tests like ELISA can also be used to detect serum antibodies produced in response to infection. During the early stage of infection (about 30 days), antibacterial drugs such as amoxicillin and doxycycline are effective. In the later stages, penicillin G, chloramphenicol, or ceftriaxone can be given intravenously.",True,Lyme Disease,Figure 20.10,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.15.png,"Figure 20.10 (a) A characteristic bull’s eye rash of Lyme disease forms at the site of a tick bite. (b) A darkfield micrograph shows Borrelia burgdorferi, the causative agent of Lyme disease. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by American Society for Microbiology)"
78560e8a-16a4-4025-94a7-8387c9690295,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,"Many of the diseases covered in this chapter involve arthropod vectors. Of these, ticks are probably the most commonly encountered in the US. Adult ticks have eight legs and two body segments, the cephalothorax and the head. They typically range from 2 mm to 4 mm in length, and feed on the blood of the host by attaching themselves to the skin. Unattached ticks should be removed and eliminated as soon as they are discovered. When removing a tick that has already attached itself, keep the following guidelines in mind to reduce the chances of exposure to pathogens:",True,Lyme Disease,,,,
29bcde39-eba2-4b3d-873c-33008dd3bb2a,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,"Culturing and direct microscopic examination of a sample of fluid from a bubo, blood, or sputum is the best way to identify Y. pestis and confirm a presumptive diagnosis of plague. Specimens may be stained using either a Gram, Giemsa, Wright, or Wayson’s staining technique (Figure 20.8). The bacteria show a characteristic bipolar staining pattern, resembling safety pins, that facilitates presumptive identification. Direct fluorescent antibody tests (rapid test of outer-membrane antigens) and serological tests like ELISA can be used to confirm the diagnosis. The confirmatory method for identifying Y. pestis isolates in the US is bacteriophage lysis.",True,Lyme Disease,Figure 20.8,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.11.png,Figure 20.8 This Wright’s stain of a blood sample from a patient with plague shows the characteristic “safety pin” appearance of Yersinia pestis. (credit: modification of work by Centers for Disease Control and Prevention)
9ffed499-76a6-4edc-aa2a-21ac22cf4309,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,"Prompt antibiotic therapy can resolve most cases of bubonic plague, but septicemic and pneumonic plague are more difficult to treat because of their shorter incubation stages. Survival often depends on an early and accurate diagnosis and an appropriate choice of antibiotic therapy. In the US, the most common antibiotics used to treat patients with plague are gentamicin, fluoroquinolones, streptomycin, levofloxacin, ciprofloxacin, and doxycycline.",True,Lyme Disease,,,,
0eb5d61d-1632-4d23-aecb-3834b38d2079,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,Lyme Disease,False,Lyme Disease,,,,
72711348-4aad-4ca6-8121-7e4d2bbf62c3,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,"Ixodes ticks have complex life cycles and deer, mice, and even birds can act as reservoirs. Over 2 years, the ticks pass through four developmental stages and require a blood meal from a host at each stage. In the spring, tick eggs hatch into six-legged larvae. These larvae do not carry B. burgdorferi initially. They may acquire the spirochete when they take their first blood meal (typically from a mouse). The larvae then overwinter and molt into eight-legged nymphs in the following spring. Nymphs take blood meals primarily from small rodents, but may also feed on humans, burrowing into the skin. The feeding period can last several days to a week, and it typically takes 24 hours for an infected nymph to transmit enough B. burgdorferi to cause infection in a human host. Nymphs ultimately mature into male and female adult ticks, which tend to feed on larger animals like deer or, occasionally, humans. The adults then mate and produce eggs to continue the cycle (Figure 20.9).",True,Lyme Disease,Figure 20.9,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.14.png,"Figure 20.9 This image shows the 2-year life cycle of the black-legged tick, the biological vector of Lyme disease. (credit “mouse”: modification of work by George Shuklin)"
456d1439-c659-46fd-b9a8-3cdbfbd7cfa7,https://open.oregonstate.education/microbiology/,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-2bacterial-infections-of-the-circulatory-and-lymphatic-systems/,"A presumptive diagnosis of Lyme disease can be made based solely on the presence of a bull’s-eye rash at the site of infection, if it is present, in addition to other associated symptoms (Figure 20.10). In addition, indirect immunofluorescent antibody (IFA) labeling can be used to visualize bacteria from blood or skin biopsy specimens. Serological tests like ELISA can also be used to detect serum antibodies produced in response to infection. During the early stage of infection (about 30 days), antibacterial drugs such as amoxicillin and doxycycline are effective. In the later stages, penicillin G, chloramphenicol, or ceftriaxone can be given intravenously.",True,Lyme Disease,Figure 20.10,20.2	Bacterial Infections of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.15.png,"Figure 20.10 (a) A characteristic bull’s eye rash of Lyme disease forms at the site of a tick bite. (b) A darkfield micrograph shows Borrelia burgdorferi, the causative agent of Lyme disease. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by American Society for Microbiology)"
cb058f0b-f7e3-42f3-9d92-03cbf5633db5,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,The Circulatory System,False,The Circulatory System,,,,
06b96bb6-f78d-40a1-8fb4-a26d027a1307,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,"The circulatory (or cardiovascular) system is a closed network of organs and vessels that moves blood around the body (Figure 20.2). The primary purposes of the circulatory system are to deliver nutrients, immune factors, and oxygen to tissues and to carry away waste products for elimination. The heart is a four-chambered pump that propels the blood throughout the body. Deoxygenated blood enters the right atrium through the superior vena cava and the inferior vena cava after returning from the body. The blood next passes through the tricuspid valve to enter the right ventricle. When the heart contracts, the blood from the right ventricle is pumped through the pulmonary arteries to the lungs. There, the blood is oxygenated at the alveoli and returns to the heart through the pulmonary veins. The oxygenated blood is received at the left atrium and proceeds through the mitral valve to the left ventricle. When the heart contracts, the oxygenated blood is pumped throughout the body via a series of thick-walled vessels called arteries. The first and largest artery is called the aorta. The arteries sequentially branch and decrease in size (and are called arterioles) until they end in a network of smaller vessels called capillaries. The capillary beds are located in the interstitial spaces within tissues and release nutrients, immune factors, and oxygen to those tissues. The capillaries connect to a series of vessels called venules, which increase in size to form the veins. The veins join together into larger vessels as they transfer blood back to the heart. The largest veins, the superior and inferior vena cava, returnthe blood to the right atrium.",True,The Circulatory System,Figure 20.2,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.2.png,"Figure 20.2 The major components of the human circulatory system include the heart, arteries, veins, and capillaries. This network delivers blood to the body’s organs and tissues. (credit top left: modification of work by Mariana Ruiz Villareal; credit bottom right: modification of work by Bruce Blaus)"
57587f3c-f0ad-4742-b430-327ba8e0c40b,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,"Other organs play important roles in the circulatory system as well. The kidneys filter the blood, removing waste products and eliminating them in the urine. The liver also filters the blood and removes damaged or defective red blood cells. The spleen filters and stores blood, removes damaged red blood cells, and is a reservoir for immune factors. All of these filtering structures serve as sites for entrapment of microorganisms and help maintain an environment free of microorganisms in the blood.",True,The Circulatory System,,,,
015f7a0f-d230-4582-9eb5-a0d2cda11ca0,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,The Lymphatic System,False,The Lymphatic System,,,,
10e11c0d-0845-4402-845b-9b378d89c096,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,"The lymphatic system is also a network of vessels that run throughout the body (Figure 20.3). However, these vessels do not form a full circulating system and are not pressurized by the heart. Rather, the lymphatic system is an open system with the fluid moving in one direction from the extremities toward two drainage points into veins just above the heart. Lymphatic fluids move more slowly than blood because they are not pressurized. Small lymph capillaries interact with blood capillaries in the interstitial spaces in tissues. Fluids from the tissues enter the lymph capillaries and are drained away (Figure 20.4). These fluids, termed lymph, also contain large numbers of white blood cells.",True,The Lymphatic System,Figure 20.3,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.3.png,Figure 20.3 The essential components of the human lymphatic system drain fluid away from tissues.
a8c94312-edf6-408f-9e45-7ba336a54c0f,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,"The lymphatic system contains two types of lymphoid tissues. The primary lymphoid tissue includes bone marrow and the thymus. Bone marrow contains the hematopoietic stem cells (HSC) that differentiate and mature into the various types of blood cells and lymphocytes. The secondary lymphoid tissues include the spleen, lymph nodes, and several areas of diffuse lymphoid tissues underlying epithelial membranes. The spleen, an encapsulated structure, filters blood and captures pathogens and antigens that pass into it (Figure 20.5). The spleen contains specialized macrophages and dendritic cells that are crucial for antigen presentation, a mechanism critical for activation of T lymphocytes and B lymphocytes. Lymph nodes are bean-shaped organs situated throughout the body. These structures contain areas called germinal centers that are rich in B and T lymphocytes. The lymph nodes also contain macrophages and dendritic cells for antigen presentation. Lymph from nearby tissues enters the lymph node through afferent lymphatic vessels and encounters these lymphocytes as it passes through; the lymph exits the lymph node through the efferent lymphatic vessels (Figure 20.5).",True,The Lymphatic System,Figure 20.5,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.5.png,Figure 20.5 (a) The spleen is a lymphatic organ located in the upper left quadrant of the abdomen near the stomach and left kidney. It contains numerous phagocytes and lymphocytes that combat and prevent circulatory infections by killing and removing pathogens from the blood. (b) Lymph nodes are masses of lymphatic tissue located along the larger lymph vessels. They contain numerous lymphocytes that kill and remove pathogens from lymphatic fluid that drains from surrounding tissues.
e01f7633-93c0-42df-8760-4525d46730d7,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,Infections of the Circulatory System,False,Infections of the Circulatory System,,,,
1df794d3-ee55-4f51-a453-977599a51d76,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,"Under normal circumstances, the circulatory system and the blood should be sterile; the circulatory system has no normal microbiota. Because the system is closed, there are no easy portals of entry into the circulatory system for microbes. Those that are able to breach the body’s physical barriers and enter the bloodstream encounter a host of circulating immune defenses, such as antibodies, complement proteins, phagocytes, and other immune cells. Microbes often gain access to the circulatory system through a break in the skin (e.g., wounds, needles, intravenous catheters, insect bites) or spread to the circulatory system from infections in other body sites. For example, microorganisms causing pneumonia or renal infection may enter the local circulation of the lung or kidney and spread from there throughout the circulatory network.",True,Infections of the Circulatory System,,,,
b2081ae4-966a-4e25-af6e-0791f8807977,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,"If microbes in the bloodstream are not quickly eliminated, they can spread rapidly throughout the body, leading to serious, even life-threatening infections. Various terms are used to describe conditions involving microbes in the circulatory system. The term bacteremia refers to bacteria in the blood. If bacteria are reproducing in the blood as they spread, this condition is called septicemia. The presence of viruses in the blood is called viremia. Microbial toxins can also be spread through the circulatory system, causing a condition termed toxemia.",True,Infections of the Circulatory System,,,,
dc4e0e62-b26f-4306-a7a9-86d74da1d862,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,"Microbes and microbial toxins in the blood can trigger an inflammatory response so severe that the inflammation damages host tissues and organs more than the infection itself. This counterproductive immune response is called systemic inflammatory response syndrome (SIRS), and it can lead to the life-threatening condition known as sepsis. Sepsis is characterized by the production of excess cytokines that leads to classic signs of inflammation such as fever, vasodilation, and edema. In a patient with sepsis, the inflammatory response becomes dysregulated and disproportionate to the threat of infection. Critical organs such as the heart, lungs, liver, and kidneys become dysfunctional, resulting in increased heart and respiratory rates, and disorientation. If not treated promptly and effectively, patients with sepsis can go into shock and die.",True,Infections of the Circulatory System,,,,
5d7528c0-7541-4a02-865f-a2f41e05b3ac,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,Infections of the Lymphatic System,False,Infections of the Lymphatic System,,,,
75c192c7-1909-4114-a855-77deac93bb1a,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,"Like the circulatory system, the lymphatic system does not have a normal microbiota, and the large numbers of immune cells typically eliminate transient microbes before they can establish an infection. Only microbes with an array of virulence factors are able to overcome these defenses and establish infection in the lymphatic system. However, when a localized infection begins to spread, the lymphatic system is often the first place the invading microbes can be detected.",True,Infections of the Lymphatic System,,,,
99365534-6497-4a1f-811f-3ddfa9ae3d4c,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,"Infections in the lymphatic system also trigger an inflammatory response. Inflammation of lymphatic vessels, called lymphangitis, can produce visible red streaks under the skin. Inflammation in the lymph nodes can cause them to swell. A swollen lymph node is referred to as a bubo, and the condition is referred to as lymphadenitis.",True,Infections of the Lymphatic System,,,,
c29ff37d-37e1-44d8-b43a-81468678f91c,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,The Lymphatic System,False,The Lymphatic System,,,,
a77b0a5e-096c-4510-9f49-7f0f3ba9de2d,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,"The lymphatic system is also a network of vessels that run throughout the body (Figure 20.3). However, these vessels do not form a full circulating system and are not pressurized by the heart. Rather, the lymphatic system is an open system with the fluid moving in one direction from the extremities toward two drainage points into veins just above the heart. Lymphatic fluids move more slowly than blood because they are not pressurized. Small lymph capillaries interact with blood capillaries in the interstitial spaces in tissues. Fluids from the tissues enter the lymph capillaries and are drained away (Figure 20.4). These fluids, termed lymph, also contain large numbers of white blood cells.",True,The Lymphatic System,Figure 20.3,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-25.3.png,Figure 20.3 The essential components of the human lymphatic system drain fluid away from tissues.
92b196c2-680b-4c4a-8e6e-a4a633169354,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,Infections of the Circulatory System,False,Infections of the Circulatory System,,,,
a31c54ba-f5ab-4f5a-b3aa-e7e2f2c03513,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,"Under normal circumstances, the circulatory system and the blood should be sterile; the circulatory system has no normal microbiota. Because the system is closed, there are no easy portals of entry into the circulatory system for microbes. Those that are able to breach the body’s physical barriers and enter the bloodstream encounter a host of circulating immune defenses, such as antibodies, complement proteins, phagocytes, and other immune cells. Microbes often gain access to the circulatory system through a break in the skin (e.g., wounds, needles, intravenous catheters, insect bites) or spread to the circulatory system from infections in other body sites. For example, microorganisms causing pneumonia or renal infection may enter the local circulation of the lung or kidney and spread from there throughout the circulatory network.",True,Infections of the Circulatory System,,,,
d0bca820-70b2-46eb-b934-363b7e5f2e0b,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,"If microbes in the bloodstream are not quickly eliminated, they can spread rapidly throughout the body, leading to serious, even life-threatening infections. Various terms are used to describe conditions involving microbes in the circulatory system. The term bacteremia refers to bacteria in the blood. If bacteria are reproducing in the blood as they spread, this condition is called septicemia. The presence of viruses in the blood is called viremia. Microbial toxins can also be spread through the circulatory system, causing a condition termed toxemia.",True,Infections of the Circulatory System,,,,
1c5f43ea-d950-4cc5-a775-b321473260d6,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,"Microbes and microbial toxins in the blood can trigger an inflammatory response so severe that the inflammation damages host tissues and organs more than the infection itself. This counterproductive immune response is called systemic inflammatory response syndrome (SIRS), and it can lead to the life-threatening condition known as sepsis. Sepsis is characterized by the production of excess cytokines that leads to classic signs of inflammation such as fever, vasodilation, and edema. In a patient with sepsis, the inflammatory response becomes dysregulated and disproportionate to the threat of infection. Critical organs such as the heart, lungs, liver, and kidneys become dysfunctional, resulting in increased heart and respiratory rates, and disorientation. If not treated promptly and effectively, patients with sepsis can go into shock and die.",True,Infections of the Circulatory System,,,,
cc1d8cd2-7e7d-4066-8e7d-05d484ecd466,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,Infections of the Lymphatic System,False,Infections of the Lymphatic System,,,,
d21577ec-423f-4c83-b4d6-b5f7edb25d6d,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,"Like the circulatory system, the lymphatic system does not have a normal microbiota, and the large numbers of immune cells typically eliminate transient microbes before they can establish an infection. Only microbes with an array of virulence factors are able to overcome these defenses and establish infection in the lymphatic system. However, when a localized infection begins to spread, the lymphatic system is often the first place the invading microbes can be detected.",True,Infections of the Lymphatic System,,,,
f3b46af1-4123-4543-96a3-a3463508cea3,https://open.oregonstate.education/microbiology/,20.1	Anatomy of the Circulatory and Lymphatic Systems,https://open.oregonstate.education/microbiology/chapter/25-1anatomy-of-the-circulatory-and-lymphatic-systems/,"Infections in the lymphatic system also trigger an inflammatory response. Inflammation of lymphatic vessels, called lymphangitis, can produce visible red streaks under the skin. Inflammation in the lymph nodes can cause them to swell. A swollen lymph node is referred to as a bubo, and the condition is referred to as lymphadenitis.",True,Infections of the Lymphatic System,,,,
aa5831eb-81a9-437a-9579-068c812eb5a6,https://open.oregonstate.education/microbiology/,19.6	Helminthic Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-6helminthic-infections-of-the-gastrointestinal-tract/,Ascariasis,False,Ascariasis,,,,
8b717484-4d67-4fc5-8f5e-1613bd323c6d,https://open.oregonstate.education/microbiology/,19.6	Helminthic Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-6helminthic-infections-of-the-gastrointestinal-tract/,"Infections caused by the large nematode roundworm Ascaris lumbricoides, a soil-transmitted helminth, are called ascariasis. Over 800 million to 1 billion people are estimated to be infected worldwide.[1] Infections are most common in warmer climates and at warmer times of year. At present, infections are uncommon in the United States. The eggs of the worms are transmitted through contaminated food and water. This may happen if food is grown in contaminated soil, including when manure is used as fertilizer.",True,Ascariasis,,,,
e01f0b7f-1948-4ccc-9e52-f83489bbc902,https://open.oregonstate.education/microbiology/,19.6	Helminthic Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-6helminthic-infections-of-the-gastrointestinal-tract/,"When an individual consumes embryonated eggs (those with a developing embryo), the eggs travel to the intestine and the larvae are able to hatch. Ascaris is able to produce proteases that allow for penetration and degradation of host tissue. The juvenile worms can then enter the circulatory system and migrate to the lungs where they enter the alveoli (air sacs). From here they crawl to the pharynx and then follow the gut lumen to return to the small intestine, where they mature into adult roundworms. Females in the host will produce and release eggs that leave the host via feces. In some cases, the worms can block ducts such as those of the pancreas or gallbladder.",True,Ascariasis,,,,
5337add9-fa03-4b26-9bc9-ccf02373459e,https://open.oregonstate.education/microbiology/,19.6	Helminthic Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-6helminthic-infections-of-the-gastrointestinal-tract/,"The infection is commonly asymptomatic. When signs and symptoms are present, they include shortness of breath, cough, nausea, diarrhea, blood in the stool, abdominal pain, weight loss, and fatigue. The roundworms may be visible in the stool. In severe cases, children with substantial infections may experience intestinal blockage.",True,Ascariasis,,,,
f967edbb-f449-488f-a065-2e68747713d0,https://open.oregonstate.education/microbiology/,19.6	Helminthic Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-6helminthic-infections-of-the-gastrointestinal-tract/,"The eggs can be identified by microscopic examination of the stool (Figure 19.17). In some cases, the worms themselves may be identified if coughed up or excreted in stool. They can also sometimes be identified by X-rays, ultrasounds, or MRIs.",True,Ascariasis,Figure 19.17,19.6	Helminthic Infections of the Gastrointestinal Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-24.32.png,"Figure 19.17 (a) Adult Ascaris lumbricoides roundworms can cause intestinal blockage. (b) This mass of A. lumbricoides worms was excreted by a child. (c) A micrograph of a fertilized egg of A. lumbricoides. Fertilized eggs can be distinguished from unfertilized eggs because they are round rather than elongated and have a thicker cell wall. (credit a: modification of work by South African Medical Research Council; credit b: modification of work by James Gathany, Centers for Disease Control and Prevention; credit c: modification of work by Centers for Disease Control and Prevention)"
a487d527-b9fd-4047-a307-afd736e4f4c7,https://open.oregonstate.education/microbiology/,19.6	Helminthic Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-6helminthic-infections-of-the-gastrointestinal-tract/,"Ascariasis is self-limiting, but can last one to two years because the worms can inhibit the body’s inflammatory response. The first line of treatment is mebendazole or albendazole. In some severe cases, surgery may be required.",True,Ascariasis,,,,
a75cd372-1f29-4802-b662-97c7bb96fac6,https://open.oregonstate.education/microbiology/,19.6	Helminthic Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-6helminthic-infections-of-the-gastrointestinal-tract/,Pinworms (Enterobiasis),False,Pinworms (Enterobiasis),,,,
0d3b2991-8b11-420e-946e-a004f9fee10b,https://open.oregonstate.education/microbiology/,19.6	Helminthic Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-6helminthic-infections-of-the-gastrointestinal-tract/,"Enterobius vermicularis, commonly called pinworms, are tiny (2–13 mm) nematodes that cause enterobiasis. Of all helminthic infections, enterobiasis is the most common in the United States, affecting as many as one-third of American children.[2] Although the signs and symptoms are generally mild, patients may experience abdominal pain and insomnia from itching of the perianal region, which frequently occurs at night when worms leave the anus to lay eggs. The itching contributes to transmission, as the disease is transmitted through the fecal-oral route. When an infected individual scratches the anal area, eggs may get under the fingernails and later be deposited near the individual’s mouth, causing reinfection, or on fomites, where they can be transferred to new hosts. After being ingested, the larvae hatch within the small intestine and then take up residence in the colon and develop into adults. From the colon, the female adult exits the body at night to lay eggs (Figure 19.18).",True,Pinworms (Enterobiasis),Figure 19.18,19.6	Helminthic Infections of the Gastrointestinal Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-24.34.png,Figure 19.18 (a) E. vermicularis are tiny nematodes commonly called pinworms. (b) This micrograph shows pinworm eggs.
73545d67-011e-4015-a203-6830e845bbbc,https://open.oregonstate.education/microbiology/,19.6	Helminthic Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-6helminthic-infections-of-the-gastrointestinal-tract/,"Infection is diagnosed in any of three ways. First, because the worms emerge at night to lay eggs, it is possible to inspect the perianal region for worms while an individual is asleep. An alternative is to use transparent tape to remove eggs from the area around the anus first thing in the morning for three days to yield eggs for microscopic examination. Finally, it may be possible to detect eggs through examination of samples from under the fingernails, where eggs may lodge due to scratching. Once diagnosis has been made, mebendazole, albendazole, and pyrantel pamoate are effective for treatment.",True,Pinworms (Enterobiasis),,,,
bb5977ba-c411-45e3-b16c-347efe5577ee,https://open.oregonstate.education/microbiology/,19.6	Helminthic Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-6helminthic-infections-of-the-gastrointestinal-tract/,Pinworms (Enterobiasis),False,Pinworms (Enterobiasis),,,,
07071749-5939-4930-8435-d768b95fa457,https://open.oregonstate.education/microbiology/,19.6	Helminthic Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-6helminthic-infections-of-the-gastrointestinal-tract/,"Infection is diagnosed in any of three ways. First, because the worms emerge at night to lay eggs, it is possible to inspect the perianal region for worms while an individual is asleep. An alternative is to use transparent tape to remove eggs from the area around the anus first thing in the morning for three days to yield eggs for microscopic examination. Finally, it may be possible to detect eggs through examination of samples from under the fingernails, where eggs may lodge due to scratching. Once diagnosis has been made, mebendazole, albendazole, and pyrantel pamoate are effective for treatment.",True,Pinworms (Enterobiasis),,,,
45ae0794-d2c0-47aa-b8ab-173229cf89b4,https://open.oregonstate.education/microbiology/,19.5	Protozoan Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-5protozoan-infections-of-the-gastrointestinal-tract/,Learning Objectives,False,Learning Objectives,,,,
c0126b15-02d1-4282-9e51-a987094e4e99,https://open.oregonstate.education/microbiology/,19.5	Protozoan Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-5protozoan-infections-of-the-gastrointestinal-tract/,Giardiasis,False,Giardiasis,,,,
d029f802-8367-4bfc-8d9d-64cf9a1c7a2e,https://open.oregonstate.education/microbiology/,19.5	Protozoan Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-5protozoan-infections-of-the-gastrointestinal-tract/,"Also called backpacker’s diarrhea or beaver fever, giardiasis is a common disease in the United States caused by the flagellated protist Giardia lamblia.. To establish infection, G. lamblia uses a large adhesive disk to attach to the intestinal mucosa. The disk is comprised of microtubules. During adhesion, the flagella of G. lamblia move in a manner that draws fluid out from under the disk, resulting in an area of lower pressure that promotes its adhesion to the intestinal epithelial cells. Due to its attachment, Giardia also blocks absorption of nutrients, including fats.",True,Giardiasis,,,,
da204e7a-6fe0-428b-80ff-8334709b7fa7,https://open.oregonstate.education/microbiology/,19.5	Protozoan Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-5protozoan-infections-of-the-gastrointestinal-tract/,"Transmission occurs through contaminated food or water or directly from person to person. Children in day-care centers are at risk due to their tendency to put items into their mouths that may be contaminated. Large outbreaks may occur if a public water supply becomes contaminated. Giardia have a resistant cyst stage in their life cycle that is able to survive cold temperatures and the chlorination treatment typically used for drinking water in municipal reservoirs. As a result, municipal water must be filtered to trap and remove these cysts. Once consumed by the host, Giardia develops into the active tropozoite.",True,Giardiasis,,,,
734ca123-7ab7-4ce5-980c-78a3dee1aed0,https://open.oregonstate.education/microbiology/,19.5	Protozoan Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-5protozoan-infections-of-the-gastrointestinal-tract/,"Infected individuals may be asymptomatic or have gastrointestinal signs and symptoms, sometimes accompanied by weight loss. Common symptoms, which appear one to three weeks after exposure, include diarrhea, nausea, stomach cramps, gas, greasy stool (because fat absorption is being blocked), and possible dehydration. The parasite remains in the colon and does not cause systemic infection. Signs and symptoms generally clear within two to six weeks. Chronic infections may develop and are often resistant to treatment. These are associated with weight loss, episodic diarrhea, and malabsorption syndrome due to the blocked nutrient absorption.",True,Giardiasis,,,,
331d30d9-72d1-49a8-8206-41f2051f296d,https://open.oregonstate.education/microbiology/,19.5	Protozoan Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-5protozoan-infections-of-the-gastrointestinal-tract/,"Diagnosis may be made using observation under the microscope. A stool ova and parasite (O&P) exam involves direct examination of a stool sample for the presence of cysts and trophozoites; it can be used to distinguish common parasitic intestinal infections. ELISA and other immunoassay tests, including commercial direct fluorescence antibody kits, are also used. The most common treatments use metronidazole as the first-line choice, followed by tinidazole. If the infection becomes chronic, the parasites may become resistant to medications.",True,Giardiasis,,,,
4bb4e24e-25cf-4223-9f74-034a0b886cb5,https://open.oregonstate.education/microbiology/,19.5	Protozoan Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-5protozoan-infections-of-the-gastrointestinal-tract/,Learning Objectives,False,Learning Objectives,,,,
14befd01-744e-4885-9115-8332de8e0351,https://open.oregonstate.education/microbiology/,19.5	Protozoan Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-5protozoan-infections-of-the-gastrointestinal-tract/,Giardiasis,False,Giardiasis,,,,
3c1e2164-0a36-4660-869a-8cb7c780a955,https://open.oregonstate.education/microbiology/,19.5	Protozoan Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-5protozoan-infections-of-the-gastrointestinal-tract/,"Also called backpacker’s diarrhea or beaver fever, giardiasis is a common disease in the United States caused by the flagellated protist Giardia lamblia.. To establish infection, G. lamblia uses a large adhesive disk to attach to the intestinal mucosa. The disk is comprised of microtubules. During adhesion, the flagella of G. lamblia move in a manner that draws fluid out from under the disk, resulting in an area of lower pressure that promotes its adhesion to the intestinal epithelial cells. Due to its attachment, Giardia also blocks absorption of nutrients, including fats.",True,Giardiasis,,,,
ec7d905c-27d9-4ee6-909c-670dc3c12254,https://open.oregonstate.education/microbiology/,19.5	Protozoan Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-5protozoan-infections-of-the-gastrointestinal-tract/,"Transmission occurs through contaminated food or water or directly from person to person. Children in day-care centers are at risk due to their tendency to put items into their mouths that may be contaminated. Large outbreaks may occur if a public water supply becomes contaminated. Giardia have a resistant cyst stage in their life cycle that is able to survive cold temperatures and the chlorination treatment typically used for drinking water in municipal reservoirs. As a result, municipal water must be filtered to trap and remove these cysts. Once consumed by the host, Giardia develops into the active tropozoite.",True,Giardiasis,,,,
78c2397e-19de-4da0-a894-92775015f528,https://open.oregonstate.education/microbiology/,19.5	Protozoan Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-5protozoan-infections-of-the-gastrointestinal-tract/,"Infected individuals may be asymptomatic or have gastrointestinal signs and symptoms, sometimes accompanied by weight loss. Common symptoms, which appear one to three weeks after exposure, include diarrhea, nausea, stomach cramps, gas, greasy stool (because fat absorption is being blocked), and possible dehydration. The parasite remains in the colon and does not cause systemic infection. Signs and symptoms generally clear within two to six weeks. Chronic infections may develop and are often resistant to treatment. These are associated with weight loss, episodic diarrhea, and malabsorption syndrome due to the blocked nutrient absorption.",True,Giardiasis,,,,
90f2dfaa-a053-48ac-b20e-c3c2a6bb5339,https://open.oregonstate.education/microbiology/,19.5	Protozoan Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-5protozoan-infections-of-the-gastrointestinal-tract/,"Diagnosis may be made using observation under the microscope. A stool ova and parasite (O&P) exam involves direct examination of a stool sample for the presence of cysts and trophozoites; it can be used to distinguish common parasitic intestinal infections. ELISA and other immunoassay tests, including commercial direct fluorescence antibody kits, are also used. The most common treatments use metronidazole as the first-line choice, followed by tinidazole. If the infection becomes chronic, the parasites may become resistant to medications.",True,Giardiasis,,,,
73cf43ec-eab0-4473-9b70-c1bf7b99c5dd,https://open.oregonstate.education/microbiology/,19.4	Viral Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-4viral-infections-of-the-gastrointestinal-tract/,Learning Objectives,False,Learning Objectives,,,,
a84069f5-7711-4295-8671-c60b59bfba97,https://open.oregonstate.education/microbiology/,19.4	Viral Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-4viral-infections-of-the-gastrointestinal-tract/,Gastroenteritis Caused by Rotaviruses,False,Gastroenteritis Caused by Rotaviruses,,,,
128e899e-15ad-4038-91fe-78c4c11bf593,https://open.oregonstate.education/microbiology/,19.4	Viral Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-4viral-infections-of-the-gastrointestinal-tract/,"Rotaviruses are double-stranded RNA viruses in the family Reoviridae. They are responsible for common diarrheal illness, although prevention through vaccination is becoming more common. The virus is primarily spread by the fecal-oral route (Figure 19.14).",True,Gastroenteritis Caused by Rotaviruses,Figure 19.14,19.4	Viral Infections of the Gastrointestinal Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-24.24.png,Figure 19.14 Rotaviruses in a fecal sample are visualized using electron microscopy. (credit: Dr. Graham Beards)
d36bb41e-82a1-48a5-a6e3-72210600e56f,https://open.oregonstate.education/microbiology/,19.4	Viral Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-4viral-infections-of-the-gastrointestinal-tract/,"Infected individuals exhibit fever, vomiting, and diarrhea. The virus can survive in the stomach following a meal, but is normally found in the small intestines, particularly the epithelial cells on the villi. Infection can cause food intolerance, especially with respect to lactose. The illness generally appears after an incubation period of about two days and lasts for approximately one week (three to eight days). Without supportive treatment, the illness can cause severe fluid loss, dehydration, and even death. Even with milder illness, repeated infections can potentially lead to malnutrition, especially in developing countries, where rotavirus infection is common due to poor sanitation and lack of access to clean drinking water. Patients (especially children) who are malnourished after an episode of diarrhea are more susceptible to future diarrheal illness, increasing their risk of death from rotavirus infection.",True,Gastroenteritis Caused by Rotaviruses,,,,
030c7a5c-ce4c-43fc-84b6-40dfc85620c0,https://open.oregonstate.education/microbiology/,19.4	Viral Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-4viral-infections-of-the-gastrointestinal-tract/,"The most common clinical tool for diagnosis is enzyme immunoassay, which detects the virus from fecal samples. Latex agglutination assays are also used. Additionally, the virus can be detected using electron microscopy and RT- PCR.",True,Gastroenteritis Caused by Rotaviruses,,,,
bad78fdd-8725-40df-a6ef-df24f865c538,https://open.oregonstate.education/microbiology/,19.4	Viral Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-4viral-infections-of-the-gastrointestinal-tract/,"Treatment is supportive with oral rehydration therapy. Preventive vaccination is also available. In the United States, rotavirus vaccines are part of the standard vaccine schedule and administration follows the guidelines of the World Health Organization (WHO). The WHO recommends that all infants worldwide receive the rotavirus vaccine, the first dose between six and 15 weeks of age and the second before 32 weeks.[4]",True,Gastroenteritis Caused by Rotaviruses,,,,
106f3f12-9980-4c12-b01b-02233db5b63f,https://open.oregonstate.education/microbiology/,19.4	Viral Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-4viral-infections-of-the-gastrointestinal-tract/,"Noroviruses, commonly identified as Norwalk viruses, are caliciviruses. Several strains can cause gastroenteritis. There are millions of cases a year, predominately in infants, young children, and the elderly. These viruses are easily transmitted and highly contagious. They are known for causing widespread infections in groups of people in confined spaces, such as on cruise ships. The viruses can be transmitted through direct contact, through touching contaminated surfaces, and through contaminated food. Because the virus is not killed by disinfectants used at standard concentrations for killing bacteria, the risk of transmission remains high, even after cleaning.",True,Gastroenteritis Caused by Rotaviruses,,,,
83bcc1cb-d25c-4272-ae54-e5dcf89e476f,https://open.oregonstate.education/microbiology/,19.4	Viral Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-4viral-infections-of-the-gastrointestinal-tract/,"The signs and symptoms of norovirus infection are similar to those for rotavirus, with watery diarrhea, mild cramps, and fever. Additionally, these viruses sometimes cause projectile vomiting. The illness is usually relatively mild, develops 12 to 48 hours after exposure, and clears within a couple of days without treatment. However, dehydration may occur.",True,Gastroenteritis Caused by Rotaviruses,,,,
4a0d21ba-58c7-4c22-abc7-23729bce624e,https://open.oregonstate.education/microbiology/,19.4	Viral Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-4viral-infections-of-the-gastrointestinal-tract/,"Norovirus can be detected using PCR or enzyme immunoassay (EIA) testing. RT-qPCR is the preferred approach as EIA is insufficiently sensitive. If EIA is used for rapid testing, diagnosis should be confirmed using PCR. No medications are available, but the illness is usually self-limiting. Rehydration therapy and electrolyte replacement may be used. Good hygiene, hand washing, and careful food preparation reduce the risk of infection.",True,Gastroenteritis Caused by Rotaviruses,,,,
11497d77-bf6c-41d8-abca-151f6e9f5612,https://open.oregonstate.education/microbiology/,19.4	Viral Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-4viral-infections-of-the-gastrointestinal-tract/,Learning Objectives,False,Learning Objectives,,,,
39db4dce-2ecd-428a-86bf-bf484d4c273c,https://open.oregonstate.education/microbiology/,19.4	Viral Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-4viral-infections-of-the-gastrointestinal-tract/,Gastroenteritis Caused by Rotaviruses,False,Gastroenteritis Caused by Rotaviruses,,,,
2edbb4db-2bd8-41ee-9799-5d3a06d74fef,https://open.oregonstate.education/microbiology/,19.4	Viral Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-4viral-infections-of-the-gastrointestinal-tract/,"Rotaviruses are double-stranded RNA viruses in the family Reoviridae. They are responsible for common diarrheal illness, although prevention through vaccination is becoming more common. The virus is primarily spread by the fecal-oral route (Figure 19.14).",True,Gastroenteritis Caused by Rotaviruses,Figure 19.14,19.4	Viral Infections of the Gastrointestinal Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-24.24.png,Figure 19.14 Rotaviruses in a fecal sample are visualized using electron microscopy. (credit: Dr. Graham Beards)
7115e14e-2727-4011-9cd8-1d4417fe8ab3,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Most bacterial gastrointestinal illness is short-lived and self-limiting; however, loss of fluids due to severe diarrheal illness can lead to dehydration that can, in some cases, be fatal without proper treatment. Oral rehydration therapy with electrolyte solutions is an essential aspect of treatment for most patients with GI disease, especially in children and infants.",True,Gastroenteritis Caused by Rotaviruses,,,,
11be00d7-39ad-403c-a58c-834e3d3fedf1,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,Staphylococcal Food Poisoning,False,Staphylococcal Food Poisoning,,,,
4b5dcb1c-68e8-46ba-a9ef-6b788a37956a,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Staphylococcal food poisoning is one form of food intoxication. When Staphylococcus aureus grows in food, it may produce enterotoxins that, when ingested, can cause symptoms such as nausea, diarrhea, cramping, and vomiting within one to six hours. In some severe cases, it may cause headache, dehydration, and changes in blood pressure and heart rate. Signs and symptoms resolve within 24 to 48 hours. S. aureus is often associated with a variety of raw or undercooked and cooked foods including meat (e.g., canned meat, ham, and sausages) and dairy products (e.g., cheeses, milk, and butter). It is also commonly found on hands and can be transmitted to prepared foods through poor hygiene, including poor handwashing and the use of contaminated food preparation surfaces, such as cutting boards. The greatest risk is for food left at a temperature below 60 °C (140 °F), which allows the bacteria to grow. Cooked foods should generally be reheated to at least 60 °C (140 °F) for safety and most raw meats should be cooked to even higher internal temperatures (Figure 19.10).",True,Staphylococcal Food Poisoning,,,,
55062df9-21fc-4b5f-98f7-dd1aecaf8673,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"There are at least 21 Staphylococcal enterotoxins and Staphylococcal enterotoxin-like toxins that can cause food intoxication. The enterotoxins are proteins that are resistant to low pH, allowing them to pass through the stomach. They are heat stable and are not destroyed by boiling at 100 °C. Even though the bacterium itself may be killed, the enterotoxins alone can cause vomiting and diarrhea, although the mechanisms are not fully understood. At least some of the symptoms may be caused by the enterotoxin functioning as a superantigen and provoking a strong immune response by activating T cell proliferation.",True,Staphylococcal Food Poisoning,,,,
43a1e9ae-9738-45d7-822e-d0f99d678c30,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"The rapid onset of signs and symptoms helps to diagnose this foodborne illness. Because the bacterium does not need to be present for the toxin to cause symptoms, diagnosis is confirmed by identifying the toxin in a food sample or in biological specimens (feces or vomitus) from the patient. Serological techniques, including ELISA, can also be used to identify the toxin in food samples.",True,Staphylococcal Food Poisoning,,,,
070513e6-89eb-4945-8909-cccc4741c243,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"The condition generally resolves relatively quickly, within 24 hours, without treatment. In some cases, supportive treatment in a hospital may be needed.",True,Staphylococcal Food Poisoning,,,,
fe53ec1a-fa55-4c72-b621-18f01d505cfc,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,E. coli Infections,True,Staphylococcal Food Poisoning,,,,
43ac3d53-1adb-4f43-9159-aaa6d350d460,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"The gram-negative rod Escherichia coli is a common member of the normal microbiota of the colon. Although the vast majority of E. coli strains are helpful commensal bacteria, some can be pathogenic and may cause dangerous diarrheal disease. The pathogenic strains have additional virulence factors such as type 1 fimbriae that promote colonization of the colon or may produce toxins. These virulence factors are acquired through horizontal gene transfer.",True,Staphylococcal Food Poisoning,,,,
2c368d78-61c9-48d1-9f8f-41ec6ca9fbd9,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Extraintestinal disease can result if the bacteria spread from the gastrointestinal tract. Although these bacteria can be spread from person to person, they are often acquired through contaminated food or water. There are six recognized pathogenic groups of E. coli, but we will focus here on the four that are most commonly transmitted through food and water.",True,Staphylococcal Food Poisoning,,,,
037da792-145c-4b6b-a5a2-a323dfd82495,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Enterotoxigenic E. coli (ETEC), also known as traveler’s diarrhea, causes diarrheal illness and is common in less developed countries. In Mexico, ETEC infection is called Montezuma’s Revenge. Following ingestion of contaminated food or water, infected individuals develop a watery diarrhea, abdominal cramps, malaise (a feeling of being unwell), and a low fever. ETEC produces a heat-stable enterotoxin similar to cholera toxin, and adhesins called colonization factors that help the bacteria to attach to the intestinal wall. Some strains of ETEC also produce heat-labile toxins. The disease is usually relatively mild and self-limiting. Diagnosis involves culturing and PCR. If needed, antibiotic treatment with fluoroquinolones, doxycycline, rifaximin, and trimethoprim-sulfamethoxazole (TMP/SMZ) may shorten infection duration. However, antibiotic resistance is a problem.",True,Staphylococcal Food Poisoning,,,,
20c73cd5-db68-4438-bc66-2b0fda1b18cf,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Enteroinvasive E. coli (EIEC) is very similar to shigellosis, including its pathogenesis of intracellular invasion into intestinal epithelial tissue. This bacterium carries a large plasmid that is involved in epithelial cell penetration. The illness is usually self-limiting, with symptoms including watery diarrhea, chills, cramps, malaise, fever, and dysentery. Culturing and PCR testing can be used for diagnosis. Antibiotic treatment is not recommended, so supportive therapy is used if needed.",True,Staphylococcal Food Poisoning,,,,
1483758b-82ed-4794-8c05-061ec01094ab,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Enteropathogenic E. coli (EPEC) can cause a potentially fatal diarrhea, especially in infants and those in less developed countries. Fever, vomiting, and diarrhea can lead to severe dehydration. These E. coli inject a protein that attaches to the surface of the intestinal epithelial cells and triggers rearrangement of host cell actin from microvilli to pedestals. The protein also happens to be the receptor for a surface protein produced by EPEC, thereby allowing E. coli to “sit” on the pedestal. As with ETEC, diagnosis involves culturing and PCR. Treatment is similar to that for ETEC.",True,Staphylococcal Food Poisoning,,,,
3e9ec320-a016-496d-8ff4-ecb037b5546d,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"The most dangerous strains are enterohemorrhagic E. coli (EHEC), which are the strains capable of causing epidemics. In particular, the strain O157:H7 has been responsible for several recent outbreaks. Recall that the O and H refer to surface antigens that contribute to pathogenicity and trigger a host immune response (“O” refers to the O-side chain of the lipopolysaccharide and the “H” refers to the flagella). Similar to EPEC, EHEC also forms pedestals. EHEC also produces a Shiga-like toxin. Because the genome of this bacterium has been sequenced, it is known that the Shiga toxin genes were most likely acquired through transduction (horizontal gene transfer). The Shiga toxin genes originated from Shigella dysenteriae. Prophage from a bacteriophage that previously infected Shigella integrated into the chromosome of E. coli. The Shiga-like toxin is often called verotoxin.",True,Staphylococcal Food Poisoning,,,,
00902cd4-c035-4622-b291-0b34febf6931,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"EHEC can cause disease ranging from relatively mild to life-threatening. Symptoms include bloody diarrhea with severe cramping, but no fever. Although it is often self-limiting, it can lead to hemorrhagic colitis and profuse bleeding. One possible complication is HUS. Diagnosis involves culture, often using MacConkey with sorbitol agar to differentiate between E. coli O157:H7, which does not ferment sorbitol, and other less virulent strains of E. coli that can ferment sorbitol.",True,Staphylococcal Food Poisoning,,,,
6aa1ad5c-7b68-4b72-97bc-0881f9e04e1f,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Antibiotic therapy is not recommended and may worsen HUS because of the toxins released when the bacteria are killed, so supportive therapies must be used. Table 19.1 summarizes the characteristics of the four most common pathogenic groups.",True,Staphylococcal Food Poisoning,,,,
c3a7c6e6-d172-4550-aabe-70564a579103,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,Peptic Ulcers,False,Peptic Ulcers,,,,
34a1f18a-3997-4e22-8342-b948673280de,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"H. pylori colonizes epithelial cells in the stomach using pili for adhesion. These bacteria produce urease, which stimulates an immune response and creates ammonia that neutralizes stomach acids to provide a more hospitable microenvironment. The infection damages the cells of the stomach lining, including those that normally produce the protective mucus that serves as a barrier between the tissue and stomach acid. As a result, inflammation (gastritis) occurs and ulcers may slowly develop. Ulcer formation can also be caused by toxin activity. It has been reported that 50% of clinical isolates of H. pylori have detectable levels of exotoxin activity in vitro.[2]",True,Peptic Ulcers,,,,
efb48945-f4e5-4746-a8d6-1db763291cf0,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Signs and symptoms include nausea, lack of appetite, bloating, burping, and weight loss. Bleeding ulcers may produce dark stools. If no treatment is provided, the ulcers can become deeper, more tissues can be involved, and stomach perforation can occur. Because perforation allows digestive enzymes and acid to leak into the body, it is a very serious condition.",True,Peptic Ulcers,,,,
90f35237-8fe1-4cd1-bc29-46d7286a5abc,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"To diagnose H. pylori infection, multiple methods are available. In a breath test, the patient swallows radiolabeled urea. If H. pylori is present, the bacteria will produce urease to break down the urea. This reaction produces radiolabeled carbon dioxide that can be detected in the patient’s breath. Blood testing can also be used to detect antibodies to H. pylori. The bacteria themselves can be detected using either a stool test or a stomach wall biopsy.",True,Peptic Ulcers,,,,
cb634a7d-77b7-4f45-9a93-839ef212648a,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Antibiotics can be used to treat the infection. However, unique to H. pylori, the recommendation from the US Food and Drug Administration is to use a triple therapy. The current protocols are 10 days of treatment with omeprazole, amoxicillin, and clarithromycin (OAC); 14 days of treatment with bismuth subsalicylate, metronidazole, and tetracycline (BMT); or 10 or 14 days of treatment with lansoprazole, amoxicillin, and clarithromycin (LAC). Omeprazole, bismuth subsalicylate, and lansoprazole are not antibiotics but are instead used to decrease acid levels because H. pylori prefers acidic environments.",True,Peptic Ulcers,,,,
acb4aa5e-4991-4776-83aa-7c929166aa35,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Although treatment is often valuable, there are also risks to H. pylori eradication. Infection with H. pylori may actually protect against some cancers, such as esophageal adenocarcinoma and gastroesophageal reflux disease.[3][4]",True,Peptic Ulcers,,,,
d4640da7-1fe0-4167-899e-5525a6b03b8a,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,Clostridium difficile,False,Clostridium difficile,,,,
b687fb06-34dd-4b89-b7e3-c0059d6d78ce,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,Clostridium difficile,False,Clostridium difficile,,,,
970da1a7-3d32-4616-ad71-33a433dda407,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Clostridium difficile is a gram-positive rod that can be a commensal bacterium as part of the normal microbiota of healthy individuals. When the normal microbiota is disrupted by long-term antibiotic use, it can allow the overgrowth of this bacterium, resulting in antibiotic-associated diarrhea caused by C. difficile. Antibiotic-associated diarrhea can also be considered a nosocomial disease. Patients at the greatest risk of C. difficile infection are those who are immunocompromised, have been in health-care settings for extended periods, are older, have recently taken antibiotics, have had gastrointestinal procedures done, or use proton pump inhibitors, which reduce stomach acidity and allow proliferation of C. difficile. Because this species can form endospores, it can survive for extended periods of time in the environment under harsh conditions and is a considerable concern in health-care settings.",True,Clostridium difficile,,,,
70779e8f-5b6f-4c72-85cd-326cdb8e1220,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"This bacterium produces two toxins, Clostridium difficile toxin A (TcdA) and Clostridium difficile toxin B (TcdB). These toxins inactivate small GTP-binding proteins, resulting in actin condensation and cell rounding, followed by cell death. Infections begin with focal necrosis, then ulceration with exudate, and can progress to pseudomembranous colitis, which involves inflammation of the colon and the development of a pseudomembrane of fibrin containing dead epithelial cells and leukocytes (Figure 19.12). Watery diarrhea, dehydration, fever, loss of appetite, and abdominal pain can result. Perforation of the colon can occur, leading to septicemia, shock, and death. C. difficile is also associated with necrotizing enterocolitis in premature babies and neutropenic enterocolitis associated with cancer therapies.",True,Clostridium difficile,Figure 19.12,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-24.21.png,"Figure 19.12 Clostridium difficile is able to colonize the mucous membrane of the colon when the normal microbiota is disrupted. The toxins TcdA and TcdB trigger an immune response, with neutrophils and monocytes migrating from the bloodstream to the site of infection. Over time, inflammation and dead cells contribute to the development of a pseudomembrane. (credit micrograph: modification of work by Janice Carr, Centers for Disease Control and Prevention)"
a41fd7e8-b1cd-4511-a88f-ebfe7f18cba6,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Diagnosis is made by considering the patient history (such as exposure to antibiotics), clinical presentation, imaging, endoscopy, lab tests, and other available data. Detecting the toxin in stool samples is used to confirm diagnosis. Although culture is preferred, it is rarely practical in clinical practice because the bacterium is an obligate anaerobe. Nucleic acid amplification tests, including PCR, are considered preferable to ELISA testing for molecular analysis.",True,Clostridium difficile,,,,
072fc0b0-fb83-432b-b49d-bd9360e1410a,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"The first step of conventional treatment is to stop antibiotic use, and then to provide supportive therapy with electrolyte replacement and fluids. Metronidazole is the preferred treatment if the C. difficile diagnosis has been confirmed. Vancomycin can also be used, but it should be reserved for patients for whom metronidazole was ineffective or who meet other criteria (e.g., under 10 years of age, pregnant, or allergic to metronidazole).",True,Clostridium difficile,,,,
1477f2f1-e60d-421d-96a5-bdf73d836c4f,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"The rapid onset of signs and symptoms helps to diagnose this foodborne illness. Because the bacterium does not need to be present for the toxin to cause symptoms, diagnosis is confirmed by identifying the toxin in a food sample or in biological specimens (feces or vomitus) from the patient. Serological techniques, including ELISA, can also be used to identify the toxin in food samples.",True,Clostridium difficile,,,,
68c704ee-1471-455f-b60f-55d8a51a8f12,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"The condition generally resolves relatively quickly, within 24 hours, without treatment. In some cases, supportive treatment in a hospital may be needed.",True,Clostridium difficile,,,,
73548cd6-ea28-4130-8bd0-ab9cc3958ff9,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,E. coli Infections,True,Clostridium difficile,,,,
8ba7ae66-d618-468f-a0c5-469c15fe6ce7,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"The gram-negative rod Escherichia coli is a common member of the normal microbiota of the colon. Although the vast majority of E. coli strains are helpful commensal bacteria, some can be pathogenic and may cause dangerous diarrheal disease. The pathogenic strains have additional virulence factors such as type 1 fimbriae that promote colonization of the colon or may produce toxins. These virulence factors are acquired through horizontal gene transfer.",True,Clostridium difficile,,,,
a9c31b11-f896-41c7-9a21-6300ce0a26cc,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Extraintestinal disease can result if the bacteria spread from the gastrointestinal tract. Although these bacteria can be spread from person to person, they are often acquired through contaminated food or water. There are six recognized pathogenic groups of E. coli, but we will focus here on the four that are most commonly transmitted through food and water.",True,Clostridium difficile,,,,
1da62ff5-978d-4111-874c-7ed5224fe8f1,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Enterotoxigenic E. coli (ETEC), also known as traveler’s diarrhea, causes diarrheal illness and is common in less developed countries. In Mexico, ETEC infection is called Montezuma’s Revenge. Following ingestion of contaminated food or water, infected individuals develop a watery diarrhea, abdominal cramps, malaise (a feeling of being unwell), and a low fever. ETEC produces a heat-stable enterotoxin similar to cholera toxin, and adhesins called colonization factors that help the bacteria to attach to the intestinal wall. Some strains of ETEC also produce heat-labile toxins. The disease is usually relatively mild and self-limiting. Diagnosis involves culturing and PCR. If needed, antibiotic treatment with fluoroquinolones, doxycycline, rifaximin, and trimethoprim-sulfamethoxazole (TMP/SMZ) may shorten infection duration. However, antibiotic resistance is a problem.",True,Clostridium difficile,,,,
1e97d1e2-d3b7-4ee1-a2d8-d1e0e8cfce98,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Enteroinvasive E. coli (EIEC) is very similar to shigellosis, including its pathogenesis of intracellular invasion into intestinal epithelial tissue. This bacterium carries a large plasmid that is involved in epithelial cell penetration. The illness is usually self-limiting, with symptoms including watery diarrhea, chills, cramps, malaise, fever, and dysentery. Culturing and PCR testing can be used for diagnosis. Antibiotic treatment is not recommended, so supportive therapy is used if needed.",True,Clostridium difficile,,,,
1a82eb98-bc0c-4c67-810d-789f06bbd625,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Enteropathogenic E. coli (EPEC) can cause a potentially fatal diarrhea, especially in infants and those in less developed countries. Fever, vomiting, and diarrhea can lead to severe dehydration. These E. coli inject a protein that attaches to the surface of the intestinal epithelial cells and triggers rearrangement of host cell actin from microvilli to pedestals. The protein also happens to be the receptor for a surface protein produced by EPEC, thereby allowing E. coli to “sit” on the pedestal. As with ETEC, diagnosis involves culturing and PCR. Treatment is similar to that for ETEC.",True,Clostridium difficile,,,,
467a70be-5950-42d2-a3e8-d2c124d0bb7c,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"The most dangerous strains are enterohemorrhagic E. coli (EHEC), which are the strains capable of causing epidemics. In particular, the strain O157:H7 has been responsible for several recent outbreaks. Recall that the O and H refer to surface antigens that contribute to pathogenicity and trigger a host immune response (“O” refers to the O-side chain of the lipopolysaccharide and the “H” refers to the flagella). Similar to EPEC, EHEC also forms pedestals. EHEC also produces a Shiga-like toxin. Because the genome of this bacterium has been sequenced, it is known that the Shiga toxin genes were most likely acquired through transduction (horizontal gene transfer). The Shiga toxin genes originated from Shigella dysenteriae. Prophage from a bacteriophage that previously infected Shigella integrated into the chromosome of E. coli. The Shiga-like toxin is often called verotoxin.",True,Clostridium difficile,,,,
df299b4a-6395-4816-8c51-e315f89242f3,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"EHEC can cause disease ranging from relatively mild to life-threatening. Symptoms include bloody diarrhea with severe cramping, but no fever. Although it is often self-limiting, it can lead to hemorrhagic colitis and profuse bleeding. One possible complication is HUS. Diagnosis involves culture, often using MacConkey with sorbitol agar to differentiate between E. coli O157:H7, which does not ferment sorbitol, and other less virulent strains of E. coli that can ferment sorbitol.",True,Clostridium difficile,,,,
b307f6ce-4eca-4590-b6fb-cd69161600da,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Antibiotic therapy is not recommended and may worsen HUS because of the toxins released when the bacteria are killed, so supportive therapies must be used. Table 19.1 summarizes the characteristics of the four most common pathogenic groups.",True,Clostridium difficile,,,,
96aae49d-1ae5-49b9-9dfc-16a91a1ae39e,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,Peptic Ulcers,False,Peptic Ulcers,,,,
15717ee1-05aa-4e10-b4ff-ce76510f306e,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"H. pylori colonizes epithelial cells in the stomach using pili for adhesion. These bacteria produce urease, which stimulates an immune response and creates ammonia that neutralizes stomach acids to provide a more hospitable microenvironment. The infection damages the cells of the stomach lining, including those that normally produce the protective mucus that serves as a barrier between the tissue and stomach acid. As a result, inflammation (gastritis) occurs and ulcers may slowly develop. Ulcer formation can also be caused by toxin activity. It has been reported that 50% of clinical isolates of H. pylori have detectable levels of exotoxin activity in vitro.[2]",True,Peptic Ulcers,,,,
fc0ff5e4-7f14-4741-81d4-e3f0b35af581,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Signs and symptoms include nausea, lack of appetite, bloating, burping, and weight loss. Bleeding ulcers may produce dark stools. If no treatment is provided, the ulcers can become deeper, more tissues can be involved, and stomach perforation can occur. Because perforation allows digestive enzymes and acid to leak into the body, it is a very serious condition.",True,Peptic Ulcers,,,,
390e0b25-150e-441d-a327-b7d00e4c1ce6,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Antibiotics can be used to treat the infection. However, unique to H. pylori, the recommendation from the US Food and Drug Administration is to use a triple therapy. The current protocols are 10 days of treatment with omeprazole, amoxicillin, and clarithromycin (OAC); 14 days of treatment with bismuth subsalicylate, metronidazole, and tetracycline (BMT); or 10 or 14 days of treatment with lansoprazole, amoxicillin, and clarithromycin (LAC). Omeprazole, bismuth subsalicylate, and lansoprazole are not antibiotics but are instead used to decrease acid levels because H. pylori prefers acidic environments.",True,Peptic Ulcers,,,,
d2c1b5c2-8e59-4a79-bac0-e4d6eed199e6,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Although treatment is often valuable, there are also risks to H. pylori eradication. Infection with H. pylori may actually protect against some cancers, such as esophageal adenocarcinoma and gastroesophageal reflux disease.[3][4]",True,Peptic Ulcers,,,,
9b7e2d5e-9864-44ef-873c-bd8a166369bf,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,Clostridium difficile,False,Clostridium difficile,,,,
2d036f0e-bc4b-4922-b935-e506dc8844b5,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"This bacterium produces two toxins, Clostridium difficile toxin A (TcdA) and Clostridium difficile toxin B (TcdB). These toxins inactivate small GTP-binding proteins, resulting in actin condensation and cell rounding, followed by cell death. Infections begin with focal necrosis, then ulceration with exudate, and can progress to pseudomembranous colitis, which involves inflammation of the colon and the development of a pseudomembrane of fibrin containing dead epithelial cells and leukocytes (Figure 19.12). Watery diarrhea, dehydration, fever, loss of appetite, and abdominal pain can result. Perforation of the colon can occur, leading to septicemia, shock, and death. C. difficile is also associated with necrotizing enterocolitis in premature babies and neutropenic enterocolitis associated with cancer therapies.",True,Clostridium difficile,Figure 19.12,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-24.21.png,"Figure 19.12 Clostridium difficile is able to colonize the mucous membrane of the colon when the normal microbiota is disrupted. The toxins TcdA and TcdB trigger an immune response, with neutrophils and monocytes migrating from the bloodstream to the site of infection. Over time, inflammation and dead cells contribute to the development of a pseudomembrane. (credit micrograph: modification of work by Janice Carr, Centers for Disease Control and Prevention)"
ce00cef2-4381-4c62-924c-f1a12f0fac5f,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"Diagnosis is made by considering the patient history (such as exposure to antibiotics), clinical presentation, imaging, endoscopy, lab tests, and other available data. Detecting the toxin in stool samples is used to confirm diagnosis. Although culture is preferred, it is rarely practical in clinical practice because the bacterium is an obligate anaerobe. Nucleic acid amplification tests, including PCR, are considered preferable to ELISA testing for molecular analysis.",True,Clostridium difficile,,,,
6e5a1178-c396-4d9b-b5ea-6fe41d644509,https://open.oregonstate.education/microbiology/,19.3	Bacterial Infections of the Gastrointestinal Tract,https://open.oregonstate.education/microbiology/chapter/24-3bacterial-infections-of-the-gastrointestinal-tract/,"The first step of conventional treatment is to stop antibiotic use, and then to provide supportive therapy with electrolyte replacement and fluids. Metronidazole is the preferred treatment if the C. difficile diagnosis has been confirmed. Vancomycin can also be used, but it should be reserved for patients for whom metronidazole was ineffective or who meet other criteria (e.g., under 10 years of age, pregnant, or allergic to metronidazole).",True,Clostridium difficile,,,,
386c72c1-ff2d-4cd8-8a6d-5c45f5d1acd2,https://open.oregonstate.education/microbiology/,19.2	Microbial Diseases of the Mouth and Oral Cavity,https://open.oregonstate.education/microbiology/chapter/24-2microbial-diseases-of-the-mouth-and-oral-cavity/,Dental Caries,False,Dental Caries,,,,
166f8277-cc99-46f2-8eb7-22d262bb7674,https://open.oregonstate.education/microbiology/,19.2	Microbial Diseases of the Mouth and Oral Cavity,https://open.oregonstate.education/microbiology/chapter/24-2microbial-diseases-of-the-mouth-and-oral-cavity/,"Cavities of the teeth, known clinically as dental caries, are microbial lesions that cause damage to the teeth. Over time, the lesion can grow through the outer enamel layer to infect the underlying dentin or even the innermost pulp. If dental caries are not treated, the infection can become an abscess that spreads to the deeper tissues of the teeth, near the roots, or to the bloodstream.",True,Dental Caries,,,,
317f1ecc-5e11-42b8-a6e2-5023fd82798b,https://open.oregonstate.education/microbiology/,19.2	Microbial Diseases of the Mouth and Oral Cavity,https://open.oregonstate.education/microbiology/chapter/24-2microbial-diseases-of-the-mouth-and-oral-cavity/,"Tooth decay results from the metabolic activity of microbes that live on the teeth. A layer of proteins and carbohydrates forms when clean teeth come into contact with saliva. Microbes are attracted to this food source and form a biofilm called plaque. The most important cariogenic species in these biofilms is Streptococcus mutans. When sucrose, a disaccharide sugar from food, is broken down by bacteria in the mouth, glucose and fructose are produced. The glucose is used to make dextran, which is part of the extracellular matrix of the biofilm. Fructose is fermented, producing organic acids such as lactic acid. These acids dissolve the minerals of the tooth, including enamel, even though it is the hardest material in the body. The acids work even more quickly on exposed dentin (Figure 19.7). Over time, the plaque biofilm can become thick and eventually calcify. When a heavy plaque deposit becomes hardened in this way, it is called tartar or dental calculus (Figure 19.8). These substantial plaque biofilms can include a variety of bacterial species, including Streptococcus and Actinomyces species.",True,Dental Caries,Figure 19.7,19.2	Microbial Diseases of the Mouth and Oral Cavity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-24.7.png,"Figure 19.7 Tooth decay occurs in stages. When bacterial biofilms (plaque) develop on teeth, the acids produced gradually dissolve the enamel, followed by the dentin. Eventually, if left untreated, the lesion may reach the pulp and cause an abscess. (credit: modification of work by “BruceBlaus”/Wikimedia Commons)"
63dfadce-5ad6-4a92-9f52-a81c2fbef9a5,https://open.oregonstate.education/microbiology/,19.2	Microbial Diseases of the Mouth and Oral Cavity,https://open.oregonstate.education/microbiology/chapter/24-2microbial-diseases-of-the-mouth-and-oral-cavity/,"Some tooth decay is visible from the outside, but it is not always possible to see all decay or the extent of the decay. X-ray imaging is used to produce radiographs that can be studied to look for deeper decay and damage to the root or bone (Figure 19.8). If not detected, the decay can reach the pulp or even spread to the bloodstream. Painful abscesses can develop.",True,Dental Caries,Figure 19.8,19.2	Microbial Diseases of the Mouth and Oral Cavity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-24.8.png,Figure 19.8 (a) Tartar (dental calculus) is visible at the bases of these teeth. The darker deposits higher on the crowns are staining. (b) This tooth shows only a small amount of visible decay. (c) An X-ray of the same tooth shows that there is a dark area representing more decay inside the tooth. (d) Removal of a portion of the crown reveals the area of damage. (e) All of the cavity must be removed before filling. (credit: modification of work by “DRosenbach”/Wikimedia Commons)
c354e680-912d-464a-9718-48a7d2b7ed3a,https://open.oregonstate.education/microbiology/,19.2	Microbial Diseases of the Mouth and Oral Cavity,https://open.oregonstate.education/microbiology/chapter/24-2microbial-diseases-of-the-mouth-and-oral-cavity/,"To prevent tooth decay, prophylactic treatment and good hygiene are important. Regular tooth brushing and flossing physically removes microbes and combats microbial growth and biofilm formation. Toothpaste contains fluoride, which becomes incorporated into the hydroxyapatite of tooth enamel, protecting it against acidity caused by fermentation of mouth microbiota. Fluoride is also bacteriostatic, thus slowing enamel degradation. Antiseptic mouthwashes commonly contain plant-derived phenolics like thymol and eucalyptol and/or heavy metals like zinc chloride. Phenolics tend to be stable and persistent on surfaces, and they act through denaturing proteins and disrupting membranes.",True,Dental Caries,,,,
5359ecfd-0ab2-4a95-b86c-68d4a08ee6cc,https://open.oregonstate.education/microbiology/,19.2	Microbial Diseases of the Mouth and Oral Cavity,https://open.oregonstate.education/microbiology/chapter/24-2microbial-diseases-of-the-mouth-and-oral-cavity/,"Regular dental cleanings allow for the detection of decay at early stages and the removal of tartar. They may also help to draw attention to other concerns, such as damage to the enamel from acidic drinks. Reducing sugar consumption may help prevent damage that results from the microbial fermentation of sugars. Additionally, sugarless candies or gum with sugar alcohols (such as xylitol) can reduce the production of acids because these are fermented to nonacidic compounds (although excess consumption may lead to gastrointestinal distress). Fluoride treatment or ingesting fluoridated water strengthens the minerals in teeth and reduces the incidence of dental caries.",True,Dental Caries,,,,
c328db6e-c2c8-477c-84ed-2e13c824abaa,https://open.oregonstate.education/microbiology/,19.2	Microbial Diseases of the Mouth and Oral Cavity,https://open.oregonstate.education/microbiology/chapter/24-2microbial-diseases-of-the-mouth-and-oral-cavity/,"If caries develop, prompt treatment prevents worsening. Smaller areas of decay can be drilled to remove affected tissue and then filled. If the pulp is affected, then a root canal may be needed to completely remove the infected tissues to avoid continued spread of the infection, which could lead to painful abscesses.",True,Dental Caries,,,,
fb8a15c2-d62c-433f-a495-b1ed82590a3c,https://open.oregonstate.education/microbiology/,19.2	Microbial Diseases of the Mouth and Oral Cavity,https://open.oregonstate.education/microbiology/chapter/24-2microbial-diseases-of-the-mouth-and-oral-cavity/,"Additionally, poor oral health can contribute to the development of disease. Increased bacterial growth in the mouth can cause inflammation and infection in other parts of the body. For example, Streptococcus in the mouth, the main contributor to biofilms on teeth, tartar, and dental caries, can spread throughout the body when there is damage to the tissues inside the mouth, as can happen during dental work. S. mutans produces a surface adhesin known as P1, which binds to salivary agglutinin on the surface of the tooth. P1 can also bind to extracellular matrix proteins including fibronectin and collagen. When Streptococcus enters the bloodstream as a result of tooth brushing or dental cleaning, it causes inflammation that can lead to the accumulation of plaque in the arteries and contribute to the development of atherosclerosis, a condition associated with cardiovascular disease, heart attack, and stroke. In some cases, bacteria that spread through the blood vessels can lodge in the heart and cause endocarditis (an example of a focal infection).",True,Dental Caries,,,,
620a1f20-3b3d-432e-815f-fcdb5af94d78,https://open.oregonstate.education/microbiology/,19.2	Microbial Diseases of the Mouth and Oral Cavity,https://open.oregonstate.education/microbiology/chapter/24-2microbial-diseases-of-the-mouth-and-oral-cavity/,"To prevent tooth decay, prophylactic treatment and good hygiene are important. Regular tooth brushing and flossing physically removes microbes and combats microbial growth and biofilm formation. Toothpaste contains fluoride, which becomes incorporated into the hydroxyapatite of tooth enamel, protecting it against acidity caused by fermentation of mouth microbiota. Fluoride is also bacteriostatic, thus slowing enamel degradation. Antiseptic mouthwashes commonly contain plant-derived phenolics like thymol and eucalyptol and/or heavy metals like zinc chloride. Phenolics tend to be stable and persistent on surfaces, and they act through denaturing proteins and disrupting membranes.",True,Dental Caries,,,,
5f8eb867-3032-45a8-b946-ab825857353f,https://open.oregonstate.education/microbiology/,19.2	Microbial Diseases of the Mouth and Oral Cavity,https://open.oregonstate.education/microbiology/chapter/24-2microbial-diseases-of-the-mouth-and-oral-cavity/,"Regular dental cleanings allow for the detection of decay at early stages and the removal of tartar. They may also help to draw attention to other concerns, such as damage to the enamel from acidic drinks. Reducing sugar consumption may help prevent damage that results from the microbial fermentation of sugars. Additionally, sugarless candies or gum with sugar alcohols (such as xylitol) can reduce the production of acids because these are fermented to nonacidic compounds (although excess consumption may lead to gastrointestinal distress). Fluoride treatment or ingesting fluoridated water strengthens the minerals in teeth and reduces the incidence of dental caries.",True,Dental Caries,,,,
2f94fc2f-9505-4fa7-9963-ebb5b992eaa3,https://open.oregonstate.education/microbiology/,19.2	Microbial Diseases of the Mouth and Oral Cavity,https://open.oregonstate.education/microbiology/chapter/24-2microbial-diseases-of-the-mouth-and-oral-cavity/,"If caries develop, prompt treatment prevents worsening. Smaller areas of decay can be drilled to remove affected tissue and then filled. If the pulp is affected, then a root canal may be needed to completely remove the infected tissues to avoid continued spread of the infection, which could lead to painful abscesses.",True,Dental Caries,,,,
efac77f9-0039-415c-9557-18152a637645,https://open.oregonstate.education/microbiology/,19.2	Microbial Diseases of the Mouth and Oral Cavity,https://open.oregonstate.education/microbiology/chapter/24-2microbial-diseases-of-the-mouth-and-oral-cavity/,"Additionally, poor oral health can contribute to the development of disease. Increased bacterial growth in the mouth can cause inflammation and infection in other parts of the body. For example, Streptococcus in the mouth, the main contributor to biofilms on teeth, tartar, and dental caries, can spread throughout the body when there is damage to the tissues inside the mouth, as can happen during dental work. S. mutans produces a surface adhesin known as P1, which binds to salivary agglutinin on the surface of the tooth. P1 can also bind to extracellular matrix proteins including fibronectin and collagen. When Streptococcus enters the bloodstream as a result of tooth brushing or dental cleaning, it causes inflammation that can lead to the accumulation of plaque in the arteries and contribute to the development of atherosclerosis, a condition associated with cardiovascular disease, heart attack, and stroke. In some cases, bacteria that spread through the blood vessels can lodge in the heart and cause endocarditis (an example of a focal infection).",True,Dental Caries,,,,
019b6233-0344-42af-a0d7-def26143b82f,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,"The digestive system contains normal microbiota, including archaea, bacteria, fungi, protists, and even viruses. Because this microbiota is important for normal functioning of the digestive system, alterations to the microbiota by antibiotics or diet can be harmful. Additionally, the introduction of pathogens to the GI tract can cause infections and diseases. In this section, we will review the microbiota found in a healthy digestive tract and the general signs and symptoms associated with oral and GI infections.",True,Dental Caries,,,,
6130041d-3816-43cf-b848-2f3ae26dd373,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,Anatomy and Normal Microbiota of the Oral Cavity,False,Anatomy and Normal Microbiota of the Oral Cavity,,,,
a223048a-75c0-4374-b562-d9efe56ac421,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,"Microbes such as bacteria and archaea are abundant in the mouth and coat all of the surfaces of the oral cavity. However, different structures, such as the teeth or cheeks, host unique communities of both aerobic and anaerobic microbes. Some factors appear to work against making the mouth hospitable to certain microbes. For example, chewing allows microbes to mix better with saliva so they can be swallowed or spit out more easily. Saliva also contains enzymes, including lysozyme, which can damage microbial cells. Recall that lysozyme is part of the first line of defense in the innate immune system and cleaves the β-(1,4) glycosidic linkages between N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM) in bacterial peptidoglycan (see Chemical Defenses). Additionally, fluids containing immunoglobulins and phagocytic cells are produced in the gingival spaces. Despite all of these chemical and mechanical activities, the mouth supports a large microbial community.",True,Anatomy and Normal Microbiota of the Oral Cavity,,,,
5c52a285-4e6e-4688-8cfe-d6954f63da5e,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,Anatomy and Normal Microbiota of the GI Tract,False,Anatomy and Normal Microbiota of the GI Tract,,,,
f509d41a-2903-4e79-8eb2-ed2b30159be3,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,"As food leaves the oral cavity, it travels through the pharynx, or the back of the throat, and moves into the esophagus, which carries the food from the pharynx to the stomach without adding any additional digestive enzymes. The stomach produces mucus to protect its lining, as well as digestive enzymes and acid to break down food. Partially digested food then leaves the stomach through the pyloric sphincter, reaching the first part of the small intestine called the duodenum. Pancreatic juice, which includes enzymes and bicarbonate ions, is released into the small intestine to neutralize the acidic material from the stomach and to assist in digestion. Bile, produced by the liver but stored in the gallbladder, is also released into the small intestine to emulsify fats so that they can travel in the watery environment of the small intestine. Digestion continues in the small intestine, where the majority of nutrients contained in the food are absorbed. Simple columnar epithelial cells called enterocytes line the lumen surface of the small intestinal folds called villi. Each enterocyte has smaller microvilli (cytoplasmic membrane extensions) on the cellular apical surface that increase the surface area to allow more absorption of nutrients to occur (Figure 19.5).",True,Anatomy and Normal Microbiota of the GI Tract,Figure 19.5,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-24.5.png,"Figure 19.5 (a) The structure of the wall of the small intestine allows for the majority of nutrient absorption in the body. (b) Villi are folds in the surface of the small intestine. Microvilli are cytoplasmic extensions on individual cells that increase the surface area for absorption. (c) A light micrograph shows the shape of the villi. (d) An electron micrograph shows the shape of the microvilli. (credit b, c, d: Modification of micrographs provided by the Regents of University of Michigan Medical School © 2012)"
388ca3d7-dfac-4f46-940d-e7a8affc22d2,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,"The environment of most of the GI tract is harsh, which serves two purposes: digestion and immunity. The stomach is an extremely acidic environment (pH 1.5–3.5) due to the gastric juices that break down food and kill many ingested microbes; this helps prevent infection from pathogens. The environment in the small intestine is less harsh and is able to support microbial communities. Microorganisms present in the small intestine can include lactobacilli, diptherioids and the fungus Candida. On the other hand, the large intestine (colon) contains a diverse and abundant microbiota that is important for normal function. These microbes include Bacteriodetes (especially the genera Bacteroides  and Prevotella) and Firmicutes (especially members of the genus Clostridium). Methanogenic archaea and some fungi are also present, among many other species of bacteria. These microbes all aid in digestion and contribute to the production of feces, the waste excreted from the digestive tract, and flatus, the gas produced from microbial fermentation of undigested food. They can also produce valuable nutrients. For example, lactic acid bacteria such as bifidobacteria can synthesize vitamins, such as vitamin B12, folate, and riboflavin, that humans cannot synthesize themselves. E. coli found in the intestine can also break down food and help the body produce vitamin K, which is important for blood coagulation.",True,Anatomy and Normal Microbiota of the GI Tract,,,,
a05071cd-a20b-46b0-9ab4-e4fa86aa7fbe,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,"The GI tract has several other methods of reducing the risk of infection by pathogens. Small aggregates of underlying lymphoid tissue in the ileum, called Peyer’s patches (Figure 19.5), detect pathogens in the intestines via microfold (M) cells, which transfer antigens from the lumen of the intestine to the lymphocytes on Peyer’s patches to induce an immune response. The Peyer’s patches then secrete IgA and other pathogen-specific antibodies into the intestinal lumen to help keep intestinal microbes at safe levels. Goblet cells, which are modified simple columnar epithelial cells, also line the GI tract (Figure 19.6). Goblet cells secrete a gel-forming mucin, which is the major component of mucus. The production of a protective layer of mucus helps reduce the risk of pathogens reaching deeper tissues.",True,Anatomy and Normal Microbiota of the GI Tract,Figure 19.5,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-24.5.png,"Figure 19.5 (a) The structure of the wall of the small intestine allows for the majority of nutrient absorption in the body. (b) Villi are folds in the surface of the small intestine. Microvilli are cytoplasmic extensions on individual cells that increase the surface area for absorption. (c) A light micrograph shows the shape of the villi. (d) An electron micrograph shows the shape of the microvilli. (credit b, c, d: Modification of micrographs provided by the Regents of University of Michigan Medical School © 2012)"
d035b2ad-5f62-4e48-bdac-6a53dcf69d00,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,"The constant movement of materials through the gastrointestinal tract also helps to move transient pathogens out of the body. In fact, feces are composed of approximately 25% microbes, 25% sloughed epithelial cells, 25% mucus, and 25% digested or undigested food. Finally, the normal microbiota provides an additional barrier to infection via a variety of mechanisms. For example, these organisms outcompete potential pathogens for space and nutrients within the intestine. This is known as competitive exclusion. Members of the microbiota may also secrete protein toxins known as bacteriocins that are able to bind to specific receptors on the surface of susceptible bacteria.",True,Anatomy and Normal Microbiota of the GI Tract,,,,
0f9f3c69-68d3-47ba-b815-ce70678a3b4a,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,General Signs and Symptoms of Oral and GI Disease,False,General Signs and Symptoms of Oral and GI Disease,,,,
87a77987-2dcb-4bec-a467-8254f1571376,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,"Despite numerous defense mechanisms that protect against infection, all parts of the digestive tract can become sites of infection or intoxication. The term food poisoning is sometimes used as a catch-all for GI infections and intoxications, but not all forms of GI disease originate with foodborne pathogens or toxins.",True,General Signs and Symptoms of Oral and GI Disease,,,,
992860a6-3783-470a-854d-c6dee23b0703,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,"In the mouth, fermentation by anaerobic microbes produces acids that damage the teeth and gums. This can lead to tooth decay, cavities, and periodontal disease, a condition characterized by chronic inflammation and erosion of the gums. Additionally, some pathogens can cause infections of the mucosa, glands, and other structures in the mouth, resulting in inflammation, sores, cankers, and other lesions. An open sore in the mouth or GI tract is typically called an ulcer.",True,General Signs and Symptoms of Oral and GI Disease,,,,
0160dfaf-7d29-4a11-9cc1-7c398619c5e8,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,"Infections and intoxications of the lower GI tract often produce symptoms such as nausea, vomiting, diarrhea, aches, and fever. In some cases, vomiting and diarrhea may cause severe dehydration and other complications that can become serious or fatal. Various clinical terms are used to describe gastrointestinal symptoms. For example, gastritis is an inflammation of the stomach lining that results in swelling and enteritis refers to inflammation of the intestinal mucosa. When the inflammation involves both the stomach lining and the intestinal lining, the condition is called gastroenteritis. Inflammation of the liver is called hepatitis. Inflammation of the colon, called colitis, commonly occurs in cases of food intoxication. Because an inflamed colon does not reabsorb water as effectively as it normally does, stools become watery, causing diarrhea. Damage to the epithelial cells of the colon can also cause bleeding and excess mucus to appear in watery stools, a condition called dysentery.",True,General Signs and Symptoms of Oral and GI Disease,,,,
06b4a384-0a70-4bba-b746-44dc8e7aa560,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,Anatomy and Normal Microbiota of the Oral Cavity,False,Anatomy and Normal Microbiota of the Oral Cavity,,,,
28353991-f3e2-4b7d-bb17-29d74c072cfe,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,"Microbes such as bacteria and archaea are abundant in the mouth and coat all of the surfaces of the oral cavity. However, different structures, such as the teeth or cheeks, host unique communities of both aerobic and anaerobic microbes. Some factors appear to work against making the mouth hospitable to certain microbes. For example, chewing allows microbes to mix better with saliva so they can be swallowed or spit out more easily. Saliva also contains enzymes, including lysozyme, which can damage microbial cells. Recall that lysozyme is part of the first line of defense in the innate immune system and cleaves the β-(1,4) glycosidic linkages between N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM) in bacterial peptidoglycan (see Chemical Defenses). Additionally, fluids containing immunoglobulins and phagocytic cells are produced in the gingival spaces. Despite all of these chemical and mechanical activities, the mouth supports a large microbial community.",True,Anatomy and Normal Microbiota of the Oral Cavity,,,,
fae228b9-0c61-4131-b1ea-246f06ddcf21,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,Anatomy and Normal Microbiota of the GI Tract,False,Anatomy and Normal Microbiota of the GI Tract,,,,
8fc1ded4-6adf-49e3-9700-cdf235c6baf1,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,"The environment of most of the GI tract is harsh, which serves two purposes: digestion and immunity. The stomach is an extremely acidic environment (pH 1.5–3.5) due to the gastric juices that break down food and kill many ingested microbes; this helps prevent infection from pathogens. The environment in the small intestine is less harsh and is able to support microbial communities. Microorganisms present in the small intestine can include lactobacilli, diptherioids and the fungus Candida. On the other hand, the large intestine (colon) contains a diverse and abundant microbiota that is important for normal function. These microbes include Bacteriodetes (especially the genera Bacteroides  and Prevotella) and Firmicutes (especially members of the genus Clostridium). Methanogenic archaea and some fungi are also present, among many other species of bacteria. These microbes all aid in digestion and contribute to the production of feces, the waste excreted from the digestive tract, and flatus, the gas produced from microbial fermentation of undigested food. They can also produce valuable nutrients. For example, lactic acid bacteria such as bifidobacteria can synthesize vitamins, such as vitamin B12, folate, and riboflavin, that humans cannot synthesize themselves. E. coli found in the intestine can also break down food and help the body produce vitamin K, which is important for blood coagulation.",True,Anatomy and Normal Microbiota of the GI Tract,,,,
e767419c-9592-4bc6-9bb8-1a24cd331138,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,"The GI tract has several other methods of reducing the risk of infection by pathogens. Small aggregates of underlying lymphoid tissue in the ileum, called Peyer’s patches (Figure 19.5), detect pathogens in the intestines via microfold (M) cells, which transfer antigens from the lumen of the intestine to the lymphocytes on Peyer’s patches to induce an immune response. The Peyer’s patches then secrete IgA and other pathogen-specific antibodies into the intestinal lumen to help keep intestinal microbes at safe levels. Goblet cells, which are modified simple columnar epithelial cells, also line the GI tract (Figure 19.6). Goblet cells secrete a gel-forming mucin, which is the major component of mucus. The production of a protective layer of mucus helps reduce the risk of pathogens reaching deeper tissues.",True,Anatomy and Normal Microbiota of the GI Tract,Figure 19.5,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-24.5.png,"Figure 19.5 (a) The structure of the wall of the small intestine allows for the majority of nutrient absorption in the body. (b) Villi are folds in the surface of the small intestine. Microvilli are cytoplasmic extensions on individual cells that increase the surface area for absorption. (c) A light micrograph shows the shape of the villi. (d) An electron micrograph shows the shape of the microvilli. (credit b, c, d: Modification of micrographs provided by the Regents of University of Michigan Medical School © 2012)"
6f528ce5-df78-4fa9-b3ee-19c18cc396e1,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,"The constant movement of materials through the gastrointestinal tract also helps to move transient pathogens out of the body. In fact, feces are composed of approximately 25% microbes, 25% sloughed epithelial cells, 25% mucus, and 25% digested or undigested food. Finally, the normal microbiota provides an additional barrier to infection via a variety of mechanisms. For example, these organisms outcompete potential pathogens for space and nutrients within the intestine. This is known as competitive exclusion. Members of the microbiota may also secrete protein toxins known as bacteriocins that are able to bind to specific receptors on the surface of susceptible bacteria.",True,Anatomy and Normal Microbiota of the GI Tract,,,,
9c2243e1-9b6d-4fa0-a684-92c0cd79c217,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,General Signs and Symptoms of Oral and GI Disease,False,General Signs and Symptoms of Oral and GI Disease,,,,
9c4abe05-37c3-4e6f-a85e-cac17b614240,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,"Despite numerous defense mechanisms that protect against infection, all parts of the digestive tract can become sites of infection or intoxication. The term food poisoning is sometimes used as a catch-all for GI infections and intoxications, but not all forms of GI disease originate with foodborne pathogens or toxins.",True,General Signs and Symptoms of Oral and GI Disease,,,,
2c3c0374-c86c-4662-8a89-e9ea80ff0c2d,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,"In the mouth, fermentation by anaerobic microbes produces acids that damage the teeth and gums. This can lead to tooth decay, cavities, and periodontal disease, a condition characterized by chronic inflammation and erosion of the gums. Additionally, some pathogens can cause infections of the mucosa, glands, and other structures in the mouth, resulting in inflammation, sores, cankers, and other lesions. An open sore in the mouth or GI tract is typically called an ulcer.",True,General Signs and Symptoms of Oral and GI Disease,,,,
b05f8e9e-1064-4f7f-b9f3-7af376995f2a,https://open.oregonstate.education/microbiology/,19.1	Anatomy and Normal Microbiota of the Digestive System,https://open.oregonstate.education/microbiology/chapter/24-1anatomy-and-normal-microbiota-of-the-digestive-system/,"Infections and intoxications of the lower GI tract often produce symptoms such as nausea, vomiting, diarrhea, aches, and fever. In some cases, vomiting and diarrhea may cause severe dehydration and other complications that can become serious or fatal. Various clinical terms are used to describe gastrointestinal symptoms. For example, gastritis is an inflammation of the stomach lining that results in swelling and enteritis refers to inflammation of the intestinal mucosa. When the inflammation involves both the stomach lining and the intestinal lining, the condition is called gastroenteritis. Inflammation of the liver is called hepatitis. Inflammation of the colon, called colitis, commonly occurs in cases of food intoxication. Because an inflamed colon does not reabsorb water as effectively as it normally does, stools become watery, causing diarrhea. Damage to the epithelial cells of the colon can also cause bleeding and excess mucus to appear in watery stools, a condition called dysentery.",True,General Signs and Symptoms of Oral and GI Disease,,,,
59399dfd-64af-4f2f-8e9c-2f8a66cc1486,https://open.oregonstate.education/microbiology/,18.6	Protozoan Infections of the Urogenital System,https://open.oregonstate.education/microbiology/chapter/23-6protozoan-infections-of-the-urogenital-system/,Protozoan Infection,False,Protozoan Infection,,,,
91a1a539-ec84-499a-845a-80811494e807,https://open.oregonstate.education/microbiology/,18.6	Protozoan Infections of the Urogenital System,https://open.oregonstate.education/microbiology/chapter/23-6protozoan-infections-of-the-urogenital-system/,"T. vaginalis is commonly found in the normal microbiota of the vagina. As with other vaginal pathogens, it can cause vaginitis when there is disruption to the normal microbiota. It is found only as a trophozoite and does not form cysts. T. vaginalis can adhere to cells using adhesins such as lipoglycans; it also has other cell-surface virulence factors, including tetraspanins that are involved in cell adhesion, motility, and tissue invasion. In addition, T. vaginalis is capable of phagocytosing other microbes of the normal microbiota, contributing to the development of an imbalance that is favorable to infection.",True,Protozoan Infection,,,,
51500aca-ea88-4384-b56e-2c539ac98a22,https://open.oregonstate.education/microbiology/,18.6	Protozoan Infections of the Urogenital System,https://open.oregonstate.education/microbiology/chapter/23-6protozoan-infections-of-the-urogenital-system/,"Both men and women can develop trichomoniasis. Men are generally asymptomatic, and although women are more likely to develop symptoms, they are often asymptomatic as well. When symptoms do occur, they are characteristic of urethritis. Men experience itching, irritation, discharge from the penis, and burning after urination or ejaculation. Women experience dysuria; itching, burning, redness, and soreness of the genitalia; and vaginal discharge. The infection may also spread to the cervix. Infection increases the risk of transmitting or acquiring HIV and is associated with pregnancy complications such as preterm birth.",True,Protozoan Infection,,,,
9c250c43-99ba-44ac-bf66-8941eedda30d,https://open.oregonstate.education/microbiology/,18.6	Protozoan Infections of the Urogenital System,https://open.oregonstate.education/microbiology/chapter/23-6protozoan-infections-of-the-urogenital-system/,"Microscopic evaluation of wet mounts is an inexpensive and convenient method of diagnosis, but the sensitivity of this method is low (Figure 18.16). Nucleic acid amplification testing (NAAT) is preferred due to its high sensitivity. Using wet mounts and then NAAT for those who initially test negative is one option to improve sensitivity.",True,Protozoan Infection,Figure 18.16,18.6	Protozoan Infections of the Urogenital System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-23.24.png,Figure 18.16 Trichomonas vaginalis is visible in this Gram stained specimen. (credit: modification of work by American Society for Microbiology)
c8230135-5dc0-424b-95a5-525b9cd759c4,https://open.oregonstate.education/microbiology/,18.6	Protozoan Infections of the Urogenital System,https://open.oregonstate.education/microbiology/chapter/23-6protozoan-infections-of-the-urogenital-system/,"Samples may be obtained for NAAT using urine, vaginal, or endocervical specimens for women and with urine and urethral swabs for men. It is also possible to use other methods such as the OSOM Trichomonas Rapid Test (an immunochromatographic test that detects antigen) and a DNA probe test for multiple species associated with vaginitis (the Affirm VPII Microbial Identification Test discussed in section 23.5).[1] T. vaginalis is sometimes detected on a Pap test, but this is not considered diagnostic due to high rates of false positives and negatives. The recommended treatment for trichomoniasis is oral metronidazole or tinidazole. Sexual partners should be treated as well.",True,Protozoan Infection,,,,
b9dda99f-fb3d-495b-a32c-f837b8f9afc4,https://open.oregonstate.education/microbiology/,18.6	Protozoan Infections of the Urogenital System,https://open.oregonstate.education/microbiology/chapter/23-6protozoan-infections-of-the-urogenital-system/,"Legal considerations further complicate such situations. The Health Insurance Portability and Accountability Act (HIPPA), passed into law in 1996, sets the standards for the protection of patient information. It requires businesses that use health information, such as insurance companies and healthcare providers, to maintain strict confidentiality of patient records. Contacting a patient’s sexual partners may therefore violate the patient’s privacy rights if the patient’s diagnosis is revealed as a result.",True,Protozoan Infection,,,,
e952656c-b72a-4e2a-9b1b-4612acd8f6d0,https://open.oregonstate.education/microbiology/,18.6	Protozoan Infections of the Urogenital System,https://open.oregonstate.education/microbiology/chapter/23-6protozoan-infections-of-the-urogenital-system/,"From an ethical standpoint, which is more important: the patient’s privacy rights or the sexual partner’s right to know that they may be at risk of a sexually transmitted disease? Does the answer depend on the severity of the disease or are the rules universal? Suppose the physician knows the identity of the sexual partner but the patient does not want that individual to be contacted. Would it be a violation of HIPPA rules to contact the individual without the patient’s consent?",True,Protozoan Infection,,,,
7d69e0dc-0580-4cde-8724-8ed07ad26909,https://open.oregonstate.education/microbiology/,18.6	Protozoan Infections of the Urogenital System,https://open.oregonstate.education/microbiology/chapter/23-6protozoan-infections-of-the-urogenital-system/,"Questions related to patient privacy become even more complicated when dealing with patients who are minors. Adolescents may be reluctant to discuss their sexual behavior or health with a health professional, especially if they believe that healthcare professionals will tell their parents. This leaves many teens at risk of having an untreated infection or of lacking the information to protect themselves and their partners. On the other hand, parents may feel that they have a right to know what is going on with their child. How should physicians handle this? Should parents always be told even if the adolescent wants confidentiality? Does this affect how the physician should handle notifying a sexual partner?",True,Protozoan Infection,,,,
e21eb561-153a-48c6-bc80-5a3e4b6d46c7,https://open.oregonstate.education/microbiology/,18.5	Fungal Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-5fungal-infections-of-the-reproductive-system/,Fungal Infection,False,Fungal Infection,,,,
43de5b1e-1517-4cb2-9c5b-f5437f16f179,https://open.oregonstate.education/microbiology/,18.5	Fungal Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-5fungal-infections-of-the-reproductive-system/,"As discussed earlier, lactobacilli in the vagina inhibit the growth of other organisms, including bacteria and Candida, but disruptions can allow Candida to increase in numbers. Typical disruptions include antibiotic therapy, illness (especially diabetes), pregnancy, and the presence of transient microbes. Immunosuppression can also play a role, and the severe immunosuppression associated with HIV infection often allows Candida to thrive. This can cause genital or vaginal candidiasis, a condition characterized by vaginitis and commonly known as a yeast infection. When a yeast infection develops, inflammation occurs along with symptoms of pruritus (itching), a thick white or yellow discharge, and odor.",True,Fungal Infection,,,,
2e755c77-a3b3-4148-8d32-23abdd5f7a77,https://open.oregonstate.education/microbiology/,18.5	Fungal Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-5fungal-infections-of-the-reproductive-system/,"Other forms of candidiasis include cutaneous candidiasis (see Mycoses of the Skin) and oral thrush (see Microbial Diseases of the Mouth and Oral Cavity). Although Candida spp. are found in the normal microbiota, Candida spp. may also be transmitted between individuals. Sexual contact is a common mode of transmission, although candidiasis is not considered an STI.",True,Fungal Infection,,,,
664ef44b-e689-4973-8c48-825b13e9b086,https://open.oregonstate.education/microbiology/,18.5	Fungal Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-5fungal-infections-of-the-reproductive-system/,"Diagnosis of vaginal candidiasis can be made using microscopic evaluation of vaginal secretions to determine whether there is an excess of Candida. Culturing approaches are less useful because Candida is part of the normal microbiota and will regularly appear. It is also easy to contaminate samples with Candida because it is so common, so care must be taken to handle clinical material appropriately. Samples can be refrigerated if there is a delay in handling. Candida is a dimorphic fungus, so it does not only exist in a yeast form; cultivation can be used to identify chlamydospores and pseudohyphae, which develop from germ tubes (Figure 18.15). The presence of the germ tube can be used in a diagnostic test in which cultured yeast cells are combined with rabbit serum and observed after a few hours for the presence of germ tubes. Molecular tests are also available if needed. The Affirm VPII Microbial Identification Test, for instance, tests simultaneously for the vaginal microbes C. albicans, G. vaginalis (see Bacterial Infections of the Urinary System), and Trichomonas vaginalis (see Protozoan Infections of the Urogenital System).",True,Fungal Infection,Figure 18.15,18.5	Fungal Infections of the Reproductive System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-23.22.png,"Figure 18.15 Candida can produce germ tubes, like the one in this micrograph, that develop into hyphae. (credit: modification of work by American Society for Microbiology)"
4cd51f36-f18d-4aea-8973-c6b079c93632,https://open.oregonstate.education/microbiology/,18.5	Fungal Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-5fungal-infections-of-the-reproductive-system/,"Topical antifungal medications for vaginal candidiasis include butoconazole, miconazole, clotrimazole, tioconazole, and nystatin. Oral treatment with fluconazole can be used. There are often no clear precipitating factors for infection, so prevention is difficult.",True,Fungal Infection,,,,
b7516a30-1d7d-4e55-831f-8fdf9a7325b3,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,Genital Herpes,False,Genital Herpes,,,,
63efc159-383a-48ae-8a32-6ce7e0f7b9e5,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"Genital herpes is a common condition caused by the herpes simplex virus (Figure 18.9), an enveloped, double- stranded DNA virus that is classified into two distinct types. Herpes simplex virus has several virulence factors, including infected cell protein (ICP) 34.5, which helps in replication and inhibits the maturation of dendritic cells as a mechanism of avoiding elimination by the immune system. In addition, surface glycoproteins on the viral envelope promote the coating of herpes simplex virus with antibodies and complement factors, allowing the virus to appear as “self” and prevent immune system activation and elimination.",True,Genital Herpes,Figure 18.9,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-23.16.png,Figure 18.9 Virions of the herpes simplex virus are shown here in this transmission electron micrograph. (credit: modification of work by Centers for Disease Control and Prevention)
09c229a8-5242-4359-a26b-41552210b901,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"There are two herpes simplex virus types. While herpes simplex virus type 1 (HSV-1) is generally associated with oral lesions like cold sores or fever blisters (see Viral Infections of the Skin and Eyes), herpes simplex virus type 2 (HSV-2) is usually associated with genital herpes. However, both viruses can infect either location as well as other parts of the body. Oral-genital contact can spread either virus from the mouth to the genital region or vice versa.",True,Genital Herpes,,,,
289c8fa8-4d56-42f2-ab40-0107370a3405,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"Many infected individuals do not develop symptoms, and thus do not realize that they carry the virus. However, in some infected individuals, fever, chills, malaise, swollen lymph nodes, and pain precede the development of fluid- filled vesicles that may be irritating and uncomfortable. When these vesicles burst, they release infectious fluid and allow transmission of HSV. In addition, open herpes lesions can increase the risk of spreading or acquiring HIV.",True,Genital Herpes,,,,
f99fb66a-2c62-45b6-95b4-3beda05d5f26,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"In men, the herpes lesions typically develop on the penis and may be accompanied by a watery discharge. In women, the vesicles develop most commonly on the vulva, but may also develop on the vagina or cervix (Figure 18.10).",True,Genital Herpes,Figure 18.10,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-23.17.png,"Figure 18.10 Genital herpes is typically characterized by lesions on the genitals (left), but lesions can also appear elsewhere on the skin or mucous membranes (right). The lesions can be large and painful or small and easily overlooked. (credit b: modification of work by Schiffer JT, Swan D, Al Sallaq R, Magaret A, Johnston C, Mark KE, Selke S, Ocbamichael N, Kuntz S, Zhu J, Robinson B, Huang ML, Jerome KR, Wald A, and Corey)"
bba5bc3d-4ba5-4989-9302-db065d7965a4,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"The symptoms are typically mild, although the lesions may be irritating or accompanied by urinary discomfort. Use of condoms may not always be an effective means of preventing transmission of genital herpes since the lesions can occur on areas other than the genitals.",True,Genital Herpes,,,,
1e3e319d-0eff-4bbe-ada7-50dbbd427882,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"Herpes simplex viruses can cause recurrent infections because the virus can become latent and then be reactivated. This occurs more commonly with HSV-2 than with HSV-1.[2] The virus moves down peripheral nerves, typically sensory neurons, to ganglia in the spine (either the trigeminal ganglion or the lumbar-sacral ganglia) and becomes latent. Reactivation can later occur, causing the formation of new vesicles. HSV-2 most effectively reactivates from the lumbar-sacral ganglia. Not everyone infected with HSV-2 experiences reactivations, which are typically associated with stressful conditions, and the frequency of reactivation varies throughout life and among individuals. Between outbreaks or when there are no obvious vesicles, the virus can still be transmitted.",True,Genital Herpes,,,,
ed5f894e-aa06-4079-b781-7f64e31715b9,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"While there is no cure or vaccine for HSV-2 infections, antiviral medications are available that manage the infection by keeping the virus in its dormant or latent phase, reducing signs and symptoms. If the medication is discontinued, then the condition returns to its original severity. The recommended medications, which may be taken at the start of an outbreak or daily as a method of prophylaxis, are acyclovir, famciclovir, and valacyclovir.",True,Genital Herpes,,,,
461a56b2-cf6d-4490-8373-3da447a536ad,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,Human Papillomas,False,Human Papillomas,,,,
4f43a19d-8216-4d82-baa3-ae83793c85a1,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"Warts of all types are caused by a variety of strains of human papillomavirus (HPV) (see Viral Infections of the Skin and Eyes). Condylomata acuminata, more commonly called genital warts or venereal warts (Figure 18.11), are an extremely prevalent STI caused by certain strains of HPV. Condylomata are irregular, soft, pink growths that are found on external genitalia or the anus.",True,Human Papillomas,Figure 18.11,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-23.18.png,"Figure 18.11 Genital warts may occur around the anus (left) or genitalia (right). (credit left, right: modification of work by Centers for Disease Control and Prevention)"
ededf014-b217-4190-80e1-3669aed76c05,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"HPV is a small, non-enveloped virus with a circular double-stranded DNA genome. Researchers have identified over 200 different strains (called types) of HPV, with approximately 40 causing STIs. While some types of HPV cause genital warts, HPV infection is often asymptomatic and self-limiting. However, genital HPV infection often co-occurs with other STIs like syphilis or gonorrhea. Additionally, some forms of HPV (not the same ones associated with genital warts) are associated with cervical cancers. At least 14 oncogenic (cancer-causing) HPV types are known to have a causal association with cervical cancers. Examples of oncogenic HPV are types 16 and 18, which are associated with 70% of cervical cancers.[3] Oncogenic HPV types can also cause oropharyngeal cancer, anal cancer, vaginal cancer, vulvar cancer, and penile cancer. Most of these cancers are caused by HPV type 16. HPV virulence factors include proteins (E6 and E7) that are capable of inactivating tumor suppressor proteins, leading to uncontrolled cell division and the development of cancer.",True,Human Papillomas,,,,
0ac0f4d3-6942-4df0-b475-e5c98317a6b7,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"HPV cannot be cultured, so molecular tests are the primary method used to detect HPV. While routine HPV screening is not recommended for men, it is included in guidelines for women. An initial screening for HPV at age 30, conducted at the same time as a Pap test, is recommended. If the tests are negative, then further HPV testing is recommended every five years. More frequent testing may be needed in some cases. The protocols used to collect, transport, and store samples vary based on both the type of HPV testing and the purpose of the testing. This should be determined in individual cases in consultation with the laboratory that will perform the testing.",True,Human Papillomas,,,,
68a41bec-158d-4ea2-810b-eb780daa1b1b,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"Because HPV testing is often conducted concurrently with Pap testing, the most common approach uses a single sample collection within one vial for both. This approach uses liquid-based cytology (LBC). The samples are then used for Pap smear cytology as well as HPV testing and genotyping. HPV can be recognized in Pap smears by the presence of cells called koilocytes (called koilocytosis or koilocytotic atypia). Koilocytes have a hyperchromatic atypical nucleus that stains darkly and a high ratio of nuclear material to cytoplasm. There is a distinct clear appearance around the nucleus called a perinuclear halo (Figure 18.12).",True,Human Papillomas,Figure 18.12,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-23.19.png,"Figure 18.12 In this image, the cervical cells on the left are normal and those on the right show enlarged nuclei and hyperchromasia (darkly stained nuclei) typical of HPV-infected koilocytes. (credit: modification of work by Ed Uthman)"
a771e533-4a8e-43b9-848e-ebb2b2c85dd0,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"Regular Pap testing can detect abnormal cells that might progress to cervical cancer, followed by biopsy and appropriate treatment. Vaccines for some of the high risk HPV types are now available. Gardasil vaccine includes types 6, 11, 16 and 18 (types 6 and 11 are associated with 90% of genital wart infections and types 16 and 18 are associated with 70% of cervical cancers). Gardasil 9 vaccinates against the previous four types and an additional five high-risk types (31, 33, 45, 52, and 58). Cervarix vaccine includes just HPV types 16 and 18. Vaccination is the most effective way to prevent infection with oncogenic HPV, but it is important to note that not all oncogenic HPV types are covered by the available vaccines. It is recommended for both boys and girls prior to sexual activity (usually between the ages of nine and fifteen).",True,Human Papillomas,,,,
10a02672-36be-46a3-bd03-d1616bc92b38,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"A recent study on the effects of HPV vaccination found a baseline HPV prevalence of 26.8% for women between the ages of 14 and 59. Among women aged 20–24, the prevalence was 44.8%; in other words, almost half of the women in this age bracket had a current infection.[4] According to the CDC, HSV-2 infection was estimated to have a prevalence of 15.5% in younger individuals (14–49 years of age) in 2007–2010, down from 20.3% in the same age group in 1988–1994. However, the CDC estimates that 87.4% of infected individuals in this age group have not been diagnosed by a physician.[5]",True,Human Papillomas,,,,
5deeb06d-4d20-43fe-ad35-1d1065c933ad,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"Another complicating factor is that many STIs can be asymptomatic or have long periods of latency. For example, the CDC estimates that among women ages 14–49 in the United States, about 2.3 million (3.1%) are infected with the sexually transmitted protozoan Trichomonas (see Protozoan Infections of the Urogenital System); however, in a study of infected women, 85% of those diagnosed with the infection were asymptomatic.[6]",True,Human Papillomas,,,,
8869c8f3-067b-4579-a2c5-57a4a487adaa,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"Even when patients are treated for symptomatic STIs, it can be difficult to obtain accurate data on the number of cases. Whereas STIs like chlamydia, gonorrhea, and syphilis are notifiable diseases—meaning each diagnosis must be reported by healthcare providers to the CDC—other STIs are not notifiable (e.g., genital herpes, genital warts, and trichomoniasis). Between the social taboos, the inconsistency of symptoms, and the lack of mandatory reporting, it can be difficult to estimate the true prevalence of STIs—but it is safe to say they are much more prevalent than most people think.",True,Human Papillomas,,,,
f3d45a2f-b4b5-4a82-a02a-2a7d527c3be3,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,Figure 18.13 summarizes the most important features of viral diseases affecting the human reproductive tract.,True,Human Papillomas,Figure 18.13,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.13-1.png,Figure 18.13 Details associated with two different viral infections of the reproductive tract.
375f328f-7bd9-4c5e-9849-a9d8f9088af9,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"Regular Pap testing can detect abnormal cells that might progress to cervical cancer, followed by biopsy and appropriate treatment. Vaccines for some of the high risk HPV types are now available. Gardasil vaccine includes types 6, 11, 16 and 18 (types 6 and 11 are associated with 90% of genital wart infections and types 16 and 18 are associated with 70% of cervical cancers). Gardasil 9 vaccinates against the previous four types and an additional five high-risk types (31, 33, 45, 52, and 58). Cervarix vaccine includes just HPV types 16 and 18. Vaccination is the most effective way to prevent infection with oncogenic HPV, but it is important to note that not all oncogenic HPV types are covered by the available vaccines. It is recommended for both boys and girls prior to sexual activity (usually between the ages of nine and fifteen).",True,Human Papillomas,,,,
fd267392-0870-4129-be04-40f841cf4130,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"A recent study on the effects of HPV vaccination found a baseline HPV prevalence of 26.8% for women between the ages of 14 and 59. Among women aged 20–24, the prevalence was 44.8%; in other words, almost half of the women in this age bracket had a current infection.[4] According to the CDC, HSV-2 infection was estimated to have a prevalence of 15.5% in younger individuals (14–49 years of age) in 2007–2010, down from 20.3% in the same age group in 1988–1994. However, the CDC estimates that 87.4% of infected individuals in this age group have not been diagnosed by a physician.[5]",True,Human Papillomas,,,,
f4415a76-15ec-49fb-bd34-4ddb0e25335b,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"Another complicating factor is that many STIs can be asymptomatic or have long periods of latency. For example, the CDC estimates that among women ages 14–49 in the United States, about 2.3 million (3.1%) are infected with the sexually transmitted protozoan Trichomonas (see Protozoan Infections of the Urogenital System); however, in a study of infected women, 85% of those diagnosed with the infection were asymptomatic.[6]",True,Human Papillomas,,,,
81e25b1a-2e62-4642-9655-69c735f67a42,https://open.oregonstate.education/microbiology/,18.4	Viral Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-4viral-infections-of-the-reproductive-system/,"Even when patients are treated for symptomatic STIs, it can be difficult to obtain accurate data on the number of cases. Whereas STIs like chlamydia, gonorrhea, and syphilis are notifiable diseases—meaning each diagnosis must be reported by healthcare providers to the CDC—other STIs are not notifiable (e.g., genital herpes, genital warts, and trichomoniasis). Between the social taboos, the inconsistency of symptoms, and the lack of mandatory reporting, it can be difficult to estimate the true prevalence of STIs—but it is safe to say they are much more prevalent than most people think.",True,Human Papillomas,,,,
805938cb-e31b-4e24-82fd-747fcbc13093,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,Bacterial Vaginitis and Vaginosis,False,Bacterial Vaginitis and Vaginosis,,,,
54c1b7a3-2076-482f-a92c-b57e07f4b737,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,"Inflammation of the vagina is called vaginitis, often caused by a bacterial infection. It is also possible to have an imbalance in the normal vaginal microbiota without inflammation called bacterial vaginosis (BV). Vaginosis may be asymptomatic or may cause mild symptoms such as a thin, white-to-yellow, homogeneous vaginal discharge, burning, odor, and itching. The major causative agent is Gardnerella vaginalis, a gram-variable to gram-negative pleomorphic bacterium. The disease is usually self-limiting, although antibiotic treatment is recommended if symptoms develop.",True,Bacterial Vaginitis and Vaginosis,,,,
58a9a700-712e-48d2-b794-7ee952047247,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,"G. vaginalis appears to be more virulent than other vaginal bacterial species potentially associated with BV. Like Lactobacillus spp., G. vaginalis is part of the normal vaginal microbiota, but when the population of Lactobacillus spp. decreases and the vaginal pH increases, G. vaginalis flourishes, causing vaginosis by attaching to vaginal epithelial cells and forming a thick protective biofilm. G. vaginalis also produces a cytotoxin called vaginolysin that lyses vaginal epithelial cells and red blood cells.",True,Bacterial Vaginitis and Vaginosis,,,,
78b3db4e-3d41-45c1-a0dd-edfa82b422c9,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,"Since G. vaginalis can also be isolated from healthy women, the “gold standard” for the diagnosis of BV is direct examination of vaginal secretions and not the culture of G. vaginalis. Diagnosis of bacterial vaginosis from vaginal secretions can be accurately made in three ways. The first is to use a DNA probe. The second method is to assay for sialidase activity, an enzyme produced by G. vaginalis and other bacteria associated with vaginosis. The third method is to assess gram-stained vaginal smears for microscopic morphology and relative numbers and types of bacteria, squamous epithelial cells, and leukocytes. By examining slides prepared from vaginal swabs, it is possible to distinguish lactobacilli (long, gram- positive rods) from other gram-negative species responsible for BV. A shift in predominance from gram-positive bacilli to gram-negative coccobacilli can indicate BV. Additionally, the slide may contain so-called clue cells, which are epithelial cells that appear to have a granular or stippled appearance due to bacterial cells attached to their surface (Figure 18.5). Presumptive diagnosis of bacterial vaginosis can involve an assessment of clinical symptoms and evaluation of vaginal fluids using Amsel’s diagnostic criteria which include 3 out of 4 of the following characteristics:",True,Bacterial Vaginitis and Vaginosis,Figure 18.5,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-23.9.png,"Figure 18.5 In this vaginal smear, the cell at the lower left is a clue cell with a unique appearance caused by the presence of bacteria on the cell. The cell on the right is a normal cell."
eccfcf5f-e67a-482b-87af-92b23ec85b82,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,"Treatment is often unnecessary because the infection often clears on its own. However, in some cases, antibiotics such as topical or oral clindamycin or metronidazole may be prescribed. Alternative treatments include oral tinidazole or clindamycin ovules (vaginal suppositories).",True,Bacterial Vaginitis and Vaginosis,,,,
88a5e77a-69b3-4604-b2da-b25c3dc7623e,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,Gonorrhea,False,Gonorrhea,,,,
337f5d77-7700-464e-9eef-3caa4f4b5fb1,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,"Many infected individuals (both men and women) are asymptomatic carriers of gonorrhea. When symptoms do occur, they manifest differently in males and females. Males may develop pain and burning during urination and discharge from the penis that may be yellow, green, or white (Figure 18.6). Less commonly, the testicles may become swollen or tender. Over time, these symptoms can increase and spread. In some cases, chronic infection develops. The disease can also develop in the rectum, causing symptoms such as discharge, soreness, bleeding, itching, and pain (especially in association with bowel movements).",True,Gonorrhea,Figure 18.6,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-23.10.png,"Figure 18.6 (a) Clinical photograph of gonococcal discharge from penis. The lesions on the skin could indicate co- infection with another STI. (b) Purulent discharge originating from the cervix and accumulating in the vagina of a patient with gonorrhea. (c) A micrograph of urethral discharge shows gram-negative diplococci (paired cells) both inside and outside the leukocytes (large cells with lobed nuclei). These results could be used to diagnose gonorrhea in a male patient, but female vaginal samples may contain other Neisseria spp. even if the patient is not infected with gonorrhoeae. (credit a, b: modification of work by Centers for Disease Control and Prevention; credit c: modification of work by American Society for Microbiology)"
e9b0c776-4596-464c-b06b-7bb5082c63cd,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,"Women may develop pelvic pain, discharge from the vagina, intermenstrual bleeding (i.e., bleeding not associated with normal menstruation), and pain or irritation associated with urination. As with men, the infection can become chronic. In women, however, chronic infection can cause increases in menstrual flow. Rectal infection can also occur, with the symptoms previously described for men. Infections that spread to the endometrium and fallopian tubes can cause pelvic inflammatory disease (PID), characterized by pain in the lower abdominal region, dysuria, vaginal discharge, and fever. PID can also lead to infertility through scarring and blockage of the fallopian tubes (salpingitis); it may also increase the risk of a life-threatening ectopic pregnancy, which occurs when a fertilized egg begins developing somewhere other than the uterus (e.g., in the fallopian tube or ovary).",True,Gonorrhea,,,,
eeb6fc4a-80e1-4d4a-8ece-b0a5d88c92a8,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,"When a gonorrhea infection disseminates throughout the body, serious complications can develop. The infection may spread through the blood (bacteremia) and affect organs throughout the body, including the heart (gonorrheal endocarditis), joints (gonorrheal arthritis), and meninges encasing the brain (meningitis).",True,Gonorrhea,,,,
f8eef861-53b1-4ae1-92eb-1844bba1ac3a,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,"Urethritis caused by N. gonorrhoeae can be difficult to treat due to antibiotic resistance. Some strains have developed resistance to the fluoroquinolones, so cephalosporins are often a first choice for treatment. Because co-infection with C. trachomatis is common, the CDC recommends treating with a combination regimen of ceftriaxone and azithromycin. Treatment of sexual partners is also recommended to avoid reinfection and spread of infection to others.[1]",True,Gonorrhea,,,,
5855a596-5e6f-423a-b026-fb481740c35f,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,"Antibiotic resistance in many pathogens is steadily increasing, causing serious concern throughout the public health community. Increased resistance has been especially notable in some species, such as Neisseria gonorrhoeae. The CDC monitors the spread of antibiotic resistance in N. gonorrhoeae, which it classifies as an urgent threat, and makes recommendations for treatment. So far, N. gonorrhoeae has shown resistance to cefixime (a cephalosporin), ceftriaxone (another cephalosporin), azithromycin, and tetracycline. Resistance to tetracycline is the most common, and was seen in 188,600 cases of gonorrhea in 2011 (out of a total 820,000 cases). In 2011, some 246,000 cases of gonorrhea involved strains of N. gonorrhoeae that were resistant to at least one antibiotic.[2] These resistance genes are spread by plasmids, and a single bacterium may be resistant to multiple antibiotics. The CDC currently recommends treatment with two medications, ceftriaxone and azithromycin, to attempt to slow the spread of resistance. If resistance to cephalosporins increases, it will be extremely difficult to control the spread of N. gonorrhoeae.",True,Gonorrhea,,,,
69c6152c-413f-41c8-a348-68e3c58cc453,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,Chlamydia,False,Chlamydia,,,,
9784c312-e9e7-40d9-a035-a7256f9f28c1,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,"Because chlamydia is widespread, often asymptomatic, and has the potential to cause substantial complications, routine screening is recommended for sexually active women who are under age 25, at high risk (i.e., not in a monogamous relationship), or beginning prenatal care.",True,Chlamydia,,,,
32710ac7-0238-436d-8c97-54a533354843,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,Urogenital infections caused by C. trachomatis can be treated using antibiotics.,True,Chlamydia,,,,
c215704a-67fe-41ac-a7b6-117c943a62c5,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,Gonorrhea,False,Gonorrhea,,,,
e01fc42a-8deb-43ba-8c89-2710d8c0f8c5,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,"Many infected individuals (both men and women) are asymptomatic carriers of gonorrhea. When symptoms do occur, they manifest differently in males and females. Males may develop pain and burning during urination and discharge from the penis that may be yellow, green, or white (Figure 18.6). Less commonly, the testicles may become swollen or tender. Over time, these symptoms can increase and spread. In some cases, chronic infection develops. The disease can also develop in the rectum, causing symptoms such as discharge, soreness, bleeding, itching, and pain (especially in association with bowel movements).",True,Gonorrhea,Figure 18.6,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-23.10.png,"Figure 18.6 (a) Clinical photograph of gonococcal discharge from penis. The lesions on the skin could indicate co- infection with another STI. (b) Purulent discharge originating from the cervix and accumulating in the vagina of a patient with gonorrhea. (c) A micrograph of urethral discharge shows gram-negative diplococci (paired cells) both inside and outside the leukocytes (large cells with lobed nuclei). These results could be used to diagnose gonorrhea in a male patient, but female vaginal samples may contain other Neisseria spp. even if the patient is not infected with gonorrhoeae. (credit a, b: modification of work by Centers for Disease Control and Prevention; credit c: modification of work by American Society for Microbiology)"
c8947145-6ef7-4ca8-9532-b8dba28aebb4,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,"Women may develop pelvic pain, discharge from the vagina, intermenstrual bleeding (i.e., bleeding not associated with normal menstruation), and pain or irritation associated with urination. As with men, the infection can become chronic. In women, however, chronic infection can cause increases in menstrual flow. Rectal infection can also occur, with the symptoms previously described for men. Infections that spread to the endometrium and fallopian tubes can cause pelvic inflammatory disease (PID), characterized by pain in the lower abdominal region, dysuria, vaginal discharge, and fever. PID can also lead to infertility through scarring and blockage of the fallopian tubes (salpingitis); it may also increase the risk of a life-threatening ectopic pregnancy, which occurs when a fertilized egg begins developing somewhere other than the uterus (e.g., in the fallopian tube or ovary).",True,Gonorrhea,,,,
dae6baf6-9aaf-4211-8866-7c58c3a7d936,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,"When a gonorrhea infection disseminates throughout the body, serious complications can develop. The infection may spread through the blood (bacteremia) and affect organs throughout the body, including the heart (gonorrheal endocarditis), joints (gonorrheal arthritis), and meninges encasing the brain (meningitis).",True,Gonorrhea,,,,
41c0ff2e-23f0-4f3c-b26f-ad0956aaf206,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,"Urethritis caused by N. gonorrhoeae can be difficult to treat due to antibiotic resistance. Some strains have developed resistance to the fluoroquinolones, so cephalosporins are often a first choice for treatment. Because co-infection with C. trachomatis is common, the CDC recommends treating with a combination regimen of ceftriaxone and azithromycin. Treatment of sexual partners is also recommended to avoid reinfection and spread of infection to others.[1]",True,Gonorrhea,,,,
2fbd3950-3459-4d35-86b3-e6659281905d,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,Chlamydia,False,Chlamydia,,,,
2d956bad-bb68-4a90-b603-4dde75dcf86b,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,"Because chlamydia is widespread, often asymptomatic, and has the potential to cause substantial complications, routine screening is recommended for sexually active women who are under age 25, at high risk (i.e., not in a monogamous relationship), or beginning prenatal care.",True,Chlamydia,,,,
d25489b5-07aa-4222-a8ea-94ee72c9ad6f,https://open.oregonstate.education/microbiology/,18.3	Bacterial Infections of the Reproductive System,https://open.oregonstate.education/microbiology/chapter/23-3bacterial-infections-of-the-reproductive-system/,Urogenital infections caused by C. trachomatis can be treated using antibiotics.,True,Chlamydia,,,,
d7fab45a-51a3-4ff8-812b-5297f18dbff7,https://open.oregonstate.education/microbiology/,18.2	Bacterial Infections of the Urinary System,https://open.oregonstate.education/microbiology/chapter/23-2bacterial-infections-of-the-urinary-system/,Learning Objectives,False,Learning Objectives,,,,
0330ac76-9c9f-488d-81ce-2f33894e8bcc,https://open.oregonstate.education/microbiology/,18.2	Bacterial Infections of the Urinary System,https://open.oregonstate.education/microbiology/chapter/23-2bacterial-infections-of-the-urinary-system/,Cystitis,False,Cystitis,,,,
7441f4e0-a224-4969-84c7-c7c21e7ab319,https://open.oregonstate.education/microbiology/,18.2	Bacterial Infections of the Urinary System,https://open.oregonstate.education/microbiology/chapter/23-2bacterial-infections-of-the-urinary-system/,"Cystitis is most often caused by a bacterial infection of the bladder, but it can also occur as a reaction to certain treatments or irritants such as radiation treatment, hygiene sprays, or spermicides. Common symptoms of cystitis include dysuria (urination accompanied by burning, discomfort, or pain), pyuria (pus in the urine), hematuria (blood in the urine), and bladder pain.",True,Cystitis,,,,
d1e8bba7-3ed9-4fdb-b3e4-6164e888967f,https://open.oregonstate.education/microbiology/,18.2	Bacterial Infections of the Urinary System,https://open.oregonstate.education/microbiology/chapter/23-2bacterial-infections-of-the-urinary-system/,"In women, bladder infections are more common because the urethra is short and located in close proximity to the anus, which can result in infections of the urinary tract by fecal bacteria. Bladder infections are also more common in the elderly because the bladder may not empty fully, causing urine to pool; the elderly may also have weaker immune systems that make them more vulnerable to infection. Conditions such as prostatitis in men or kidney stones in both men and women can impact proper drainage of urine and increase risk of bladder infections. Catheterization can also increase the risk of bladder infection.",True,Cystitis,,,,
e7f3b419-7ae4-4a84-8d16-2439e8336cb7,https://open.oregonstate.education/microbiology/,18.2	Bacterial Infections of the Urinary System,https://open.oregonstate.education/microbiology/chapter/23-2bacterial-infections-of-the-urinary-system/,"Gram-negative bacteria cause most bladder infections, although there are gram-positive pathogens associated with cystitis as well. Routine manual urinalysis using a urine dipstick or test strip can be used for rapid screening of infection. These test strips (Figure 18.4) are either held in a urine stream or dipped in a sample of urine to test for the presence of nitrites, leukocyte esterase, protein, or blood that can indicate an active bacterial infection.",True,Cystitis,Figure 18.4,18.2	Bacterial Infections of the Urinary System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-23.5.png,"Figure 18.4 A urine dipstick is compared against a color key to determine levels of various chemicals, proteins, or cells in the urine. Abnormal levels may indicate an infection. (credit: modification of work by Suzanne Wakim)"
400cbaf4-c9cd-4302-ac9b-1d5eb015edf0,https://open.oregonstate.education/microbiology/,18.2	Bacterial Infections of the Urinary System,https://open.oregonstate.education/microbiology/chapter/23-2bacterial-infections-of-the-urinary-system/,"Low specificity, sensitivity, or both, associated with these rapid screening tests require that care be taken in interpretation of results and in their use in diagnosis of urinary tract infections. Therefore, positive LE or nitrite results are followed by a urine culture to confirm a bladder infection. Urine culture is generally accomplished using blood agar and MacConkey agar, and it is important to culture a clean catch of urine to minimize contamination with normal microbiota of the penis and vagina. A clean catch of urine is accomplished by first washing the labia and urethral opening of female patients or the penis of male patients. The patient then releases a small amount of urine into the toilet bowl before stopping the flow of urine. Finally, the patient resumes urination, this time filling the container used to collect the specimen.",True,Cystitis,,,,
34ce474b-f2ff-41dd-ac22-04544a2ca61e,https://open.oregonstate.education/microbiology/,18.2	Bacterial Infections of the Urinary System,https://open.oregonstate.education/microbiology/chapter/23-2bacterial-infections-of-the-urinary-system/,"Bacterial cystitis is commonly treated with antibiotics. Pain medications may provide relief for patients with dysuria. Treatment is more difficult in elderly patients, who experience a higher rate of complications such as sepsis and kidney infections.",True,Cystitis,,,,
c7f1803e-da6c-4318-9b38-6703899128de,https://open.oregonstate.education/microbiology/,18.2	Bacterial Infections of the Urinary System,https://open.oregonstate.education/microbiology/chapter/23-2bacterial-infections-of-the-urinary-system/,Learning Objectives,False,Learning Objectives,,,,
591821e6-8771-46ce-91c7-40f74f152815,https://open.oregonstate.education/microbiology/,18.2	Bacterial Infections of the Urinary System,https://open.oregonstate.education/microbiology/chapter/23-2bacterial-infections-of-the-urinary-system/,Cystitis,False,Cystitis,,,,
c7c01c23-b5e6-4f92-b0e4-bc5fc0e6e470,https://open.oregonstate.education/microbiology/,18.2	Bacterial Infections of the Urinary System,https://open.oregonstate.education/microbiology/chapter/23-2bacterial-infections-of-the-urinary-system/,"Cystitis is most often caused by a bacterial infection of the bladder, but it can also occur as a reaction to certain treatments or irritants such as radiation treatment, hygiene sprays, or spermicides. Common symptoms of cystitis include dysuria (urination accompanied by burning, discomfort, or pain), pyuria (pus in the urine), hematuria (blood in the urine), and bladder pain.",True,Cystitis,,,,
79b3a2b6-f7ca-41d0-ae9c-87a4b9f1a2ac,https://open.oregonstate.education/microbiology/,18.2	Bacterial Infections of the Urinary System,https://open.oregonstate.education/microbiology/chapter/23-2bacterial-infections-of-the-urinary-system/,"In women, bladder infections are more common because the urethra is short and located in close proximity to the anus, which can result in infections of the urinary tract by fecal bacteria. Bladder infections are also more common in the elderly because the bladder may not empty fully, causing urine to pool; the elderly may also have weaker immune systems that make them more vulnerable to infection. Conditions such as prostatitis in men or kidney stones in both men and women can impact proper drainage of urine and increase risk of bladder infections. Catheterization can also increase the risk of bladder infection.",True,Cystitis,,,,
117ad3bc-4446-4e09-a520-69aa4f91325c,https://open.oregonstate.education/microbiology/,18.2	Bacterial Infections of the Urinary System,https://open.oregonstate.education/microbiology/chapter/23-2bacterial-infections-of-the-urinary-system/,"Gram-negative bacteria cause most bladder infections, although there are gram-positive pathogens associated with cystitis as well. Routine manual urinalysis using a urine dipstick or test strip can be used for rapid screening of infection. These test strips (Figure 18.4) are either held in a urine stream or dipped in a sample of urine to test for the presence of nitrites, leukocyte esterase, protein, or blood that can indicate an active bacterial infection.",True,Cystitis,Figure 18.4,18.2	Bacterial Infections of the Urinary System,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-23.5.png,"Figure 18.4 A urine dipstick is compared against a color key to determine levels of various chemicals, proteins, or cells in the urine. Abnormal levels may indicate an infection. (credit: modification of work by Suzanne Wakim)"
2304013a-68db-4467-9674-c93ae4c8d4e8,https://open.oregonstate.education/microbiology/,18.2	Bacterial Infections of the Urinary System,https://open.oregonstate.education/microbiology/chapter/23-2bacterial-infections-of-the-urinary-system/,"Low specificity, sensitivity, or both, associated with these rapid screening tests require that care be taken in interpretation of results and in their use in diagnosis of urinary tract infections. Therefore, positive LE or nitrite results are followed by a urine culture to confirm a bladder infection. Urine culture is generally accomplished using blood agar and MacConkey agar, and it is important to culture a clean catch of urine to minimize contamination with normal microbiota of the penis and vagina. A clean catch of urine is accomplished by first washing the labia and urethral opening of female patients or the penis of male patients. The patient then releases a small amount of urine into the toilet bowl before stopping the flow of urine. Finally, the patient resumes urination, this time filling the container used to collect the specimen.",True,Cystitis,,,,
69696381-64f2-47db-9e9e-248afbf32216,https://open.oregonstate.education/microbiology/,18.2	Bacterial Infections of the Urinary System,https://open.oregonstate.education/microbiology/chapter/23-2bacterial-infections-of-the-urinary-system/,"Bacterial cystitis is commonly treated with antibiotics. Pain medications may provide relief for patients with dysuria. Treatment is more difficult in elderly patients, who experience a higher rate of complications such as sepsis and kidney infections.",True,Cystitis,,,,
e7d53634-6ace-4012-95c3-992702dd7e25,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,Anatomy of the Urinary Tract,False,Anatomy of the Urinary Tract,,,,
00597a17-78aa-4df7-9ad5-15b9a5d9bb57,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"The basic structures of the urinary tract are common in males and females. However, there are unique locations for these structures in females and males, and there is a significant amount of overlap between the urinary and genital structures in males. Figure 18.2 illustrates the urinary anatomy common to females and males.",True,Anatomy of the Urinary Tract,Figure 18.2,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-23.2.png,Figure 18.2 These structures of the human urinary system are present in both males and females.
af83b6c9-26b1-4773-a611-8a5fafe70591,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"The kidneys carry out the urinary system’s primary functions of filtering the blood and maintaining water and electrolyte balance. The kidneys are composed of millions of filtration units called nephrons. Each nephron is in intimate contact with blood through a specialized capillary bed called the glomerulus (plural glomeruli). Fluids, electrolytes, and molecules from the blood pass from the glomerulus into the nephron, creating the filtrate that becomes urine. Urine that collects in each kidney empties through a ureter and drains to the urinary bladder, which stores urine. Urine is released from the bladder to the urethra, which transports it to be excreted from the body through the urinary meatus, the opening of the urethra.",True,Anatomy of the Urinary Tract,,,,
4198027a-5444-43b4-8609-2f67096db36c,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,Anatomy of the Reproductive System,False,Anatomy of the Reproductive System,,,,
1dd91d7b-dcb7-4dbe-bfe2-43c88d2bde27,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"The male reproductive system (Figure 18.3) is located in close proximity to the urinary system, and the urethra is part of both systems. The testes are responsible for the production of sperm. The epididymis is a coiled tube that collects sperm from the testes and passes it on to the vas deferens. The epididymis is also the site of sperm maturation after they leave the testes. The seminal vesicles and prostate are accessory glands that produce fluid that supports sperm. During ejaculation, the vas deferens releases this mixture of fluid and sperm, called semen, into the urethra, which extends to the end of the penis.",True,Anatomy of the Reproductive System,Figure 18.3,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-23.4.png,"Figure 18.3 The female reproductive system is located in close proximity to the urinary system. In males, the urethra is shared by the reproductive and urinary systems."
215e9693-21f6-414c-976d-6b96fe21baf7,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"The female reproductive system is located near the urinary system (Figure 18.3). The external genitalia (vulva) in females open to the vagina, a muscular passageway that connects to the cervix. The cervix is the lower part of the uterus (the organ where a fertilized egg will implant and develop). The cervix is a common site of infection, especially for viruses that may lead to cervical cancer. The uterus leads to the fallopian tubes and eventually to the ovaries. Ovaries are the site of ova (egg) production, as well as the site of estrogen and progesterone production that are involved in maturation and maintenance of reproductive organs, preparation of the uterus for pregnancy, and regulation of the menstrual cycle.",True,Anatomy of the Reproductive System,Figure 18.3,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-23.4.png,"Figure 18.3 The female reproductive system is located in close proximity to the urinary system. In males, the urethra is shared by the reproductive and urinary systems."
fb12d620-f4a5-4e33-8027-a59444975e84,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,Normal Microbiota of the Urogenital System,False,Normal Microbiota of the Urogenital System,,,,
1e310439-1306-4e98-be9d-b758080124be,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"The normal microbiota of different body sites provides an important nonspecific defense against infectious diseases (see Physical Defenses), and the urogenital tract is no exception. In both men and women, however, the kidneys are sterile. Although urine does contain some antibacterial components, bacteria will grow in urine left out at room temperature. Therefore, it is primarily the flushing action that keeps the ureters and bladder free of microbes.",True,Normal Microbiota of the Urogenital System,,,,
97b7b9ec-c7aa-46cb-9c6f-4790b1384ac9,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"Below the bladder, the normal microbiota of the male urogenital system is found primarily within the distal urethra and includes bacterial species that are commonly associated with the skin microbiota. In women, the normal microbiota is found within the distal one third of the urethra and the vagina. The normal microbiota of the vagina becomes established shortly after birth and is a complex and dynamic population of bacteria that fluctuates in response to environmental changes. Members of the vaginal microbiota play an important role in the nonspecific defense against vaginal infections and sexually transmitted infections by occupying cellular binding sites and competing for nutrients. In addition, the production of lactic acid by members of the microbiota provides an acidic environment within the vagina that also serves as a defense against infections. For the majority of women, the lactic-acid–producing bacteria in the vagina are dominated by a variety of species of Lactobacillus. Lactobacillus spp. use glycogen from vaginal epithelial cells for metabolism and production of lactic acid. This process is tightly regulated by the hormone estrogen. Increased levels of estrogen correlate with increased levels of vaginal glycogen, increased production of lactic acid, and a lower vaginal pH. Therefore, decreases in estrogen during the menstrual cycle and with menopause are associated with decreased levels of vaginal glycogen and lactic acid, and a higher pH. In addition to producing lactic acid, Lactobacillus spp. also contribute to the defenses against infectious disease through their production of hydrogen peroxide and bacteriocins (antibacterial peptides).",True,Normal Microbiota of the Urogenital System,,,,
d8597acd-2603-4ba3-93c4-2cdf65ad4852,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,General Signs and Symptoms of Urogenital Infections,False,General Signs and Symptoms of Urogenital Infections,,,,
204613f8-b74a-4852-8538-62bf098ec4f8,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"Infections of the urinary tract most commonly cause inflammation of the bladder (cystitis) or of the urethra (urethritis). Urethritis can be associated with cystitis, but can also be caused by sexually transmitted infections. Symptoms of urethritis in men include burning sensation while urinating, discharge from the penis, and blood in the semen or the urine. In women, urethritis is associated with painful and frequent urination, vaginal discharge, fever, chills, and abdominal pain. The symptoms of cystitis are similar to those of urethritis. When urethritis is caused by a sexually transmitted pathogen, additional symptoms involving the genitalia can occur. These can include painful vesicles (blisters), warts, and ulcers. Ureteritis, a rare infection of the ureter, can also occur with cystitis. These infections can be acute or chronic. Infections of the kidney may develop from a lower urinary tract infection; the upper urinary tract, including the ureters, is often affected. Signs and symptoms of a kidney infection include fever, chills, nausea, vomiting, lower back pain, and frequent painful urination.",True,General Signs and Symptoms of Urogenital Infections,,,,
0586c793-ab64-4d66-9141-7dff52f688da,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"Infections occurring within the reproductive structures of males include epididymitis, orchitis, and prostatitis. Bacterial infections may cause inflammation of the epididymis, called epididymitis. This inflammation causes pain in the scrotum, testicles, and groin; swelling, redness, and warm skin in these areas may also be observed. Inflammation of the testicle, called orchitis, is usually caused by a bacterial infection spreading from the epididymis, but it can also be a complication of mumps, a viral disease. The symptoms are similar to those of epididymitis, and it is not uncommon for them both to occur together, in which case the condition is called epididymo-orchitis. Inflammation of the prostate gland, called prostatitis, can result from a bacterial infection. The signs and symptoms of prostatitis include fever, chills, and pain in the bladder, testicles, and penis. Patients may also experience burning during urination, difficulty emptying the bladder, and painful ejaculation.",True,General Signs and Symptoms of Urogenital Infections,,,,
9ce48074-4280-4f2d-b971-175a41ffc6e6,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"Because of its proximity to the exterior, the vagina is a common site for infections in women. The general term for any inflammation of the vagina is vaginitis. Vaginitis often develops as a result of an overgrowth of bacteria or fungi that normally reside in the vaginal microbiota, although it can also result from infections by transient pathogens. Bacterial infections of the vagina are called bacterial vaginosis, whereas fungal infections (typically involving Candida spp.) are called yeast infections. Dynamic changes affecting the normal microbiota, acid production, and pH variations can be involved in the initiation of the microbial overgrowth and the development of vaginitis. Although some individuals may have no symptoms, vaginosis and vaginitis can be associated with discharge, odor, itching, and burning.",True,General Signs and Symptoms of Urogenital Infections,,,,
34fd68f4-5cc4-4052-9a43-5a896895d3b0,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"Pelvic inflammatory disease (PID) is an infection of the female reproductive organs including the uterus, cervix, fallopian tubes, and ovaries. Inflammation of the fallopian tubes, called salpingitis, is the most serious form of PID. Symptoms of PID can vary between women and include pain in the lower abdomen, vaginal discharge, fever, chills, nausea, diarrhea, vomiting, and painful urination.",True,General Signs and Symptoms of Urogenital Infections,,,,
93913d2d-c672-4eeb-b2fa-5294efabcc0c,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,General Causes and Modes of Transmission of Urogenital Infections,False,General Causes and Modes of Transmission of Urogenital Infections,,,,
4053714c-66d2-4721-a646-e92817ec98d3,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"Hormonal changes, particularly shifts in estrogen in women due to pregnancy or menopause, can increase susceptibility to urogenital infections. As discussed earlier, estrogen plays an important role in regulating the availability of glycogen and subsequent production of lactic acid by Lactobacillus species. Low levels of estrogen are associated with an increased vaginal pH and an increased risk of bacterial vaginosis and yeast infections. Estrogen also plays a role in maintaining the elasticity, strength, and thickness of the vaginal wall, and keeps the vaginal wall lubricated, reducing dryness. Low levels of estrogen are associated with thinning of the vaginal wall. This thinning increases the risk of tears and abrasions, which compromise the protective barrier and increase susceptibility to pathogens.",True,General Causes and Modes of Transmission of Urogenital Infections,,,,
2cc91300-5895-4ebd-8e00-075ce37594d6,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"Another common cause of urogenital infections in females is fecal contamination that occurs because of the close proximity of the anus and the urethra. Escherichia coli, an important member of the digestive tract microbiota, is the most common cause of urinary tract infections (urethritis and cystitis) in women; it generally causes infection when it is introduced to the urethra in fecal matter. Good hygiene can reduce the risk of urinary tract infections by this route. In men, urinary tract infections are more commonly associated with other conditions, such as an enlarged prostate, kidney stones, or placement of a urinary catheter. All of these conditions impair the normal emptying of the bladder, which serves to flush out microbes capable of causing infection.",True,General Causes and Modes of Transmission of Urogenital Infections,,,,
5d2455ef-2121-4e7a-afd5-a4d755faab95,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"Infections that are transmitted between individuals through sexual contact are called sexually transmitted infections (STIs) or sexually transmitted diseases (STDs). (The CDC prefers the term STD, but WHO prefers STI,[1] which encompasses infections that result in disease as well as those that are subclinical or asymptomatic.) STIs often affect the external genitalia and skin, where microbes are easily transferred through physical contact. Lymph nodes in the genital region may also become swollen as a result of infection. However, many STIs have systemic effects as well, causing symptoms that range from mild (e.g., general malaise) to severe (e.g., liver damage or serious immunosuppression).",True,General Causes and Modes of Transmission of Urogenital Infections,,,,
d2e7951a-a8b2-4736-9f96-78a1b5b1d412,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,Anatomy of the Reproductive System,False,Anatomy of the Reproductive System,,,,
f43d437e-59fc-4c9e-98d0-9846186f81cb,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"The female reproductive system is located near the urinary system (Figure 18.3). The external genitalia (vulva) in females open to the vagina, a muscular passageway that connects to the cervix. The cervix is the lower part of the uterus (the organ where a fertilized egg will implant and develop). The cervix is a common site of infection, especially for viruses that may lead to cervical cancer. The uterus leads to the fallopian tubes and eventually to the ovaries. Ovaries are the site of ova (egg) production, as well as the site of estrogen and progesterone production that are involved in maturation and maintenance of reproductive organs, preparation of the uterus for pregnancy, and regulation of the menstrual cycle.",True,Anatomy of the Reproductive System,Figure 18.3,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-23.4.png,"Figure 18.3 The female reproductive system is located in close proximity to the urinary system. In males, the urethra is shared by the reproductive and urinary systems."
c9e29e65-c0ae-4c76-81dd-c230f8f6ce22,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,Normal Microbiota of the Urogenital System,False,Normal Microbiota of the Urogenital System,,,,
76f4a9c5-0ad7-4d73-8ef0-64c72b0ddf35,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"The normal microbiota of different body sites provides an important nonspecific defense against infectious diseases (see Physical Defenses), and the urogenital tract is no exception. In both men and women, however, the kidneys are sterile. Although urine does contain some antibacterial components, bacteria will grow in urine left out at room temperature. Therefore, it is primarily the flushing action that keeps the ureters and bladder free of microbes.",True,Normal Microbiota of the Urogenital System,,,,
6a47ea0a-49a8-44f6-9665-5a9058d8e1b8,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"Below the bladder, the normal microbiota of the male urogenital system is found primarily within the distal urethra and includes bacterial species that are commonly associated with the skin microbiota. In women, the normal microbiota is found within the distal one third of the urethra and the vagina. The normal microbiota of the vagina becomes established shortly after birth and is a complex and dynamic population of bacteria that fluctuates in response to environmental changes. Members of the vaginal microbiota play an important role in the nonspecific defense against vaginal infections and sexually transmitted infections by occupying cellular binding sites and competing for nutrients. In addition, the production of lactic acid by members of the microbiota provides an acidic environment within the vagina that also serves as a defense against infections. For the majority of women, the lactic-acid–producing bacteria in the vagina are dominated by a variety of species of Lactobacillus. Lactobacillus spp. use glycogen from vaginal epithelial cells for metabolism and production of lactic acid. This process is tightly regulated by the hormone estrogen. Increased levels of estrogen correlate with increased levels of vaginal glycogen, increased production of lactic acid, and a lower vaginal pH. Therefore, decreases in estrogen during the menstrual cycle and with menopause are associated with decreased levels of vaginal glycogen and lactic acid, and a higher pH. In addition to producing lactic acid, Lactobacillus spp. also contribute to the defenses against infectious disease through their production of hydrogen peroxide and bacteriocins (antibacterial peptides).",True,Normal Microbiota of the Urogenital System,,,,
169d8a41-9ce7-46bd-8f81-93a08eb446fd,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,General Signs and Symptoms of Urogenital Infections,False,General Signs and Symptoms of Urogenital Infections,,,,
855735a4-9775-49d1-a740-597966da2b49,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"Infections occurring within the reproductive structures of males include epididymitis, orchitis, and prostatitis. Bacterial infections may cause inflammation of the epididymis, called epididymitis. This inflammation causes pain in the scrotum, testicles, and groin; swelling, redness, and warm skin in these areas may also be observed. Inflammation of the testicle, called orchitis, is usually caused by a bacterial infection spreading from the epididymis, but it can also be a complication of mumps, a viral disease. The symptoms are similar to those of epididymitis, and it is not uncommon for them both to occur together, in which case the condition is called epididymo-orchitis. Inflammation of the prostate gland, called prostatitis, can result from a bacterial infection. The signs and symptoms of prostatitis include fever, chills, and pain in the bladder, testicles, and penis. Patients may also experience burning during urination, difficulty emptying the bladder, and painful ejaculation.",True,General Signs and Symptoms of Urogenital Infections,,,,
644d3b76-b706-4d67-b831-c55944d5d14b,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"Because of its proximity to the exterior, the vagina is a common site for infections in women. The general term for any inflammation of the vagina is vaginitis. Vaginitis often develops as a result of an overgrowth of bacteria or fungi that normally reside in the vaginal microbiota, although it can also result from infections by transient pathogens. Bacterial infections of the vagina are called bacterial vaginosis, whereas fungal infections (typically involving Candida spp.) are called yeast infections. Dynamic changes affecting the normal microbiota, acid production, and pH variations can be involved in the initiation of the microbial overgrowth and the development of vaginitis. Although some individuals may have no symptoms, vaginosis and vaginitis can be associated with discharge, odor, itching, and burning.",True,General Signs and Symptoms of Urogenital Infections,,,,
70c51f63-c8ae-4711-8886-bc9e2d99d689,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"Pelvic inflammatory disease (PID) is an infection of the female reproductive organs including the uterus, cervix, fallopian tubes, and ovaries. Inflammation of the fallopian tubes, called salpingitis, is the most serious form of PID. Symptoms of PID can vary between women and include pain in the lower abdomen, vaginal discharge, fever, chills, nausea, diarrhea, vomiting, and painful urination.",True,General Signs and Symptoms of Urogenital Infections,,,,
dc97ad64-382d-4e73-be5e-670d4b34224d,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,General Causes and Modes of Transmission of Urogenital Infections,False,General Causes and Modes of Transmission of Urogenital Infections,,,,
e21d0400-1523-43d8-a5ef-2cc45c33b666,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"Hormonal changes, particularly shifts in estrogen in women due to pregnancy or menopause, can increase susceptibility to urogenital infections. As discussed earlier, estrogen plays an important role in regulating the availability of glycogen and subsequent production of lactic acid by Lactobacillus species. Low levels of estrogen are associated with an increased vaginal pH and an increased risk of bacterial vaginosis and yeast infections. Estrogen also plays a role in maintaining the elasticity, strength, and thickness of the vaginal wall, and keeps the vaginal wall lubricated, reducing dryness. Low levels of estrogen are associated with thinning of the vaginal wall. This thinning increases the risk of tears and abrasions, which compromise the protective barrier and increase susceptibility to pathogens.",True,General Causes and Modes of Transmission of Urogenital Infections,,,,
a74a72f2-fe69-4ad5-99fb-7ec75ec8d4fc,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"Another common cause of urogenital infections in females is fecal contamination that occurs because of the close proximity of the anus and the urethra. Escherichia coli, an important member of the digestive tract microbiota, is the most common cause of urinary tract infections (urethritis and cystitis) in women; it generally causes infection when it is introduced to the urethra in fecal matter. Good hygiene can reduce the risk of urinary tract infections by this route. In men, urinary tract infections are more commonly associated with other conditions, such as an enlarged prostate, kidney stones, or placement of a urinary catheter. All of these conditions impair the normal emptying of the bladder, which serves to flush out microbes capable of causing infection.",True,General Causes and Modes of Transmission of Urogenital Infections,,,,
d75f1a63-d20f-4f2a-a970-97248a49f5eb,https://open.oregonstate.education/microbiology/,18.1	Anatomy and Normal Microbiota of the Urogenital Tract,https://open.oregonstate.education/microbiology/chapter/23-1anatomy-and-normal-microbiota-of-the-urogenital-tract/,"Infections that are transmitted between individuals through sexual contact are called sexually transmitted infections (STIs) or sexually transmitted diseases (STDs). (The CDC prefers the term STD, but WHO prefers STI,[1] which encompasses infections that result in disease as well as those that are subclinical or asymptomatic.) STIs often affect the external genitalia and skin, where microbes are easily transferred through physical contact. Lymph nodes in the genital region may also become swollen as a result of infection. However, many STIs have systemic effects as well, causing symptoms that range from mild (e.g., general malaise) to severe (e.g., liver damage or serious immunosuppression).",True,General Causes and Modes of Transmission of Urogenital Infections,,,,
36b26288-8221-4ea1-a831-e0b3fc8dd4b7,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,The Common Cold,False,The Common Cold,,,,
9e28d209-ddb9-409d-ad27-4762060c24ff,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"The common cold is a generic term for a variety of mild viral infections of the nasal cavity. More than 200 different viruses are known to cause the common cold. The most common groups of cold viruses include rhinoviruses, coronaviruses, and adenoviruses. These infections are widely disseminated in the human population and are transmitted through direct contact and droplet transmission. Coughing and sneezing efficiently produce infectious aerosols, and rhinoviruses are known to persist on environmental surfaces for up to a week.[1]",True,The Common Cold,,,,
47d1679a-5040-43c3-bed4-835fcbff6ab5,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Viral contact with the nasal mucosa or eyes can lead to infection. Rhinoviruses tend to replicate best between 33 °C (91.4 °F) and 35 °C (95 °F), somewhat below normal body temperature (37 °C [98.6 °F]). As a consequence, they tend to infect the cooler tissues of the nasal cavities. Colds are marked by an irritation of the mucosa that leads to an inflammatory response. This produces common signs and symptoms such as nasal excess nasal secretions (runny nose), congestion, sore throat, coughing, and sneezing. The absence of high fever is typically used to differentiate common colds from other viral infections, like influenza. Some colds may progress to cause otitis media, pharyngitis, or laryngitis, and patients may also experience headaches and body aches. The disease, however, is self-limiting and typically resolves within 1–2 weeks.",True,The Common Cold,,,,
f5610265-de65-4152-b816-6709d638b2f7,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"There are no effective antiviral treatments for the common cold and antibacterial drugs should not be prescribed unless secondary bacterial infections have been established. Many of the viruses that cause colds are related, so immunity develops throughout life. Given the number of viruses that cause colds, however, individuals are never likely to develop immunity to all causes of the common cold.",True,The Common Cold,,,,
4d01f893-09f8-4993-92d8-9181dedb19be,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,Influenza,False,Influenza,,,,
904eb05e-3ee5-4f62-9d5e-9bed17008b77,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Commonly known as the flu, influenza is a common viral disease of the lower respiratory system caused by an orthomyxovirus. Influenza is pervasive worldwide and causes 3,000–50,000 deaths each year in the United States. The annual mortality rate can vary greatly depending on the virulence of the strain(s) responsible for seasonal epidemics.[2]",True,Influenza,,,,
83627a96-ba7e-4504-95d7-2291cca4ddb3,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Influenza infections are most typically characterized by fever, chills, and body aches. This is followed by symptoms similar to the common cold that may last a week or more. Table 17.2 compares the signs and symptoms of influenza and the common cold.",True,Influenza,,,,
61672d95-6299-459b-8274-807bb2e6dcbf,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"In general, influenza is self-limiting. However, serious cases can lead to pneumonia and other complications that can be fatal. Such cases are more common in the very young and the elderly; however, certain strains of influenza virus (like the 1918–1919 variant discussed later in this chapter) are more lethal to young adults than to the very young or old. Strains that affect young adults are believed to involve a cytokine storm—a positive feedback loop that forms between cytokine production and leukocytes. This cytokine storm produces an acute inflammatory response that leads to rapid fluid accumulation in the lungs, culminating in pulmonary failure. In such cases, the ability to mount a vigorous immune response is actually detrimental to the patient. The very young and very old are less susceptible to this effect because their immune systems are less robust.",True,Influenza,,,,
14f2b806-34b2-4043-ac3b-3eb066111a27,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"A complication of influenza that occurs primarily in children and teenagers is Reye syndrome. This sequela causes swelling in the liver and brain, and may progress to neurological damage, coma, or death. Reye syndrome may follow other viral infections, like chickenpox, and has been associated with the use of aspirin. For this reason, the CDC and other agencies recommend that aspirin and products containing aspirin never be used to treat viral illnesses in children younger than age 19 years.[3]",True,Influenza,,,,
d30841ef-3094-4079-b328-3f90d75c5962,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"The influenza virus is primarily transmitted by direct contact and inhalation of aerosols. The RNA genome of this virus exists as seven or eight segments, each coated with ribonucleoprotein and encoding one or two specific viral proteins. The influenza virus is surrounded by a lipid membrane envelope, and two of the main antigens of the influenza virus are the spike proteins hemagglutinin (H) and neuraminidase (N), as shown in Figure 17.15. These spike proteins play important roles in the viral infectious cycle.",True,Influenza,Figure 17.15,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.17.png,"Figure 17.15 The illustration shows the structure of an influenza virus. The viral envelope is studded with copies of the proteins neuraminidase and hemagglutinin, and surrounds the individual seven or eight RNA genome segments. (credit: modification of work by Dan Higgins, Centers for Disease Control and Prevention)"
d30841ef-3094-4079-b328-3f90d75c5962,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"The influenza virus is primarily transmitted by direct contact and inhalation of aerosols. The RNA genome of this virus exists as seven or eight segments, each coated with ribonucleoprotein and encoding one or two specific viral proteins. The influenza virus is surrounded by a lipid membrane envelope, and two of the main antigens of the influenza virus are the spike proteins hemagglutinin (H) and neuraminidase (N), as shown in Figure 17.15. These spike proteins play important roles in the viral infectious cycle.",True,Influenza,Figure 17.15,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.14-1.png,Figure 17.15
29365e74-5c5a-4e39-b40d-c97138b01c78,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"There are three genetically related influenza viruses, called A, B, and C. The influenza A viruses have different subtypes based on the structure of their hemagglutinin and neuraminidase proteins. There are currently 18 known subtypes of hemagglutinin and 11 known subtypes of neuraminidase. Influenza viruses are serologically characterized by the type of H and N proteins that they possess. Of the nearly 200 different combinations of H and N, only a few, such as the H1N1 strain, are associated with human disease. The influenza viruses A, B, and C make up three of the five major groups of orthomyxoviruses. The differences between the three types of influenza are summarized in Table 17.3. The most virulent group is the influenza A viruses, which cause seasonal pandemics of influenza each year. Influenza A virus can infect a variety of animals, including pigs, horses, pigs, and even whales and dolphins. Influenza B virus is less virulent and is sometimes associated with epidemic outbreaks. Influenza C virus generally produces the mildest disease symptoms and is rarely connected with epidemics. Neither influenza B virus nor influenza C virus has significant animal reservoirs.",True,Influenza,,,,
bfd4a707-0dbc-424f-8098-a7cdc8f27e5a,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Influenza virus infections elicit a strong immune response, particularly to the hemagglutinin protein, which would protect the individual if they encountered the same virus. Unfortunately, the antigenic properties of the virus change relatively rapidly, so new strains are evolving that immune systems previously challenged by influenza virus cannot recognize. When an influenza virus gains a new hemagglutinin or neuraminidase type, it is able to evade the host’s immune response and be successfully transmitted, often leading to an epidemic.",True,Influenza,,,,
06a3cfaa-6f4f-4eb0-a2f2-6fcfebc40b2a,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"There are two mechanisms by which these evolutionary changes may occur. The mechanisms of antigen drift and antigenic shift for influenza virus have been described in Virulence Factors of Bacterial and Viral Pathogens. Of these two genetic processes, it is viruses produced by antigenic shift that have the potential to be extremely virulent because individuals previously infected by other strains are unlikely to produce any protective immune response against these novel variants.",True,Influenza,,,,
c0b39b86-d5e5-43a4-9408-57dea978de97,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"The most lethal influenza pandemic in recorded history occurred from 1918 through 1919. Near the end of World War I, an antigenic shift involving the recombination of avian and human viruses is thought to have produced a new H1N1 virus. This strain rapidly spread worldwide and is commonly claimed to have killed as many as 40 million to 50 million people—more than double the number killed in the war. Although referred to as the Spanish flu, this disease is thought to have originated in the United States. Regardless of its source, the conditions of World War I greatly contributed to the spread of this disease. Crowding, poor sanitation, and rapid mobilization of large numbers of personnel and animals facilitated the dissemination of the new virus once it appeared.",True,Influenza,,,,
026b2911-5fa5-42ad-a236-b42c14329d2e,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Laboratory diagnosis of influenza is typically performed using a variety of RIDTs. These tests are inoculated by point-of-care personnel and give results within 15–20 minutes. Unfortunately, these tests have variable sensitivity and commonly yield false-negative results. Other tests include hemagglutination of erythrocytes (due to hemagglutinin action) or complement fixation. Patient serum antibodies against influenza viruses can also be detected in blood samples. Because influenza is self-limiting disease, diagnosis through these more time-consuming and expensive methods is not typically used.",True,Influenza,,,,
7da9a766-9e4d-4cfd-90ed-431afe4529ad,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Three drugs that inhibit influenza neuraminidase activity are available: inhaled zanamivir, oral oseltamivir, and intravenous peramivir. If taken at the onset of symptoms, these drugs can shorten the course of the disease. These drugs are thought to impair the ability of the virus to efficiently exit infected host cells. A more effective means of controlling influenza outbreaks, though, is vaccination. Every year, new influenza vaccines are developed to be effective against the strains expected to be predominant. This is determined in February by a review of the dominant strains around the world from a network of reporting sites; their reports are used to generate a recommendation for the vaccine combination for the following winter in the northern hemisphere. In September, a similar recommendation is made for the winter in the southern hemisphere.[4] These recommendations are used by vaccine manufacturers to formulate each year’s vaccine. In most cases, three or four viruses are selected—the two most prevalent influenza A strains and one or two influenza B strains. The chosen strains are typically cultivated in eggs and used to produce either an inactivated or a live attenuated vaccine (e.g., FluMist). For individuals 18 years or older with an allergy to egg products, a recombinant egg-free trivalent vaccine is available. Most of the influenza vaccines over the past decade have had an effectiveness of about 50%.[5]",True,Influenza,,,,
af6f44cb-1a94-4d7b-a952-28f88c5289fb,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"During the spring of 2013, a new strain of H7N9 influenza was reported in China. A total of 132 people were infected. Of those infected, 44 (33%) died. A genetic analysis of the virus suggested that this strain arose from the reassortment of three different influenza viruses: a domestic duck H7N3 virus, a wild bird H7N9 virus, and a domestic poultry H9N2 virus. The virus was detected in the Chinese domestic bird flocks and contact with this reservoir is thought to have been the primary source of infection. This strain of influenza was not able to spread from person to person. Therefore, the disease did not become a global problem. This case does, though, illustrate the potential threat that influenza still represents. If a strain like the H7N9 virus were to undergo another antigenic shift, it could become more communicable in the human population. With a mortality rate of 33%, such a pandemic would be disastrous. For this reason, organizations like the World Health Organization and the Centers for Disease Control and Prevention keep all known influenza outbreaks under constant surveillance.",True,Influenza,,,,
9ffc73f7-ff5d-40d6-a6d4-49a92a0ffe3d,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,Viral Respiratory Diseases Causing Skin Rashes,False,Viral Respiratory Diseases Causing Skin Rashes,,,,
c3ba095a-bc7a-40ac-9bba-9197d2523fdc,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Measles, rubella (German measles), and chickenpox are three important viral diseases often associated with skin rashes. However, their symptoms are systemic, and because their portal of entry is the respiratory tract, they can be considered respiratory infections.",True,Viral Respiratory Diseases Causing Skin Rashes,,,,
06a687c5-dfb1-4163-b71b-ed696160b1a6,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,Measles (Rubeola),False,Measles (Rubeola),,,,
2460ab79-a339-481e-8854-7bb0d58d57ef,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"The measles virus (MeV) causes the highly contagious disease measles, also known as rubeola, which is a major cause of childhood mortality worldwide. Although vaccination efforts have greatly reduced the incidence of measles in much of the world, epidemics are still common in unvaccinated populations in certain countries.[6]",True,Measles (Rubeola),,,,
05f633ee-8661-4fd0-a287-e1374173b1b3,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"The measles virus is a single-stranded, negative-strand RNA virus and, like the influenza virus, it possesses an envelope with spikes of embedded hemagglutinin. The infection is spread by direct contact with infectious secretions or inhalation of airborne droplets spread by breathing, coughing, or sneezing. Measles is initially characterized by a high fever, conjunctivitis, and a sore throat. The virus then moves systemically through the bloodstream and causes a characteristic rash. The measles rash initially forms on the face and later spreads to the extremities. The red, raised macular rash will eventually become confluent and can last for several days. At the same time, extremely high fevers (higher than 40.6 °C [105 °F]) can occur. Another diagnostic sign of measles infections is Koplik’s spots, white spots that form on the inner lining of inflamed cheek tissues (Figure 17.16).",True,Measles (Rubeola),Figure 17.16,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.18.png,"Figure 17.16 (a) Measles typically presents as a raised macular rash that begins on the face and spreads to the extremities. (b) Koplik’s spots on the oral mucosa are also characteristic of measles. (c) A thin-section transmission electron micrograph of a measles virion. (credit a, b, c: modification of work by Centers for Disease Control and Prevention)"
5ff67608-54a1-420e-ad0a-b54202d4f5a2,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Although measles is usually self-limiting, it can lead to pneumonia, encephalitis, and death. In addition, the inhibition of immune system cells by the measles virus predisposes patients to secondary infections. In severe infections with highly virulent strains, measles fatality rates can be as high as 10% to 15%. There were more than 145,000 measles deaths (mostly young children) worldwide in 2013.[7]",True,Measles (Rubeola),,,,
e581b724-8fcc-4363-b682-775826026435,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,The preliminary diagnosis of measles is typically based on the appearance of the rash and Koplik’s spots. Hemagglutination inhibition tests and serological tests may be used to confirm measles infections in low-prevalence settings.,True,Measles (Rubeola),,,,
aa6b78af-9163-4f46-8101-6aa1c51554c1,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"There are no effective treatments for measles. Vaccination is widespread in developed countries as part of the measles, mumps, and rubella (MMR) vaccine. As a result, there are typically fewer than 200 cases of measles in the United States annually.[8] When it is seen, it is often associated with children who have not been vaccinated.",True,Measles (Rubeola),,,,
61c1e29c-4a85-4e68-adf9-4d7ca458163b,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Several factors could conceivably lead to a strong comeback of measles in the U.S. Measles is still an epidemic disease in many locations worldwide. Air travel enables infected individuals to rapidly translocate these infections globally. Compounding this problem, low vaccination rates in some local areas in the United States (such as in Amish communities) provide populations of susceptible hosts for the virus to establish itself. Finally, measles has been a low-prevalence infection in the U.S. for some time. As a consequence, physicians are not as likely to recognize the initial symptoms and make accurate diagnoses. Until vaccination rates become high enough to ensure herd immunity, measles is likely to be an ongoing problem in the United States.",True,Measles (Rubeola),,,,
6ab66c98-9089-47da-8a62-9ce69c560434,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Chickenpox, also known as varicella, was once a common viral childhood disease. The causative agent of chickenpox, the varicella-zoster virus, is a member of the herpesvirus family. In children, the disease is mild and self- limiting, and is easily transmitted by direct contact or inhalation of material from the skin lesions. In adults, however, chickenpox infections can be much more severe and can lead to pneumonia and birth defects in the case of infected pregnant women. Reye syndrome, mentioned earlier in this chapter, is also a serious complication associated with chickenpox, generally in children.",True,Measles (Rubeola),,,,
0297ab4d-4bf4-4fc2-9155-9a33c7f9cc8a,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Once infected, most individuals acquire a lifetime immunity to future chickenpox outbreaks. For this reason, parents once held “chickenpox parties” for their children. At these events, uninfected children were intentionally exposed to an infected individual so they would contract the disease earlier in life, when the incidence of complications is very low, rather than risk a more severe infection later.",True,Measles (Rubeola),,,,
33229380-3b71-45d4-b8f1-3e49965c199f,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"After the initial viral exposure, chickenpox has an incubation period of about 2 weeks. The initial infection of the respiratory tract leads to viremia and eventually produces fever and chills. A pustular rash then develops on the face, progresses to the trunk, and then the extremities, although most form on the trunk (Figure 17.17). Eventually, the lesions burst and form a crusty scab. Individuals with chickenpox are infectious from about 2 days before the outbreak of the rash until all the lesions have scabbed over.",True,Measles (Rubeola),Figure 17.17,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.20.png,"Figure 17.17 (a) The characteristic appearance of the pustular chickenpox rash is concentrated on the trunk region. (b) This transmission electron micrograph shows a viroid of human herpesvirus 3, the virus that causes chickenpox in children and shingles when it is reactivated in adults. (credit b: modification of work by Centers for Disease Control and Prevention)"
5a0fc3dd-e322-4345-ae89-b0692826d3c5,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Like other herpesviruses, the varicella-zoster virus can become dormant in nerve cells. While the pustular vesicles are developing, the virus moves along sensory nerves to the dorsal ganglia in the spinal cord. Once there, the varicella-zoster virus can remain latent for decades. These dormant viruses may be reactivated later in life by a variety of stimuli, including stress, aging, and immunosuppression. Once reactivated, the virus moves along sensory nerves to the skin of the face or trunk. This results in the production of the painful lesions in a condition known as shingles (Figure 17.18). These symptoms generally last for 2–6 weeks, and may recur more than once. Postherpetic neuralgia, pain signals sent from damaged nerves long after the other symptoms have subsided, is also possible. In addition, the virus can spread to other organs in immunocompromised individuals. A person with shingles lesions can transmit the virus to a nonimmune contact, and the newly infected individual would develop chickenpox as the primary infection. Shingles cannot be transmitted from one person to another.",True,Measles (Rubeola),Figure 17.18,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.21.png,Figure 17.18 (a) An individual suffering from shingles. (b) The rash is formed because of the reactivation of a varicella-zoster infection that was initially contracted in childhood. (credit a: modification of work by National Institute of Allergy and Infectious Diseases (NIAID); credit b: modification of work by Centers for Disease Control and Prevention)
15094f01-9b70-430e-aa21-4ec4fd0d2903,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"The primary diagnosis of chickenpox in children is mainly based on the presentation of a pustular rash of the trunk. Serological and PCR-based tests are available to confirm the initial diagnosis. Treatment for chickenpox infections in children is usually not required. In patients with shingles, acyclovir treatment can often reduce the severity and length of symptoms, and diminish the risk of postherpetic neuralgia. An effective vaccine is now available for chickenpox. A vaccine is also available for adults older than 60 years who were infected with chickenpox in their youth. This vaccine reduces the likelihood of a shingles outbreak by boosting the immune defenses that are keeping the latent infection in check and preventing reactivation.",True,Measles (Rubeola),,,,
2eee6efd-8442-4d8b-bd83-1c89ef63ad72,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"A complication of influenza that occurs primarily in children and teenagers is Reye syndrome. This sequela causes swelling in the liver and brain, and may progress to neurological damage, coma, or death. Reye syndrome may follow other viral infections, like chickenpox, and has been associated with the use of aspirin. For this reason, the CDC and other agencies recommend that aspirin and products containing aspirin never be used to treat viral illnesses in children younger than age 19 years.[3]",True,Measles (Rubeola),,,,
5d21bfdb-11c1-4737-9bcb-3aac17478acc,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"The influenza virus is primarily transmitted by direct contact and inhalation of aerosols. The RNA genome of this virus exists as seven or eight segments, each coated with ribonucleoprotein and encoding one or two specific viral proteins. The influenza virus is surrounded by a lipid membrane envelope, and two of the main antigens of the influenza virus are the spike proteins hemagglutinin (H) and neuraminidase (N), as shown in Figure 17.15. These spike proteins play important roles in the viral infectious cycle.",True,Measles (Rubeola),Figure 17.15,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.17.png,"Figure 17.15 The illustration shows the structure of an influenza virus. The viral envelope is studded with copies of the proteins neuraminidase and hemagglutinin, and surrounds the individual seven or eight RNA genome segments. (credit: modification of work by Dan Higgins, Centers for Disease Control and Prevention)"
5d21bfdb-11c1-4737-9bcb-3aac17478acc,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"The influenza virus is primarily transmitted by direct contact and inhalation of aerosols. The RNA genome of this virus exists as seven or eight segments, each coated with ribonucleoprotein and encoding one or two specific viral proteins. The influenza virus is surrounded by a lipid membrane envelope, and two of the main antigens of the influenza virus are the spike proteins hemagglutinin (H) and neuraminidase (N), as shown in Figure 17.15. These spike proteins play important roles in the viral infectious cycle.",True,Measles (Rubeola),Figure 17.15,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.14-1.png,Figure 17.15
3b12c560-855f-4390-bce5-a4534cf38c81,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"There are three genetically related influenza viruses, called A, B, and C. The influenza A viruses have different subtypes based on the structure of their hemagglutinin and neuraminidase proteins. There are currently 18 known subtypes of hemagglutinin and 11 known subtypes of neuraminidase. Influenza viruses are serologically characterized by the type of H and N proteins that they possess. Of the nearly 200 different combinations of H and N, only a few, such as the H1N1 strain, are associated with human disease. The influenza viruses A, B, and C make up three of the five major groups of orthomyxoviruses. The differences between the three types of influenza are summarized in Table 17.3. The most virulent group is the influenza A viruses, which cause seasonal pandemics of influenza each year. Influenza A virus can infect a variety of animals, including pigs, horses, pigs, and even whales and dolphins. Influenza B virus is less virulent and is sometimes associated with epidemic outbreaks. Influenza C virus generally produces the mildest disease symptoms and is rarely connected with epidemics. Neither influenza B virus nor influenza C virus has significant animal reservoirs.",True,Measles (Rubeola),,,,
e0ce109a-7ba3-46d8-800b-8dfe9637bb18,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Influenza virus infections elicit a strong immune response, particularly to the hemagglutinin protein, which would protect the individual if they encountered the same virus. Unfortunately, the antigenic properties of the virus change relatively rapidly, so new strains are evolving that immune systems previously challenged by influenza virus cannot recognize. When an influenza virus gains a new hemagglutinin or neuraminidase type, it is able to evade the host’s immune response and be successfully transmitted, often leading to an epidemic.",True,Measles (Rubeola),,,,
0cdb5593-7ea0-462c-9c10-2bc78bb2982a,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"The most lethal influenza pandemic in recorded history occurred from 1918 through 1919. Near the end of World War I, an antigenic shift involving the recombination of avian and human viruses is thought to have produced a new H1N1 virus. This strain rapidly spread worldwide and is commonly claimed to have killed as many as 40 million to 50 million people—more than double the number killed in the war. Although referred to as the Spanish flu, this disease is thought to have originated in the United States. Regardless of its source, the conditions of World War I greatly contributed to the spread of this disease. Crowding, poor sanitation, and rapid mobilization of large numbers of personnel and animals facilitated the dissemination of the new virus once it appeared.",True,Measles (Rubeola),,,,
84509d86-8345-4ccf-a60b-1544e31f5b86,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Laboratory diagnosis of influenza is typically performed using a variety of RIDTs. These tests are inoculated by point-of-care personnel and give results within 15–20 minutes. Unfortunately, these tests have variable sensitivity and commonly yield false-negative results. Other tests include hemagglutination of erythrocytes (due to hemagglutinin action) or complement fixation. Patient serum antibodies against influenza viruses can also be detected in blood samples. Because influenza is self-limiting disease, diagnosis through these more time-consuming and expensive methods is not typically used.",True,Measles (Rubeola),,,,
4bcebbca-8bf7-4882-a599-5ca4b4c07d38,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Three drugs that inhibit influenza neuraminidase activity are available: inhaled zanamivir, oral oseltamivir, and intravenous peramivir. If taken at the onset of symptoms, these drugs can shorten the course of the disease. These drugs are thought to impair the ability of the virus to efficiently exit infected host cells. A more effective means of controlling influenza outbreaks, though, is vaccination. Every year, new influenza vaccines are developed to be effective against the strains expected to be predominant. This is determined in February by a review of the dominant strains around the world from a network of reporting sites; their reports are used to generate a recommendation for the vaccine combination for the following winter in the northern hemisphere. In September, a similar recommendation is made for the winter in the southern hemisphere.[4] These recommendations are used by vaccine manufacturers to formulate each year’s vaccine. In most cases, three or four viruses are selected—the two most prevalent influenza A strains and one or two influenza B strains. The chosen strains are typically cultivated in eggs and used to produce either an inactivated or a live attenuated vaccine (e.g., FluMist). For individuals 18 years or older with an allergy to egg products, a recombinant egg-free trivalent vaccine is available. Most of the influenza vaccines over the past decade have had an effectiveness of about 50%.[5]",True,Measles (Rubeola),,,,
bf098e2f-bae5-4f13-a815-a0b88816111b,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,Viral Respiratory Diseases Causing Skin Rashes,False,Viral Respiratory Diseases Causing Skin Rashes,,,,
1cadcb61-92f8-47ec-9acd-d572c1b51171,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Measles, rubella (German measles), and chickenpox are three important viral diseases often associated with skin rashes. However, their symptoms are systemic, and because their portal of entry is the respiratory tract, they can be considered respiratory infections.",True,Viral Respiratory Diseases Causing Skin Rashes,,,,
9bae5a82-5878-4c8a-a693-cde184bd3e18,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"The measles virus (MeV) causes the highly contagious disease measles, also known as rubeola, which is a major cause of childhood mortality worldwide. Although vaccination efforts have greatly reduced the incidence of measles in much of the world, epidemics are still common in unvaccinated populations in certain countries.[6]",True,Viral Respiratory Diseases Causing Skin Rashes,,,,
b143364a-6d4f-4374-999b-42b42817d193,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"The measles virus is a single-stranded, negative-strand RNA virus and, like the influenza virus, it possesses an envelope with spikes of embedded hemagglutinin. The infection is spread by direct contact with infectious secretions or inhalation of airborne droplets spread by breathing, coughing, or sneezing. Measles is initially characterized by a high fever, conjunctivitis, and a sore throat. The virus then moves systemically through the bloodstream and causes a characteristic rash. The measles rash initially forms on the face and later spreads to the extremities. The red, raised macular rash will eventually become confluent and can last for several days. At the same time, extremely high fevers (higher than 40.6 °C [105 °F]) can occur. Another diagnostic sign of measles infections is Koplik’s spots, white spots that form on the inner lining of inflamed cheek tissues (Figure 17.16).",True,Viral Respiratory Diseases Causing Skin Rashes,Figure 17.16,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.18.png,"Figure 17.16 (a) Measles typically presents as a raised macular rash that begins on the face and spreads to the extremities. (b) Koplik’s spots on the oral mucosa are also characteristic of measles. (c) A thin-section transmission electron micrograph of a measles virion. (credit a, b, c: modification of work by Centers for Disease Control and Prevention)"
47805c38-b981-4067-9ea8-f388d77f1c47,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Although measles is usually self-limiting, it can lead to pneumonia, encephalitis, and death. In addition, the inhibition of immune system cells by the measles virus predisposes patients to secondary infections. In severe infections with highly virulent strains, measles fatality rates can be as high as 10% to 15%. There were more than 145,000 measles deaths (mostly young children) worldwide in 2013.[7]",True,Viral Respiratory Diseases Causing Skin Rashes,,,,
c2078311-7c5f-4eb6-9c53-7e5b9cb3100c,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,The preliminary diagnosis of measles is typically based on the appearance of the rash and Koplik’s spots. Hemagglutination inhibition tests and serological tests may be used to confirm measles infections in low-prevalence settings.,True,Viral Respiratory Diseases Causing Skin Rashes,,,,
76bb7b2f-9313-4f75-b3b9-da5cd0186070,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"There are no effective treatments for measles. Vaccination is widespread in developed countries as part of the measles, mumps, and rubella (MMR) vaccine. As a result, there are typically fewer than 200 cases of measles in the United States annually.[8] When it is seen, it is often associated with children who have not been vaccinated.",True,Viral Respiratory Diseases Causing Skin Rashes,,,,
d6ab7e03-97d3-4b91-9692-6c15c3cb9d24,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Several factors could conceivably lead to a strong comeback of measles in the U.S. Measles is still an epidemic disease in many locations worldwide. Air travel enables infected individuals to rapidly translocate these infections globally. Compounding this problem, low vaccination rates in some local areas in the United States (such as in Amish communities) provide populations of susceptible hosts for the virus to establish itself. Finally, measles has been a low-prevalence infection in the U.S. for some time. As a consequence, physicians are not as likely to recognize the initial symptoms and make accurate diagnoses. Until vaccination rates become high enough to ensure herd immunity, measles is likely to be an ongoing problem in the United States.",True,Viral Respiratory Diseases Causing Skin Rashes,,,,
5eef601c-f60b-47c1-98d8-0e2c0a25b8dc,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"Once infected, most individuals acquire a lifetime immunity to future chickenpox outbreaks. For this reason, parents once held “chickenpox parties” for their children. At these events, uninfected children were intentionally exposed to an infected individual so they would contract the disease earlier in life, when the incidence of complications is very low, rather than risk a more severe infection later.",True,Viral Respiratory Diseases Causing Skin Rashes,,,,
52d34393-8461-46af-8243-2ce03ec17766,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"After the initial viral exposure, chickenpox has an incubation period of about 2 weeks. The initial infection of the respiratory tract leads to viremia and eventually produces fever and chills. A pustular rash then develops on the face, progresses to the trunk, and then the extremities, although most form on the trunk (Figure 17.17). Eventually, the lesions burst and form a crusty scab. Individuals with chickenpox are infectious from about 2 days before the outbreak of the rash until all the lesions have scabbed over.",True,Viral Respiratory Diseases Causing Skin Rashes,Figure 17.17,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.20.png,"Figure 17.17 (a) The characteristic appearance of the pustular chickenpox rash is concentrated on the trunk region. (b) This transmission electron micrograph shows a viroid of human herpesvirus 3, the virus that causes chickenpox in children and shingles when it is reactivated in adults. (credit b: modification of work by Centers for Disease Control and Prevention)"
662a53dd-1f5b-46af-a044-3656fc62686a,https://open.oregonstate.education/microbiology/,17.3	Viral Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-3viral-infections-of-the-respiratory-tract/,"The primary diagnosis of chickenpox in children is mainly based on the presentation of a pustular rash of the trunk. Serological and PCR-based tests are available to confirm the initial diagnosis. Treatment for chickenpox infections in children is usually not required. In patients with shingles, acyclovir treatment can often reduce the severity and length of symptoms, and diminish the risk of postherpetic neuralgia. An effective vaccine is now available for chickenpox. A vaccine is also available for adults older than 60 years who were infected with chickenpox in their youth. This vaccine reduces the likelihood of a shingles outbreak by boosting the immune defenses that are keeping the latent infection in check and preventing reactivation.",True,Viral Respiratory Diseases Causing Skin Rashes,,,,
506204e0-db6b-46fd-a5c2-c9fbde004fa2,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,Streptococcal Infections,False,Streptococcal Infections,,,,
054e3fa8-71db-41f7-8d16-ff35b0ae6a47,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"A common upper respiratory infection, streptococcal pharyngitis (strep throat) is caused by Streptococcus pyogenes. This gram-positive bacterium appears as chains of cocci, as seen in Figure 17.5. Rebecca Lancefield serologically classified streptococci in the 1930s using carbohydrate antigens from the bacterial cell walls. S. pyogenes is the sole member of the Lancefield group A streptococci and is often referred to as GAS, or group A strep.",True,Streptococcal Infections,Figure 17.5,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.5.png,Figure 17.5 This scanning electron micrograph of Streptococcus pyogenes shows the characteristic cellular phenotype resembling chains of cocci. (credit: modification of work by U.S. Centers for Disease Control and Prevention – Medical Illustrator)
0e20d406-926d-4de7-989d-013f229217de,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Similar to streptococcal infections of the skin, the mucosal membranes of the pharynx are damaged by the release of a variety of exoenzymes and exotoxins by this extracellular pathogen. Many strains of S. pyogenes can degrade connective tissues by using hyaluronidase, collagenase and streptokinase. Streptokinase activates plasmin, which leads to degradation of fibrin and, in turn, dissolution of blood clots, which assists in the spread of the pathogen. Released toxins include streptolysins that can destroy red and white blood cells. The classic signs of streptococcal pharyngitis are a fever higher than 38 °C (100.4 °F); intense pharyngeal pain; erythema associated with pharyngeal inflammation; and swollen, dark-red palatine tonsils, often dotted with patches of pus; and petechiae (microcapillary hemorrhages) on the soft or hard palate (roof of the mouth) (Figure 17.6). The submandibular lymph nodes beneath the angle of the jaw are also often swollen during strep throat.",True,Streptococcal Infections,Figure 17.6,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.6.png,Figure 17.6 Streptococcal infections of the respiratory tract may cause localized pharyngitis or systemic signs and symptoms. (a) The characteristic appearance of strep throat: bright red arches of inflammation with the presence of dark-red spots (petechiae). (b) Scarlet fever presents as a rash on the skin. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by Alicia Williams)
ac293ef2-9b40-4976-93dc-0ebd3a0e0cce,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Some strains of group A streptococci produce erythrogenic toxin. This exotoxin is encoded by a temperate bacteriophage (bacterial virus) and is an example of phage conversion (see The Viral Life Cycle). The toxin attacks the plasma membranes of capillary endothelial cells and leads to scarlet fever (or scarlatina), a disseminated fine red rash on the skin, and strawberry tongue, a red rash on the tongue (Figure 17.6). Severe cases may even lead tostreptococcal toxic shock syndrome (STSS), which results from massive superantigen production that leads to septic shock and death.",True,Streptococcal Infections,Figure 17.6,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.6.png,Figure 17.6 Streptococcal infections of the respiratory tract may cause localized pharyngitis or systemic signs and symptoms. (a) The characteristic appearance of strep throat: bright red arches of inflammation with the presence of dark-red spots (petechiae). (b) Scarlet fever presents as a rash on the skin. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by Alicia Williams)
baa81416-5a50-4f41-9c39-2c2814f40e8a,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"S. pyogenes can be easily spread by direct contact or droplet transmission through coughing and sneezing. The disease can be diagnosed quickly using a rapid enzyme immunoassay for the group A antigen. However, due to a significant rate of false-negative results (up to 30%[2]), culture identification is still the gold standard to confirm pharyngitis due to S. pyogenes. S. pyogenes can be identified as a catalase-negative, beta hemolytic bacterium that is susceptible to 0.04 units of bacitracin. Antibiotic resistance is limited for this bacterium, so most β-lactams remain effective; oral amoxicillin and intramuscular penicillin G are those most commonly prescribed.",True,Streptococcal Infections,,,,
bacc8288-9ce3-40b0-98d3-a7ba5c73905e,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"One reason strep throat infections are aggressively treated with antibiotics is because they can lead to serious sequelae, later clinical consequences of a primary infection. It is estimated that 1%–3% of untreated S. pyogenes infections can be followed by nonsuppurative (without the production of pus) sequelae that develop 1–3 weeks after the acute infection has resolved. Two such sequelae are acute rheumatic fever and acute glomerulonephritis.",True,Streptococcal Infections,,,,
9683095a-94ef-48d7-a0de-8d093229cd86,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Acute rheumatic fever can follow pharyngitis caused by specific rheumatogenic strains of S. pyogenes (strains 1, 3, 5, 6, and 18). Although the exact mechanism responsible for this sequela remains unclear, molecular mimicry between the M protein of rheumatogenic strains of S. pyogenes and heart tissue is thought to initiate the autoimmune attack. The most serious and lethal clinical manifestation of rheumatic fever is damage to and inflammation of the heart (carditis). Acute glomerulonephritis also results from an immune response to streptococcal antigens following pharyngitis and cutaneous infections. Acute glomerulonephritis develops within 6–10 days after pharyngitis, but can take up to 21 days after a cutaneous infection. Similar to acute rheumatic fever, there are strong associations between specific nephritogenic strains of S. pyogenes and acute glomerulonephritis, and evidence suggests a role for antigen mimicry and autoimmunity. However, the primary mechanism of acute glomerulonephritis appears to be the formation of immune complexes between S. pyogenes antigens and antibodies, and their deposition between endothelial cells of the glomeruli of kidney. Inflammatory response against the immune complexes leads to damage and inflammation of the glomeruli (glomerulonephritis).",True,Streptococcal Infections,,,,
ff884b8f-487e-48bc-857c-e17a4ed6c3a7,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,Acute Otitis Media,False,Acute Otitis Media,,,,
bbeb3170-d07b-44ca-995e-1fc2487f8f8f,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"An infection of the middle ear is called acute otitis media (AOM), but often it is simply referred to as an earache. The condition is most common between ages 3 months and 3 years. In the United States, AOM is the second-leading cause of visits to pediatricians by children younger than age 5 years, and it is the leading indication for antibiotic prescription.[3]",True,Acute Otitis Media,,,,
423b747a-bbfd-4026-ad16-91819667485a,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"AOM is characterized by the formation and accumulation of pus in the middle ear. Unable to drain, the pus builds up, resulting in moderate to severe bulging of the tympanic membrane and otalgia (ear pain). Inflammation resulting from the infection leads to swelling of the eustachian tubes, and may also lead to fever, nausea, vomiting, and diarrhea, particularly in infants. Infants and toddlers who cannot yet speak may exhibit nonverbal signs suggesting AOM, such as holding, tugging, or rubbing of the ear, as well as uncharacteristic crying or distress in response to the pain.",True,Acute Otitis Media,,,,
aa6eb866-c0e6-43d1-968b-6fe9f22c5e5e,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"AOM can be caused by a variety of bacteria. Among neonates, S. pneumoniae is the most common cause of AOM, but Escherichia coli, Enterococcus spp., and group B Streptococcus species can also be involved. In older infants and children younger than 14 years old, the most common bacterial causes are S. pneumoniae, Haemophilus influenzae, or Moraxella catarrhalis. Among S. pneumoniae infections, encapsulated strains are frequent causes of AOM. By contrast, the strains of H. influenzae and M. cattarhalis that are responsible for AOM do not possess a capsule. Rather than direct tissue damage by these pathogens, bacterial components such as lipopolysaccharide (LPS) in gram- negative pathogens induce an inflammatory response that causes swelling, pus, and tissue damage within the middle ear (Figure 17.7).",True,Acute Otitis Media,Figure 17.7,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.7.png,"Figure 17.7 (a) A healthy tympanic membrane; the middle ear bones can be seen behind the membrane. (b) An ear with chronic inflammation that has resulted in a torn membrane, erosion of the inner ear bones, and mucus buildup. (credit a: modification of work by “DrER.tv”/YouTube; credit b: modification of work by Li Mg, Hotez PJ, Vrabec JT, Donovan DT)"
f60c7bd6-b79c-41fc-b341-4b0d56ed739f,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Any blockage of the eustachian tubes, with or without infection, can cause fluid to become trapped and accumulate in the middle ear. This is referred to as otitis media with effusion (OME). The accumulated fluid offers an excellent reservoir for microbial growth and, consequently, secondary bacterial infections often ensue. This can lead to recurring and chronic earaches, which are especially common in young children. The higher incidence in children can be attributed to many factors. Children have more upper respiratory infections, in general, and their eustachian tubes are also shorter and drain at a shallower angle. Young children also tend to spend more time lying down than adults, which facilitates drainage from the nasopharynx through the eustachian tube and into the middle ear. Bottle feeding while lying down enhances this risk because the sucking action on the bottle causes negative pressure to build up within the eustachian tube, promoting the movement of fluid and bacteria from the nasopharynx.",True,Acute Otitis Media,,,,
df7274d1-9dc8-4458-9fb2-c3c2108de6f2,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Diagnosis is typically made based on clinical signs and symptoms, without laboratory testing to determine the specific causative agent. Antibiotics are frequently prescribed for the treatment of AOM. High-dose amoxicillin is the first-line drug, but with increasing resistance concerns, macrolides and cephalosporins may also be used. The pneumococcal conjugate vaccine (PCV13) contains serotypes that are important causes of AOM, and vaccination has been shown to decrease the incidence of AOM. Vaccination against influenza has also been shown to decrease the risk for AOM, likely because viral infections like influenza predispose patients to secondary infections with S. pneumoniae. Although there is a conjugate vaccine available for the invasive serotype B of H. influenzae, this vaccine does not impact the incidence of H. influenzae AOM. Because unencapsulated strains of H. influenzae and M. catarrhalis are involved in AOM, vaccines against bacterial cellular factors other than capsules will need to be developed.",True,Acute Otitis Media,,,,
4fe2dba9-85bf-468c-856b-dc2817c6f1d0,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,Bacterial Pneumonia,False,Bacterial Pneumonia,,,,
7145273a-8579-4505-b587-848dfb0ffdc0,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Pneumonia is a general term for infections of the lungs that lead to inflammation and accumulation of fluids and white blood cells in the alveoli. Pneumonia can be caused by bacteria, viruses, fungi, and other organisms, although the vast majority of pneumonias are bacterial in origin. Bacterial pneumonia is a prevalent, potentially serious infection; it caused more 50,000 deaths in the United States in 2014.[4] As the alveoli fill with fluids and white blood cells (consolidation), air exchange becomes impaired and patients experience respiratory distress (Figure 17.8). In addition, pneumonia can lead to pleurisy, an infection of the pleural membrane surrounding the lungs, which can make breathing very painful. Although many different bacteria can cause pneumonia under the right circumstances, three bacterial species cause most clinical cases: Streptococcus pneumoniae, H. influenzae, and Mycoplasma pneumoniae. In addition to these, we will also examine some of the less common causes of pneumonia.",True,Bacterial Pneumonia,Figure 17.8,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.9.png,Figure 17.8 A chest radiograph of a patient with pneumonia shows the consolidations (lesions) present as opaque patches. (credit: modification of work by Centers for Disease Control and Prevention)
e080a96d-b848-4b5f-8a09-a5b22bbfbed5,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"The most common cause of community-acquired bacterial pneumonia is Streptococcus pneumoniae. This gram- positive, alpha hemolytic streptococcus is commonly found as part of the normal microbiota of the human respiratory tract. The cells tend to be somewhat lancet-shaped and typically appear as pairs (Figure 17.9). The pneumococci initially colonize the bronchioles of the lungs. Eventually, the infection spreads to the alveoli, where the microbe’s polysaccharide capsule interferes with phagocytic clearance. Other virulence factors include autolysins like Lyt A, which degrade the microbial cell wall, resulting in cell lysis and the release of cytoplasmic virulence factors. One of these factors, pneumolysin O, is important in disease progression; this pore-forming protein damages host cells, promotes bacterial adherence, and enhances pro-inflammatory cytokine production. The resulting inflammatory response causes the alveoli to fill with exudate rich in neutrophils and red blood cells. As a consequence, infected individuals develop a productive cough with bloody sputum.",True,Bacterial Pneumonia,Figure 17.9,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.10.png,"Figure 17.9 (a) This micrograph of Streptococcus pneumoniae grown from a blood culture shows the characteristic lancet-shaped diplococcal morphology. (b) A colorized scanning electron micrograph of S. pneumoniae. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by Janice Carr, Centers for Disease Control and Prevention)"
f5b42ae4-20b5-4be7-8d83-413144291fce,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Pneumococci can be presumptively identified by their distinctive gram-positive, lancet-shaped cell morphology and diplococcal arrangement. In blood agar cultures, the organism demonstrates alpha hemolytic colonies that are autolytic after 24 to 48 hours. In addition, S. pneumoniae is extremely sensitive to optochin and colonies are rapidly destroyed by the addition of 10% solution of sodium deoxycholate. All clinical pneumococcal isolates are serotyped using the quellung reaction with typing antisera produced by the CDC. Positive quellung reactions are considered definitive identification of pneumococci.",True,Bacterial Pneumonia,,,,
3547ba98-00a6-4cf6-9380-bbc726c6c14d,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Antibiotics remain the mainstay treatment for pneumococci. β-Lactams like penicillin are the first-line drugs, but resistance to β-lactams is a growing problem. When β-lactam resistance is a concern, macrolides and fluoroquinolones may be prescribed. However, S. pneumoniae resistance to macrolides and fluoroquinolones is increasing as well, limiting the therapeutic options for some infections. There are currently two pneumococcal vaccines available: pneumococcal conjugate vaccine (PCV13) and pneumococcal polysaccharide vaccine (PPSV23). These are generally given to the most vulnerable populations of individuals: children younger than 2 years and adults older than 65 years.",True,Bacterial Pneumonia,,,,
7184108c-dab9-4800-ba1e-09efe950f7e9,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,Haemophilus Pneumonia,False,Haemophilus Pneumonia,,,,
5b065729-2e01-4342-b06b-4082b3f4fd48,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Encapsulated strains of Haemophilus influenzae are known for causing meningitis, but nonencapsulated strains are important causes of pneumonia. This small, gram-negative coccobacillus is found in the pharynx of the majority of healthy children; however, Haemophilus pneumonia is primarily seen in the elderly. Like other pathogens that cause pneumonia, H. influenzae is spread by droplets and aerosols produced by coughing. A fastidious organism, H. influenzae will only grow on media with available factor X (hemin) and factor V (NAD), like chocolate agar (Figure 17.10). Serotyping must be performed to confirm identity of H. influenzae isolates.",True,Haemophilus Pneumonia,Figure 17.10,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.11.png,Figure 17.10 Culture of Haemophilus influenzae on a chocolate agar plate. (credit: modification of work by Centers for Disease Control and Prevention)
08cb179f-0a7e-4181-aa6a-cd37222e8480,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Infections of the alveoli by H. influenzae result in inflammation and accumulation of fluids. Increasing resistance to β-lactams, macrolides, and tetracyclines presents challenges for the treatment of Haemophilus pneumonia. Resistance to the fluoroquinolones is rare among isolates of H. influenzae but has been observed. As discussed for AOM, a vaccine directed against nonencapsulated H. influenzae, if developed, would provide protection against pneumonia caused by this pathogen.",True,Haemophilus Pneumonia,,,,
b55155e7-a54b-4671-8f5b-c4250a333aaf,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Primary atypical pneumonia is caused by Mycoplasma pneumoniae. This bacterium is not part of the respiratory tract’s normal microbiota and can cause epidemic disease outbreaks. Also known as walking pneumonia, mycoplasma pneumonia infections are common in crowded environments like college campuses and military bases. It is spread by aerosols formed when coughing or sneezing. The disease is often mild, with a low fever and persistent cough. These bacteria, which do not have cell walls, use a specialized attachment organelle to bind to ciliated cells. In the process, epithelial cells are damaged and the proper function of the cilia is hindered (Figure 17.11).",True,Haemophilus Pneumonia,Figure 17.11,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.12.png,Figure 17.11 The micrograph shows Mycoplasma pneumoniae using their specialized receptors to attach to epithelial cells in the trachea of an infected hamster. (credit: modification of work by American Society for Microbiology)
4498d32e-cbfe-4b16-8a5e-6d7e78bb25bf,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Tracy is a 6-year old who developed a serious cough that would not seem to go away. After 2 weeks, her parents became concerned and took her to the pediatrician, who suspected a case of bacterial pneumonia. Tests confirmed that the cause was Haemophilus influenzae. Fortunately, Tracy responded well to antibiotic treatment and eventually made a full recovery.",True,Haemophilus Pneumonia,,,,
0dc83912-ebfd-403e-ad51-a40cb7db53ec,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Because there had been several other cases of bacterial pneumonia at Tracy’s elementary school, local health officials urged parents to have their children screened. Of the children who were screened, it was discovered that greater than 50% carried H. influenzae in their nasal cavities, yet all but two of them were asymptomatic.",True,Haemophilus Pneumonia,,,,
2602cb1c-649c-4b1a-bfdb-86303d8680da,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Why is it that some individuals become seriously ill from bacterial infections that seem to have little or no effect on others? The pathogenicity of an organism—its ability to cause host damage—is not solely a property of the microorganism. Rather, it is the product of a complex relationship between the microbe’s virulence factors and the immune defenses of the individual. Preexisting conditions and environmental factors such as exposure to secondhand smoke can make some individuals more susceptible to infection by producing conditions favorable to microbial growth or compromising the immune system. In addition, individuals may have genetically determined immune factors that protect them—or not—from particular strains of pathogens. The interactions between these host factors and the pathogenicity factors produced by the microorganism ultimately determine the outcome of the infection. A clearer understanding of these interactions may allow for better identification of at-risk individuals and prophylactic interventions in the future.",True,Haemophilus Pneumonia,,,,
5ff5c4fd-5670-40b9-addb-80ef50caa507,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Mycoplasma grow very slowly when cultured. Therefore, penicillin and thallium acetate are added to agar to prevent the overgrowth by faster-growing potential contaminants. Since M. pneumoniae does not have a cell wall, it is resistant to these substances. Without a cell wall, the microbial cells appear pleomorphic. M. pneumoniae infections tend to be self-limiting but may also respond well to macrolide antibiotic therapy. β-lactams, which target cell wall synthesis, are not indicated for treatment of infections with this pathogen.",True,Haemophilus Pneumonia,,,,
19a75659-b65e-4755-b541-ad447157fa0f,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,Tuberculosis,False,Tuberculosis,,,,
e72a4773-9c52-4657-9192-d5107af0f070,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Tuberculosis (TB) is one of the deadliest infectious diseases in human history. Although tuberculosis infection rates in the United States are extremely low, the CDC estimates that about one-third of the world’s population is infected with Mycobacterium tuberculosis, the causal organism of TB, with 9.6 million new TB cases and 1.5 million deaths worldwide in 2014.[5]",True,Tuberculosis,,,,
779b048d-db3b-495f-a1a5-5ce5d54ea8db,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"M. tuberculosis is an acid-fast, high G + C, gram-positive, nonspore-forming rod. Its cell wall is rich in waxy mycolic acids, which make the cells impervious to polar molecules. It also causes these organisms to grow slowly.",True,Tuberculosis,,,,
343d3467-3d98-46a1-b4fc-1b44179e98d5,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"M. tuberculosis causes a chronic granulomatous disease that can infect any area of the body, although it is typically associated with the lungs. M. tuberculosis is spread by inhalation of respiratory droplets or aerosols from an infected person. The infectious dose of M. tuberculosis is only 10 cells.[6]",True,Tuberculosis,,,,
fd7c5894-751f-412d-b673-28c6e988a1d1,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"After inhalation, the bacteria enter the alveoli (Figure 17.12). The cells are phagocytized by macrophages but can survive and multiply within these phagocytes because of the protection by the waxy mycolic acid in their cell walls. If not eliminated by macrophages, the infection can progress, causing an inflammatory response and an accumulation of neutrophils and macrophages in the area. Several weeks or months may pass before an immunological response is mounted by T cells and B cells. Eventually, the lesions in the alveoli become walled off, forming small round lesions called tubercles. Bacteria continue to be released into the center of the tubercles and the chronic immune response results in tissue damage and induction of apoptosis (programmed host-cell death) in a process called liquefaction. This creates a caseous center, or air pocket, where the aerobic M. tuberculosis can grow and multiply. Tubercles may eventually rupture and bacterial cells can invade pulmonary capillaries; from there, bacteria can spread through the bloodstream to other organs, a condition known as miliary tuberculosis. The rupture of tubercles also facilitates transmission of the bacteria to other individuals via droplet aerosols that exit the body in coughs. Because these droplets can be very small and stay aloft for a long time, special precautions are necessary when caring for patients with TB, such as the use of face masks and negative-pressure ventilation and filtering systems.",True,Tuberculosis,Figure 17.12,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.13.png,"Figure 17.12 In the infectious cycle of tuberculosis, the immune response of most infected individuals (approximately 90%) results in the formation of tubercles in which the infection is walled off.[footnote]G. Kaplan et al. “Mycobacterium tuberculosis Growth at the Cavity Surface: A Microenvironment with Failed Immunity.” Infection and Immunity 71 no.12 (2003):7099–7108.[/footnote] The remainder will suffer progressive primary tuberculosis. The sequestered bacteria may be reactivated to form secondary tuberculosis in immunocompromised patients at a later time. (credit: modification of work by Centers for Disease Control and Prevention)"
6f03b756-26ca-423f-b432-180b59c13384,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Eventually, most lesions heal to form calcified Ghon complexes. These structures are visible on chest radiographs and are a useful diagnostic feature. But even after the disease has apparently ended, viable bacteria remain sequestered in these locations. Release of these organisms at a later time can produce reactivation tuberculosis (or secondary TB). This is mainly observed in people with alcoholism, the elderly, or in otherwise immunocompromised individuals (Figure 17.12).",True,Tuberculosis,Figure 17.12,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.13.png,"Figure 17.12 In the infectious cycle of tuberculosis, the immune response of most infected individuals (approximately 90%) results in the formation of tubercles in which the infection is walled off.[footnote]G. Kaplan et al. “Mycobacterium tuberculosis Growth at the Cavity Surface: A Microenvironment with Failed Immunity.” Infection and Immunity 71 no.12 (2003):7099–7108.[/footnote] The remainder will suffer progressive primary tuberculosis. The sequestered bacteria may be reactivated to form secondary tuberculosis in immunocompromised patients at a later time. (credit: modification of work by Centers for Disease Control and Prevention)"
105bb5f3-9ca3-4e82-ad0b-b8892969c9fd,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Because TB is a chronic disease, chemotherapeutic treatments often continue for months or years. Multidrug resistant (MDR-TB) and extensively drug-resistant (XDR-TB) strains of M. tuberculosis are a growing clinical concern. These strains can arise due to misuse or mismanagement of antibiotic therapies. Therefore, it is imperative that proper multidrug protocols are used to treat these infections. Common antibiotics included in these mixtures are isoniazid, rifampin, ethambutol, and pyrazinamide.",True,Tuberculosis,,,,
b4dd6120-a070-4695-b87a-ed670e907d36,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"A TB vaccine is available that is based on the so-called bacillus Calmette-Guérin (BCG) strain of M. bovis commonly found in cattle. In the United States, the BCG vaccine is only given to health-care workers and members of the military who are at risk of exposure to active cases of TB. It is used more broadly worldwide. Many individuals born in other countries have been vaccinated with BCG strain. BCG is used in many countries with a high prevalence of TB, to prevent childhood tuberculous meningitis and miliary disease.",True,Tuberculosis,,,,
2ad9bb45-0066-4f9b-8ab9-72a45c17ddd8,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"The Mantoux tuberculin skin test (Figure 17.13) is regularly used in the United States to screen for potential TB exposure (see Hypersensitivities). However, prior vaccinations with the BCG vaccine can cause false-positive results. Chest radiographs to detect Ghon complex formation are required, therefore, to confirm exposure.",True,Tuberculosis,Figure 17.13,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.14.png,"Figure 17.13 (a) The Mantoux skin test for tuberculosis involves injecting the subject with tuberculin protein derivative. The injection should initially produce a raised wheal. (b) The test should be read in 48–72 hours. A positive result is indicated by redness, swelling, or hardness; the size of the responding region is measured to determine the final result. (credit a, b: modification of work by Centers for Disease Control and Prevention)"
be95a358-2648-4435-9692-7807e0cf5cb2,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,These short animations (https://openstax.org/l/22mycotublegpnean) discuss the infection strategies of Mycobacterium tuberculosis and Legionella pneumophila.,True,Tuberculosis,,,,
95df85a2-4a8c-4c28-8c2b-2f91d5cfa8a3,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,Pertussis (Whooping Cough),False,Pertussis (Whooping Cough),,,,
c52620f9-245a-49a4-a1e0-6f7db29afa41,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"The causative agent of pertussis, commonly called whooping cough, is Bordetella pertussis, a gram-negative coccobacillus. The disease is characterized by mucus accumulation in the lungs that leads to a long period of severe coughing. Sometimes, following a bout of coughing, a sound resembling a “whoop” is produced as air is inhaled through the inflamed and restricted airway—hence the name whooping cough. Although adults can be infected, the symptoms of this disease are most pronounced in infants and children. Pertussis is highly communicable through droplet transmission, so the uncontrollable coughing produced is an efficient means of transmitting the disease in a susceptible population.",True,Pertussis (Whooping Cough),,,,
ce522a28-2177-41c3-aa30-456c82a64efe,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Following inhalation, B. pertussis specifically attaches to epithelial cells using an adhesin, filamentous hemagglutinin. The bacteria then grow at the site of infection and cause disease symptoms through the production of exotoxins. One of the main virulence factors of this organism is an A-B exotoxin called the pertussis toxin (PT). When PT enters the host cells, it increases the cyclic adenosine monophosphate (cAMP) levels and disrupts cellular signaling. PT is known to enhance inflammatory responses involving histamine and serotonin. In addition to PT, B. pertussis produces a tracheal cytotoxin that damages ciliated epithelial cells and results in accumulation of mucus in the lungs. The mucus can support the colonization and growth of other microbes and, as a consequence, secondary infections are common. Together, the effects of these factors produce the cough that characterizes this infection.",True,Pertussis (Whooping Cough),,,,
6ed42b47-ed59-494d-a9ac-e43fc1bbf945,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"A pertussis infection can be divided into three distinct stages. The initial infection, termed the catarrhal stage, is relatively mild and unremarkable. The signs and symptoms may include nasal congestion, a runny nose, sneezing, and a low-grade fever. This, however, is the stage in which B. pertussis is most infectious. In the paroxysmal stage, mucus accumulation leads to uncontrollable coughing spasms that can last for several minutes and frequently induce vomiting. The paroxysmal stage can last for several weeks. A long convalescence stage follows the paroxysmal stage, during which time patients experience a chronic cough that can last for up to several months. In fact, the disease is sometimes called the 100-day cough.",True,Pertussis (Whooping Cough),,,,
d756b6a1-101b-408c-bf98-a9a6d6a37482,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"In infants, coughing can be forceful enough to cause fractures to the ribs, and prolonged infections can lead to death. The CDC reported 20 pertussis-related deaths in 2012,[7] but that number had declined to five by 2015.[8]",True,Pertussis (Whooping Cough),,,,
57c71315-2088-4a1d-b039-45efa518625b,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"During the first 2 weeks of infection, laboratory diagnosis is best performed by culturing the organism directly from a nasopharyngeal (NP) specimen collected from the posterior nasopharynx. The NP specimen is streaked onto Bordet- Gengou medium. The specimens must be transported to the laboratory as quickly as possible, even if transport media are used. Transport times of longer than 24 hours reduce the viability of B. pertussis significantly.",True,Pertussis (Whooping Cough),,,,
be09317c-4a9a-46b1-82a6-07d3f63f2625,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Pertussis is generally a self-limiting disease. Antibiotic therapy with erythromycin or tetracycline is only effective at the very earliest stages of disease. Antibiotics given later in the infection, and prophylactically to uninfected individuals, reduce the rate of transmission. Active vaccination is a better approach to control this disease. The DPT vaccine was once in common use in the United States. In that vaccine, the P component consisted of killed whole-cell B. pertussis preparations. Because of some adverse effects, that preparation has now been superseded by the DTaP and Tdap vaccines. In both of these new vaccines, the “aP” component is a pertussis toxoid.",True,Pertussis (Whooping Cough),,,,
cc2abb6f-be16-440f-8ebe-b7456086fa46,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Widespread vaccination has greatly reduced the number of reported cases and prevented large epidemics of pertussis. Recently, however, pertussis has begun to reemerge as a childhood disease in some states because of declining vaccination rates and an increasing population of susceptible children.",True,Pertussis (Whooping Cough),,,,
2d5780ec-b53c-4ac0-91d2-e42f32755630,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,This webpage (https://openstax.org/l/22pertussaudio) contains an audio clip of the distinctive “whooping” sound associated with pertussis in infants.,True,Pertussis (Whooping Cough),,,,
9d4e132e-b4ed-4008-97bc-fde794adc23f,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"This interactive map (https://openstax.org/l/22intmapprevacc) shows outbreaks of vaccine preventable diseases, including pertussis, around the world.",True,Pertussis (Whooping Cough),,,,
64bd694a-c7d9-430e-8c3b-603f256c8179,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,Acute Otitis Media,False,Acute Otitis Media,,,,
309403d0-feab-41ea-8b19-811c42244905,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"AOM is characterized by the formation and accumulation of pus in the middle ear. Unable to drain, the pus builds up, resulting in moderate to severe bulging of the tympanic membrane and otalgia (ear pain). Inflammation resulting from the infection leads to swelling of the eustachian tubes, and may also lead to fever, nausea, vomiting, and diarrhea, particularly in infants. Infants and toddlers who cannot yet speak may exhibit nonverbal signs suggesting AOM, such as holding, tugging, or rubbing of the ear, as well as uncharacteristic crying or distress in response to the pain.",True,Acute Otitis Media,,,,
9d8e07cd-963b-42f4-98a1-b472db1d5cec,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"AOM can be caused by a variety of bacteria. Among neonates, S. pneumoniae is the most common cause of AOM, but Escherichia coli, Enterococcus spp., and group B Streptococcus species can also be involved. In older infants and children younger than 14 years old, the most common bacterial causes are S. pneumoniae, Haemophilus influenzae, or Moraxella catarrhalis. Among S. pneumoniae infections, encapsulated strains are frequent causes of AOM. By contrast, the strains of H. influenzae and M. cattarhalis that are responsible for AOM do not possess a capsule. Rather than direct tissue damage by these pathogens, bacterial components such as lipopolysaccharide (LPS) in gram- negative pathogens induce an inflammatory response that causes swelling, pus, and tissue damage within the middle ear (Figure 17.7).",True,Acute Otitis Media,Figure 17.7,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.7.png,"Figure 17.7 (a) A healthy tympanic membrane; the middle ear bones can be seen behind the membrane. (b) An ear with chronic inflammation that has resulted in a torn membrane, erosion of the inner ear bones, and mucus buildup. (credit a: modification of work by “DrER.tv”/YouTube; credit b: modification of work by Li Mg, Hotez PJ, Vrabec JT, Donovan DT)"
b1489cbc-0c6f-42a7-9994-b5471de3f2dd,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Any blockage of the eustachian tubes, with or without infection, can cause fluid to become trapped and accumulate in the middle ear. This is referred to as otitis media with effusion (OME). The accumulated fluid offers an excellent reservoir for microbial growth and, consequently, secondary bacterial infections often ensue. This can lead to recurring and chronic earaches, which are especially common in young children. The higher incidence in children can be attributed to many factors. Children have more upper respiratory infections, in general, and their eustachian tubes are also shorter and drain at a shallower angle. Young children also tend to spend more time lying down than adults, which facilitates drainage from the nasopharynx through the eustachian tube and into the middle ear. Bottle feeding while lying down enhances this risk because the sucking action on the bottle causes negative pressure to build up within the eustachian tube, promoting the movement of fluid and bacteria from the nasopharynx.",True,Acute Otitis Media,,,,
f7c75d33-701a-4b36-95e0-ea46f4d0ed56,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Diagnosis is typically made based on clinical signs and symptoms, without laboratory testing to determine the specific causative agent. Antibiotics are frequently prescribed for the treatment of AOM. High-dose amoxicillin is the first-line drug, but with increasing resistance concerns, macrolides and cephalosporins may also be used. The pneumococcal conjugate vaccine (PCV13) contains serotypes that are important causes of AOM, and vaccination has been shown to decrease the incidence of AOM. Vaccination against influenza has also been shown to decrease the risk for AOM, likely because viral infections like influenza predispose patients to secondary infections with S. pneumoniae. Although there is a conjugate vaccine available for the invasive serotype B of H. influenzae, this vaccine does not impact the incidence of H. influenzae AOM. Because unencapsulated strains of H. influenzae and M. catarrhalis are involved in AOM, vaccines against bacterial cellular factors other than capsules will need to be developed.",True,Acute Otitis Media,,,,
19b2e994-63d2-4f45-b2b9-0aa62846de80,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,Bacterial Pneumonia,False,Bacterial Pneumonia,,,,
d8b9ad27-7b83-4802-8763-fd7c290fadd1,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"The most common cause of community-acquired bacterial pneumonia is Streptococcus pneumoniae. This gram- positive, alpha hemolytic streptococcus is commonly found as part of the normal microbiota of the human respiratory tract. The cells tend to be somewhat lancet-shaped and typically appear as pairs (Figure 17.9). The pneumococci initially colonize the bronchioles of the lungs. Eventually, the infection spreads to the alveoli, where the microbe’s polysaccharide capsule interferes with phagocytic clearance. Other virulence factors include autolysins like Lyt A, which degrade the microbial cell wall, resulting in cell lysis and the release of cytoplasmic virulence factors. One of these factors, pneumolysin O, is important in disease progression; this pore-forming protein damages host cells, promotes bacterial adherence, and enhances pro-inflammatory cytokine production. The resulting inflammatory response causes the alveoli to fill with exudate rich in neutrophils and red blood cells. As a consequence, infected individuals develop a productive cough with bloody sputum.",True,Bacterial Pneumonia,Figure 17.9,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.10.png,"Figure 17.9 (a) This micrograph of Streptococcus pneumoniae grown from a blood culture shows the characteristic lancet-shaped diplococcal morphology. (b) A colorized scanning electron micrograph of S. pneumoniae. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by Janice Carr, Centers for Disease Control and Prevention)"
f21e8bd0-7b34-47ab-b82d-dc95ad9a1b0b,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Antibiotics remain the mainstay treatment for pneumococci. β-Lactams like penicillin are the first-line drugs, but resistance to β-lactams is a growing problem. When β-lactam resistance is a concern, macrolides and fluoroquinolones may be prescribed. However, S. pneumoniae resistance to macrolides and fluoroquinolones is increasing as well, limiting the therapeutic options for some infections. There are currently two pneumococcal vaccines available: pneumococcal conjugate vaccine (PCV13) and pneumococcal polysaccharide vaccine (PPSV23). These are generally given to the most vulnerable populations of individuals: children younger than 2 years and adults older than 65 years.",True,Bacterial Pneumonia,,,,
cc310b35-d866-4e75-b716-2ef02cd8b9d2,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Encapsulated strains of Haemophilus influenzae are known for causing meningitis, but nonencapsulated strains are important causes of pneumonia. This small, gram-negative coccobacillus is found in the pharynx of the majority of healthy children; however, Haemophilus pneumonia is primarily seen in the elderly. Like other pathogens that cause pneumonia, H. influenzae is spread by droplets and aerosols produced by coughing. A fastidious organism, H. influenzae will only grow on media with available factor X (hemin) and factor V (NAD), like chocolate agar (Figure 17.10). Serotyping must be performed to confirm identity of H. influenzae isolates.",True,Bacterial Pneumonia,Figure 17.10,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.11.png,Figure 17.10 Culture of Haemophilus influenzae on a chocolate agar plate. (credit: modification of work by Centers for Disease Control and Prevention)
6abb11d3-7c62-42d7-918c-d2f44d61192f,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Infections of the alveoli by H. influenzae result in inflammation and accumulation of fluids. Increasing resistance to β-lactams, macrolides, and tetracyclines presents challenges for the treatment of Haemophilus pneumonia. Resistance to the fluoroquinolones is rare among isolates of H. influenzae but has been observed. As discussed for AOM, a vaccine directed against nonencapsulated H. influenzae, if developed, would provide protection against pneumonia caused by this pathogen.",True,Bacterial Pneumonia,,,,
6d07c944-6852-47d4-96c7-267329bdddb0,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Because there had been several other cases of bacterial pneumonia at Tracy’s elementary school, local health officials urged parents to have their children screened. Of the children who were screened, it was discovered that greater than 50% carried H. influenzae in their nasal cavities, yet all but two of them were asymptomatic.",True,Bacterial Pneumonia,,,,
90cbb877-c22b-432b-9e2d-1d72bb532863,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Why is it that some individuals become seriously ill from bacterial infections that seem to have little or no effect on others? The pathogenicity of an organism—its ability to cause host damage—is not solely a property of the microorganism. Rather, it is the product of a complex relationship between the microbe’s virulence factors and the immune defenses of the individual. Preexisting conditions and environmental factors such as exposure to secondhand smoke can make some individuals more susceptible to infection by producing conditions favorable to microbial growth or compromising the immune system. In addition, individuals may have genetically determined immune factors that protect them—or not—from particular strains of pathogens. The interactions between these host factors and the pathogenicity factors produced by the microorganism ultimately determine the outcome of the infection. A clearer understanding of these interactions may allow for better identification of at-risk individuals and prophylactic interventions in the future.",True,Bacterial Pneumonia,,,,
4a1077e6-ac6f-4bf8-90fb-7340c962db3d,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Mycoplasma grow very slowly when cultured. Therefore, penicillin and thallium acetate are added to agar to prevent the overgrowth by faster-growing potential contaminants. Since M. pneumoniae does not have a cell wall, it is resistant to these substances. Without a cell wall, the microbial cells appear pleomorphic. M. pneumoniae infections tend to be self-limiting but may also respond well to macrolide antibiotic therapy. β-lactams, which target cell wall synthesis, are not indicated for treatment of infections with this pathogen.",True,Bacterial Pneumonia,,,,
561f4dfe-55a2-4e6b-ac49-d95529dc1bc9,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,Tuberculosis,False,Tuberculosis,,,,
cf198fb1-85bd-46ea-b27a-2668025f1624,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Tuberculosis (TB) is one of the deadliest infectious diseases in human history. Although tuberculosis infection rates in the United States are extremely low, the CDC estimates that about one-third of the world’s population is infected with Mycobacterium tuberculosis, the causal organism of TB, with 9.6 million new TB cases and 1.5 million deaths worldwide in 2014.[5]",True,Tuberculosis,,,,
51c07bc7-a6dd-4b4d-bccb-a8ceb99aa2ca,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"M. tuberculosis is an acid-fast, high G + C, gram-positive, nonspore-forming rod. Its cell wall is rich in waxy mycolic acids, which make the cells impervious to polar molecules. It also causes these organisms to grow slowly.",True,Tuberculosis,,,,
8588b1de-9fe6-4cd9-8760-19de032d19f2,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"M. tuberculosis causes a chronic granulomatous disease that can infect any area of the body, although it is typically associated with the lungs. M. tuberculosis is spread by inhalation of respiratory droplets or aerosols from an infected person. The infectious dose of M. tuberculosis is only 10 cells.[6]",True,Tuberculosis,,,,
e42b5070-3a9b-46b2-b46e-161bf529b376,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"After inhalation, the bacteria enter the alveoli (Figure 17.12). The cells are phagocytized by macrophages but can survive and multiply within these phagocytes because of the protection by the waxy mycolic acid in their cell walls. If not eliminated by macrophages, the infection can progress, causing an inflammatory response and an accumulation of neutrophils and macrophages in the area. Several weeks or months may pass before an immunological response is mounted by T cells and B cells. Eventually, the lesions in the alveoli become walled off, forming small round lesions called tubercles. Bacteria continue to be released into the center of the tubercles and the chronic immune response results in tissue damage and induction of apoptosis (programmed host-cell death) in a process called liquefaction. This creates a caseous center, or air pocket, where the aerobic M. tuberculosis can grow and multiply. Tubercles may eventually rupture and bacterial cells can invade pulmonary capillaries; from there, bacteria can spread through the bloodstream to other organs, a condition known as miliary tuberculosis. The rupture of tubercles also facilitates transmission of the bacteria to other individuals via droplet aerosols that exit the body in coughs. Because these droplets can be very small and stay aloft for a long time, special precautions are necessary when caring for patients with TB, such as the use of face masks and negative-pressure ventilation and filtering systems.",True,Tuberculosis,Figure 17.12,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.13.png,"Figure 17.12 In the infectious cycle of tuberculosis, the immune response of most infected individuals (approximately 90%) results in the formation of tubercles in which the infection is walled off.[footnote]G. Kaplan et al. “Mycobacterium tuberculosis Growth at the Cavity Surface: A Microenvironment with Failed Immunity.” Infection and Immunity 71 no.12 (2003):7099–7108.[/footnote] The remainder will suffer progressive primary tuberculosis. The sequestered bacteria may be reactivated to form secondary tuberculosis in immunocompromised patients at a later time. (credit: modification of work by Centers for Disease Control and Prevention)"
0e33eee2-0695-4fae-af95-3ab691590709,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Eventually, most lesions heal to form calcified Ghon complexes. These structures are visible on chest radiographs and are a useful diagnostic feature. But even after the disease has apparently ended, viable bacteria remain sequestered in these locations. Release of these organisms at a later time can produce reactivation tuberculosis (or secondary TB). This is mainly observed in people with alcoholism, the elderly, or in otherwise immunocompromised individuals (Figure 17.12).",True,Tuberculosis,Figure 17.12,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.13.png,"Figure 17.12 In the infectious cycle of tuberculosis, the immune response of most infected individuals (approximately 90%) results in the formation of tubercles in which the infection is walled off.[footnote]G. Kaplan et al. “Mycobacterium tuberculosis Growth at the Cavity Surface: A Microenvironment with Failed Immunity.” Infection and Immunity 71 no.12 (2003):7099–7108.[/footnote] The remainder will suffer progressive primary tuberculosis. The sequestered bacteria may be reactivated to form secondary tuberculosis in immunocompromised patients at a later time. (credit: modification of work by Centers for Disease Control and Prevention)"
a435e520-d4f0-4dcf-bc8f-04f099184ce0,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Because TB is a chronic disease, chemotherapeutic treatments often continue for months or years. Multidrug resistant (MDR-TB) and extensively drug-resistant (XDR-TB) strains of M. tuberculosis are a growing clinical concern. These strains can arise due to misuse or mismanagement of antibiotic therapies. Therefore, it is imperative that proper multidrug protocols are used to treat these infections. Common antibiotics included in these mixtures are isoniazid, rifampin, ethambutol, and pyrazinamide.",True,Tuberculosis,,,,
4c308800-a64f-4a21-bb4e-c0ae129f7009,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"A TB vaccine is available that is based on the so-called bacillus Calmette-Guérin (BCG) strain of M. bovis commonly found in cattle. In the United States, the BCG vaccine is only given to health-care workers and members of the military who are at risk of exposure to active cases of TB. It is used more broadly worldwide. Many individuals born in other countries have been vaccinated with BCG strain. BCG is used in many countries with a high prevalence of TB, to prevent childhood tuberculous meningitis and miliary disease.",True,Tuberculosis,,,,
acfe925f-3be5-4a39-98f1-3a3b63fbc7e2,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"The Mantoux tuberculin skin test (Figure 17.13) is regularly used in the United States to screen for potential TB exposure (see Hypersensitivities). However, prior vaccinations with the BCG vaccine can cause false-positive results. Chest radiographs to detect Ghon complex formation are required, therefore, to confirm exposure.",True,Tuberculosis,Figure 17.13,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.14.png,"Figure 17.13 (a) The Mantoux skin test for tuberculosis involves injecting the subject with tuberculin protein derivative. The injection should initially produce a raised wheal. (b) The test should be read in 48–72 hours. A positive result is indicated by redness, swelling, or hardness; the size of the responding region is measured to determine the final result. (credit a, b: modification of work by Centers for Disease Control and Prevention)"
07cc3b82-f931-4847-9b80-76c829f0f27d,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,Pertussis (Whooping Cough),False,Pertussis (Whooping Cough),,,,
164d1f11-06d3-4701-a4b2-2d831a8b974e,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"The causative agent of pertussis, commonly called whooping cough, is Bordetella pertussis, a gram-negative coccobacillus. The disease is characterized by mucus accumulation in the lungs that leads to a long period of severe coughing. Sometimes, following a bout of coughing, a sound resembling a “whoop” is produced as air is inhaled through the inflamed and restricted airway—hence the name whooping cough. Although adults can be infected, the symptoms of this disease are most pronounced in infants and children. Pertussis is highly communicable through droplet transmission, so the uncontrollable coughing produced is an efficient means of transmitting the disease in a susceptible population.",True,Pertussis (Whooping Cough),,,,
0b32e3b2-b3cc-49d1-ba5e-e4a744b1e0fe,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Following inhalation, B. pertussis specifically attaches to epithelial cells using an adhesin, filamentous hemagglutinin. The bacteria then grow at the site of infection and cause disease symptoms through the production of exotoxins. One of the main virulence factors of this organism is an A-B exotoxin called the pertussis toxin (PT). When PT enters the host cells, it increases the cyclic adenosine monophosphate (cAMP) levels and disrupts cellular signaling. PT is known to enhance inflammatory responses involving histamine and serotonin. In addition to PT, B. pertussis produces a tracheal cytotoxin that damages ciliated epithelial cells and results in accumulation of mucus in the lungs. The mucus can support the colonization and growth of other microbes and, as a consequence, secondary infections are common. Together, the effects of these factors produce the cough that characterizes this infection.",True,Pertussis (Whooping Cough),,,,
bbc1e4c0-be6c-4a86-bf74-fa22e6dd45a6,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"A pertussis infection can be divided into three distinct stages. The initial infection, termed the catarrhal stage, is relatively mild and unremarkable. The signs and symptoms may include nasal congestion, a runny nose, sneezing, and a low-grade fever. This, however, is the stage in which B. pertussis is most infectious. In the paroxysmal stage, mucus accumulation leads to uncontrollable coughing spasms that can last for several minutes and frequently induce vomiting. The paroxysmal stage can last for several weeks. A long convalescence stage follows the paroxysmal stage, during which time patients experience a chronic cough that can last for up to several months. In fact, the disease is sometimes called the 100-day cough.",True,Pertussis (Whooping Cough),,,,
c6a46c3b-8a42-452b-a872-749a4df2b2cd,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"In infants, coughing can be forceful enough to cause fractures to the ribs, and prolonged infections can lead to death. The CDC reported 20 pertussis-related deaths in 2012,[7] but that number had declined to five by 2015.[8]",True,Pertussis (Whooping Cough),,,,
980cb094-6c40-4c07-a4f9-976d671775df,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"During the first 2 weeks of infection, laboratory diagnosis is best performed by culturing the organism directly from a nasopharyngeal (NP) specimen collected from the posterior nasopharynx. The NP specimen is streaked onto Bordet- Gengou medium. The specimens must be transported to the laboratory as quickly as possible, even if transport media are used. Transport times of longer than 24 hours reduce the viability of B. pertussis significantly.",True,Pertussis (Whooping Cough),,,,
40470a89-3f9d-4bca-8c4b-00c70f0a2189,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Pertussis is generally a self-limiting disease. Antibiotic therapy with erythromycin or tetracycline is only effective at the very earliest stages of disease. Antibiotics given later in the infection, and prophylactically to uninfected individuals, reduce the rate of transmission. Active vaccination is a better approach to control this disease. The DPT vaccine was once in common use in the United States. In that vaccine, the P component consisted of killed whole-cell B. pertussis preparations. Because of some adverse effects, that preparation has now been superseded by the DTaP and Tdap vaccines. In both of these new vaccines, the “aP” component is a pertussis toxoid.",True,Pertussis (Whooping Cough),,,,
db79b303-a08c-4a0b-b505-273b2fe65032,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"Widespread vaccination has greatly reduced the number of reported cases and prevented large epidemics of pertussis. Recently, however, pertussis has begun to reemerge as a childhood disease in some states because of declining vaccination rates and an increasing population of susceptible children.",True,Pertussis (Whooping Cough),,,,
73220014-d181-4694-81bd-ff8ba436e340,https://open.oregonstate.education/microbiology/,17.2	Bacterial Infections of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/22-2bacterial-infections-of-the-respiratory-tract/,"This interactive map (https://openstax.org/l/22intmapprevacc) shows outbreaks of vaccine preventable diseases, including pertussis, around the world.",True,Pertussis (Whooping Cough),,,,
b5029fe8-49fb-488d-ba04-c3e14e6abf0a,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,Anatomy of the Upper Respiratory System,False,Anatomy of the Upper Respiratory System,,,,
dd688146-8ec7-4008-ae51-a4a912b167fc,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,"The respiratory system can be conceptually divided into upper and lower regions at the point of the epiglottis, the structure that seals off the lower respiratory system from the pharynx during swallowing (Figure 17.2). The upper respiratory system is in direct contact with the external environment. The nares (or nostrils) are the external openings of the nose that lead back into the nasal cavity, a large air-filled space behind the nares. These anatomical sites constitute the primary opening and first section of the respiratory tract, respectively. The nasal cavity is lined with hairs that trap large particles, like dust and pollen, and prevent their access to deeper tissues. The nasal cavity is also lined with a mucous membrane and Bowman’s glands that produce mucus to help trap particles and microorganisms for removal. The nasal cavity is connected to several other air-filled spaces. The sinuses, a set of four, paired small cavities in the skull, communicate with the nasal cavity through a series of small openings. The nasopharynx is part of the upper throat extending from the posterior nasal cavity. The nasopharynx carries air inhaled through the nose. The middle ear is connected to the nasopharynx through the eustachian tube. The middle ear is separated from the outer ear by the tympanic membrane, or ear drum. And finally, the lacrimal glands drain to the nasal cavity through the nasolacrimal ducts (tear ducts). The open connections between these sites allow microorganisms to move from the nasal cavity to the sinuses, middle ears (and back), and down into the lower respiratory tract from the nasopharynx.",True,Anatomy of the Upper Respiratory System,Figure 17.2,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.2.png,"Figure 17.2 (a) The ear is connected to the upper respiratory tract by the eustachian tube, which opens to the nasopharynx. (b) The structures of the upper respiratory tract."
e724018d-2195-4550-906f-cc127e5f066b,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,"The oral cavity is a secondary opening for the respiratory tract. The oral and nasal cavities connect through the fauces to the pharynx, or throat. The pharynx can be divided into three regions: the nasopharynx, the oropharynx, and the laryngopharynx. Air inhaled through the mouth does not pass through the nasopharynx; it proceeds first through the oropharynx and then through the laryngopharynx. The palatine tonsils, which consist of lymphoid tissue, are located within the oropharynx. The laryngopharynx, the last portion of the pharynx, connects to the larynx, which contains the vocal fold (Figure 17.2).",True,Anatomy of the Upper Respiratory System,Figure 17.2,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.2.png,"Figure 17.2 (a) The ear is connected to the upper respiratory tract by the eustachian tube, which opens to the nasopharynx. (b) The structures of the upper respiratory tract."
1f0cf1f5-7fd5-4c39-85e4-64aac358c44d,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,Anatomy of the Lower Respiratory System,False,Anatomy of the Lower Respiratory System,,,,
465ba5f1-8d59-41f1-ab74-324dfecee20a,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,"The lower respiratory system begins below the epiglottis in the larynx or voice box (Figure 17.3). The trachea, or windpipe, is a cartilaginous tube extending from the larynx that provides an unobstructed path for air to reach the lungs. The trachea bifurcates into the left and right bronchi as it reaches the lungs. These paths branch repeatedly to form smaller and more extensive networks of tubes, the bronchioles. The terminal bronchioles formed in this tree- like network end in cul-de-sacs called the alveoli. These structures are surrounded by capillary networks and are the site of gas exchange in the respiratory system. Human lungs contain on the order of 400,000,000 alveoli. The outer surface of the lungs is protected with a double-layered pleural membrane. This structure protects the lungs and provides lubrication to permit the lungs to move easily during respiration.",True,Anatomy of the Lower Respiratory System,Figure 17.3,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.3.png,Figure 17.3 The structures of the lower respiratory tract are identified in this illustration. (credit: modification of work by National Cancer Institute)
c8c6f92f-e0ee-42f3-a1f8-3c4022ed5a14,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,Defenses of the Respiratory System,False,Defenses of the Respiratory System,,,,
c1761f70-bb10-4b42-bdc9-a5a5b91fed9a,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,"The upper respiratory system is under constant surveillance by mucosa-associated lymphoid tissue (MALT), including the adenoids and tonsils. Other mucosal defenses include secreted antibodies (IgA), lysozyme, surfactant, and antimicrobial peptides called defensins. Meanwhile, the lower respiratory tract is protected by alveolar macrophages. These phagocytes efficiently kill any microbes that manage to evade the other defenses. The combined action of these factors renders the lower respiratory tract nearly devoid of colonized microbes.",True,Defenses of the Respiratory System,,,,
d55a9d91-28fb-4038-b60f-9e42f9a67514,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,Normal Microbiota of the Respiratory System,False,Normal Microbiota of the Respiratory System,,,,
273efbdb-d02b-43ba-a055-2601cfaf9e5e,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,"The upper respiratory tract contains an abundant and diverse microbiota. The most common bacteria identified include Staphylococcus epidermidis, viridans group streptococci (VGS), Corynebacterium spp. (diphtheroids), Propionibacterium spp., and Haemophilus spp. In addition, many healthy humans asymptomatically carry potential pathogens in the upper respiratory tract. As much as 20% of the population carry Staphylococcus aureus  in their nostrils.[1]",True,Normal Microbiota of the Respiratory System,,,,
cd837339-90b0-4eea-8fbd-b390d2b45615,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,"The lower respiratory tract, by contrast, is scantily populated with microbes. It is not clear at this time if these small populations of bacteria constitute a normal microbiota or if they are transients.",True,Normal Microbiota of the Respiratory System,,,,
efeff022-a243-4ded-b04f-db301992a612,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,"Many members of the respiratory system’s normal microbiota are opportunistic pathogens. To proliferate and cause host damage, they first must overcome the immune defenses of respiratory tissues. Many mucosal pathogens produce virulence factors such as adhesins that mediate attachment to host epithelial cells, or polysaccharide capsules that allow microbes to evade phagocytosis. The endotoxins of gram-negative bacteria can stimulate a strong inflammatory response that damages respiratory cells. Other pathogens produce exotoxins, and still others have the ability to survive within the host cells. Once an infection of the respiratory tract is established, it tends to impair the mucociliary escalator, limiting the body’s ability to expel the invading microbes, thus making it easier for pathogens to multiply and spread.",True,Normal Microbiota of the Respiratory System,,,,
64e68674-e4c1-4e88-a6fe-c391abf80ecd,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,"Vaccines have been developed for many of the most serious bacterial and viral pathogens. Several of the most important respiratory pathogens and their vaccines, if available, are summarized in Table 17.1. Components of these vaccines will be explained later in the chapter.",True,Normal Microbiota of the Respiratory System,,,,
66c5fd0f-50fe-493c-a849-058d0cf647c8,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,Signs and Symptoms of Respiratory Infection,False,Signs and Symptoms of Respiratory Infection,,,,
aee1391d-61e8-45d2-8e20-a23c21c297f6,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,Anatomy of the Lower Respiratory System,False,Anatomy of the Lower Respiratory System,,,,
7700ef76-0e8e-46bd-aa55-6a3f45ea9d64,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,"The lower respiratory system begins below the epiglottis in the larynx or voice box (Figure 17.3). The trachea, or windpipe, is a cartilaginous tube extending from the larynx that provides an unobstructed path for air to reach the lungs. The trachea bifurcates into the left and right bronchi as it reaches the lungs. These paths branch repeatedly to form smaller and more extensive networks of tubes, the bronchioles. The terminal bronchioles formed in this tree- like network end in cul-de-sacs called the alveoli. These structures are surrounded by capillary networks and are the site of gas exchange in the respiratory system. Human lungs contain on the order of 400,000,000 alveoli. The outer surface of the lungs is protected with a double-layered pleural membrane. This structure protects the lungs and provides lubrication to permit the lungs to move easily during respiration.",True,Anatomy of the Lower Respiratory System,Figure 17.3,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-22.3.png,Figure 17.3 The structures of the lower respiratory tract are identified in this illustration. (credit: modification of work by National Cancer Institute)
1b759f8d-9397-46d0-a8c5-315c22b1daff,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,Defenses of the Respiratory System,False,Defenses of the Respiratory System,,,,
65cdf78f-a3a7-43e7-8f94-98fd72c9ae7a,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,Normal Microbiota of the Respiratory System,False,Normal Microbiota of the Respiratory System,,,,
794791da-c0dc-40ad-aedb-17a31307db04,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,"The upper respiratory tract contains an abundant and diverse microbiota. The most common bacteria identified include Staphylococcus epidermidis, viridans group streptococci (VGS), Corynebacterium spp. (diphtheroids), Propionibacterium spp., and Haemophilus spp. In addition, many healthy humans asymptomatically carry potential pathogens in the upper respiratory tract. As much as 20% of the population carry Staphylococcus aureus  in their nostrils.[1]",True,Normal Microbiota of the Respiratory System,,,,
02918310-a8f3-4286-a73f-9e1973a4633c,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,"Many members of the respiratory system’s normal microbiota are opportunistic pathogens. To proliferate and cause host damage, they first must overcome the immune defenses of respiratory tissues. Many mucosal pathogens produce virulence factors such as adhesins that mediate attachment to host epithelial cells, or polysaccharide capsules that allow microbes to evade phagocytosis. The endotoxins of gram-negative bacteria can stimulate a strong inflammatory response that damages respiratory cells. Other pathogens produce exotoxins, and still others have the ability to survive within the host cells. Once an infection of the respiratory tract is established, it tends to impair the mucociliary escalator, limiting the body’s ability to expel the invading microbes, thus making it easier for pathogens to multiply and spread.",True,Normal Microbiota of the Respiratory System,,,,
d41d4775-209d-48e6-aa41-1f81f5f6b605,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,"Vaccines have been developed for many of the most serious bacterial and viral pathogens. Several of the most important respiratory pathogens and their vaccines, if available, are summarized in Table 17.1. Components of these vaccines will be explained later in the chapter.",True,Normal Microbiota of the Respiratory System,,,,
559e1207-4acb-4e0f-b600-594339adbc84,https://open.oregonstate.education/microbiology/,17.1	Anatomy and Normal Microbiota of the Respiratory Tract,https://open.oregonstate.education/microbiology/chapter/916/,Signs and Symptoms of Respiratory Infection,False,Signs and Symptoms of Respiratory Infection,,,,
2b60e77f-b8f6-4766-9779-fa5db30de77c,https://open.oregonstate.education/microbiology/,16.5	Helminthic Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-5protozoan-and-helminthic-infections-of-the-skin-and-eyes/,Loiasis,False,Loiasis,,,,
bfba3d72-c087-48f8-aaac-220cf49d8a01,https://open.oregonstate.education/microbiology/,16.5	Helminthic Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-5protozoan-and-helminthic-infections-of-the-skin-and-eyes/,"The helminth Loa loa, also known as the African eye worm, is a nematode that can cause loiasis, a disease endemic to West and Central Africa. The disease does not occur outside that region except when carried by travelers. There is evidence that individual genetic differences affect susceptibility to developing loiasis after infection by the Loa loa worm. Even in areas in which Loa loa worms are common, the disease is generally found in less than 30% of the population.[1] It has been suggested that travelers who spend time in the region may be somewhat more susceptible to developing symptoms than the native population, and the presentation of infection may differ.[2]",True,Loiasis,,,,
f88481e1-93eb-4ddd-8c6c-612a4e080f23,https://open.oregonstate.education/microbiology/,16.5	Helminthic Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-5protozoan-and-helminthic-infections-of-the-skin-and-eyes/,"The parasite is spread by deerflies (genus Chrysops), which can ingest the larvae from an infected human via a blood meal (Figure 16.24). When the deerfly bites other humans, it deposits the larvae into their bloodstreams. After about five months in the human body, some larvae develop into adult worms, which can grow to several centimeters in length and live for years in the subcutaneous tissue of the host.",True,Loiasis,Figure 16.24,16.5	Helminthic Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.36.png,"Figure 16.24 This Loa loa worm, measuring about 55 mm long, was extracted from the conjunctiva of a patient with loiasis. The Loa loa has a complex life cycle. Biting deerflies native to the rain forests of Central and West Africa transmit the larvae between humans. (credit a: modification of work by Eballe AO, Epée E, Koki G, Owono D, Mvogo CE, Bella AL; credit b: modification of work by NIAID; credit c: modification of work by Centers for Disease Controland Prevention)"
c8071db6-8322-434d-ac34-50deaeb7d2de,https://open.oregonstate.education/microbiology/,16.5	Helminthic Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-5protozoan-and-helminthic-infections-of-the-skin-and-eyes/,"The name “eye worm” alludes to the visible migration of worms across the conjunctiva of the eye. Adult worms live in the subcutaneous tissues and can travel at about 1 cm per hour. They can often be observed when migrating through the eye, and sometimes under the skin; in fact, this is generally how the disease is diagnosed. It is also possible to test for antibodies, but the presence of antibodies does not necessarily indicate a current infection; it only means that the individual was exposed at some time. Some patients are asymptomatic, but in others the migrating worms can cause fever and areas of allergic inflammation known as Calabar swellings. Worms migrating through the conjunctiva can cause temporary eye pain and itching, but generally there is no lasting damage to the eye. Some patients experience a range of other symptoms, such as widespread itching, hives, and joint and muscle pain.",True,Loiasis,,,,
bd9a3557-391d-4371-bae4-d5fd775fa797,https://open.oregonstate.education/microbiology/,16.5	Helminthic Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-5protozoan-and-helminthic-infections-of-the-skin-and-eyes/,"Worms can be surgically removed from the eye or the skin, but this treatment only relieves discomfort; it does not cure the infection, which involves many worms. The preferred treatment is diethylcarbamazine, but this medication produces severe side effects in some individuals, such as brain inflammation and possible death in patients with heavy infections. Albendazole is also sometimes used if diethylcarbamazine is not appropriate or not successful. If left untreated for many years, loiasis can damage the kidneys, heart, and lungs, though these symptoms are rare.",True,Loiasis,,,,
cff11472-7b91-4322-9ab0-228a7bdeb073,https://open.oregonstate.education/microbiology/,16.5	Helminthic Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-5protozoan-and-helminthic-infections-of-the-skin-and-eyes/,The protozoan Acanthamoeba and the helminth Loa loa are two parasites capable of causing infections of the skin and eyes. Figure 16.25 summarizes the characteristics of some common fungal infections of the skin.,True,Loiasis,Figure 16.25,16.5	Helminthic Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.25.png,"Figure 16.25 Details associated with loiasis, a parasitic skin and eye infection."
3dc76445-2255-4b3a-94d7-2ddce090879a,https://open.oregonstate.education/microbiology/,16.4	Mycoses of the Skin,https://open.oregonstate.education/microbiology/chapter/21-4mycoses-of-the-skin/,"Fungal infections, also called mycoses, can be divided into classes based on their invasiveness. Mycoses that cause superficial infections of the epidermis, hair, and nails, are called cutaneous mycoses. Mycoses that penetrate the epidermis and the dermis to infect deeper tissues are called subcutaneous mycoses. Mycoses that spread throughout the body are called systemic mycoses.",True,Loiasis,,,,
c9bfad20-1ea5-4e4a-9e67-21ddfed27e36,https://open.oregonstate.education/microbiology/,16.4	Mycoses of the Skin,https://open.oregonstate.education/microbiology/chapter/21-4mycoses-of-the-skin/,Tineas,False,Tineas,,,,
a94a6647-03c3-49e7-ac7b-617b26ba6088,https://open.oregonstate.education/microbiology/,16.4	Mycoses of the Skin,https://open.oregonstate.education/microbiology/chapter/21-4mycoses-of-the-skin/,"A group of cutaneous mycoses called tineas are caused by dermatophytes, fungal molds that require keratin, a protein found in skin, hair, and nails, for growth. There are three genera of dermatophytes, all of which can cause cutaneous mycoses: Trichophyton, Epidermophyton, and Microsporum. Tineas on most areas of the body are generally called ringworm, but tineas in specific locations may have distinctive names and symptoms (see Table 16.3 and Figure 16.22). Keep in mind that these names—even though they are Latinized—refer to locations on the body, not causative organisms. Tineas can be caused by different dermatophytes in most areas of the body.",True,Tineas,Figure 16.22,16.4	Mycoses of the Skin,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.29.png,"Figure 16.22 Tineas are superficial cutaneous mycoses and are common. (a) Tinea barbae (barber’s itch) occurs on the lower face. (b) Tinea pedis (athlete’s foot) occurs on the feet, causing itching, burning, and dry, cracked skin between the toes. (c) A close-up view of tinea corporis (ringworm) caused by Trichophyton mentagrophytes. (credit a, c: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by Al Hasan M, Fitzgerald SM, Saoudian M, Krishnaswamy G)"
2e4c5d2d-4885-45f0-97dd-6f8974adead2,https://open.oregonstate.education/microbiology/,16.4	Mycoses of the Skin,https://open.oregonstate.education/microbiology/chapter/21-4mycoses-of-the-skin/,"Dermatophytes are commonly found in the environment and in soils and are frequently transferred to the skin via contact with other humans and animals. Fungal spores can also spread on hair. Many dermatophytes grow well in moist, dark environments. For example, tinea pedis (athlete’s foot) commonly spreads in public showers, and the causative fungi grow well in the dark, moist confines of sweaty shoes and socks. Likewise, tinea cruris (jock itch) often spreads in communal living environments and thrives in warm, moist undergarments.",True,Tineas,,,,
53e65ac0-a349-4752-88e4-e78f74b9e534,https://open.oregonstate.education/microbiology/,16.4	Mycoses of the Skin,https://open.oregonstate.education/microbiology/chapter/21-4mycoses-of-the-skin/,"Tineas on the body (tinea corporis) often produce lesions that grow radially and heal towards the center. This causes the formation of a red ring, leading to the misleading name of ringworm.",True,Tineas,,,,
716b621c-53e9-4a65-8c47-d71d7a4d29e4,https://open.oregonstate.education/microbiology/,16.4	Mycoses of the Skin,https://open.oregonstate.education/microbiology/chapter/21-4mycoses-of-the-skin/,"Several approaches may be used to diagnose tineas. A Wood’s lamp (also called a black lamp) with a wavelength of 365 nm is often used. When directed on a tinea, the ultraviolet light emitted from the Wood’s lamp causes the fungal elements (spores and hyphae) to fluoresce. Direct microscopic evaluation of specimens from skin scrapings, hair, or nails can also be used to detect fungi. Generally, these specimens are prepared in a wet mount using a potassium hydroxide solution (10%–20% aqueous KOH), which dissolves the keratin in hair, nails, and skin cells to allow for visualization of the hyphae and fungal spores. The specimens may be grown on Sabouraud dextrose CC (chloramphenicol/cyclohexamide), a selective agar that supports dermatophyte growth while inhibiting the growth of bacteria and saprophytic fungi. Macroscopic colony morphology is often used to initially identify the genus of the dermatophyte; identification can be further confirmed by visualizing the microscopic morphology using either a slide culture or a sticky tape prep stained with lactophenol cotton blue.",True,Tineas,,,,
a949ff96-1374-4d72-8384-4286a6cb7300,https://open.oregonstate.education/microbiology/,16.4	Mycoses of the Skin,https://open.oregonstate.education/microbiology/chapter/21-4mycoses-of-the-skin/,"Various antifungal treatments can be effective against tineas. Allylamine ointments that include terbinafine are commonly used; miconazole and clotrimazole are also available for topical treatment, and griseofulvin is used orally.",True,Tineas,,,,
86b9a995-9651-48dd-baf7-bb84541eba81,https://open.oregonstate.education/microbiology/,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-3viral-infections-of-the-skin-and-eyes/,Learning Objectives,False,Learning Objectives,,,,
3a6d2a59-06cb-4fce-97f2-fb9e546bab7d,https://open.oregonstate.education/microbiology/,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-3viral-infections-of-the-skin-and-eyes/,"Numerous types of viral infections cause rashes or lesions on the skin; however, in many cases these skin conditions result from infections that originate in other body systems. In this chapter, we will limit the discussion to viral skin infections that use the skin as a portal of entry. Later chapters will discuss viral infections such as chickenpox, measles, and rubella—diseases that cause skin rashes but invade the body through portals of entry other than the skin.",True,Learning Objectives,,,,
9fbe4c34-60ec-465a-a50d-094ead800fc5,https://open.oregonstate.education/microbiology/,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-3viral-infections-of-the-skin-and-eyes/,Papillomas,False,Papillomas,,,,
7b5d5274-0c97-46b6-8c3b-be34178cf097,https://open.oregonstate.education/microbiology/,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-3viral-infections-of-the-skin-and-eyes/,"Papillomas (warts) are the expression of common skin infections by human papillomavirus (HPV) and are transmitted by direct contact. There are many types of HPV, and they lead to a variety of different presentations, such as common warts, plantar warts, flat warts, and filiform warts. HPV can also cause sexually-transmitted genital warts, which will be discussed in Urogenital System Infections. Vaccination is available for some strains of HPV.",True,Papillomas,,,,
60b04707-657c-4e52-80ac-0b483362da9b,https://open.oregonstate.education/microbiology/,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-3viral-infections-of-the-skin-and-eyes/,"Common warts tend to develop on fingers, the backs of hands, and around nails in areas with broken skin. In contrast, plantar warts (also called foot warts) develop on the sole of the foot and can grow inwards, causing pain and pressure during walking. Flat warts can develop anywhere on the body, are often numerous, and are relatively smooth and small compared with other wart types. Filiform warts are long, threadlike warts that grow quickly.",True,Papillomas,,,,
ce582152-10e1-4282-a050-8c39def8bef6,https://open.oregonstate.education/microbiology/,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-3viral-infections-of-the-skin-and-eyes/,"In some cases, the immune system may be strong enough to prevent warts from forming or to eradicate established warts. However, treatment of established warts is typically required. There are many available treatments for warts, and their effectiveness varies. Common warts can be frozen off with liquid nitrogen. Topical applications of salicylic acid may also be effective. Other options are electrosurgery (burning), curettage (cutting), excision, painting with cantharidin (which causes the wart to die so it can more easily be removed), laser treatments, treatment with bleomycin, chemical peels, and immunotherapy (Figure 16.19).",True,Papillomas,Figure 16.19,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.25.png,Figure 16.19 Warts can vary in shape and in location. (a) Multiple plantar warts have grown on this toe. (b) A filiform wart has grown on this eyelid.
e4a55906-1b2a-4c86-b1ae-340959b84535,https://open.oregonstate.education/microbiology/,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-3viral-infections-of-the-skin-and-eyes/,"Infection by HSV-1 commonly manifests as cold sores or fever blisters, usually on or around the lips (Figure 16.20). HSV-1 is highly contagious, with some studies suggesting that up to 65% of the US population is infected; however, many infected individuals are asymptomatic.[1] Moreover, the virus can be latent for long periods, residing in the trigeminal nerve ganglia between recurring bouts of symptoms. Recurrence can be triggered by stress or environmental conditions (systemic or affecting the skin). When lesions are present, they may blister, break open, and crust. The virus can be spread through direct contact, even when a patient is asymptomatic.",True,Papillomas,Figure 16.20,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.26.png,Figure 16.20 This cold sore was caused by HSV-1. (credit: Centers for Disease Control and Prevention)
6b3d304b-0ce4-4adc-9353-2c44a857919c,https://open.oregonstate.education/microbiology/,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-3viral-infections-of-the-skin-and-eyes/,"While the lips, mouth, and face are the most common sites for HSV-1 infections, lesions can spread to other areas of the body. Wrestlers and other athletes involved in contact sports may develop lesions on the neck, shoulders, and trunk. This condition is often called herpes gladiatorum. Herpes lesions that develop on the fingers are often called herpetic whitlow.",True,Papillomas,,,,
84355319-cc9a-477d-9ccc-1d97450dab6b,https://open.oregonstate.education/microbiology/,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-3viral-infections-of-the-skin-and-eyes/,"HSV-1 infections are commonly diagnosed from their appearance, although laboratory testing can confirm the diagnosis. There is no cure, but antiviral medications such as acyclovir, penciclovir, famciclovir, and valacyclovir are used to reduce symptoms and risk of transmission. Topical medications, such as creams with n-docosanol and penciclovir, can also be used to reduce symptoms such as itching, burning, and tingling.",True,Papillomas,,,,
1cc75a04-fac4-4c29-a8f6-acdf97540678,https://open.oregonstate.education/microbiology/,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-3viral-infections-of-the-skin-and-eyes/,Learning Objectives,False,Learning Objectives,,,,
09c206c7-10b6-4780-b0d2-855346bc3c33,https://open.oregonstate.education/microbiology/,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-3viral-infections-of-the-skin-and-eyes/,"Numerous types of viral infections cause rashes or lesions on the skin; however, in many cases these skin conditions result from infections that originate in other body systems. In this chapter, we will limit the discussion to viral skin infections that use the skin as a portal of entry. Later chapters will discuss viral infections such as chickenpox, measles, and rubella—diseases that cause skin rashes but invade the body through portals of entry other than the skin.",True,Learning Objectives,,,,
9b7ff2b0-f108-4830-88c9-a0374a2d1435,https://open.oregonstate.education/microbiology/,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-3viral-infections-of-the-skin-and-eyes/,Papillomas,False,Papillomas,,,,
2921e8d9-0c78-40f1-b519-6e1edb4de53a,https://open.oregonstate.education/microbiology/,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-3viral-infections-of-the-skin-and-eyes/,"Papillomas (warts) are the expression of common skin infections by human papillomavirus (HPV) and are transmitted by direct contact. There are many types of HPV, and they lead to a variety of different presentations, such as common warts, plantar warts, flat warts, and filiform warts. HPV can also cause sexually-transmitted genital warts, which will be discussed in Urogenital System Infections. Vaccination is available for some strains of HPV.",True,Papillomas,,,,
aff7ff0b-0704-47a8-81b7-291925a799f6,https://open.oregonstate.education/microbiology/,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-3viral-infections-of-the-skin-and-eyes/,"Common warts tend to develop on fingers, the backs of hands, and around nails in areas with broken skin. In contrast, plantar warts (also called foot warts) develop on the sole of the foot and can grow inwards, causing pain and pressure during walking. Flat warts can develop anywhere on the body, are often numerous, and are relatively smooth and small compared with other wart types. Filiform warts are long, threadlike warts that grow quickly.",True,Papillomas,,,,
4c5dd2e4-529c-408a-b3ce-791c2225c1d6,https://open.oregonstate.education/microbiology/,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-3viral-infections-of-the-skin-and-eyes/,"In some cases, the immune system may be strong enough to prevent warts from forming or to eradicate established warts. However, treatment of established warts is typically required. There are many available treatments for warts, and their effectiveness varies. Common warts can be frozen off with liquid nitrogen. Topical applications of salicylic acid may also be effective. Other options are electrosurgery (burning), curettage (cutting), excision, painting with cantharidin (which causes the wart to die so it can more easily be removed), laser treatments, treatment with bleomycin, chemical peels, and immunotherapy (Figure 16.19).",True,Papillomas,Figure 16.19,16.3	Viral Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.25.png,Figure 16.19 Warts can vary in shape and in location. (a) Multiple plantar warts have grown on this toe. (b) A filiform wart has grown on this eyelid.
18232339-e764-4301-8eba-4926b4f3cf2f,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"In this section, we will examine some of the most important bacterial infections of the skin and eyes and discuss how biofilms can contribute to and exacerbate such infections. Key features of bacterial skin and eye infections are also summarized in the Disease Profile boxes throughout this section.",True,Papillomas,,,,
49b085e8-0dc1-4b72-a09c-37bc5b226b09,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Staphylococcal Infections of the Skin,False,Staphylococcal Infections of the Skin,,,,
efe8227b-6033-4d36-9bca-7150243da753,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Staphylococcus species are commonly found on the skin, with S. epidermidis and S. hominis being prevalent in the normal microbiota. S. aureus is also commonly found in the nasal passages and on healthy skin, but pathogenic strains are often the cause of a broad range of infections of the skin and other body systems.",True,Staphylococcal Infections of the Skin,,,,
1fcaebf6-0e4f-46a1-bae7-1afe42f2b52b,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"S. aureus is quite contagious. It is spread easily through skin-to-skin contact, and because many people are chronic nasal carriers (asymptomatic individuals who carry S. aureus in their nares), the bacteria can easily be transferred from the nose to the hands and then to fomites or other individuals. Because it is so contagious, S. aureus is prevalent in most community settings. This prevalence is particularly problematic in hospitals, where antibiotic- resistant strains of the bacteria may be present, and where immunocompromised patients may be more susceptible to infection. Resistant strains include methicillin-resistant S. aureus (MRSA), which can be acquired through health- care settings (hospital-acquired MRSA, or HA-MRSA) or in the community (community-acquired MRSA, or CA- MRSA). Hospital patients often arrive at health-care facilities already colonized with antibiotic-resistant strains of S. aureus that can be transferred to health-care providers and other patients. Some hospitals have attempted to detect these individuals in order to institute prophylactic measures, but they have had mixed success (see Eye on Ethics: Screening Patients for MRSA).",True,Staphylococcal Infections of the Skin,,,,
c2ac3515-dff6-46ab-b14a-337071fde1e1,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"When a staphylococcal infection develops, choice of medication is important. As discussed above, many staphylococci (such as MRSA) are resistant to some or many antibiotics. Thus, antibiotic sensitivity is measured to identify the most suitable antibiotic. However, even before receiving the results of sensitivity analysis, suspected S. aureus infections are often initially treated with drugs known to be effective against MRSA, such as trimethoprim- sulfamethoxazole (TMP/SMZ), clindamycin, a tetracycline (doxycycline or minocycline), or linezolid.",True,Staphylococcal Infections of the Skin,,,,
472ad659-4485-458e-baa2-c7b5d7879c37,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"The pathogenicity of staphylococcal infections is often enhanced by characteristic chemicals secreted by some strains. Staphylococcal virulence factors include hemolysins called staphylolysins, which are cytotoxic for many types of cells, including skin cells and white blood cells. Virulent strains of S. aureus are also coagulase-positive, meaning they produce coagulase, a plasma-clotting protein that is involved in abscess formation. They may also produce leukocidins, which kill white blood cells and can contribute to the production of pus and Protein A, which inhibits phagocytosis by binding to the constant region of antibodies. Some virulent strains of S. aureus also produce other toxins, such as toxic shock syndrome toxin-1 (see Virulence Factors of Bacterial and Viral Pathogens).",True,Staphylococcal Infections of the Skin,,,,
9871bf2d-1a54-4c50-a591-789102ddbb11,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"To confirm the causative agent of a suspected staphylococcal skin infection, samples from the wound are cultured. Under the microscope, gram-positive Staphylococcus species have cellular arrangements that form grapelike clusters; when grown on blood agar, colonies have a unique pigmentation ranging from opaque white to cream. A catalase test is used to distinguish Staphylococcus from Streptococcus, which is also a genus of gram-positive cocci and a common cause of skin infections. Staphylococcus species are catalase-positive while Streptococcus species are catalase-negative.",True,Staphylococcal Infections of the Skin,,,,
4269b3b5-921a-443e-8d50-771f24016092,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Other tests are performed on samples from the wound in order to distinguish coagulase-positive species of Staphylococcus (CoPS) such as S. aureus from common coagulase-negative species (CoNS) such as S. epidermidis. Although CoNS are less likely than CoPS to cause human disease, they can cause infections when they enter the body, as can sometimes occur via catheters, indwelling medical devices, and wounds. Passive agglutination testing can be used to distinguish CoPS from CoNS. If the sample is coagulase-positive, the sample is generally presumed to contain S. aureus. Additional genetic testing would be necessary to identify the particular strain of S. aureus.",True,Staphylococcal Infections of the Skin,,,,
8fc3da8a-e2a6-4aa3-a331-160b9a5feb01,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Another way to distinguish CoPS from CoNS is by culturing the sample on mannitol salt agar (MSA). Staphylococcus species readily grow on this medium because they are tolerant of the high concentration of sodium chloride (7.5% NaCl). However, CoPS such as S. aureus ferment mannitol (which will be evident on a MSA plate), whereas CoNS such as S. epidermidis do not ferment mannitol but can be distinguished by the fermentation of other sugars such as lactose, malonate, and raffinose (Figure 16.7).",True,Staphylococcal Infections of the Skin,Figure 16.7,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.9.png,"Figure 16.7 (a) A mannitol salt agar plate is used to distinguish different species of staphylococci. In this plate, S. aureus is on the left and S. epidermidis is in the right. Because S. aureus is capable of fermenting mannitol, it produces acids that cause the color to change to yellow. (b) This scanning electron micrograph shows the characteristic grapelike clusters of S. aureus. (credit a: modification of work by “ScienceProfOnline”/YouTube; credit b: modification of work by Centers for Disease Control and Prevention)"
68f3411a-af59-450f-aec0-ac32e8526936,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"In an attempt to control the spread of MRSA, hospitals have tried screening patients for MRSA. If patients test positive following a nasal swab test, they can undergo decolonization using chlorhexidine washes or intranasal mupirocin. Some studies have reported substantial reductions in MRSA disease following implementation of these protocols, while others have not. This is partly because there is no standard protocol for these procedures. Several different MRSA identification tests may be used, some involving slower culturing techniques and others rapid testing. Other factors, such as the effectiveness of general hand-washing protocols, may also play a role in helping to prevent MRSA transmission. There are still other questions that need to be addressed: How frequently should patients be screened? Which individuals should be tested? From where on the body should samples be collected? Will increased resistance develop from the decolonization procedures?",True,Staphylococcal Infections of the Skin,,,,
a1c37094-5081-40f9-95d8-0edb62ad6fc1,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Even if identification and decolonization procedures are perfected, ethical questions will remain. Should patients have the right to decline testing? Should a patient who tests positive for MRSA have the right to decline the decolonization procedure, and if so, should hospitals have the right to refuse treatment to the patient? How do we balance the individual’s right to receive care with the rights of other patients who could be exposed to disease as a result?",True,Staphylococcal Infections of the Skin,,,,
e1612423-0eef-4470-b05e-624908a374b8,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Superficial Staphylococcal Infections,False,Superficial Staphylococcal Infections,,,,
626dcce0-872e-4abf-9ed6-228a443f6eb7,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"S. aureus is often associated with pyoderma, skin infections that are purulent. Pus formation occurs because many strains of S. aureus produce leukocidins, which kill white blood cells. These purulent skin infections may initially manifest as folliculitis, but can lead to furuncles or deeper abscesses called carbuncles.",True,Superficial Staphylococcal Infections,,,,
b346afe9-33d7-426f-b4f0-c4a490189e03,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Folliculitis generally presents as bumps and pimples that may be itchy, red, and/or pus-filled. In some cases, folliculitis is self-limiting, but if it continues for more than a few days, worsens, or returns repeatedly, it may require medical treatment. Sweat, skin injuries, ingrown hairs, tight clothing, irritation from shaving, and skin conditions can all contribute to folliculitis. Avoidance of tight clothing and skin irritation can help to prevent infection, but topical antibiotics (and sometimes other treatments) may also help. Folliculitis can be identified by skin inspection; treatment is generally started without first culturing and identifying the causative agent.",True,Superficial Staphylococcal Infections,,,,
0b9fec2d-1f20-486a-953d-404e07cea802,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"In contrast, furuncles (boils) are deeper infections (Figure 16.8). They are most common in those individuals (especially young adults and teenagers) who play contact sports, share athletic equipment, have poor nutrition, live in close quarters, or have weakened immune systems. Good hygiene and skin care can often help to prevent furuncles from becoming more infective, and they generally resolve on their own. However, if furuncles spread, increase in number or size, or lead to systemic symptoms such as fever and chills, then medical care is needed. They may sometimes need to be drained (at which time the pathogens can be cultured) and treated with antibiotics.",True,Superficial Staphylococcal Infections,Figure 16.8,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.10.png,Figure 16.8 Furuncles (boils) and carbuncles are infections of the skin often caused by Staphylococcus bacteria. (a) A furuncle contains pus and exhibits swelling. (b) A carbuncle is a pus-filled lesion that is typically deeper than the furuncle. It often forms from multiple furuncles. (credit a: modification of work by “Mahdouch”/Wikimedia Commons; credit b: modification of work by “Drvgaikwad”/Wikimedia Commons)
3ba479de-d735-4055-9641-d47e19a807ca,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"When multiple boils develop into a deeper lesion, it is called a carbuncle (Figure 16.8). Because carbuncles are deeper, they are more commonly associated with systemic symptoms and a general feeling of illness. Larger, recurrent, or worsening carbuncles require medical treatment, as do those associated with signs of illness such as fever. Carbuncles generally need to be drained and treated with antibiotics. While carbuncles are relatively easy to identify visually, culturing and laboratory analysis of the wound may be recommended for some infections because antibiotic resistance is relatively common.",True,Superficial Staphylococcal Infections,Figure 16.8,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.10.png,Figure 16.8 Furuncles (boils) and carbuncles are infections of the skin often caused by Staphylococcus bacteria. (a) A furuncle contains pus and exhibits swelling. (b) A carbuncle is a pus-filled lesion that is typically deeper than the furuncle. It often forms from multiple furuncles. (credit a: modification of work by “Mahdouch”/Wikimedia Commons; credit b: modification of work by “Drvgaikwad”/Wikimedia Commons)
0e050826-cd30-47bc-a94e-b955f43ca24e,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Proper hygiene is important to prevent these types of skin infections or to prevent the progression of existing infections.,True,Superficial Staphylococcal Infections,,,,
d7f49493-5b18-4991-a23f-31fc19509a2e,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Staphylococcal scalded skin syndrome (SSSS) is another superficial infection caused by S. aureus that is most commonly seen in young children, especially infants. Bacterial exotoxins first produce erythema (redness of the skin) and then severe peeling of the skin, as might occur after scalding (Figure 16.9). SSSS is diagnosed by examining characteristics of the skin (which may rub off easily), using blood tests to check for elevated white blood cell counts, culturing, and other methods. Intravenous antibiotics and fluid therapy are used as treatment.",True,Superficial Staphylococcal Infections,Figure 16.9,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.11.png,"Figure 16.9 A newborn with staphylococcal scalded skin syndrome (SSSS), which results in large regions of peeling, dead skin. (credit: modification of work by D Jeyakumari, R Gopal, M Eswaran, and C MaheshKumar)"
19f52b7a-ff38-4e91-bca8-3c1398cc53c1,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Impetigo,False,Impetigo,,,,
f4b5dab0-6a57-40b3-8ec2-1683f2ae4c0f,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"The skin infection impetigo causes the formation of vesicles, pustules, and possibly bullae, often around the nose and mouth. Bullae are large, fluid-filled blisters that measure at least 5 mm in diameter. Impetigo can be diagnosed as either nonbullous or bullous. In nonbullous impetigo, vesicles and pustules rupture and become encrusted sores. Typically the crust is yellowish, often with exudate draining from the base of the lesion. In bullous impetigo, the bullae fill and rupture, resulting in larger, draining, encrusted lesions (Figure 16.10).",True,Impetigo,Figure 16.10,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.12.png,"Figure 16.10 Impetigo is characterized by vesicles, pustules, or bullae that rupture, producing encrusted sores. (credit: modification of work by FDA)"
e28f9c7a-6657-44e5-84ef-3911f913f5e7,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Especially common in children, impetigo is particularly concerning because it is highly contagious. Impetigo can be caused by S. aureus alone, by Streptococcus pyogenes alone, or by coinfection of S. aureus and S. pyogenes. Impetigo is often diagnosed through observation of its characteristic appearance, although culture and susceptibility testing may also be used.",True,Impetigo,,,,
ee0bcecb-3ac7-43db-bfe7-cabea2ee06f4,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Topical or oral antibiotic treatment is typically effective in treating most cases of impetigo. However, cases caused by S. pyogenes can lead to serious sequelae (pathological conditions resulting from infection, disease, injury, therapy, or other trauma) such as acute glomerulonephritis (AGN), which is severe inflammation in the kidneys.",True,Impetigo,,,,
62b71a47-951a-458a-8375-e0675530fb47,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Nosocomial S. epidermidis Infections,True,Impetigo,,,,
40586217-1946-460b-8450-3565b1fbf076,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,S. epidermidis,True,Impetigo,,,,
56fd32a4-02e4-49c0-97cb-b213cf1c75ac,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Though not as virulent as S. aureus, the staphylococcus S. epidermidis can cause serious opportunistic infections. Such infections usually occur only in hospital settings. S. epidermidis is usually a harmless resident of the normal skin microbiota. However, health-care workers can inadvertently transfer S. epidermidis to medical devices that are inserted into the body, such as catheters, prostheses, and indwelling medical devices. Once it has bypassed the skin barrier, S. epidermidis can cause infections inside the body that can be difficult to treat. Like S. aureus, S. epidermidis is resistant to many antibiotics, and localized infections can become systemic if not treated quickly. To reduce the risk of nosocomial (hospital-acquired) S. epidermidis, health-care workers must follow strict procedures for handling and sterilizing medical devices before and during surgical procedures.",True,Impetigo,,,,
d44afc7a-b212-4de5-9f22-06eedc088831,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Streptococcal Infections of the Skin,False,Streptococcal Infections of the Skin,,,,
04fbc31e-2b55-4597-81a8-6cd5923d475f,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Streptococcus are gram-positive cocci with a microscopic morphology that resembles chains of bacteria. Colonies are typically small (1–2 mm in diameter), translucent, entire edge, with a slightly raised elevation that can be either nonhemolytic, alpha-hemolytic, or beta-hemolytic when grown on blood agar (Figure 16.11). Additionally, they are facultative anaerobes that are catalase-negative.",True,Streptococcal Infections of the Skin,Figure 16.11,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.13.png,Figure 16.11 Streptococcus pyogenes forms chains of cocci. (credit: modification of work by Centers for Disease Control and Prevention)
d70e6d9b-895e-41ad-8007-025aed77244c,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"The genus Streptococcus includes important pathogens that are categorized in serological Lancefield groups based on the distinguishing characteristics of their surface carbohydrates. The most clinically important streptococcal species in humans is S. pyogenes, also known as group A streptococcus (GAS). S. pyogenes produces a variety of extracellular enzymes, including streptolysins O and S, hyaluronidase, and streptokinase. These enzymes can aid in transmission and contribute to the inflammatory response.[1] S. pyogenes also produces a capsule and M protein, a streptococcal cell wall protein. These virulence factors help the bacteria to avoid phagocytosis while provoking a substantial immune response that contributes to symptoms associated with streptococcal infections.",True,Streptococcal Infections of the Skin,,,,
fa505980-d650-4ec5-a80d-df033acd26a1,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"S. pyogenes causes a wide variety of diseases not only in the skin, but in other organ systems as well. Examples of diseases elsewhere in the body include pharyngitis and scarlet fever.",True,Streptococcal Infections of the Skin,,,,
ae81dce0-5731-46e2-8e69-946c62c3893d,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Cellulitis, Erysipelas, and Erythema Nosodum",False,"Cellulitis, Erysipelas, and Erythema Nosodum",,,,
d503e6b7-6c5e-4010-acbb-568f6e2af43d,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Common streptococcal conditions of the skin include cellulitis and erysipelas. An infection that develops in the dermis or hypodermis can cause cellulitis, which presents as a reddened area of the skin that is warm to the touch and painful. The causative agent is often S. pyogenes, which may breach the epidermis through a cut or abrasion, although cellulitis may also be caused by staphylococci (Figure 16.12).",True,"Cellulitis, Erysipelas, and Erythema Nosodum",Figure 16.12,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.14.png,"Figure 16.12 S. pyogenes can cause a variety of skin conditions once it breaches the skin barrier through a cut or wound. (a) Cellulitis presents as a painful, red rash. (b) Erysipelas presents as a raised rash, usually with clear borders. (c) Erythema nodosum is characterized by red lumps or nodules, typically on the lower legs. (credit a: modification of work by “Bassukas ID, Gaitanis G, Zioga A, Boboyianni C, Stergiopoulou C; credit b: modification of work by Centers for Disease Control and Prevention; credit c: modification of work by Dean C, Crow WT)"
5794c275-3ad9-435b-8bf2-f08efb4e538f,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"In general, streptococcal infections are best treated through identification of the specific pathogen followed by treatment based upon that particular pathogen’s susceptibility to different antibiotics. Many immunological tests, including agglutination reactions and ELISAs, can be used to detect streptococci. Penicillin is commonly prescribed for treatment of cellulitis and erysipelas because resistance is not widespread in streptococci at this time. Recommended treatments may include nonsteroidal anti-inflammatory drugs (NSAIDs), cool wet compresses, elevation, and bed rest.",True,"Cellulitis, Erysipelas, and Erythema Nosodum",,,,
c3e957c1-a89d-429b-8b11-854de75108f9,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Necrotizing Fasciitis,False,Necrotizing Fasciitis,,,,
93187f5e-9157-42bd-8462-9aef0e6e7eaf,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Streptococcal infections that start in the skin can sometimes spread elsewhere, resulting in a rare but potentially life-threatening condition called necrotizing fasciitis, sometimes referred to as flesh-eating bacterial syndrome. S. pyogenes is one of several species that can cause this rare but potentially-fatal condition; others include Klebsiella, Clostridium, Escherichia coli, S. aureus, and Aeromonas hydrophila.",True,Necrotizing Fasciitis,,,,
34c6436d-52ff-4123-9578-8308fbfafe51,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Necrotizing fasciitis occurs when the fascia, a thin layer of connective tissue between the skin and muscle, becomes infected. Severe invasive necrotizing fasciitis due to Streptococcus pyogenes occurs when virulence factors that are responsible for adhesion and invasion overcome host defenses. S. pyogenes invasins allow bacterial cells to adhere to tissues and establish infection. Bacterial proteases unique to S. pyogenes aggressively infiltrate and destroy host tissues, inactivate complement, and prevent neutrophil migration to the site of infection. The infection and resulting tissue death can spread very rapidly, as large areas of skin become detached and die. Treatment generally requires debridement (surgical removal of dead or infected tissue) or amputation of infected limbs to stop the spread of the infection; surgical treatment is supplemented with intravenous antibiotics and other therapies (Figure 16.13).",True,Necrotizing Fasciitis,Figure 16.13,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.15.png,"Figure 16.13 (a) The left leg of this patient shows the clinical features of necrotizing fasciitis. (b) The same patient’s leg is surgically debrided to remove the infection. (credit a, b: modification of work by Piotr Smuszkiewicz, Iwona Trojanowska, and Hanna Tomczak)"
916f3774-0a62-4485-aadd-161e9e9568ab,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Necrotizing fasciitis does not always originate from a skin infection; in some cases there is no known portal of entry.,True,Necrotizing Fasciitis,,,,
2b0b117f-8f5c-448c-8a2c-2a0f7c250e85,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Acne,False,Acne,,,,
4bb582f6-e149-4f96-93c0-f4c99a16d0fc,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"One of the most ubiquitous skin conditions is acne. Acne afflicts nearly 80% of teenagers and young adults, but it can be found in individuals of all ages. Higher incidence among adolescents is due to hormonal changes that can result in overproduction of sebum.",True,Acne,,,,
6533e6c2-cddb-4fb6-a041-938a3b110cb4,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Acne occurs when hair follicles become clogged by shed skin cells and sebum, causing non-inflammatory lesions called comedones. Comedones (singular “comedo”) can take the form of whitehead and blackhead pimples. Whiteheads are covered by skin, whereas blackhead pimples are not; the black color occurs when lipids in the clogged follicle become exposed to the air and oxidize (Figure 16.14).",True,Acne,Figure 16.14,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.18.png,"Figure 16.14 (a) Acne is characterized by whitehead and blackhead comedones that result from clogged hair follicles. (b) Blackheads, visible as black spots on the skin, have a dark appearance due to the oxidation of lipids in sebum via exposure to the air. (credit a: modification of work by Bruce Blaus)"
c4cb3d47-3998-4cb2-bef1-16952cd2c928,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Often comedones lead to infection by Propionibacterium acnes, a gram-positive, non-spore-forming, aerotolerant anaerobic bacillus found on skin that consumes components of sebum. P. acnes secretes enzymes that damage the hair follicle, causing inflammatory lesions that may include papules, pustules, nodules, or pseudocysts, depending on their size and severity.",True,Acne,,,,
aaed37e0-bd4e-46a2-9405-f97b3a582faa,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Treatment of acne depends on the severity of the case. There are multiple ways to grade acne severity, but three levels are usually considered based on the number of comedones, the number of inflammatory lesions, and the types of lesions. Mild acne is treated with topical agents that may include salicylic acid (which helps to remove old skin cells) or retinoids (which have multiple mechanisms, including the reduction of inflammation). Moderate acne may be treated with antibiotics (erythromycin, clindamycin), acne creams (e.g., benzoyl peroxide), and hormones. Severe acne may require treatment using strong medications such as isotretinoin (a retinoid that reduces oil buildup, among other effects, but that also has serious side effects such as photosensitivity). Other treatments, such as phototherapy and laser therapy to kill bacteria and possibly reduce oil production, are also sometimes used.",True,Acne,,,,
91acfd5f-7bfc-41bf-a1e8-4b944683d670,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Anthrax,False,Anthrax,,,,
2c474d5c-8b2f-472a-9969-77c2cd1191e0,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"The vast majority of anthrax cases (95–99%) occur when anthrax endospores enter the body through abrasions of the skin.[2] This form of the disease is called cutaneous anthrax. It is characterized by the formation of a nodule on the skin; the cells within the nodule die, forming a black eschar, a mass of dead skin tissue (Figure 16.15). The localized infection can eventually lead to bacteremia and septicemia. If untreated, cutaneous anthrax can cause death in 20% of patients.[3] Once in the skin tissues, B. anthracis endospores germinate and produce a capsule, which prevents the bacteria from being phagocytized, and two binary exotoxins that cause edema and tissue damage.",True,Anthrax,Figure 16.15,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.19.png,"Figure 16.15 (a) Cutaneous anthrax is an infection of the skin by B. anthracis, which produces tissue-damaging exotoxins. Dead tissues accumulating in this nodule have produced a small black eschar. (b) Colonies of B. anthracis grown on sheep’s blood agar. (credit a, b: modification of work by Centers for Disease Control and Prevention)"
de71a66b-cff5-4b4b-a36c-8389ac521128,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Less commonly, anthrax infections can be initiated through other portals of entry such as the digestive tract (gastrointestinal anthrax) or respiratory tract (pulmonary anthrax or inhalation anthrax). Typically, cases of noncutaneous anthrax are more difficult to treat than the cutaneous form. The mortality rate for gastrointestinal anthrax can be up to 40%, even with treatment. Inhalation anthrax, which occurs when anthrax spores are inhaled, initially causes influenza-like symptoms, but mortality rates are approximately 45% in treated individuals and 85% in those not treated. A relatively new form of the disease, injection anthrax, has been reported in Europe in intravenous drug users; it occurs when drugs are contaminated with B. anthracis. Patients with injection anthrax show signs and symptoms of severe soft tissue infection that differ clinically from cutaneous anthrax. This often delays diagnosis and treatment, and leads to a high mortality rate.[4]",True,Anthrax,,,,
d626ffe8-417e-482b-8f9d-d22a44029add,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"B. anthracis colonies on blood agar have a rough texture and serrated edges that eventually form an undulating band (Figure 16.15). Broad spectrum antibiotics such as penicillin, erythromycin, and tetracycline are often effective treatments.",True,Anthrax,Figure 16.15,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.19.png,"Figure 16.15 (a) Cutaneous anthrax is an infection of the skin by B. anthracis, which produces tissue-damaging exotoxins. Dead tissues accumulating in this nodule have produced a small black eschar. (b) Colonies of B. anthracis grown on sheep’s blood agar. (credit a, b: modification of work by Centers for Disease Control and Prevention)"
b94915ee-8fb9-4ffe-bcac-969889ba9f46,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Unfortunately, B. anthracis has been used as a biological weapon and remains on the United Nations’ list of potential agents of bioterrorism.[5] Over a period of several months in 2001, a number of letters were mailed to members of the news media and the United States Congress. As a result, 11 individuals developed cutaneous anthrax and another 11 developed inhalation anthrax. Those infected included recipients of the letters, postal workers, and two other individuals. Five of those infected with pulmonary anthrax died. The anthrax spores had been carefully prepared to aerosolize, showing that the perpetrator had a high level of expertise in microbiology.[6]",True,Anthrax,,,,
181429ee-27a2-4edf-a8a5-53dc93ba1743,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"A vaccine is available to protect individuals from anthrax. However, unlike most routine vaccines, the current anthrax vaccine is unique in both its formulation and the protocols dictating who receives it.[7] The vaccine is administered through five intramuscular injections over a period of 18 months, followed by annual boosters. The US Food and Drug Administration (FDA) has only approved administration of the vaccine prior to exposure for at-risk adults, such as individuals who work with anthrax in a laboratory, some individuals who handle animals or animal products (e.g., some veterinarians), and some members of the United States military. The vaccine protects against cutaneous and inhalation anthrax using cell-free filtrates of microaerophilic cultures of an avirulent, nonencapsulated strain of B. anthracis.[8] The FDA has not approved the vaccine for routine use after exposure to anthrax, but if there were ever an anthrax emergency in the United States, patients could be given anthrax vaccine after exposure to help prevent disease.",True,Anthrax,,,,
9629ae4f-1c5f-436d-8fc8-82cda180b0ad,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Bacterial infections of the skin can cause a wide range of symptoms and syndromes, ranging from the superficial and relatively harmless to the severe and even fatal. Most bacterial skin infections can be diagnosed by culturing the bacteria and treated with antibiotics. Antimicrobial susceptibility testing is also often necessary because many strains of bacteria have developed antibiotic resistance. Figure 16.16 summarizes the characteristics of some common bacterial skin infections.",True,Anthrax,Figure 16.16,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.16-1.png,Figure 16.16. Details associated with various bacterial infections of the skin.
c87b7ae4-d552-4c48-bb07-c352b590a369,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Bacterial Conjunctivitis,False,Bacterial Conjunctivitis,,,,
f9791657-e250-4bd4-9a3b-5874e0bbda7d,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Like the skin, the surface of the eye comes in contact with the outside world and is somewhat prone to infection by bacteria in the environment. Bacterial conjunctivitis (pinkeye) is a condition characterized by inflammation of the conjunctiva, often accompanied by a discharge of sticky fluid (described as acute purulent conjunctivitis) (Figure 16.17). Conjunctivitis can affect one eye or both, and it usually does not affect vision permanently. Bacterial conjunctivitis is most commonly caused by Haemophilus influenzae, but can also be caused by other species such as Moraxella catarrhalis, S. pneumoniae, and S. aureus. The causative agent may be identified using bacterial cultures, Gram stain, and diagnostic biochemical, antigenic, or nucleic acid profile tests of the isolated pathogen. Bacterial conjunctivitis is very contagious, being transmitted via secretions from infected individuals, but it is also self-limiting.",True,Bacterial Conjunctivitis,Figure 16.17,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.21.png,"Figure 16.17 Acute, purulent, bacterial conjunctivitis causes swelling and redness in the conjunctiva, the membrane lining the whites of the eyes and the inner eyelids. It is often accompanied by a yellow, green, or white discharge, which can dry and become encrusted on the eyelashes. (credit: “Tanalai”/Wikimedia Commons)"
b454d950-11f8-4b70-8615-f3f24a26c60d,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Bacterial conjunctivitis usually resolves in a few days, but topical antibiotics are sometimes prescribed. Because this condition is so contagious, medical attention is recommended whenever it is suspected. Individuals who use contact lenses should discontinue their use when conjunctivitis is suspected. Certain symptoms, such as blurred vision, eye pain, and light sensitivity, can be associated with serious conditions and require medical attention.",True,Bacterial Conjunctivitis,,,,
363f2e3a-0f26-48c2-9c8c-c63837c20d94,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"A number of bacteria are able to cause infection when introduced to the mucosa of the eye. In general, bacterial eye infections can lead to inflammation, irritation, and discharge, but they vary in severity. Some are typically short-lived, and others can become chronic and lead to permanent eye damage. Prevention requires limiting exposure to contagious pathogens. When infections do occur, prompt treatment with antibiotics can often limit or prevent permanent damage. Figure 16.18 summarizes the characteristics of some common bacterial infections of the eyes.",True,Bacterial Conjunctivitis,Figure 16.18,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/08/Fig.-16.18.png,"Figure 16.18 Details associated with acute bacterial conjunctivitis, a bacterial infection of the eyes."
62f44ffa-8a3a-4098-b7a6-be2472ec107d,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"In an attempt to control the spread of MRSA, hospitals have tried screening patients for MRSA. If patients test positive following a nasal swab test, they can undergo decolonization using chlorhexidine washes or intranasal mupirocin. Some studies have reported substantial reductions in MRSA disease following implementation of these protocols, while others have not. This is partly because there is no standard protocol for these procedures. Several different MRSA identification tests may be used, some involving slower culturing techniques and others rapid testing. Other factors, such as the effectiveness of general hand-washing protocols, may also play a role in helping to prevent MRSA transmission. There are still other questions that need to be addressed: How frequently should patients be screened? Which individuals should be tested? From where on the body should samples be collected? Will increased resistance develop from the decolonization procedures?",True,Bacterial Conjunctivitis,,,,
e6217168-4a3e-40dc-946c-0dde1818f8b1,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Even if identification and decolonization procedures are perfected, ethical questions will remain. Should patients have the right to decline testing? Should a patient who tests positive for MRSA have the right to decline the decolonization procedure, and if so, should hospitals have the right to refuse treatment to the patient? How do we balance the individual’s right to receive care with the rights of other patients who could be exposed to disease as a result?",True,Bacterial Conjunctivitis,,,,
bf239861-19a4-4ccd-bdfd-45f6ea0c48fc,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Superficial Staphylococcal Infections,False,Superficial Staphylococcal Infections,,,,
ef4a31c5-8741-49c0-b43a-1a48bd033cd5,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Folliculitis generally presents as bumps and pimples that may be itchy, red, and/or pus-filled. In some cases, folliculitis is self-limiting, but if it continues for more than a few days, worsens, or returns repeatedly, it may require medical treatment. Sweat, skin injuries, ingrown hairs, tight clothing, irritation from shaving, and skin conditions can all contribute to folliculitis. Avoidance of tight clothing and skin irritation can help to prevent infection, but topical antibiotics (and sometimes other treatments) may also help. Folliculitis can be identified by skin inspection; treatment is generally started without first culturing and identifying the causative agent.",True,Superficial Staphylococcal Infections,,,,
0112de8d-c269-465d-a356-8e5964a60a82,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"In contrast, furuncles (boils) are deeper infections (Figure 16.8). They are most common in those individuals (especially young adults and teenagers) who play contact sports, share athletic equipment, have poor nutrition, live in close quarters, or have weakened immune systems. Good hygiene and skin care can often help to prevent furuncles from becoming more infective, and they generally resolve on their own. However, if furuncles spread, increase in number or size, or lead to systemic symptoms such as fever and chills, then medical care is needed. They may sometimes need to be drained (at which time the pathogens can be cultured) and treated with antibiotics.",True,Superficial Staphylococcal Infections,Figure 16.8,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.10.png,Figure 16.8 Furuncles (boils) and carbuncles are infections of the skin often caused by Staphylococcus bacteria. (a) A furuncle contains pus and exhibits swelling. (b) A carbuncle is a pus-filled lesion that is typically deeper than the furuncle. It often forms from multiple furuncles. (credit a: modification of work by “Mahdouch”/Wikimedia Commons; credit b: modification of work by “Drvgaikwad”/Wikimedia Commons)
a1d6f9e5-aec1-493f-87af-1534db430331,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"When multiple boils develop into a deeper lesion, it is called a carbuncle (Figure 16.8). Because carbuncles are deeper, they are more commonly associated with systemic symptoms and a general feeling of illness. Larger, recurrent, or worsening carbuncles require medical treatment, as do those associated with signs of illness such as fever. Carbuncles generally need to be drained and treated with antibiotics. While carbuncles are relatively easy to identify visually, culturing and laboratory analysis of the wound may be recommended for some infections because antibiotic resistance is relatively common.",True,Superficial Staphylococcal Infections,Figure 16.8,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.10.png,Figure 16.8 Furuncles (boils) and carbuncles are infections of the skin often caused by Staphylococcus bacteria. (a) A furuncle contains pus and exhibits swelling. (b) A carbuncle is a pus-filled lesion that is typically deeper than the furuncle. It often forms from multiple furuncles. (credit a: modification of work by “Mahdouch”/Wikimedia Commons; credit b: modification of work by “Drvgaikwad”/Wikimedia Commons)
9f50e914-072d-4b9e-88b2-d7b5dfe459d0,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Proper hygiene is important to prevent these types of skin infections or to prevent the progression of existing infections.,True,Superficial Staphylococcal Infections,,,,
dab92c43-634f-4c0f-a972-21753af448dd,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Staphylococcal scalded skin syndrome (SSSS) is another superficial infection caused by S. aureus that is most commonly seen in young children, especially infants. Bacterial exotoxins first produce erythema (redness of the skin) and then severe peeling of the skin, as might occur after scalding (Figure 16.9). SSSS is diagnosed by examining characteristics of the skin (which may rub off easily), using blood tests to check for elevated white blood cell counts, culturing, and other methods. Intravenous antibiotics and fluid therapy are used as treatment.",True,Superficial Staphylococcal Infections,Figure 16.9,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.11.png,"Figure 16.9 A newborn with staphylococcal scalded skin syndrome (SSSS), which results in large regions of peeling, dead skin. (credit: modification of work by D Jeyakumari, R Gopal, M Eswaran, and C MaheshKumar)"
223f75a9-b711-44e8-97eb-e2472d7f9c5f,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Impetigo,False,Impetigo,,,,
d2673965-eb89-47f6-ba7e-a14c1f401c2d,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Especially common in children, impetigo is particularly concerning because it is highly contagious. Impetigo can be caused by S. aureus alone, by Streptococcus pyogenes alone, or by coinfection of S. aureus and S. pyogenes. Impetigo is often diagnosed through observation of its characteristic appearance, although culture and susceptibility testing may also be used.",True,Impetigo,,,,
37133762-28e5-4e27-9b6c-6af4fb24c3ce,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Topical or oral antibiotic treatment is typically effective in treating most cases of impetigo. However, cases caused by S. pyogenes can lead to serious sequelae (pathological conditions resulting from infection, disease, injury, therapy, or other trauma) such as acute glomerulonephritis (AGN), which is severe inflammation in the kidneys.",True,Impetigo,,,,
c751ea16-95e7-4b98-b6ce-c915a61a08a7,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Nosocomial S. epidermidis Infections,True,Impetigo,,,,
175aff66-ffdc-4521-bf6c-04bd0f0f1efd,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Though not as virulent as S. aureus, the staphylococcus S. epidermidis can cause serious opportunistic infections. Such infections usually occur only in hospital settings. S. epidermidis is usually a harmless resident of the normal skin microbiota. However, health-care workers can inadvertently transfer S. epidermidis to medical devices that are inserted into the body, such as catheters, prostheses, and indwelling medical devices. Once it has bypassed the skin barrier, S. epidermidis can cause infections inside the body that can be difficult to treat. Like S. aureus, S. epidermidis is resistant to many antibiotics, and localized infections can become systemic if not treated quickly. To reduce the risk of nosocomial (hospital-acquired) S. epidermidis, health-care workers must follow strict procedures for handling and sterilizing medical devices before and during surgical procedures.",True,Impetigo,,,,
2a0e7cda-a7eb-4e1f-87cb-c978e71da2ac,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Streptococcal Infections of the Skin,False,Streptococcal Infections of the Skin,,,,
cec66fd5-816f-42b5-87bd-85b3b12b013f,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"The genus Streptococcus includes important pathogens that are categorized in serological Lancefield groups based on the distinguishing characteristics of their surface carbohydrates. The most clinically important streptococcal species in humans is S. pyogenes, also known as group A streptococcus (GAS). S. pyogenes produces a variety of extracellular enzymes, including streptolysins O and S, hyaluronidase, and streptokinase. These enzymes can aid in transmission and contribute to the inflammatory response.[1] S. pyogenes also produces a capsule and M protein, a streptococcal cell wall protein. These virulence factors help the bacteria to avoid phagocytosis while provoking a substantial immune response that contributes to symptoms associated with streptococcal infections.",True,Streptococcal Infections of the Skin,,,,
907e9d8a-fb5c-41bf-b0f6-54b8396ec428,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"S. pyogenes causes a wide variety of diseases not only in the skin, but in other organ systems as well. Examples of diseases elsewhere in the body include pharyngitis and scarlet fever.",True,Streptococcal Infections of the Skin,,,,
e12a4c58-275b-44cd-a558-c57cd78e9484,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Cellulitis, Erysipelas, and Erythema Nosodum",False,"Cellulitis, Erysipelas, and Erythema Nosodum",,,,
514d90b4-22f0-44d5-acaa-a35849c08269,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"In general, streptococcal infections are best treated through identification of the specific pathogen followed by treatment based upon that particular pathogen’s susceptibility to different antibiotics. Many immunological tests, including agglutination reactions and ELISAs, can be used to detect streptococci. Penicillin is commonly prescribed for treatment of cellulitis and erysipelas because resistance is not widespread in streptococci at this time. Recommended treatments may include nonsteroidal anti-inflammatory drugs (NSAIDs), cool wet compresses, elevation, and bed rest.",True,"Cellulitis, Erysipelas, and Erythema Nosodum",,,,
2de858fe-34b6-4edf-9f12-6f8f213b7757,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Necrotizing Fasciitis,False,Necrotizing Fasciitis,,,,
b5331d79-4113-4f51-bfa7-c6f2aeeabadd,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Streptococcal infections that start in the skin can sometimes spread elsewhere, resulting in a rare but potentially life-threatening condition called necrotizing fasciitis, sometimes referred to as flesh-eating bacterial syndrome. S. pyogenes is one of several species that can cause this rare but potentially-fatal condition; others include Klebsiella, Clostridium, Escherichia coli, S. aureus, and Aeromonas hydrophila.",True,Necrotizing Fasciitis,,,,
0d9094f7-631b-4aba-b403-ec3d4dc667a6,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Necrotizing fasciitis occurs when the fascia, a thin layer of connective tissue between the skin and muscle, becomes infected. Severe invasive necrotizing fasciitis due to Streptococcus pyogenes occurs when virulence factors that are responsible for adhesion and invasion overcome host defenses. S. pyogenes invasins allow bacterial cells to adhere to tissues and establish infection. Bacterial proteases unique to S. pyogenes aggressively infiltrate and destroy host tissues, inactivate complement, and prevent neutrophil migration to the site of infection. The infection and resulting tissue death can spread very rapidly, as large areas of skin become detached and die. Treatment generally requires debridement (surgical removal of dead or infected tissue) or amputation of infected limbs to stop the spread of the infection; surgical treatment is supplemented with intravenous antibiotics and other therapies (Figure 16.13).",True,Necrotizing Fasciitis,Figure 16.13,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.15.png,"Figure 16.13 (a) The left leg of this patient shows the clinical features of necrotizing fasciitis. (b) The same patient’s leg is surgically debrided to remove the infection. (credit a, b: modification of work by Piotr Smuszkiewicz, Iwona Trojanowska, and Hanna Tomczak)"
a41ea7eb-9ad8-4680-a028-3d79b177b28f,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Necrotizing fasciitis does not always originate from a skin infection; in some cases there is no known portal of entry.,True,Necrotizing Fasciitis,,,,
b342eb43-9739-4384-b2b9-f373fe9ea583,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Acne,False,Acne,,,,
5c489c7f-bca0-43dc-b9d7-1e2912ba8c33,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Acne occurs when hair follicles become clogged by shed skin cells and sebum, causing non-inflammatory lesions called comedones. Comedones (singular “comedo”) can take the form of whitehead and blackhead pimples. Whiteheads are covered by skin, whereas blackhead pimples are not; the black color occurs when lipids in the clogged follicle become exposed to the air and oxidize (Figure 16.14).",True,Acne,Figure 16.14,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.18.png,"Figure 16.14 (a) Acne is characterized by whitehead and blackhead comedones that result from clogged hair follicles. (b) Blackheads, visible as black spots on the skin, have a dark appearance due to the oxidation of lipids in sebum via exposure to the air. (credit a: modification of work by Bruce Blaus)"
95613edd-30ff-4dc3-b282-33ece640d186,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Often comedones lead to infection by Propionibacterium acnes, a gram-positive, non-spore-forming, aerotolerant anaerobic bacillus found on skin that consumes components of sebum. P. acnes secretes enzymes that damage the hair follicle, causing inflammatory lesions that may include papules, pustules, nodules, or pseudocysts, depending on their size and severity.",True,Acne,,,,
4b502692-2859-4b92-b6c4-da29db150abe,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Treatment of acne depends on the severity of the case. There are multiple ways to grade acne severity, but three levels are usually considered based on the number of comedones, the number of inflammatory lesions, and the types of lesions. Mild acne is treated with topical agents that may include salicylic acid (which helps to remove old skin cells) or retinoids (which have multiple mechanisms, including the reduction of inflammation). Moderate acne may be treated with antibiotics (erythromycin, clindamycin), acne creams (e.g., benzoyl peroxide), and hormones. Severe acne may require treatment using strong medications such as isotretinoin (a retinoid that reduces oil buildup, among other effects, but that also has serious side effects such as photosensitivity). Other treatments, such as phototherapy and laser therapy to kill bacteria and possibly reduce oil production, are also sometimes used.",True,Acne,,,,
4050348f-b404-4ca4-b51e-827c84a5e3bb,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Anthrax,False,Anthrax,,,,
8ba052ce-a8dd-4c21-9ea3-9bf55ad4f7d5,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"The vast majority of anthrax cases (95–99%) occur when anthrax endospores enter the body through abrasions of the skin.[2] This form of the disease is called cutaneous anthrax. It is characterized by the formation of a nodule on the skin; the cells within the nodule die, forming a black eschar, a mass of dead skin tissue (Figure 16.15). The localized infection can eventually lead to bacteremia and septicemia. If untreated, cutaneous anthrax can cause death in 20% of patients.[3] Once in the skin tissues, B. anthracis endospores germinate and produce a capsule, which prevents the bacteria from being phagocytized, and two binary exotoxins that cause edema and tissue damage.",True,Anthrax,Figure 16.15,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.19.png,"Figure 16.15 (a) Cutaneous anthrax is an infection of the skin by B. anthracis, which produces tissue-damaging exotoxins. Dead tissues accumulating in this nodule have produced a small black eschar. (b) Colonies of B. anthracis grown on sheep’s blood agar. (credit a, b: modification of work by Centers for Disease Control and Prevention)"
fe1b4f7c-7642-4a03-b4d0-6e384a3d8fd2,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"B. anthracis colonies on blood agar have a rough texture and serrated edges that eventually form an undulating band (Figure 16.15). Broad spectrum antibiotics such as penicillin, erythromycin, and tetracycline are often effective treatments.",True,Anthrax,Figure 16.15,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.19.png,"Figure 16.15 (a) Cutaneous anthrax is an infection of the skin by B. anthracis, which produces tissue-damaging exotoxins. Dead tissues accumulating in this nodule have produced a small black eschar. (b) Colonies of B. anthracis grown on sheep’s blood agar. (credit a, b: modification of work by Centers for Disease Control and Prevention)"
a363e822-8962-47ce-9251-ee94b2d3e19a,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Unfortunately, B. anthracis has been used as a biological weapon and remains on the United Nations’ list of potential agents of bioterrorism.[5] Over a period of several months in 2001, a number of letters were mailed to members of the news media and the United States Congress. As a result, 11 individuals developed cutaneous anthrax and another 11 developed inhalation anthrax. Those infected included recipients of the letters, postal workers, and two other individuals. Five of those infected with pulmonary anthrax died. The anthrax spores had been carefully prepared to aerosolize, showing that the perpetrator had a high level of expertise in microbiology.[6]",True,Anthrax,,,,
a0211ff2-a04d-48d0-8b23-8ad78fb5210c,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"A vaccine is available to protect individuals from anthrax. However, unlike most routine vaccines, the current anthrax vaccine is unique in both its formulation and the protocols dictating who receives it.[7] The vaccine is administered through five intramuscular injections over a period of 18 months, followed by annual boosters. The US Food and Drug Administration (FDA) has only approved administration of the vaccine prior to exposure for at-risk adults, such as individuals who work with anthrax in a laboratory, some individuals who handle animals or animal products (e.g., some veterinarians), and some members of the United States military. The vaccine protects against cutaneous and inhalation anthrax using cell-free filtrates of microaerophilic cultures of an avirulent, nonencapsulated strain of B. anthracis.[8] The FDA has not approved the vaccine for routine use after exposure to anthrax, but if there were ever an anthrax emergency in the United States, patients could be given anthrax vaccine after exposure to help prevent disease.",True,Anthrax,,,,
26d68eb4-66e3-4db8-9f9a-441744c8159c,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,Bacterial Conjunctivitis,False,Bacterial Conjunctivitis,,,,
11f0b2d1-e391-4bdf-98b5-6c7812c6b04a,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Like the skin, the surface of the eye comes in contact with the outside world and is somewhat prone to infection by bacteria in the environment. Bacterial conjunctivitis (pinkeye) is a condition characterized by inflammation of the conjunctiva, often accompanied by a discharge of sticky fluid (described as acute purulent conjunctivitis) (Figure 16.17). Conjunctivitis can affect one eye or both, and it usually does not affect vision permanently. Bacterial conjunctivitis is most commonly caused by Haemophilus influenzae, but can also be caused by other species such as Moraxella catarrhalis, S. pneumoniae, and S. aureus. The causative agent may be identified using bacterial cultures, Gram stain, and diagnostic biochemical, antigenic, or nucleic acid profile tests of the isolated pathogen. Bacterial conjunctivitis is very contagious, being transmitted via secretions from infected individuals, but it is also self-limiting.",True,Bacterial Conjunctivitis,Figure 16.17,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.21.png,"Figure 16.17 Acute, purulent, bacterial conjunctivitis causes swelling and redness in the conjunctiva, the membrane lining the whites of the eyes and the inner eyelids. It is often accompanied by a yellow, green, or white discharge, which can dry and become encrusted on the eyelashes. (credit: “Tanalai”/Wikimedia Commons)"
190c45e9-22da-4456-8de0-d2efacce4415,https://open.oregonstate.education/microbiology/,16.2	Bacterial Infections of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-2bacterial-infections-of-the-skin-and-eyes/,"Bacterial conjunctivitis usually resolves in a few days, but topical antibiotics are sometimes prescribed. Because this condition is so contagious, medical attention is recommended whenever it is suspected. Individuals who use contact lenses should discontinue their use when conjunctivitis is suspected. Certain symptoms, such as blurred vision, eye pain, and light sensitivity, can be associated with serious conditions and require medical attention.",True,Bacterial Conjunctivitis,,,,
e6c71a7f-6764-4278-89c6-716b2296e768,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,Layers of the Skin,False,Layers of the Skin,,,,
cbaa9f9d-10fb-4d06-9bae-25198dcf23e6,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"Human skin is made up of several layers and sublayers. The two main layers are the epidermis and the dermis. These layers cover a third layer of tissue called the hypodermis, which consists of fibrous and adipose connective tissue (Figure 16.2).",True,Layers of the Skin,Figure 16.2,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.2.png,"Figure 16.2 (a) A micrograph of a section through human skin shows the epidermis and dermis. (b) The major layers of human skin are the epidermis, dermis, and hypodermis. (credit b: modification of work by National Cancer Institute)"
4add977f-01ec-4b45-868b-c95cb10ed56c,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"The epidermis is the outermost layer of the skin, and it is relatively thin. The exterior surface of the epidermis, called the stratum corneum, primarily consists of dead skin cells. This layer of dead cells limits direct contact between the outside world and live cells. The stratum corneum is rich in keratin, a tough, fibrous protein that is also found in hair and nails. Keratin helps make the outer surface of the skin relatively tough and waterproof. It also helps to keep the surface of the skin dry, which reduces microbial growth. However, some microbes are still able to live on the surface of the skin, and some of these can be shed with dead skin cells in the process of desquamation, which is the shedding and peeling of skin that occurs as a normal process but that may be accelerated when infection is present.",True,Layers of the Skin,,,,
32207b29-9ee3-48fd-afcf-202e0a2ba01f,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"Beneath the epidermis lies a thicker skin layer called the dermis. The dermis contains connective tissue and embedded structures such as blood vessels, nerves, and muscles. Structures called hair follicles (from which hair grows) are located within the dermis, even though much of their structure consists of epidermal tissue. The dermis also contains the two major types of glands found in human skin: sweat glands (tubular glands that produce sweat) and sebaceous glands (which are associated with hair follicles and produce sebum, a lipid-rich substance containing proteins and minerals).",True,Layers of the Skin,,,,
67e5a352-8325-47aa-a3bb-4ef9733acdc2,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"Perspiration (sweat) provides some moisture to the epidermis, which can increase the potential for microbial growth. For this reason, more microbes are found on the regions of the skin that produce the most sweat, such as the skin of the underarms and groin. However, in addition to water, sweat also contains substances that inhibit microbial growth, such as salts, lysozyme, and antimicrobial peptides. Sebum also serves to protect the skin and reduce water loss. Although some of the lipids and fatty acids in sebum inhibit microbial growth, sebum contains compounds that provide nutrition for certain microbes.",True,Layers of the Skin,,,,
047fb44c-7aaa-4803-a6ff-45c75e5f0e2d,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,Normal Microbiota of the Skin,False,Normal Microbiota of the Skin,,,,
2e6b739d-01a2-4d19-a551-b723d3cec71a,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"The skin is home to a wide variety of normal microbiota, consisting of commensal organisms that derive nutrition from skin cells and secretions such as sweat and sebum. The normal microbiota of skin tends to inhibit transient- microbe colonization by producing antimicrobial substances and outcompeting other microbes that land on the surface of the skin. This helps to protect the skin from pathogenic infection.",True,Normal Microbiota of the Skin,,,,
594652f1-5581-4e4e-9fce-d7e396aa79f3,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"The skin’s properties differ from one region of the body to another, as does the composition of the skin’s microbiota. The availability of nutrients and moisture partly dictates which microorganisms will thrive in a particular region of the skin. Relatively moist skin, such as that of the nares (nostrils) and underarms, has a much different microbiota than the dryer skin on the arms, legs, hands, and top of the feet. Some areas of the skin have higher densities of sebaceous glands. These sebum-rich areas, which include the back, the folds at the side of the nose, and the back of the neck, harbor distinct microbial communities that are less diverse than those found on other parts of the body.",True,Normal Microbiota of the Skin,,,,
9781ae51-25aa-473d-87c9-e985f7ff7783,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"Different types of bacteria dominate the dry, moist, and sebum-rich regions of the skin. The most abundant microbes typically found in the dry and sebaceous regions are Betaproteobacteria and Propionibacteria, respectively. In the moist regions, Corynebacterium and Staphylococcus are most commonly found (Figure 16.3). Viruses and fungi are also found on the skin, with Malassezia being the most common type of fungus found as part of the normal microbiota. The role and populations of viruses in the microbiota, known as viromes, are still not well understood, and there are limitations to the techniques used to identify them.",True,Normal Microbiota of the Skin,Figure 16.3,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.3.png,"Figure 16.3 The normal microbiota varies on different regions of the skin, especially in dry versus moist areas. The figure shows the major organisms commonly found in different locations of a healthy individual’s skin and external mucosa. Note that there is significant variation among individuals. (credit: modification of work by National Human Genome Research Institute)"
ee4eaa88-d160-401f-9675-f2f72b729d63,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,Infections of the Skin,False,Infections of the Skin,,,,
bced84e2-8240-43a4-901c-db2fa59c6ee2,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"While the microbiota of the skin can play a protective role, it can also cause harm in certain cases. Often, an opportunistic pathogen residing in the skin microbiota of one individual may be transmitted to another individual more susceptible to an infection. For example, methicillin-resistant Staphylococcus aureus (MRSA) can often take upresidence in the nares of health care workers and hospital patients; though harmless on intact, healthy skin, MRSA can cause infections if introduced into other parts of the body, as might occur during surgery or via a post-surgical incision or wound. This is one reason why clean surgical sites are so important.",True,Infections of the Skin,,,,
70a0bdaa-c63e-4302-8ae3-5a96bc50d9dc,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"Injury or damage to the skin can allow microbes to enter deeper tissues, where nutrients are more abundant and the environment is more conducive to bacterial growth. Wound infections are common after a puncture or laceration that damages the physical barrier of the skin. Microbes may infect structures in the dermis, such as hair follicles and glands, causing a localized infection, or they may reach the bloodstream, which can lead to a systemic infection.",True,Infections of the Skin,,,,
328af9dc-bfb3-4ec4-ac7f-fab77ed94da6,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"In some cases, infectious microbes can cause a variety of rashes or lesions that differ in their physical characteristics. These rashes can be the result of inflammation reactions or direct responses to toxins produced by the microbes. Table 16.1 lists some of the medical terminology used to describe skin lesions and rashes based on their characteristics. It is important to note that many different diseases can lead to skin conditions of very similar appearance; thus the terms used in the table are generally not exclusive to a particular type of infection or disease.",True,Infections of the Skin,,,,
04ce6448-3853-4fbe-8adf-da262fbb6386,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,Anatomy and Microbiota of the Eye,False,Anatomy and Microbiota of the Eye,,,,
216636c2-db99-40f4-a39b-e102018cf34f,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"Although the eye and skin have distinct anatomy, they are both in direct contact with the external environment. An important component of the eye is the nasolacrimal drainage system, which serves as a conduit for the fluid of the eye, called tears. Tears flow from the external eye to the nasal cavity by the lacrimal apparatus, which is composed of the structures involved in tear production (Figure 16.4). The lacrimal gland, above the eye, secretes tears to keep the eye moist. There are two small openings, one on the inside edge of the upper eyelid and one on the inside edge of the lower eyelid, near the nose. Each of these openings is called a lacrimal punctum. Together, these lacrimal puncta collect tears from the eye that are then conveyed through lacrimal ducts to a reservoir for tears called the lacrimal sac, also known as the dacrocyst or tear sac.",True,Anatomy and Microbiota of the Eye,Figure 16.4,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.6.png,Figure 16.4 The lacrimal apparatus includes the structures of the eye associated with tear production and drainage. (credit: modification of work by “Evidence Based Medical Educator Inc.”/YouTube)
006c7a78-8068-4348-9496-34782623d426,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"From the sac, tear fluid flows via a nasolacrimal duct to the inner nose. Each nasolacrimal duct is located underneath the skin and passes through the bones of the face into the nose. Chemicals in tears, such as defensins, lactoferrin, and lysozyme, help to prevent colonization by pathogens. In addition, mucins facilitate removal of microbes from the surface of the eye.",True,Anatomy and Microbiota of the Eye,,,,
7d526cce-29a1-4ad5-9138-83bf941fba4f,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"The surfaces of the eyeball and inner eyelid are mucous membranes called conjunctiva. The normal conjunctival microbiota has not been well characterized, but does exist. One small study (part of the Ocular Microbiome project) found twelve genera that were consistently present in the conjunctiva.[1] These microbes are thought to help defend the membranes against pathogens. However, it is still unclear which microbes may be transient and which may form a stable microbiota.[2]",True,Anatomy and Microbiota of the Eye,,,,
dbf79b2d-efb0-457a-b137-15e47fe14f8b,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,Use of contact lenses can cause changes in the normal microbiota of the conjunctiva by introducing another surface into the natural anatomy of the eye. Research is currently underway to better understand how contact lenses may impact the normal microbiota and contribute to eye disease.,True,Anatomy and Microbiota of the Eye,,,,
286715f1-b6ed-43b8-adea-e9af089490b5,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"The watery material inside of the eyeball is called the vitreous humor. Unlike the conjunctiva, it is protected from contact with the environment and is almost always sterile, with no normal microbiota (Figure 16.5).",True,Anatomy and Microbiota of the Eye,Figure 16.5,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.7.png,"Figure 16.5 Some microbes live on the conjunctiva of the human eye, but the vitreous humor is sterile."
c76b610e-790f-4349-b6d7-ef1a64d8c7a3,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,Infections of the Eye,False,Infections of the Eye,,,,
70aa9eb4-195d-40b7-8aac-d2afad01092b,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"The conjunctiva is a frequent site of infection of the eye; like other mucous membranes, it is also a common portal of entry for pathogens. Inflammation of the conjunctiva is called conjunctivitis, although it is commonly known as pinkeye because of the pink appearance in the eye. Infections of deeper structures, beneath the cornea, are less common (Figure 16.6). Conjunctivitis occurs in multiple forms. It may be acute or chronic. Acute purulent conjunctivitis is associated with pus formation, while acute hemorrhagic conjunctivitis is associated with bleeding in the conjunctiva. The term blepharitis refers to an inflammation of the eyelids, while keratitis refers to an inflammation of the cornea (Figure 16.6); keratoconjunctivitis is an inflammation of both the cornea and the conjunctiva, and dacryocystitis is an inflammation of the lacrimal sac that can often occur when a nasolacrimal duct is blocked.",True,Infections of the Eye,Figure 16.6,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.8.png,"Figure 16.6 (a) Conjunctivitis is inflammation of the conjunctiva. (b) Blepharitis is inflammation of the eyelids. (c) Keratitis is inflammation of the cornea. (credit a: modification of work by Lopez-Prats MJ, Sanz Marco E, Hidalgo- Mora JJ, Garcia-Delpech S, Diaz-Llopis M; credit b, c: modification of work by Centers for Disease Control and Prevention)"
a6d03133-49d1-4c10-99cb-979aed2d2ba5,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"Infections leading to conjunctivitis, blepharitis, keratoconjunctivitis, or dacryocystitis may be caused by bacteria or viruses, but allergens, pollutants, or chemicals can also irritate the eye and cause inflammation of various structures. Viral infection is a more likely cause of conjunctivitis in cases with symptoms such as fever and watery discharge that occurs with upper respiratory infection and itchy eyes.",True,Infections of the Eye,,,,
9f576c67-c52c-4052-8526-4db1dbe2455b,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,Normal Microbiota of the Skin,False,Normal Microbiota of the Skin,,,,
a0e1dc06-5f8c-471a-9190-1219f2765d14,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"The skin is home to a wide variety of normal microbiota, consisting of commensal organisms that derive nutrition from skin cells and secretions such as sweat and sebum. The normal microbiota of skin tends to inhibit transient- microbe colonization by producing antimicrobial substances and outcompeting other microbes that land on the surface of the skin. This helps to protect the skin from pathogenic infection.",True,Normal Microbiota of the Skin,,,,
e3fa9e0c-0080-4ac1-b80e-a1d7f6a321c4,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"The skin’s properties differ from one region of the body to another, as does the composition of the skin’s microbiota. The availability of nutrients and moisture partly dictates which microorganisms will thrive in a particular region of the skin. Relatively moist skin, such as that of the nares (nostrils) and underarms, has a much different microbiota than the dryer skin on the arms, legs, hands, and top of the feet. Some areas of the skin have higher densities of sebaceous glands. These sebum-rich areas, which include the back, the folds at the side of the nose, and the back of the neck, harbor distinct microbial communities that are less diverse than those found on other parts of the body.",True,Normal Microbiota of the Skin,,,,
2c4e04cd-448c-4c3b-a437-e4de16ff62d7,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"Different types of bacteria dominate the dry, moist, and sebum-rich regions of the skin. The most abundant microbes typically found in the dry and sebaceous regions are Betaproteobacteria and Propionibacteria, respectively. In the moist regions, Corynebacterium and Staphylococcus are most commonly found (Figure 16.3). Viruses and fungi are also found on the skin, with Malassezia being the most common type of fungus found as part of the normal microbiota. The role and populations of viruses in the microbiota, known as viromes, are still not well understood, and there are limitations to the techniques used to identify them.",True,Normal Microbiota of the Skin,Figure 16.3,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.3.png,"Figure 16.3 The normal microbiota varies on different regions of the skin, especially in dry versus moist areas. The figure shows the major organisms commonly found in different locations of a healthy individual’s skin and external mucosa. Note that there is significant variation among individuals. (credit: modification of work by National Human Genome Research Institute)"
3ec9c816-84b7-4f8c-b387-6342e9d3464b,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,Infections of the Skin,False,Infections of the Skin,,,,
3d15c932-7957-4d68-af62-f79552aa1634,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"While the microbiota of the skin can play a protective role, it can also cause harm in certain cases. Often, an opportunistic pathogen residing in the skin microbiota of one individual may be transmitted to another individual more susceptible to an infection. For example, methicillin-resistant Staphylococcus aureus (MRSA) can often take upresidence in the nares of health care workers and hospital patients; though harmless on intact, healthy skin, MRSA can cause infections if introduced into other parts of the body, as might occur during surgery or via a post-surgical incision or wound. This is one reason why clean surgical sites are so important.",True,Infections of the Skin,,,,
1e566b02-8410-4637-bc9c-837f4e4982b4,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"Injury or damage to the skin can allow microbes to enter deeper tissues, where nutrients are more abundant and the environment is more conducive to bacterial growth. Wound infections are common after a puncture or laceration that damages the physical barrier of the skin. Microbes may infect structures in the dermis, such as hair follicles and glands, causing a localized infection, or they may reach the bloodstream, which can lead to a systemic infection.",True,Infections of the Skin,,,,
b32db2fb-06ef-4c57-9638-665c92a31e5e,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"In some cases, infectious microbes can cause a variety of rashes or lesions that differ in their physical characteristics. These rashes can be the result of inflammation reactions or direct responses to toxins produced by the microbes. Table 16.1 lists some of the medical terminology used to describe skin lesions and rashes based on their characteristics. It is important to note that many different diseases can lead to skin conditions of very similar appearance; thus the terms used in the table are generally not exclusive to a particular type of infection or disease.",True,Infections of the Skin,,,,
8ff25ae7-7d85-4955-9435-8feb7d4a7ec5,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,Anatomy and Microbiota of the Eye,False,Anatomy and Microbiota of the Eye,,,,
a677ccc8-7d27-4a16-907f-b6ee0e31c8b1,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"Although the eye and skin have distinct anatomy, they are both in direct contact with the external environment. An important component of the eye is the nasolacrimal drainage system, which serves as a conduit for the fluid of the eye, called tears. Tears flow from the external eye to the nasal cavity by the lacrimal apparatus, which is composed of the structures involved in tear production (Figure 16.4). The lacrimal gland, above the eye, secretes tears to keep the eye moist. There are two small openings, one on the inside edge of the upper eyelid and one on the inside edge of the lower eyelid, near the nose. Each of these openings is called a lacrimal punctum. Together, these lacrimal puncta collect tears from the eye that are then conveyed through lacrimal ducts to a reservoir for tears called the lacrimal sac, also known as the dacrocyst or tear sac.",True,Anatomy and Microbiota of the Eye,Figure 16.4,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.6.png,Figure 16.4 The lacrimal apparatus includes the structures of the eye associated with tear production and drainage. (credit: modification of work by “Evidence Based Medical Educator Inc.”/YouTube)
2375fa74-c25b-4fef-a035-49cd95fbb499,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"From the sac, tear fluid flows via a nasolacrimal duct to the inner nose. Each nasolacrimal duct is located underneath the skin and passes through the bones of the face into the nose. Chemicals in tears, such as defensins, lactoferrin, and lysozyme, help to prevent colonization by pathogens. In addition, mucins facilitate removal of microbes from the surface of the eye.",True,Anatomy and Microbiota of the Eye,,,,
162cdb27-b8e6-4b2b-a3ae-cffc51b5a03b,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,Use of contact lenses can cause changes in the normal microbiota of the conjunctiva by introducing another surface into the natural anatomy of the eye. Research is currently underway to better understand how contact lenses may impact the normal microbiota and contribute to eye disease.,True,Anatomy and Microbiota of the Eye,,,,
7ffc97b2-b8a6-4e69-9e6f-4430cd1c08b7,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"The watery material inside of the eyeball is called the vitreous humor. Unlike the conjunctiva, it is protected from contact with the environment and is almost always sterile, with no normal microbiota (Figure 16.5).",True,Anatomy and Microbiota of the Eye,Figure 16.5,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-21.7.png,"Figure 16.5 Some microbes live on the conjunctiva of the human eye, but the vitreous humor is sterile."
6167815f-42f0-49b6-add8-8d982155405f,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,Infections of the Eye,False,Infections of the Eye,,,,
eda59edd-276c-4e1d-8768-104053c8660e,https://open.oregonstate.education/microbiology/,16.1	Anatomy and Normal Microbiota of the Skin and Eyes,https://open.oregonstate.education/microbiology/chapter/21-1anatomy-and-normal-microbiota-of-the-skin-and-eyes/,"Infections leading to conjunctivitis, blepharitis, keratoconjunctivitis, or dacryocystitis may be caused by bacteria or viruses, but allergens, pollutants, or chemicals can also irritate the eye and cause inflammation of various structures. Viral infection is a more likely cause of conjunctivitis in cases with symptoms such as fever and watery discharge that occurs with upper respiratory infection and itchy eyes.",True,Infections of the Eye,,,,
a402ec40-9c0a-414f-bf65-2aa8a2163c8e,https://open.oregonstate.education/microbiology/,15.3	Organ Transplantation and Rejection,https://open.oregonstate.education/microbiology/chapter/19-3organ-transplantation-and-rejection/,"Traditional cancer treatment uses radiation and/or chemotherapy to destroy cancer cells; however, these treatments can have unwanted side effects because they harm normal cells as well as cancer cells. Newer, promising therapies attempt to enlist the patient’s immune system to target cancer cells specifically. It is known that the immune system can recognize and destroy cancerous cells, and some researchers and immunologists also believe, based on the results of their experiments, that many cancers are eliminated by the body’s own defenses before they can become a health problem. This idea is not universally accepted by researchers, however, and needs further investigation for verification.",True,Infections of the Eye,,,,
133dd909-5543-4502-8047-7682a14f0d38,https://open.oregonstate.education/microbiology/,15.3	Organ Transplantation and Rejection,https://open.oregonstate.education/microbiology/chapter/19-3organ-transplantation-and-rejection/,Cell-Mediated Response to Tumors,False,Cell-Mediated Response to Tumors,,,,
5069a7d6-31d2-43ef-8620-236c41addc6d,https://open.oregonstate.education/microbiology/,15.3	Organ Transplantation and Rejection,https://open.oregonstate.education/microbiology/chapter/19-3organ-transplantation-and-rejection/,"Cell-mediated immune responses can be directed against cancer cells, many of which do not have the normal complement of self-proteins, making them a target for elimination. Abnormal cancer cells may also present tumor antigens. These tumor antigens are not a part of the screening process used to eliminate lymphocytes during development; thus, even though they are self-antigens, they can stimulate and drive adaptive immune responses against abnormal cells.",True,Cell-Mediated Response to Tumors,,,,
ffe50c23-73ea-4d8a-b707-1640f48bfc60,https://open.oregonstate.education/microbiology/,15.3	Organ Transplantation and Rejection,https://open.oregonstate.education/microbiology/chapter/19-3organ-transplantation-and-rejection/,"Presentation of tumor antigens can stimulate naïve helper T cells to become activated by cytokines such as IL-12 and differentiate into TH1cells. TH1 cells release cytokines that can activate natural killer (NK) cells and enhance the killing of activated cytotoxic T cells. Both NK cells and cytotoxic T cells can recognize and target cancer cells, and induce apoptosis through the action of perforins and granzymes. In addition, activated cytotoxic T cells can bind to cell-surface proteins on abnormal cells and induce apoptosis by a second killing mechanism called the CD95 (Fas) cytotoxic pathway.",True,Cell-Mediated Response to Tumors,,,,
ed411cfd-ceab-41db-992d-9a00a3cc2c0c,https://open.oregonstate.education/microbiology/,15.3	Organ Transplantation and Rejection,https://open.oregonstate.education/microbiology/chapter/19-3organ-transplantation-and-rejection/,"Despite these mechanisms for removing cancerous cells from the body, cancer remains a common cause of death. Unfortunately, malignant tumors tend to actively suppress the immune response in various ways. In some cancers, the immune cells themselves are cancerous. In leukemia, lymphocytes that would normally facilitate the immune response become abnormal. In other cancers, the cancerous cells can become resistant to induction of apoptosis. This may occur through the expression of membrane proteins that shut off cytotoxic T cells or that induce regulatory T cells that can shut down immune responses.",True,Cell-Mediated Response to Tumors,,,,
ae2e5886-e2fa-4164-9f29-2fbde406ade2,https://open.oregonstate.education/microbiology/,15.3	Organ Transplantation and Rejection,https://open.oregonstate.education/microbiology/chapter/19-3organ-transplantation-and-rejection/,"The mechanisms by which cancer cells alter immune responses are still not yet fully understood, and this is a very active area of research. As scientists’ understanding of adaptive immunity improves, cancer therapies that harness the body’s immune defenses may someday be more successful in treating and eliminating cancer.",True,Cell-Mediated Response to Tumors,,,,
af99a0ae-33cb-4e87-a119-a814d4516839,https://open.oregonstate.education/microbiology/,15.3	Organ Transplantation and Rejection,https://open.oregonstate.education/microbiology/chapter/19-3organ-transplantation-and-rejection/,Cancer Vaccines,False,Cancer Vaccines,,,,
19b85d1e-8aff-441d-b5ad-20a49f123cb2,https://open.oregonstate.education/microbiology/,15.3	Organ Transplantation and Rejection,https://open.oregonstate.education/microbiology/chapter/19-3organ-transplantation-and-rejection/,"There are two types of cancer vaccines: preventive and therapeutic. Preventive vaccines are used to prevent cancer from occurring, whereas therapeutic vaccines are used to treat patients with cancer. Most preventive cancer vaccines target viral infections that are known to lead to cancer. These include vaccines against human papillomavirus (HPV) and hepatitis B, which help prevent cervical and liver cancer, respectively.",True,Cancer Vaccines,,,,
c59800d5-b2f2-42d9-b239-0213bd4e35f5,https://open.oregonstate.education/microbiology/,15.3	Organ Transplantation and Rejection,https://open.oregonstate.education/microbiology/chapter/19-3organ-transplantation-and-rejection/,"Most therapeutic cancer vaccines are in the experimental stage. They exploit tumor-specific antigens to stimulate the immune system to selectively attack cancer cells. Specifically, they aim to enhance TH1 function and interaction with cytotoxic T cells, which, in turn, results in more effective attack on abnormal tumor cells. In some cases, researchers have used genetic engineering to develop antitumor vaccines in an approach similar to that used for DNA vaccines. The vaccine contains a recombinant plasmid with genes for tumor antigens; theoretically, the tumor gene would not induce new cancer because it is not functional, but it could trick the immune system into targeting the tumor gene product as a foreign invader.",True,Cancer Vaccines,,,,
1ce0a2cc-526e-49d0-99db-d90222900a75,https://open.oregonstate.education/microbiology/,15.3	Organ Transplantation and Rejection,https://open.oregonstate.education/microbiology/chapter/19-3organ-transplantation-and-rejection/,"The first FDA-approved therapeutic cancer vaccine was sipuleucel-T (Provenge), approved in 2010 to treat certain cases of prostate cancer.[1] This unconventional vaccine is custom designed using the patient’s own cells. APCs are removed from the patient and cultured with a tumor-specific molecule; the cells are then returned to the patient. This approach appears to enhance the patient’s immune response against the cancer cells. Another therapeutic cancer vaccine (talimogene laherparepvec, also called T-VEC or Imlygic) was approved by the FDA in 2015 for treatment of melanoma, a form of skin cancer. This vaccine contains a virus that is injected into tumors, where it infects and lyses the tumor cells. The virus also induces a response in lesions or tumors besides those into which the vaccine is injected, indicating that it is stimulating a more general (as opposed to local) antitumor immune response in the patient.",True,Cancer Vaccines,,,,
01e7edf9-8ff9-410d-8bde-53a08563df30,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"Autoimmune diseases are those in which the body is attacked by its own specific adaptive immune response. In normal, healthy states, the immune system induces tolerance, which is a lack of an anti-self immune response. However, with autoimmunity, there is a loss of immune tolerance, and the mechanisms responsible for autoimmune diseases include type II, III, and IV hypersensitivity reactions. Autoimmune diseases can have a variety of mixed symptoms that flare up and disappear, making diagnosis difficult.",True,Cancer Vaccines,,,,
c5eecb0c-b196-4a90-943e-d802f99fa8d1,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"The causes of autoimmune disease are a combination of the individual’s genetic makeup and the effect of environmental influences, such as sunlight, infections, medications, and environmental chemicals. However, the vagueness of this list reflects our poor understanding of the etiology of these diseases. Except in a very few specific diseases, the initiation event(s) of most autoimmune states has not been fully characterized.",True,Cancer Vaccines,,,,
3f8a804d-0c2b-47c6-915b-f1daea940156,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"There are several possible causes for the origin of autoimmune diseases and autoimmunity is likely due to several factors. Evidence now suggests that regulatory T and B cells play an essential role in the maintenance of tolerance and prevention of autoimmune responses. The regulatory T cells are especially important for inhibiting autoreactive T cells that are not eliminated during thymic selection and escape the thymus (see T Lymphocytes and Cellular Immunity). In addition, antigen mimicry between pathogen antigens and our own self antigens can lead to cross- reactivity and autoimmunity. Hidden self-antigens may become exposed because of trauma, drug interactions, or disease states, and trigger an autoimmune response. All of these factors could contribute to autoimmunity. Ultimately, damage to tissues and organs in the autoimmune disease state comes as a result of inflammatory responses that are inappropriate; therefore, treatment often includes immunosuppressive drugs and corticosteroids.",True,Cancer Vaccines,,,,
961df6a9-8315-42d7-abb8-0b07f9470868,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,Organ-Specific Autoimmune Diseases,False,Organ-Specific Autoimmune Diseases,,,,
af3adf25-e6fd-40ca-b8ea-87c9c380a737,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"Some autoimmune diseases are considered organ specific, meaning that the immune system targets specific organs or tissues. Examples of organ-specific autoimmune diseases include celiac disease, Graves disease, Hashimoto thyroiditis, type I diabetes mellitus, and Addison disease.",True,Organ-Specific Autoimmune Diseases,,,,
7a50376f-f85d-408c-8391-cbf6db2c7e4c,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,Celiac Disease,False,Celiac Disease,,,,
4ff1fe6d-23b9-4f5c-84d3-ecd14d73a83d,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"Celiac disease is largely a disease of the small intestine, although other organs may be affected. People in their 30s and 40s, and children are most commonly affected, but celiac disease can begin at any age. It results from a reaction to proteins, commonly called gluten, found mainly in wheat, barley, rye, and some other grains. The disease has several genetic causes (predispositions) and poorly understood environmental influences. On exposure to gluten, the body produces various autoantibodies and an inflammatory response. The inflammatory response in the small intestine leads to a reduction in the depth of the microvilli of the mucosa, which hinders absorption and can lead to weight loss and anemia. The disease is also characterized by diarrhea and abdominal pain, symptoms that are often misdiagnosed as irritable bowel syndrome.",True,Celiac Disease,,,,
9d60f832-6258-491f-8cd1-9e8c1f46bed4,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"Diagnosis of celiac disease is accomplished from serological tests for the presence of primarily IgA antibodies to components of gluten, the transglutinaminase enzyme, and autoantibodies to endomysium, a connective tissue surrounding muscle fibers. Serological tests are typically followed up with endoscopy and biopsy of the duodenal mucosa. Serological screening surveys have found about 1% of individuals in the United Kingdom are positive even though they do not all display symptoms.[1] This early recognition allows for more careful monitoring and prevention of severe disease.",True,Celiac Disease,,,,
c39fbee3-f607-4cb8-bfb0-f27e2751c033,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"Celiac disease is treated with complete removal of gluten-containing foods from the diet, which results in improved symptoms and reduced risk of complications. Other theoretical approaches include breeding grains that do not contain the immunologically reactive components or developing dietary supplements that contain enzymes that break down the protein components that cause the immune response.[2]",True,Celiac Disease,,,,
edcab63b-669b-440c-bfb0-4200a91ec43f,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,Type 1 Diabetes,False,Type 1 Diabetes,,,,
8a3884be-90b9-41cd-b3d3-a840b5da4eb0,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"Juvenile diabetes, or type 1 diabetes mellitus, is usually diagnosed in children and young adults. It is a T-cell- dependent autoimmune disease characterized by the selective destruction of the β cells of the islets of Langerhans in the pancreas by CD4 TH1-mediated CD8 T cells, anti-β-cell antibodies, and macrophage activity. There is also evidence that viral infections can have either a potentiating or inhibitory role in the development of type 1 diabetes (T1D) mellitus. The destruction of the β cells causes a lack of insulin production by the pancreas. In T1D, β- cell destruction may take place over several years, but symptoms of hyperglycemia, extreme increase in thirst and urination, weight loss, and extreme fatigue usually have a sudden onset, and diagnosis usually does not occur until most β cells have already been destroyed.",True,Type 1 Diabetes,,,,
8e434150-7cb6-4b27-8786-93ef39c32666,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,Autoimmune Addison Disease,False,Autoimmune Addison Disease,,,,
cada73d4-652f-4d65-bdba-b278e41dbb5a,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"Destruction of the adrenal glands (the glands lying above the kidneys that produce glucocorticoids, mineralocorticoids, and sex steroids) is the cause of Addison disease, also called primary adrenal insufficiency (PAI). Today, up to 80% of Addison disease cases are diagnosed as autoimmune Addison disease (AAD), which is caused by an autoimmune response to adrenal tissues disrupting adrenal function. Disruption of adrenal function causes impaired metabolic processes that require normal steroid hormone levels, causing signs and symptoms throughout the body. The adrenal cortex cells are targeted, destroyed, and replaced with fibrous tissue by immune-mediated inflammation. In some patients, at least 90% of the adrenal cortex is destroyed before symptoms become diagnostic.",True,Autoimmune Addison Disease,,,,
1d66269a-c391-483e-bb87-d4d8b12a6d88,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"Symptoms of AAD include weakness, nausea, decreased appetite, weight loss, hyperpigmentation (Figure 15.11), hyperkalemia (elevated blood potassium levels), hyponatremia (decreased blood sodium levels), hypoglycemia (decreased levels of blood sugar), hypotension (decreased blood pressure), anemia, lymphocytosis (decreased levels of white blood cells), and fatigue. Under extreme stress, such as surgery, accidental trauma, or infection, patients with AAD may experience an adrenal crisis that causes the patient to vomit, experience abdominal pain, back or leg cramps, and even severe hypotension leading to shock.",True,Autoimmune Addison Disease,Figure 15.11,15.2	Autoimmune Disorders,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-19.15.png,Figure 15.11 Hyperpigmentation is a sign of Addison disease. (credit: modification of work by Petros Perros)
15136536-bd6d-4855-8848-afade26df65b,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,Systemic Autoimmune Diseases,False,Systemic Autoimmune Diseases,,,,
bebdd103-681d-436c-ac4e-b21a55766991,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,Multiple Sclerosis,False,Multiple Sclerosis,,,,
5a07453b-3569-491f-9008-4c1d0d56c2b3,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"Multiple sclerosis (MS) is an autoimmune central nervous system disease that affects the brain and spinal cord. Lesions in multiple locations within the central nervous system are a hallmark of multiple sclerosis and are caused by infiltration of immune cells across the blood-brain barrier. The immune cells include T cells that promote inflammation, demyelination, and neuron degeneration, all of which disrupt neuronal signaling. Symptoms of MS include visual disturbances; muscle weakness; difficulty with coordination and balance; sensations such as numbness, prickling, or “pins and needles”; and cognitive and memory problems.",True,Multiple Sclerosis,,,,
ccadd85a-881a-478e-b9fa-7835deda0b43,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,Psoriasis,False,Psoriasis,,,,
7e8645b5-ce11-4460-9bf8-7eb0a3448fb4,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"Psoriasis is a skin disease that causes itchy or sore patches of thick, red skin with silvery scales on elbows, knees, scalp, back, face, palms, feet, and sometimes other areas. Some individuals with psoriasis also get a form of arthritis called psoriatic arthritis, in which the joints can become inflamed. Psoriasis results from the complex interplay between keratinocytes, dendritic cells, and T cells, and the cytokines produced by these various cells. In a process called cell turnover, skin cells that grow deep in the skin rise to the surface. Normally, this process takes a month. In psoriasis, as a result of cytokine activation, cell turnover happens in just a few days. The thick inflamed patches of skin that are characteristic of psoriasis develop because the skin cells rise too fast.",True,Psoriasis,,,,
ae7ed6af-37ca-4e66-85d2-ed5b21b18485,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,Rheumatoid Arthritis,False,Rheumatoid Arthritis,,,,
4866460e-e9fc-451b-a5dd-dd3104774ed6,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"The most common chronic inflammatory joint disease is rheumatoid arthritis (RA) (Figure 15.12) and it is still a major medical challenge because of unsolved questions related to the environmental and genetic causes of the disease. RA involves type III hypersensitivity reactions and the activation of CD4 T cells, resulting in chronic release of the inflammatory cytokines IL-1, IL-6, and tumor necrosis factor-α (TNF-α). The activated CD4 T cells also stimulate the production of rheumatoid factor (RF) antibodies and anticyclic citrullinated peptide antibodies (anti- CCP) that form immune complexes. Increased levels of acute-phase proteins, such as C-reactive protein (CRP), are also produced as part of the inflammatory process and participate in complement fixation with the antibodies on the immune complexes. The formation of immune complexes and reaction to the immune factors cause an inflammatory process in joints, particularly in the hands, feet, and legs. Diagnosis of RA is based on elevated levels of RF, anti- CCP, quantitative CRP, and the erythrocyte sedimentation rate (ESR) (modified Westergren). In addition, radiographs, ultrasound, or magnetic resonance imaging scans can identify joint damage, such as erosions, a loss of bone within the joint, and narrowing of joint space.",True,Rheumatoid Arthritis,Figure 15.12,15.2	Autoimmune Disorders,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-19.17.png,Figure 15.12 The radiograph (left) and photograph (right) show damage to the hands typical of rheumatoid arthritis. (credit right: modification of work by “handarmdoc”/Flickr)
f79d2578-6fc6-43dc-8763-78c0db40b238,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,Systemic Lupus Erythematosus,False,Systemic Lupus Erythematosus,,,,
e8a9f60e-09c2-4a57-b0bd-fe4ff6e0f7b2,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"The damage and pathology of systemic lupus erythematosus (SLE) is caused by type III hypersensitivity reactions. Autoantibodies produced in SLE are directed against nuclear and cytoplasmic proteins. Anti-nuclear antibodies (ANAs) are present in more than 95% of patients with SLE,[3] with additional autoantibodies including anti- double–stranded DNA (ds-DNA) and anti-Sm antibodies (antibodies to small nuclear ribonucleoprotein). Anti-ds- DNA and anti-Sm antibodies are unique to patients with SLE; thus, their presence is included in the classification criteria of SLE. Cellular interaction with autoantibodies leads to nuclear and cellular destruction, with components released after cell death leading to the formation of immune complexes.",True,Systemic Lupus Erythematosus,,,,
c4f5376f-9704-4f91-b1c8-d816f5e6ba34,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"Because autoantibodies in SLE can target a wide variety of cells, symptoms of SLE can occur in many body locations. However, the most common symptoms include fatigue, fever with no other cause, hair loss, and a sunlight-sensitive “butterfly” or wolf-mask (lupus) rash that is found in about 50% of people with SLE (Figure 15.13). The rash is most often seen over the cheeks and bridge of the nose, but can be widespread. Other symptoms may appear depending on affected areas. The joints may be affected, leading to arthritis of the fingers, hands, wrists, and knees. Effects on the brain and nervous system can lead to headaches, numbness, tingling, seizures, vision problems, and personality changes. There may also be abdominal pain, nausea, vomiting, arrhythmias, shortness of breath, and blood in the sputum. Effects on the skin can lead to additional areas of skin lesions, and vasoconstriction can cause color changes in the fingers when they are cold (Raynaud phenomenon). Effects on the kidneys can lead to edema in the legs and weight gain. A diagnosis of SLE depends on identification of four of 11 of the most common symptoms and confirmed production of an array of autoantibodies unique to SLE. A positive test for ANAs alone is not diagnostic.",True,Systemic Lupus Erythematosus,Figure 15.13,15.2	Autoimmune Disorders,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-19.18.png,"Figure 15.13 (a) Systemic lupus erythematosus is characterized by autoimmunity to the individual’s own DNA and/ or proteins. (b) This patient is presenting with a butterfly rash, one of the characteristic signs of lupus. (credit a: modification of work by Mikael Häggström; credit b: modification of work by Shrestha D, Dhakal AK, Shiva RK, Shakya A, Shah SC, Shakya H)"
546c047e-2cef-4979-b44c-561da9744064,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"Table 15.6 summarizes the causes, signs, and symptoms of select autoimmune diseases.",True,Systemic Lupus Erythematosus,,,,
220c8164-9bf3-4f63-a1d9-4fee2fdec56b,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,Systemic Autoimmune Diseases,False,Systemic Autoimmune Diseases,,,,
6f3268cb-ff1d-4fea-ba7c-5f0839af3ce3,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"Multiple sclerosis (MS) is an autoimmune central nervous system disease that affects the brain and spinal cord. Lesions in multiple locations within the central nervous system are a hallmark of multiple sclerosis and are caused by infiltration of immune cells across the blood-brain barrier. The immune cells include T cells that promote inflammation, demyelination, and neuron degeneration, all of which disrupt neuronal signaling. Symptoms of MS include visual disturbances; muscle weakness; difficulty with coordination and balance; sensations such as numbness, prickling, or “pins and needles”; and cognitive and memory problems.",True,Systemic Autoimmune Diseases,,,,
3608380b-23c4-41a7-aa0d-294613457e78,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"Psoriasis is a skin disease that causes itchy or sore patches of thick, red skin with silvery scales on elbows, knees, scalp, back, face, palms, feet, and sometimes other areas. Some individuals with psoriasis also get a form of arthritis called psoriatic arthritis, in which the joints can become inflamed. Psoriasis results from the complex interplay between keratinocytes, dendritic cells, and T cells, and the cytokines produced by these various cells. In a process called cell turnover, skin cells that grow deep in the skin rise to the surface. Normally, this process takes a month. In psoriasis, as a result of cytokine activation, cell turnover happens in just a few days. The thick inflamed patches of skin that are characteristic of psoriasis develop because the skin cells rise too fast.",True,Systemic Autoimmune Diseases,,,,
53ad425d-77f9-486f-b25f-134d989ed5e2,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"The most common chronic inflammatory joint disease is rheumatoid arthritis (RA) (Figure 15.12) and it is still a major medical challenge because of unsolved questions related to the environmental and genetic causes of the disease. RA involves type III hypersensitivity reactions and the activation of CD4 T cells, resulting in chronic release of the inflammatory cytokines IL-1, IL-6, and tumor necrosis factor-α (TNF-α). The activated CD4 T cells also stimulate the production of rheumatoid factor (RF) antibodies and anticyclic citrullinated peptide antibodies (anti- CCP) that form immune complexes. Increased levels of acute-phase proteins, such as C-reactive protein (CRP), are also produced as part of the inflammatory process and participate in complement fixation with the antibodies on the immune complexes. The formation of immune complexes and reaction to the immune factors cause an inflammatory process in joints, particularly in the hands, feet, and legs. Diagnosis of RA is based on elevated levels of RF, anti- CCP, quantitative CRP, and the erythrocyte sedimentation rate (ESR) (modified Westergren). In addition, radiographs, ultrasound, or magnetic resonance imaging scans can identify joint damage, such as erosions, a loss of bone within the joint, and narrowing of joint space.",True,Systemic Autoimmune Diseases,Figure 15.12,15.2	Autoimmune Disorders,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-19.17.png,Figure 15.12 The radiograph (left) and photograph (right) show damage to the hands typical of rheumatoid arthritis. (credit right: modification of work by “handarmdoc”/Flickr)
dbe6c743-7e66-4cc9-8115-57132aeb5d7c,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"Because autoantibodies in SLE can target a wide variety of cells, symptoms of SLE can occur in many body locations. However, the most common symptoms include fatigue, fever with no other cause, hair loss, and a sunlight-sensitive “butterfly” or wolf-mask (lupus) rash that is found in about 50% of people with SLE (Figure 15.13). The rash is most often seen over the cheeks and bridge of the nose, but can be widespread. Other symptoms may appear depending on affected areas. The joints may be affected, leading to arthritis of the fingers, hands, wrists, and knees. Effects on the brain and nervous system can lead to headaches, numbness, tingling, seizures, vision problems, and personality changes. There may also be abdominal pain, nausea, vomiting, arrhythmias, shortness of breath, and blood in the sputum. Effects on the skin can lead to additional areas of skin lesions, and vasoconstriction can cause color changes in the fingers when they are cold (Raynaud phenomenon). Effects on the kidneys can lead to edema in the legs and weight gain. A diagnosis of SLE depends on identification of four of 11 of the most common symptoms and confirmed production of an array of autoantibodies unique to SLE. A positive test for ANAs alone is not diagnostic.",True,Systemic Autoimmune Diseases,Figure 15.13,15.2	Autoimmune Disorders,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-19.18.png,"Figure 15.13 (a) Systemic lupus erythematosus is characterized by autoimmunity to the individual’s own DNA and/ or proteins. (b) This patient is presenting with a butterfly rash, one of the characteristic signs of lupus. (credit a: modification of work by Mikael Häggström; credit b: modification of work by Shrestha D, Dhakal AK, Shiva RK, Shakya A, Shah SC, Shakya H)"
b2f66146-205e-4216-9d02-90f0f8337f10,https://open.oregonstate.education/microbiology/,15.2	Autoimmune Disorders,https://open.oregonstate.education/microbiology/chapter/19-2autoimmune-disorders/,"Table 15.6 summarizes the causes, signs, and symptoms of select autoimmune diseases.",True,Systemic Autoimmune Diseases,,,,
784dee2a-a1ee-4e30-93e0-92d682e2b089,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,Type I Hypersensitivities,False,Type I Hypersensitivities,,,,
cc767bc7-e315-4f77-96ee-541881d953c5,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"When a presensitized individual is exposed to an allergen, it can lead to a rapid immune response that occurs almost immediately. Such a response is called an allergy and is classified as a type I hypersensitivity. Allergens may be seemingly harmless substances such as animal dander, molds, or pollen. Allergens may also be substances considered innately more hazardous, such as insect venom or therapeutic drugs. Food intolerances can also yield allergic reactions as individuals become sensitized to foods such as peanuts or shellfish (Figure 15.2). Regardless of the allergen, the first exposure activates a primary IgE antibody response that sensitizes an individual to type I hypersensitivity reaction upon subsequent exposure.",True,Type I Hypersensitivities,Figure 15.2,15.1	Hypersensitivities,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-19.2.png,"Figure 15.2 (a) Allergens in plant pollen, shown here in a colorized electron micrograph, may trigger allergic rhinitis or hay fever in sensitive individuals. (b) Skin rashes are often associated with allergic reactions. (c) Peanuts can be eaten safely by most people but can provoke severe allergic reactions in sensitive individuals."
e6025304-acd0-49db-82ce-a4c001b3e947,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"For susceptible individuals, a first exposure to an allergen activates a strong TH2 cell response (Figure 15.3). Cytokines interleukin (IL)-4 and IL-13 from the TH2 cells activate B cells specific to the same allergen, resulting in clonal proliferation, differentiation into plasma cells, and antibody-class switch from production of IgM to production of IgE. The fragment crystallizable (Fc) regions of the IgE antibodies bind to specific receptors on the surface of mast cells throughout the body. It is estimated that each mast cell can bind up to 500,000 IgE molecules, with each IgE molecule having two allergen-specific fragment antigen-binding (Fab) sites available for binding allergen on subsequent exposures. By the time this occurs, the allergen is often no longer present and there is no allergic reaction, but the mast cells are primed for a subsequent exposure and the individual is sensitized to the allergen.",True,Type I Hypersensitivities,Figure 15.3,15.1	Hypersensitivities,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-19.3.png,"Figure 15.3 On first exposure to an allergen in a susceptible individual, antigen-presenting cells process and present allergen epitopes with major histocompatibility complex (MHC) II to T helper cells. B cells also process and present the same allergen epitope to TH2 cells, which release cytokines IL-4 and IL-13 to stimulate proliferation and differentiation into IgE-secreting plasma cells. The IgE molecules bind to mast cells with their Fc region, sensitizing the mast cells for activation with subsequent exposure to the allergen. With each subsequent exposure, the allergen cross-links IgE molecules on the mast cells, activating the mast cells and causing the release of preformed chemical mediators from granules (degranulation), as well as newly formed chemical mediators that collectively cause the signs and symptoms of type I hypersensitivity reactions."
f879e11d-1d47-41a3-aedf-756ea81cc7fa,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"On subsequent exposure, allergens bind to multiple IgE molecules on mast cells, cross-linking the IgE molecules. Within minutes, this cross-linking of IgE activates the mast cells and triggers degranulation, a reaction in which the contents of the granules in the mast cell are released into the extracellular environment. Preformed components that are released from granules include histamine, serotonin, and bradykinin (Table 15.1). The activated mast cells also release newly formed lipid mediators (leukotrienes and prostaglandins from membrane arachadonic acid metabolism) and cytokines such as tumor necrosis factor (Table 15.2).",True,Type I Hypersensitivities,,,,
ca8ce6eb-dea0-47ba-83b2-a81b1ff60f1a,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"The chemical mediators released by mast cells collectively cause the inflammation and signs and symptoms associated with type I hypersensitivity reactions. Histamine stimulates mucus secretion in nasal passages and tear formation from lacrimal glands, promoting the runny nose and watery eyes of allergies. Interaction of histamine with nerve endings causes itching and sneezing. The vasodilation caused by several of the mediators can result in hives, headaches, angioedema (swelling that often affects the lips, throat, and tongue), and hypotension (low blood pressure). Bronchiole constriction caused by some of the chemical mediators leads to wheezing, dyspnea (difficulty breathing), coughing, and, in more severe cases, cyanosis (bluish color to the skin or mucous membranes). Vomiting can result from stimulation of the vomiting center in the cerebellum by histamine and serotonin. Histamine can also cause relaxation of intestinal smooth muscles and diarrhea.",True,Type I Hypersensitivities,,,,
ffac944d-ebef-4e30-8e75-12c36403cc35,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Late-phase reactions in type I hypersensitivities may develop 4–12 hours after the early phase and are mediated by eosinophils, neutrophils, and lymphocytes that have been recruited by chemotactic factors released from mast cells. Activation of these recruited cells leads to the release of more chemical mediators that cause tissue damage and late- phase symptoms of swelling and redness of the skin, coughing, wheezing, and nasal discharge.",True,Type I Hypersensitivities,,,,
7a63319b-2ecf-442f-b4a6-600ed2f07ae2,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Individuals who possess genes for maladaptive traits, such as intense type I hypersensitivity reactions to otherwise harmless components of the environment, would be expected to suffer reduced reproductive success. With this kind of evolutionary selective pressure, such traits would not be expected to persist in a population. This suggests that type I hypersensitivities may have an adaptive function. There is evidence that the IgE produced during type I hypersensitivity reactions is actually meant to counter helminth infections.[2] Helminths are one of few organisms that possess proteins that are targeted by IgE. In addition, there is evidence that helminth infections at a young age reduce the likelihood of type I hypersensitivities to innocuous substances later in life. Thus it may be that allergies are an unfortunate consequence of strong selection in the mammalian lineage or earlier for a defense against parasitic worms.",True,Type I Hypersensitivities,,,,
b8244541-f10b-4c6e-a40f-f4348eb2a334,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"The hygiene hypothesis was first suggested in 1989 by David Strachan[4], who observed an inverse relationship between the number of older children in a family and the incidence of hay fever. Although hay fever in children had increased dramatically during the mid-20th century, incidence was significantly lower in families with more children. Strachan proposed that the lower incidence of allergies in large families could be linked to infections acquired from older siblings, suggesting that these infections made children less susceptible to allergies. Strachan also argued that trends toward smaller families and a greater emphasis on cleanliness in the 20th century had decreased exposure to pathogens and thus led to higher overall rates of allergies, asthma, and other immune disorders.",True,Type I Hypersensitivities,,,,
1d486e99-872b-4ea6-8408-c433a571f395,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Other researchers have observed an inverse relationship between the incidence of immune disorders and infectious diseases that are now rare in industrialized countries but still common in less industrialized countries.[5] In developed nations, children under the age of 5 years are not exposed to many of the microbes, molecules, and antigens they almost certainly would have encountered a century ago. The lack of early challenges to the immune system by organisms with which humans and their ancestors evolved may result in failures in immune system functioning later in life.",True,Type I Hypersensitivities,,,,
aef4cf5f-f7e0-4265-960c-e2c985d9c891,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,Type II (Cytotoxic) Hypersensitivities,False,Type II (Cytotoxic) Hypersensitivities,,,,
cad849d7-ef6a-44c2-8bec-99e648172094,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Immune reactions categorized as type II hypersensitivities, or cytotoxic hypersensitivities, are mediated by IgG and IgM antibodies binding to cell-surface antigens or matrix-associated antigens on basement membranes. These antibodies can either activate complement, resulting in an inflammatory response and lysis of the targeted cells, or they can be involved in antibody-dependent cell-mediated cytotoxicity (ADCC) with cytotoxic T cells.",True,Type II (Cytotoxic) Hypersensitivities,,,,
a2fc5221-fca1-437f-969a-9629397fbe67,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"In some cases, the antigen may be a self-antigen, in which case the reaction would also be described as an autoimmune disease. (Autoimmune diseases are described in Autoimmune Disorders). In other cases, antibodies may bind to naturally occurring, but exogenous, cell-surface molecules such as antigens associated with blood typing found on red blood cells (RBCs). This leads to the coating of the RBCs by antibodies, activation of the complement cascade, and complement-mediated lysis of RBCs, as well as opsonization of RBCs for phagocytosis. Two examples of type II hypersensitivity reactions involving RBCs are hemolytic transfusion reaction (HTR) and hemolytic disease of the newborn (HDN). These type II hypersensitivity reactions, which will be discussed in greater detail, are summarized in Table 15.4.",True,Type II (Cytotoxic) Hypersensitivities,,,,
6d35355a-1d94-4747-9d7e-e2ad38c7cf61,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Immunohematology is the study of blood and blood-forming tissue in relation to the immune response. Antibody- initiated responses against blood cells are type II hypersensitivities, thus falling into the field of immunohematology. For students first learning about immunohematology, understanding the immunological mechanisms involved is made even more challenging by the complex nomenclature system used to identify different blood-group antigens, often called blood types. The first blood-group antigens either used alphabetical names or were named for the first person known to produce antibodies to the red blood cell antigen (e.g., Kell, Duffy, or Diego). However, in 1980, the International Society of Blood Transfusion (ISBT) Working Party on Terminology created a standard for blood-group terminology in an attempt to more consistently identify newly discovered blood group antigens. New antigens are now given a number and assigned to a blood-group system, collection, or series. However, even with this effort, blood-group nomenclature is still inconsistent.",True,Type II (Cytotoxic) Hypersensitivities,,,,
1e274060-ad54-4dbd-af6c-0704170875fe,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"The recognition that individuals have different blood types was first described by Karl Landsteiner (1868–1943) in the early 1900s, based on his observation that serum from one person could cause a clumping of RBCs from another. These studies led Landsteiner to the identification of four distinct blood types. Subsequent research by other scientists determined that the four blood types were based on the presence or absence of surface carbohydrates “A” and “B,” and this provided the foundation for the ABO blood group system that is still in use today (Figure 15.4). The functions of these antigens are unknown, but some have been associated with normal biochemical functions of the cell. Furthermore, ABO blood types are inherited as alleles (one from each parent), and they display patterns of dominant and codominant inheritance. The alleles for A and B blood types are codominant to each other, and both are dominant over blood type O. Therefore, individuals with genotypes of AA or AO have type A blood and express the A carbohydrate antigen on the surface of their RBCs. People with genotypes of BB or BO have type B blood and express the B carbohydrate antigen on the surface of their RBCs. Those with a genotype of AB have type AB blood and express both A and B carbohydrate antigens on the surface of their RBCs. Finally, individuals with a genotype of OO have type O blood and lack A and B carbohydrate on the surface of their RBCs.",True,Type II (Cytotoxic) Hypersensitivities,Figure 15.4,15.1	Hypersensitivities,https://open.oregonstate.education/app/uploads/sites/8/2023/04/Figure-15.4v2.png,Figure 15.4. This figure shows the isohemagglutinins and antigens associated with the different human blood types.
c11c045f-c32b-47dc-b990-d8a74043ef12,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"It is important to note that the RBCs of all four ABO blood types share a common protein receptor molecule, and it is the addition of specific carbohydrates to the protein receptors that determines A, B, and AB blood types. The genes that are inherited for the A, B, and AB blood types encode enzymes that add the carbohydrate component to the protein receptor. Individuals with O blood type still have the protein receptor but lack the enzymes that would add carbohydrates that would make their red blood cell type A, B, or AB.",True,Type II (Cytotoxic) Hypersensitivities,,,,
99d198d8-bd72-4a48-bfbe-23fa7d9b9618,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"IgM antibodies in plasma that cross-react with blood group antigens not present on an individual’s own RBCs are called isohemagglutinins (Figure 15.4). Isohemagglutinins are produced within the first few weeks after birth and persist throughout life. These antibodies are produced in response to exposure to environmental antigens from food and microorganisms. A person with type A blood has A antigens on the surface of their RBCs and will produce anti-B antibodies to environmental antigens that resemble the carbohydrate component of B antigens. A person with type B blood has B antigens on the surface of their RBCs and will produce anti-A antibodies to environmental antigens that are similar to the carbohydrate component of A antigens. People with blood type O lack both A and B antigens on their RBCs and, therefore, produce both anti-A and anti-B antibodies. Conversely, people with AB blood type have both A and B antigens on their RBCs and, therefore, lack anti-A and anti-B antibodies.",True,Type II (Cytotoxic) Hypersensitivities,Figure 15.4,15.1	Hypersensitivities,https://open.oregonstate.education/app/uploads/sites/8/2023/04/Figure-15.4v2.png,Figure 15.4. This figure shows the isohemagglutinins and antigens associated with the different human blood types.
7dea048c-891e-45e3-85ef-bdda5f85d775,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"A patient may require a blood transfusion because they lack sufficient RBCs (anemia) or because they have experienced significant loss of blood volume through trauma or disease. Although the blood transfusion is given to help the patient, it is essential that the patient receive a transfusion with matching ABO blood type. A transfusion with an incompatible ABO blood type may lead to a strong, potentially lethal type II hypersensitivity cytotoxic response called hemolytic transfusion reaction (HTR) (Figure 15.5).",True,Type II (Cytotoxic) Hypersensitivities,Figure 15.5,15.1	Hypersensitivities,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-19.5.png,"Figure 15.5 A type II hypersensitivity hemolytic transfusion reaction (HTR) leading to hemolytic anemia. Blood from a type A donor is administered to a patient with type B blood. The anti-A isohemagglutinin IgM antibodies in the recipient bind to and agglutinate the incoming donor type A red blood cells. The bound anti-A antibodies activate the classical complement cascade, resulting in destruction of the donor red blood cells."
a98cf443-cd57-4311-a5d3-cdb4c39f62d4,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"For instance, if a person with type B blood receives a transfusion of type A blood, their anti-A antibodies will bind to and agglutinate the transfused RBCs. In addition, activation of the classical complement cascade will lead to a strong inflammatory response, and the complement membrane attack complex (MAC) will mediate massive hemolysis of the transfused RBCs. The debris from damaged and destroyed RBCs can occlude blood vessels in the alveoli of the lungs and the glomeruli of the kidneys. Within 1 to 24 hours of an incompatible transfusion, the patient experiences fever, chills, pruritus (itching), urticaria (hives), dyspnea, hemoglobinuria (hemoglobin in the urine), and hypotension (low blood pressure). In the most serious reactions, dangerously low blood pressure can lead to shock, multi-organ failure, and death of the patient.",True,Type II (Cytotoxic) Hypersensitivities,,,,
922e8f32-d783-449e-8455-c347c1277561,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Hospitals, medical centers, and associated clinical laboratories typically use hemovigilance systems to minimize the risk of HTRs due to clerical error. Hemovigilance systems are procedures that track transfusion information from the donor source and blood products obtained to the follow-up of recipient patients. Hemovigilance systems used in many countries identify HTRs and their outcomes through mandatory reporting (e.g., to the Food and Drug Administration in the United States), and this information is valuable to help prevent such occurrences in the future. For example, if an HTR is found to be the result of laboratory or clerical error, additional blood products collected from the donor at that time can be located and labeled correctly to avoid additional HTRs. As a result of these measures, HTR-associated deaths in the United States occur in about one per 2 million transfused units.[6]",True,Type II (Cytotoxic) Hypersensitivities,,,,
8cd314db-394b-4850-8349-aa63f8a66e2b,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,Rh Factors,False,Rh Factors,,,,
504b3529-834e-43b2-8a3d-7ba6ef37f7d0,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Like ABO incompatibilities, blood transfusions from a donor with the wrong Rh factor antigens can cause a type II hypersensitivity HTR. However, in contrast to the IgM isohemagglutinins produced early in life through exposure to environmental antigens, production of anti-Rh factor antibodies requires the exposure of an individual with Rh− blood to Rh+ positive RBCs and activation of a primary antibody response. Although this primary antibody response can cause an HTR in the transfusion patient, the hemolytic reaction would be delayed up to 2 weeks during the extended lag period of a primary antibody response (B Lymphocytes and Humoral Immunity). However, if the patient receives a subsequent transfusion with Rh+ RBCs, a more rapid HTR would occur with anti-Rh factor antibody already present in the blood. Furthermore, the rapid secondary antibody response would provide even more anti-Rh factor antibodies for the HTR.",True,Rh Factors,,,,
7e34002f-1efd-4241-b56b-a956c9fcd0d0,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Rh factor incompatibility between mother and fetus can also cause a type II hypersensitivity hemolytic reaction, referred to as hemolytic disease of the newborn (HDN) (Figure 15.6). If an Rh− woman carries an Rh+ baby to term, the mother’s immune system can be exposed to Rh+ fetal red blood cells. This exposure will usually occur during the last trimester of pregnancy and during the delivery process. If this exposure occurs, the Rh+ fetal RBCs will activate a primary adaptive immune response in the mother, and anti-Rh factor IgG antibodies will be produced. IgG antibodies are the only class of antibody that can cross the placenta from mother to fetus; however, in most cases, the first Rh+ baby is unaffected by these antibodies because the first exposure typically occurs late enough in the pregnancy that the mother does not have time to mount a sufficient primary antibody response before the baby is born.",True,Rh Factors,Figure 15.6,15.1	Hypersensitivities,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-19.6.png,"Figure 15.6 (a) When an Rh− mother has an Rh+ fetus, fetal erythrocytes are introduced into the mother ’s circulatory system before or during birth, leading to production of anti-Rh IgG antibodies. These antibodies remain in the mother and, if she becomes pregnant with a second Rh+ baby, they can cross the placenta and attach to fetal Rh+ erythrocytes. Complement-mediated hemolysis of fetal erythrocytes results in a lack of sufficient cells for proper oxygenation of the fetus. (b) HDN can be prevented by administering Rho(D) immune globulin during and after each pregnancy with an Rh+ fetus. The immune globulin binds fetal Rh+ RBCs that gain access to the mother ’s bloodstream, preventing activation of her primary immune response."
b3de54f7-c0ec-446b-95d8-93428bbd6e62,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"If a subsequent pregnancy with an Rh+ fetus occurs, however, the mother’s second exposure to the Rh factor antigens causes a strong secondary antibody response that produces larger quantities of anti-Rh factor IgG. These antibodies can cross the placenta from mother to fetus and cause HDN, a potentially lethal condition for the baby (Figure 15.6).",True,Rh Factors,Figure 15.6,15.1	Hypersensitivities,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-19.6.png,"Figure 15.6 (a) When an Rh− mother has an Rh+ fetus, fetal erythrocytes are introduced into the mother ’s circulatory system before or during birth, leading to production of anti-Rh IgG antibodies. These antibodies remain in the mother and, if she becomes pregnant with a second Rh+ baby, they can cross the placenta and attach to fetal Rh+ erythrocytes. Complement-mediated hemolysis of fetal erythrocytes results in a lack of sufficient cells for proper oxygenation of the fetus. (b) HDN can be prevented by administering Rho(D) immune globulin during and after each pregnancy with an Rh+ fetus. The immune globulin binds fetal Rh+ RBCs that gain access to the mother ’s bloodstream, preventing activation of her primary immune response."
e8aa5301-3606-420c-9fe4-6a9cc356843b,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Prior to the development of techniques for diagnosis and prevention, Rh factor incompatibility was the most common cause of HDN, resulting in thousands of infant deaths each year worldwide.[7] For this reason, the Rh factors of prospective parents are regularly screened, and treatments have been developed to prevent HDN caused by Rh incompatibility. To prevent Rh factor-mediated HDN, human Rho(D) immune globulin (e.g., RhoGAM) is injected intravenously or intramuscularly into the mother during the 28th week of pregnancy and within 72 hours after delivery. Additional doses may be administered after events that may result in transplacental hemorrhage (e.g., umbilical blood sampling, chorionic villus sampling, abdominal trauma, amniocentesis). This treatment is initiated during the first pregnancy with an Rh+ fetus. The anti-Rh antibodies in Rho(D) immune globulin will bind to the Rh factor of any fetal RBCs that gain access to the mother’s bloodstream, preventing these Rh+ cells from activating the mother’s primary antibody response. Without a primary anti-Rh factor antibody response, the next pregnancy with an Rh+ will have minimal risk of HDN. However, the mother will need to be retreated with Rho(D) immune globulin during that pregnancy to prevent a primary anti-Rh antibody response that could threaten subsequent pregnancies.",True,Rh Factors,,,,
20ad0f1c-d3b5-4e8d-95c2-b41951e42ffa,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,Type III Hypersensitivities,False,Type III Hypersensitivities,,,,
4a505a29-ca71-437d-8aea-5a3c5f7d5791,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Type III hypersensitivities are immune-complex reactions that were first characterized by Nicolas Maurice Arthus (1862–1945) in 1903. To produce antibodies for experimental procedures, Arthus immunized rabbits by injecting them with serum from horses. However, while immunizing rabbits repeatedly with horse serum, Arthus noticed a previously unreported and unexpected localized subcutaneous hemorrhage with edema at the site of injection. This reaction developed within 3 to10 hours after injection. This localized reaction to non-self serum proteins was called an Arthus reaction. An Arthus reaction occurs when soluble antigens bind with IgG in a ratio that results in the accumulation of antigen-antibody aggregates called immune complexes.",True,Type III Hypersensitivities,,,,
fbf514a8-e4b3-4a26-9e27-bba574c059ed,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"A unique characteristic of type III hypersensitivity is antibody excess (primarily IgG), coupled with a relatively low concentration of antigen, resulting in the formation of small immune complexes that deposit on the surface of the epithelial cells lining the inner lumen of small blood vessels or on the surfaces of tissues (Figure 15.7). This immune complex accumulation leads to a cascade of inflammatory events that include the following:",True,Type III Hypersensitivities,Figure 15.7,15.1	Hypersensitivities,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-19.7.png,"Figure 15.7 Type III hypersensitivities and the systems they affect. (a) Immune complexes form and deposit in tissue. Complement activation, stimulation of an inflammatory response, and recruitment and activation of neutrophils result in damage to blood vessels, heart tissue, joints, skin, and/or kidneys. (b) If the kidneys are damaged by a type III hypersensitivity reaction, dialysis may be required."
5a171316-57b4-4abb-9c9f-0da51cc99e06,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Because these immune complexes are not an optimal size and are deposited on cell surfaces, they cannot be phagocytosed in the usual way by neutrophils and macrophages, which, in turn, are often described as “frustrated.” Although phagocytosis does not occur, neutrophil degranulation results in the release of lysosomal enzymes that causeextracellular destruction of the immune complex, damaging localized cells in the process. Activation of coagulation pathways also occurs, resulting in thrombi (blood clots) that occlude blood vessels and cause ischemia that can lead to vascular necrosis and localized hemorrhage.",True,Type III Hypersensitivities,,,,
577cabb7-5dd1-44bf-8137-a8f9e00ee1cc,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Systemic type III hypersensitivity (serum sickness) occurs when immune complexes deposit in various body sites, resulting in a more generalized systemic inflammatory response. These immune complexes involve non-self proteins such as antibodies produced in animals for artificial passive immunity (see Vaccines), certain drugs, or microbial antigens that are continuously released over time during chronic infections (e.g., subacute bacterial endocarditis, chronic viral hepatitis). The mechanisms of serum sickness are similar to those described in localized type III hypersensitivity but involve widespread activation of mast cells, complement, neutrophils, and macrophages, which causes tissue destruction in areas such as the kidneys, joints, and blood vessels. As a result of tissue destruction, symptoms of serum sickness include chills, fever, rash, vasculitis, and arthritis. Development of glomerulonephritis or hepatitis is also possible.",True,Type III Hypersensitivities,,,,
703933bf-a446-4bc5-ab52-fd692898a966,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,Autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis can also involve damaging type III hypersensitivity reactions when auto-antibodies form immune complexes with self antigens. These conditions are discussed in Autoimmune Disorders.,True,Type III Hypersensitivities,,,,
309276d4-cb08-4df7-9f31-b3b22a079a4d,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,Type IV Hypersensitivities,False,Type IV Hypersensitivities,,,,
ef306697-c076-40b7-8e5e-f67dc128f1c8,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Type IV hypersensitivities are not mediated by antibodies like the other three types of hypersensitivities. Rather, type IV hypersensitivities are regulated by T cells and involve the action of effector cells. These types of hypersensitivities can be organized into three subcategories based on T-cell subtype, type of antigen, and the resulting effector mechanism (Table 15.5).",True,Type IV Hypersensitivities,,,,
e9b0666b-787c-40e5-993e-452a2425dcf2,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"In the first type IV subcategory, CD4 TH1-mediated reactions are described as delayed-type hypersensitivities (DTH). The sensitization step involves the introduction of antigen into the skin and phagocytosis by local antigen presenting cells (APCs). The APCs activate helper T cells, stimulating clonal proliferation and differentiation into memory TH1 cells. Upon subsequent exposure to the antigen, these sensitized memory TH1 cells release cytokines that activate macrophages, and activated macrophages are responsible for much of the tissue damage. Examples of this TH1-mediated hypersensitivity are observed in tuberculin the Mantoux skin test and contact dermatitis, such as occurs in latex allergy reactions.",True,Type IV Hypersensitivities,,,,
3bdf0dd4-8829-4821-b463-fdba2fef3d7a,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"In the second type IV subcategory, CD4 TH2-mediated reactions result in chronic asthma or chronic allergic rhinitis. In these cases, the soluble antigen is first inhaled, resulting in eosinophil recruitment and activation with the release of cytokines and inflammatory mediators.",True,Type IV Hypersensitivities,,,,
230699c2-deb9-422b-8d5d-f19a5b9e6154,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"In the third type IV subcategory, CD8 cytotoxic T lymphocyte (CTL)-mediated reactions are associated with tissue transplant rejection and contact dermatitis (Figure 15.8). For this form of cell-mediated hypersensitivity, APCs process and present the antigen with MHC I to naïve CD8 T cells. When these naïve CD8 T cells are activated, they proliferate and differentiate into CTLs. Activated TH1 cells can also enhance the activation of the CTLs. The activated CTLs then target and induce granzyme-mediated apoptosis in cells presenting the same antigen with MHC I. These target cells could be “self” cells that have absorbed the foreign antigen (such as with contact dermatitis due to poison ivy), or they could be transplanted tissue cells displaying foreign antigen from the donor.",True,Type IV Hypersensitivities,Figure 15.8,15.1	Hypersensitivities,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-19.8.png,"Figure 15.8 Exposure to hapten antigens in poison ivy can cause contact dermatitis, a type IV hypersensitivity. (a) The first exposure to poison ivy does not result in a reaction. However, sensitization stimulates helper T cells, leading to production of memory helper T cells that can become reactivated on future exposures. (b) Upon secondary exposure, the memory helper T cells become reactivated, producing inflammatory cytokines that stimulate macrophages and cytotoxic T cells to induce an inflammatory lesion at the exposed site. This lesion, which will persist until the allergen is removed, can inflict significant tissue damage if it continues long enough."
9d5ac471-7a18-467b-b6f5-35183535c60b,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"The tips of all the needles in the array are coated with tuberculin, a protein extract of TB bacteria, effectively introducing the tuberculin into the skin. One to 3 days later, the area can be examined for a delayed hypersensitivity reaction, signs of which include swelling and redness.",True,Type IV Hypersensitivities,,,,
25b18058-5222-4a58-a134-1995683f5af9,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"As you can imagine, scarification was not a pleasant experience,[9] and the numerous skin punctures put the patient at risk of developing bacterial infection of the skin. Mantoux modified Pirquet’s test to use a single subcutaneous injection of purified tuberculin material. A positive test, which is indicated by a delayed localized swelling at the injection site, does not necessarily mean that the patient is currently infected with active TB. Because type IV (delayed-type) hypersensitivity is mediated by reactivation of memory T cells, such cells may have been created recently (due to an active current infection) or years prior (if a patient had TB and had spontaneously cleared it, or if it had gone into latency). However, the test can be used to confirm infection in cases in which symptoms in the patient or findings on a radiograph suggest its presence.",True,Type IV Hypersensitivities,,,,
5dfd7b00-a522-4025-8a61-7536bfe1ccc7,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"On subsequent exposure, allergens bind to multiple IgE molecules on mast cells, cross-linking the IgE molecules. Within minutes, this cross-linking of IgE activates the mast cells and triggers degranulation, a reaction in which the contents of the granules in the mast cell are released into the extracellular environment. Preformed components that are released from granules include histamine, serotonin, and bradykinin (Table 15.1). The activated mast cells also release newly formed lipid mediators (leukotrienes and prostaglandins from membrane arachadonic acid metabolism) and cytokines such as tumor necrosis factor (Table 15.2).",True,Type IV Hypersensitivities,,,,
0058a2e7-36c7-46bb-a15b-9dcbca029b95,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"The chemical mediators released by mast cells collectively cause the inflammation and signs and symptoms associated with type I hypersensitivity reactions. Histamine stimulates mucus secretion in nasal passages and tear formation from lacrimal glands, promoting the runny nose and watery eyes of allergies. Interaction of histamine with nerve endings causes itching and sneezing. The vasodilation caused by several of the mediators can result in hives, headaches, angioedema (swelling that often affects the lips, throat, and tongue), and hypotension (low blood pressure). Bronchiole constriction caused by some of the chemical mediators leads to wheezing, dyspnea (difficulty breathing), coughing, and, in more severe cases, cyanosis (bluish color to the skin or mucous membranes). Vomiting can result from stimulation of the vomiting center in the cerebellum by histamine and serotonin. Histamine can also cause relaxation of intestinal smooth muscles and diarrhea.",True,Type IV Hypersensitivities,,,,
dc62059c-7473-4ff3-99fa-dcd1d3b1ccbc,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Late-phase reactions in type I hypersensitivities may develop 4–12 hours after the early phase and are mediated by eosinophils, neutrophils, and lymphocytes that have been recruited by chemotactic factors released from mast cells. Activation of these recruited cells leads to the release of more chemical mediators that cause tissue damage and late- phase symptoms of swelling and redness of the skin, coughing, wheezing, and nasal discharge.",True,Type IV Hypersensitivities,,,,
3d2dd583-9ab3-4e77-8e68-43247ef6ba29,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Individuals who possess genes for maladaptive traits, such as intense type I hypersensitivity reactions to otherwise harmless components of the environment, would be expected to suffer reduced reproductive success. With this kind of evolutionary selective pressure, such traits would not be expected to persist in a population. This suggests that type I hypersensitivities may have an adaptive function. There is evidence that the IgE produced during type I hypersensitivity reactions is actually meant to counter helminth infections.[2] Helminths are one of few organisms that possess proteins that are targeted by IgE. In addition, there is evidence that helminth infections at a young age reduce the likelihood of type I hypersensitivities to innocuous substances later in life. Thus it may be that allergies are an unfortunate consequence of strong selection in the mammalian lineage or earlier for a defense against parasitic worms.",True,Type IV Hypersensitivities,,,,
09f74621-8eee-47bb-b4f0-41f11acf76f6,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"The hygiene hypothesis was first suggested in 1989 by David Strachan[4], who observed an inverse relationship between the number of older children in a family and the incidence of hay fever. Although hay fever in children had increased dramatically during the mid-20th century, incidence was significantly lower in families with more children. Strachan proposed that the lower incidence of allergies in large families could be linked to infections acquired from older siblings, suggesting that these infections made children less susceptible to allergies. Strachan also argued that trends toward smaller families and a greater emphasis on cleanliness in the 20th century had decreased exposure to pathogens and thus led to higher overall rates of allergies, asthma, and other immune disorders.",True,Type IV Hypersensitivities,,,,
b9b97f08-6a98-4122-8ce2-2bdfd0d8f9de,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Other researchers have observed an inverse relationship between the incidence of immune disorders and infectious diseases that are now rare in industrialized countries but still common in less industrialized countries.[5] In developed nations, children under the age of 5 years are not exposed to many of the microbes, molecules, and antigens they almost certainly would have encountered a century ago. The lack of early challenges to the immune system by organisms with which humans and their ancestors evolved may result in failures in immune system functioning later in life.",True,Type IV Hypersensitivities,,,,
f93939c5-2142-48ff-bcc0-c67bf1ad3a49,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,Type II (Cytotoxic) Hypersensitivities,False,Type II (Cytotoxic) Hypersensitivities,,,,
922a96cd-c82d-4408-9ab6-46254f3f6987,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"In some cases, the antigen may be a self-antigen, in which case the reaction would also be described as an autoimmune disease. (Autoimmune diseases are described in Autoimmune Disorders). In other cases, antibodies may bind to naturally occurring, but exogenous, cell-surface molecules such as antigens associated with blood typing found on red blood cells (RBCs). This leads to the coating of the RBCs by antibodies, activation of the complement cascade, and complement-mediated lysis of RBCs, as well as opsonization of RBCs for phagocytosis. Two examples of type II hypersensitivity reactions involving RBCs are hemolytic transfusion reaction (HTR) and hemolytic disease of the newborn (HDN). These type II hypersensitivity reactions, which will be discussed in greater detail, are summarized in Table 15.4.",True,Type II (Cytotoxic) Hypersensitivities,,,,
8dd7b2d8-d90e-4583-a6bb-3553c38999e0,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Immunohematology is the study of blood and blood-forming tissue in relation to the immune response. Antibody- initiated responses against blood cells are type II hypersensitivities, thus falling into the field of immunohematology. For students first learning about immunohematology, understanding the immunological mechanisms involved is made even more challenging by the complex nomenclature system used to identify different blood-group antigens, often called blood types. The first blood-group antigens either used alphabetical names or were named for the first person known to produce antibodies to the red blood cell antigen (e.g., Kell, Duffy, or Diego). However, in 1980, the International Society of Blood Transfusion (ISBT) Working Party on Terminology created a standard for blood-group terminology in an attempt to more consistently identify newly discovered blood group antigens. New antigens are now given a number and assigned to a blood-group system, collection, or series. However, even with this effort, blood-group nomenclature is still inconsistent.",True,Type II (Cytotoxic) Hypersensitivities,,,,
ebbac80b-acf8-451d-9a2d-4dbe5979b9fc,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"It is important to note that the RBCs of all four ABO blood types share a common protein receptor molecule, and it is the addition of specific carbohydrates to the protein receptors that determines A, B, and AB blood types. The genes that are inherited for the A, B, and AB blood types encode enzymes that add the carbohydrate component to the protein receptor. Individuals with O blood type still have the protein receptor but lack the enzymes that would add carbohydrates that would make their red blood cell type A, B, or AB.",True,Type II (Cytotoxic) Hypersensitivities,,,,
10673dfc-2cb3-495e-9867-d5fbe820e304,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"IgM antibodies in plasma that cross-react with blood group antigens not present on an individual’s own RBCs are called isohemagglutinins (Figure 15.4). Isohemagglutinins are produced within the first few weeks after birth and persist throughout life. These antibodies are produced in response to exposure to environmental antigens from food and microorganisms. A person with type A blood has A antigens on the surface of their RBCs and will produce anti-B antibodies to environmental antigens that resemble the carbohydrate component of B antigens. A person with type B blood has B antigens on the surface of their RBCs and will produce anti-A antibodies to environmental antigens that are similar to the carbohydrate component of A antigens. People with blood type O lack both A and B antigens on their RBCs and, therefore, produce both anti-A and anti-B antibodies. Conversely, people with AB blood type have both A and B antigens on their RBCs and, therefore, lack anti-A and anti-B antibodies.",True,Type II (Cytotoxic) Hypersensitivities,Figure 15.4,15.1	Hypersensitivities,https://open.oregonstate.education/app/uploads/sites/8/2023/04/Figure-15.4v2.png,Figure 15.4. This figure shows the isohemagglutinins and antigens associated with the different human blood types.
ac390211-139d-4046-8571-41aee483eeba,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"For instance, if a person with type B blood receives a transfusion of type A blood, their anti-A antibodies will bind to and agglutinate the transfused RBCs. In addition, activation of the classical complement cascade will lead to a strong inflammatory response, and the complement membrane attack complex (MAC) will mediate massive hemolysis of the transfused RBCs. The debris from damaged and destroyed RBCs can occlude blood vessels in the alveoli of the lungs and the glomeruli of the kidneys. Within 1 to 24 hours of an incompatible transfusion, the patient experiences fever, chills, pruritus (itching), urticaria (hives), dyspnea, hemoglobinuria (hemoglobin in the urine), and hypotension (low blood pressure). In the most serious reactions, dangerously low blood pressure can lead to shock, multi-organ failure, and death of the patient.",True,Type II (Cytotoxic) Hypersensitivities,,,,
9752ba78-dc12-45ef-b0e8-5f7326a3d394,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Hospitals, medical centers, and associated clinical laboratories typically use hemovigilance systems to minimize the risk of HTRs due to clerical error. Hemovigilance systems are procedures that track transfusion information from the donor source and blood products obtained to the follow-up of recipient patients. Hemovigilance systems used in many countries identify HTRs and their outcomes through mandatory reporting (e.g., to the Food and Drug Administration in the United States), and this information is valuable to help prevent such occurrences in the future. For example, if an HTR is found to be the result of laboratory or clerical error, additional blood products collected from the donor at that time can be located and labeled correctly to avoid additional HTRs. As a result of these measures, HTR-associated deaths in the United States occur in about one per 2 million transfused units.[6]",True,Type II (Cytotoxic) Hypersensitivities,,,,
90951cd2-dea8-4c17-b213-7bf3e9ed6a9c,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Like ABO incompatibilities, blood transfusions from a donor with the wrong Rh factor antigens can cause a type II hypersensitivity HTR. However, in contrast to the IgM isohemagglutinins produced early in life through exposure to environmental antigens, production of anti-Rh factor antibodies requires the exposure of an individual with Rh− blood to Rh+ positive RBCs and activation of a primary antibody response. Although this primary antibody response can cause an HTR in the transfusion patient, the hemolytic reaction would be delayed up to 2 weeks during the extended lag period of a primary antibody response (B Lymphocytes and Humoral Immunity). However, if the patient receives a subsequent transfusion with Rh+ RBCs, a more rapid HTR would occur with anti-Rh factor antibody already present in the blood. Furthermore, the rapid secondary antibody response would provide even more anti-Rh factor antibodies for the HTR.",True,Type II (Cytotoxic) Hypersensitivities,,,,
83a9797f-4a5f-4005-b038-ffb2e8f4f7fb,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Rh factor incompatibility between mother and fetus can also cause a type II hypersensitivity hemolytic reaction, referred to as hemolytic disease of the newborn (HDN) (Figure 15.6). If an Rh− woman carries an Rh+ baby to term, the mother’s immune system can be exposed to Rh+ fetal red blood cells. This exposure will usually occur during the last trimester of pregnancy and during the delivery process. If this exposure occurs, the Rh+ fetal RBCs will activate a primary adaptive immune response in the mother, and anti-Rh factor IgG antibodies will be produced. IgG antibodies are the only class of antibody that can cross the placenta from mother to fetus; however, in most cases, the first Rh+ baby is unaffected by these antibodies because the first exposure typically occurs late enough in the pregnancy that the mother does not have time to mount a sufficient primary antibody response before the baby is born.",True,Type II (Cytotoxic) Hypersensitivities,Figure 15.6,15.1	Hypersensitivities,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-19.6.png,"Figure 15.6 (a) When an Rh− mother has an Rh+ fetus, fetal erythrocytes are introduced into the mother ’s circulatory system before or during birth, leading to production of anti-Rh IgG antibodies. These antibodies remain in the mother and, if she becomes pregnant with a second Rh+ baby, they can cross the placenta and attach to fetal Rh+ erythrocytes. Complement-mediated hemolysis of fetal erythrocytes results in a lack of sufficient cells for proper oxygenation of the fetus. (b) HDN can be prevented by administering Rho(D) immune globulin during and after each pregnancy with an Rh+ fetus. The immune globulin binds fetal Rh+ RBCs that gain access to the mother ’s bloodstream, preventing activation of her primary immune response."
6cd90546-1074-41ef-b360-02d32671ccde,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"If a subsequent pregnancy with an Rh+ fetus occurs, however, the mother’s second exposure to the Rh factor antigens causes a strong secondary antibody response that produces larger quantities of anti-Rh factor IgG. These antibodies can cross the placenta from mother to fetus and cause HDN, a potentially lethal condition for the baby (Figure 15.6).",True,Type II (Cytotoxic) Hypersensitivities,Figure 15.6,15.1	Hypersensitivities,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-19.6.png,"Figure 15.6 (a) When an Rh− mother has an Rh+ fetus, fetal erythrocytes are introduced into the mother ’s circulatory system before or during birth, leading to production of anti-Rh IgG antibodies. These antibodies remain in the mother and, if she becomes pregnant with a second Rh+ baby, they can cross the placenta and attach to fetal Rh+ erythrocytes. Complement-mediated hemolysis of fetal erythrocytes results in a lack of sufficient cells for proper oxygenation of the fetus. (b) HDN can be prevented by administering Rho(D) immune globulin during and after each pregnancy with an Rh+ fetus. The immune globulin binds fetal Rh+ RBCs that gain access to the mother ’s bloodstream, preventing activation of her primary immune response."
3145e4e8-f06b-4af4-b8b8-83c5c097b28d,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Prior to the development of techniques for diagnosis and prevention, Rh factor incompatibility was the most common cause of HDN, resulting in thousands of infant deaths each year worldwide.[7] For this reason, the Rh factors of prospective parents are regularly screened, and treatments have been developed to prevent HDN caused by Rh incompatibility. To prevent Rh factor-mediated HDN, human Rho(D) immune globulin (e.g., RhoGAM) is injected intravenously or intramuscularly into the mother during the 28th week of pregnancy and within 72 hours after delivery. Additional doses may be administered after events that may result in transplacental hemorrhage (e.g., umbilical blood sampling, chorionic villus sampling, abdominal trauma, amniocentesis). This treatment is initiated during the first pregnancy with an Rh+ fetus. The anti-Rh antibodies in Rho(D) immune globulin will bind to the Rh factor of any fetal RBCs that gain access to the mother’s bloodstream, preventing these Rh+ cells from activating the mother’s primary antibody response. Without a primary anti-Rh factor antibody response, the next pregnancy with an Rh+ will have minimal risk of HDN. However, the mother will need to be retreated with Rho(D) immune globulin during that pregnancy to prevent a primary anti-Rh antibody response that could threaten subsequent pregnancies.",True,Type II (Cytotoxic) Hypersensitivities,,,,
d6e38be5-280d-45fa-9c1f-2bd9111dfbe0,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,Type III Hypersensitivities,False,Type III Hypersensitivities,,,,
8d489c0d-1b8f-461f-aa44-a80dc6c5e8e7,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"A unique characteristic of type III hypersensitivity is antibody excess (primarily IgG), coupled with a relatively low concentration of antigen, resulting in the formation of small immune complexes that deposit on the surface of the epithelial cells lining the inner lumen of small blood vessels or on the surfaces of tissues (Figure 15.7). This immune complex accumulation leads to a cascade of inflammatory events that include the following:",True,Type III Hypersensitivities,Figure 15.7,15.1	Hypersensitivities,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-19.7.png,"Figure 15.7 Type III hypersensitivities and the systems they affect. (a) Immune complexes form and deposit in tissue. Complement activation, stimulation of an inflammatory response, and recruitment and activation of neutrophils result in damage to blood vessels, heart tissue, joints, skin, and/or kidneys. (b) If the kidneys are damaged by a type III hypersensitivity reaction, dialysis may be required."
c0fce338-0819-4e3b-be0e-6fb73ebda873,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Because these immune complexes are not an optimal size and are deposited on cell surfaces, they cannot be phagocytosed in the usual way by neutrophils and macrophages, which, in turn, are often described as “frustrated.” Although phagocytosis does not occur, neutrophil degranulation results in the release of lysosomal enzymes that causeextracellular destruction of the immune complex, damaging localized cells in the process. Activation of coagulation pathways also occurs, resulting in thrombi (blood clots) that occlude blood vessels and cause ischemia that can lead to vascular necrosis and localized hemorrhage.",True,Type III Hypersensitivities,,,,
d6601845-7765-45e8-8183-41a6ea22b145,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Systemic type III hypersensitivity (serum sickness) occurs when immune complexes deposit in various body sites, resulting in a more generalized systemic inflammatory response. These immune complexes involve non-self proteins such as antibodies produced in animals for artificial passive immunity (see Vaccines), certain drugs, or microbial antigens that are continuously released over time during chronic infections (e.g., subacute bacterial endocarditis, chronic viral hepatitis). The mechanisms of serum sickness are similar to those described in localized type III hypersensitivity but involve widespread activation of mast cells, complement, neutrophils, and macrophages, which causes tissue destruction in areas such as the kidneys, joints, and blood vessels. As a result of tissue destruction, symptoms of serum sickness include chills, fever, rash, vasculitis, and arthritis. Development of glomerulonephritis or hepatitis is also possible.",True,Type III Hypersensitivities,,,,
83947e38-340e-44fb-b7c9-2f1d7d8edc3e,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,Autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis can also involve damaging type III hypersensitivity reactions when auto-antibodies form immune complexes with self antigens. These conditions are discussed in Autoimmune Disorders.,True,Type III Hypersensitivities,,,,
f2a17378-56fd-447f-824a-c7d474b2a4d9,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,Type IV Hypersensitivities,False,Type IV Hypersensitivities,,,,
57aaee9a-fd33-4b6f-9165-55901f0eb991,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"Type IV hypersensitivities are not mediated by antibodies like the other three types of hypersensitivities. Rather, type IV hypersensitivities are regulated by T cells and involve the action of effector cells. These types of hypersensitivities can be organized into three subcategories based on T-cell subtype, type of antigen, and the resulting effector mechanism (Table 15.5).",True,Type IV Hypersensitivities,,,,
9f257c67-535b-48bf-a822-f62c1c4e2669,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"In the first type IV subcategory, CD4 TH1-mediated reactions are described as delayed-type hypersensitivities (DTH). The sensitization step involves the introduction of antigen into the skin and phagocytosis by local antigen presenting cells (APCs). The APCs activate helper T cells, stimulating clonal proliferation and differentiation into memory TH1 cells. Upon subsequent exposure to the antigen, these sensitized memory TH1 cells release cytokines that activate macrophages, and activated macrophages are responsible for much of the tissue damage. Examples of this TH1-mediated hypersensitivity are observed in tuberculin the Mantoux skin test and contact dermatitis, such as occurs in latex allergy reactions.",True,Type IV Hypersensitivities,,,,
f7719e2e-d315-4690-bb4c-81cb5b39764f,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"In the second type IV subcategory, CD4 TH2-mediated reactions result in chronic asthma or chronic allergic rhinitis. In these cases, the soluble antigen is first inhaled, resulting in eosinophil recruitment and activation with the release of cytokines and inflammatory mediators.",True,Type IV Hypersensitivities,,,,
f445c029-6c01-4310-aba5-cb5d147adc56,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"In the third type IV subcategory, CD8 cytotoxic T lymphocyte (CTL)-mediated reactions are associated with tissue transplant rejection and contact dermatitis (Figure 15.8). For this form of cell-mediated hypersensitivity, APCs process and present the antigen with MHC I to naïve CD8 T cells. When these naïve CD8 T cells are activated, they proliferate and differentiate into CTLs. Activated TH1 cells can also enhance the activation of the CTLs. The activated CTLs then target and induce granzyme-mediated apoptosis in cells presenting the same antigen with MHC I. These target cells could be “self” cells that have absorbed the foreign antigen (such as with contact dermatitis due to poison ivy), or they could be transplanted tissue cells displaying foreign antigen from the donor.",True,Type IV Hypersensitivities,Figure 15.8,15.1	Hypersensitivities,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-19.8.png,"Figure 15.8 Exposure to hapten antigens in poison ivy can cause contact dermatitis, a type IV hypersensitivity. (a) The first exposure to poison ivy does not result in a reaction. However, sensitization stimulates helper T cells, leading to production of memory helper T cells that can become reactivated on future exposures. (b) Upon secondary exposure, the memory helper T cells become reactivated, producing inflammatory cytokines that stimulate macrophages and cytotoxic T cells to induce an inflammatory lesion at the exposed site. This lesion, which will persist until the allergen is removed, can inflict significant tissue damage if it continues long enough."
3ec7e4a5-2f48-45b8-924a-4b4bdf059ee4,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"The tips of all the needles in the array are coated with tuberculin, a protein extract of TB bacteria, effectively introducing the tuberculin into the skin. One to 3 days later, the area can be examined for a delayed hypersensitivity reaction, signs of which include swelling and redness.",True,Type IV Hypersensitivities,,,,
27ec87f8-daa1-4ff4-9db1-e61e929f6657,https://open.oregonstate.education/microbiology/,15.1	Hypersensitivities,https://open.oregonstate.education/microbiology/chapter/19-1hypersensitivities/,"As you can imagine, scarification was not a pleasant experience,[9] and the numerous skin punctures put the patient at risk of developing bacterial infection of the skin. Mantoux modified Pirquet’s test to use a single subcutaneous injection of purified tuberculin material. A positive test, which is indicated by a delayed localized swelling at the injection site, does not necessarily mean that the patient is currently infected with active TB. Because type IV (delayed-type) hypersensitivity is mediated by reactivation of memory T cells, such cells may have been created recently (due to an active current infection) or years prior (if a patient had TB and had spontaneously cleared it, or if it had gone into latency). However, the test can be used to confirm infection in cases in which symptoms in the patient or findings on a radiograph suggest its presence.",True,Type IV Hypersensitivities,,,,
8f0a2508-39e1-456f-9500-09823c70a02c,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,Classifications of Adaptive Immunity,False,Classifications of Adaptive Immunity,,,,
e33674f8-7f2a-4e20-b2f1-ea73779f1051,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"All forms of adaptive immunity can be described as either active or passive. Active immunity refers to the activation of an individual’s own adaptive immune defenses, whereas passive immunity refers to the transfer of adaptive immune defenses from another individual or animal. Active and passive immunity can be further subdivided based on whether the protection is acquired naturally or artificially.",True,Classifications of Adaptive Immunity,,,,
26076dc9-5ba2-42ad-8753-1722420828ab,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Natural active immunity is adaptive immunity that develops after natural exposure to a pathogen (Figure 14.24). Examples would include the lifelong immunity that develops after recovery from a chickenpox or measles infection (although an acute infection is not always necessary to activate adaptive immunity). The length of time that an individual is protected can vary substantially depending upon the pathogen and antigens involved. For example, activation of adaptive immunity by protein spike structures during an intracellular viral infection can activate lifelong immunity, whereas activation by carbohydrate capsule antigens during an extracellular bacterial infection may activate shorter-term immunity.",True,Classifications of Adaptive Immunity,Figure 14.24,14.5	Vaccines,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.24.png,"Figure 14.24 The four classifications of immunity. (credit top left photo: modification of work by USDA; credit top right photo: modification of work by “Michaelberry”/Wikimedia; credit bottom left photo: modification of work by Centers for Disease Control and Prevention; credit bottom right photo: modification of work by Friskila Silitonga, Indonesia, Centers for Disease Control and Prevention)"
b98d90ef-7df9-4113-869e-26c88baa8049,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Natural passive immunity involves the natural passage of antibodies from a mother to her child before and after birth. IgG is the only antibody class that can cross the placenta from mother’s blood to the fetal blood supply. Placental transfer of IgG is an important passive immune defense for the infant, lasting up to six months after birth. Secretory IgA can also be transferred from mother to infant through breast milk.",True,Classifications of Adaptive Immunity,,,,
91ef6cdc-ea54-4f25-ac09-d8239323cd24,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Artificial passive immunity refers to the transfer of antibodies produced by a donor (human or animal) to another individual. This transfer of antibodies may be done as a prophylactic measure (i.e., to prevent disease after exposure to a pathogen) or as a strategy for treating an active infection. For example, artificial passive immunity is commonly used for post-exposure prophylaxis against rabies, hepatitis A, hepatitis B, and chickenpox (in high risk individuals). Active infections treated by artificial passive immunity include cytomegalovirus infections in immunocompromised patients and Ebola virus infections. In 1995, eight patients in the Democratic Republic of the Congo with active Ebola infections were treated with blood transfusions from patients who were recovering from Ebola. Only one of the eight patients died (a 12.5% mortality rate), which was much lower than the expected 80% mortality rate for Ebola in untreated patients.[1] Artificial passive immunity is also used for the treatment of diseases caused by bacterial toxins, including tetanus, botulism, and diphtheria.",True,Classifications of Adaptive Immunity,,,,
19b8c309-5184-454a-a0af-e95edab9dee3,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Artificial active immunity is the foundation for vaccination. It involves the activation of adaptive immunity through the deliberate exposure of an individual to weakened or inactivated pathogens, or preparations consisting of key pathogen antigens.",True,Classifications of Adaptive Immunity,,,,
2371f309-d1eb-429f-ad7b-6d26f43977e5,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"The four kinds of immunity just described result from an individual’s adaptive immune system. For any given disease, an individual may be considered immune or susceptible depending on his or her ability to mount an effective immune response upon exposure. Thus, any given population is likely to have some individuals who are immune and other individuals who are susceptible. If a population has very few susceptible individuals, even those susceptible individuals will be protected by a phenomenon called herd immunity. Herd immunity has nothing to do with an individual’s ability to mount an effective immune response; rather, it occurs because there are too few susceptible individuals in a population for the disease to spread effectively.",True,Classifications of Adaptive Immunity,,,,
6e2beb80-738c-46be-b1ac-4cbdf8db1bed,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Vaccination programs create herd immunity by greatly reducing the number of susceptible individuals in a population. Even if some individuals in the population are not vaccinated, as long as a certain percentage is immune (either naturally or artificially), the few susceptible individuals are unlikely to be exposed to the pathogen. However, because new individuals are constantly entering populations (for example, through birth or relocation), vaccination programs are necessary to maintain herd immunity.",True,Classifications of Adaptive Immunity,,,,
54b699a2-66de-4e03-b031-150210a1c11d,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"It is believed that this growing number of unvaccinated individuals has led to new outbreaks of whooping cough and measles. We would expect that herd immunity would protect those unvaccinated in our population, but herd immunity can only be maintained if enough individuals are being vaccinated.",True,Classifications of Adaptive Immunity,,,,
4af40791-19fd-4756-8fb9-a7cbefef4200,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Vaccination is clearly beneficial for public health. But from the individual parent’s perspective the view can be murkier. Vaccines, like all medical interventions, have associated risks, and while the risks of vaccination may be extremely low compared to the risks of infection, parents may not always understand or accept the consensus of the medical community. Do such parents have a right to withhold vaccination from their children? Should they be allowed to put their children—and society at large—at risk?",True,Classifications of Adaptive Immunity,,,,
6ea0bdf7-a471-4fa1-9481-94511011a349,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Many governments insist on childhood vaccinations as a condition for entering public school, but it has become easy in most states to opt out of the requirement or to keep children out of the public system. Since the 1970s, West Virginia and Mississippi have had in place a stringent requirement for childhood vaccination, without exceptions, and neither state has had a case of measles since the early 1990s. California lawmakers recently passed a similar law in response to a measles outbreak in 2015, making it much more difficult for parents to opt out of vaccines if their children are attending public schools. Given this track record and renewed legislative efforts, should other states adopt similarly strict requirements?",True,Classifications of Adaptive Immunity,,,,
9b5a8532-38f7-48de-96ec-7d4de0965f89,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"What role should health-care providers play in promoting or enforcing universal vaccination? Studies have shown that many parents’ minds can be changed in response to information delivered by health-care workers, but is it the place of health-care workers to try to persuade parents to have their children vaccinated? Some health-care providers are understandably reluctant to treat unvaccinated patients. Do they have the right to refuse service to patients who decline vaccines? Do insurance companies have the right to deny coverage to antivaxxers? These are all ethical questions that policymakers may be forced to address as more parents skirt vaccination norms.",True,Classifications of Adaptive Immunity,,,,
15041a5f-c283-4b61-aee5-61ccf9b4ee5c,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,Variolation and Vaccination,False,Variolation and Vaccination,,,,
ead7d13e-68a3-41fc-b1a4-79773b46a845,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Thousands of years ago, it was first recognized that individuals who survived a smallpox infection were immune to subsequent infections. The practice of inoculating individuals to actively protect them from smallpox appears to have originated in the 10th century in China, when the practice of variolation was described. Variolation refers to the deliberate inoculation of individuals with infectious material from scabs or pustules of smallpox victims. Infectious materials were either injected into the skin or introduced through the nasal route. The infection that developed was usually milder than naturally acquired smallpox, and recovery from the milder infection provided protection against the more serious disease.",True,Variolation and Vaccination,,,,
dc7e038a-146e-4415-8136-7d2f84d6281d,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Although the majority of individuals treated by variolation developed only mild infections, the practice was not without risks. More serious and sometimes fatal infections did occur, and because smallpox was contagious, infections resulting from variolation could lead to epidemics. Even so, the practice of variolation for smallpox prevention spread to other regions, including India, Africa, and Europe.",True,Variolation and Vaccination,,,,
2715a9e8-a7a8-4433-8e89-ef7503720db3,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Although variolation had been practiced for centuries, the English physician Edward Jenner (1749–1823) is generally credited with developing the modern process of vaccination. Jenner observed that milkmaids who developed cowpox, a disease similar to smallpox but milder, were immune to the more serious smallpox. This led Jenner to hypothesize that exposure to a less virulent pathogen could provide immune protection against a more virulent pathogen, providing a safer alternative to variolation. In 1796, Jenner tested his hypothesis by obtaining infectious samples from a milkmaid’s active cowpox lesion and injecting the materials into a young boy (Figure 14.25). The boy developed a mild infection that included a low-grade fever, discomfort in his axillae (armpit) and loss of appetite. When the boy was later infected with infectious samples from smallpox lesions, he did not contract smallpox.[3] This new approach was termed vaccination, a name deriving from the use of cowpox (Latin vacca meaning “cow”) to protect against smallpox. Today, we know that Jenner’s vaccine worked because the cowpox virus is genetically and antigenically related to the Variola viruses that caused smallpox. Exposure to cowpox antigens resulted in a primary response and the production of memory cells that identical or related epitopes of Variola virus upon a later exposure to smallpox.",True,Variolation and Vaccination,Figure 14.25,14.5	Vaccines,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.26.png,"Figure 14.25 (a) A painting of Edward Jenner depicts a cow and a milkmaid in the background. (b) Lesions on a patient infected with cowpox, a zoonotic disease caused by a virus closely related to the one that causes smallpox. (credit b: modification of work by the Centers for Disease Control and Prevention)"
25000c9f-2cf0-4161-af92-a7369f832bb2,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"The success of Jenner’s smallpox vaccination led other scientists to develop vaccines for other diseases. Perhaps the most notable was Louis Pasteur, who developed vaccines for rabies, cholera, and anthrax. During the 20th and 21st centuries, effective vaccines were developed to prevent a wide range of diseases caused by viruses (e.g., chickenpox and shingles, hepatitis, measles, mumps, polio, and yellow fever) and bacteria (e.g., diphtheria, pneumococcal pneumonia, tetanus, and whooping cough,).",True,Variolation and Vaccination,,,,
83d49ebc-98ce-4093-9d40-30cd7d9a9834,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,Classes of Vaccines,False,Classes of Vaccines,,,,
ca5cc710-fe7b-4caa-a4c1-b548c66d5b2c,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"For a vaccine to provide protection against a disease, it must expose an individual to pathogen-specific antigens that will stimulate a protective adaptive immune response. By its very nature, this entails some risk. As with any pharmaceutical drug, vaccines have the potential to cause adverse effects. However, the ideal vaccine causes no severe adverse effects and poses no risk of contracting the disease that it is intended to prevent. Various types of vaccines have been developed with these goals in mind. These different classes of vaccines are described in the next section and summarized in Table 14.3.",True,Classes of Vaccines,,,,
2bb531b6-1251-49fd-a377-66bb0df296b7,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,Live Attenuated Vaccines,False,Live Attenuated Vaccines,,,,
439a6aed-04b4-4659-85bd-a4cc30479d0f,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,Live attenuated vaccines expose an individual to a weakened strain of a pathogen with the goal of establishing a subclinical infection that will activate the adaptive immune defenses. Pathogens are attenuated to decrease their virulence using methods such as genetic manipulation (to eliminate key virulence factors) or long-term culturing in an unnatural host or environment (to promote mutations and decrease virulence).,True,Live Attenuated Vaccines,,,,
71472d60-4fa7-43ec-96f0-91cc1f9e6937,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"By establishing an active infection, live attenuated vaccines stimulate a more comprehensive immune response than some other types of vaccines. Live attenuated vaccines activate both cellular and humoral immunity and stimulate the development of memory for long-lasting immunity. In some cases, vaccination of one individual with a live attenuated pathogen can even lead to natural transmission of the attenuated pathogen to other individuals. This can cause the other individuals to also develop an active, subclinical infection that activates their adaptive immune defenses.",True,Live Attenuated Vaccines,,,,
3bedbc9f-0518-423a-bb3f-b5bd4688a69a,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,Disadvantages associated with live attenuated vaccines include the challenges associated with long-term storage and transport as well as the potential for a patient to develop signs and symptoms of disease during the active infection (particularly in immunocompromised patients). There is also a risk of the attenuated pathogen reverting back to full virulence. Table 14.3 lists examples live attenuated vaccines.,True,Live Attenuated Vaccines,,,,
0c99c581-9b97-4329-ae6f-afc03eb384a5,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,Inactivated Vaccines,False,Inactivated Vaccines,,,,
702f79e2-2c5a-49a5-a3b5-9bbbc8484200,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Inactivated vaccines contain whole pathogens that have been killed or inactivated with heat, chemicals, or radiation. For inactivated vaccines to be effective, the inactivation process must not affect the structure of key antigens on the pathogen.",True,Inactivated Vaccines,,,,
0b100f54-3195-4a96-9ffd-50e8ae12fcbf,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Because the pathogen is killed or inactive, inactivated vaccines do not produce an active infection, and the resulting immune response is weaker and less comprehensive than that provoked by a live attenuated vaccine. Typically the response involves only humoral immunity, and the pathogen cannot be transmitted to other individuals. In addition, inactivated vaccines usually require higher doses and multiple boosters, possibly causing inflammatory reactions at the site of injection.",True,Inactivated Vaccines,,,,
567891f2-56c3-46c9-a84e-96da2c8d0647,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Despite these disadvantages, inactivated vaccines do have the advantages of long-term storage stability and ease of transport. Also, there is no risk of causing severe active infections. However, inactivated vaccines are not without their side effects. Table 14.3 lists examples of inactivated vaccines.",True,Inactivated Vaccines,,,,
858008e3-6350-4479-83d7-287aaa3e73b1,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,Subunit Vaccines,False,Subunit Vaccines,,,,
4f3ea5fc-797d-45e2-8876-0f7257f06a36,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Whereas live attenuated and inactive vaccines expose an individual to a weakened or dead pathogen, subunit vaccines only expose the patient to the key antigens of a pathogen—not whole cells or viruses. Subunit vaccines can be produced either by chemically degrading a pathogen and isolating its key antigens or by producing the antigens through genetic engineering. Because these vaccines contain only the essential antigens of a pathogen, the risk of side effects is relatively low. Table 14.3 lists examples of subunit vaccines.",True,Subunit Vaccines,,,,
d92a4a3e-bb9d-4c1a-8b97-ff345fa025e5,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,Toxoid Vaccines,False,Toxoid Vaccines,,,,
02ac5299-3a3c-4a9d-8b42-ec3cd8de1d44,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Like subunit vaccines, toxoid vaccines do not introduce a whole pathogen to the patient; they contain inactivated bacterial toxins, called toxoids. Toxoid vaccines are used to prevent diseases in which bacterial toxins play an important role in pathogenesis. These vaccines activate humoral immunity that neutralizes the toxins. Table 14.3 lists examples of toxoid vaccines.",True,Toxoid Vaccines,,,,
d3a3192d-147f-4011-928a-5f04280555e1,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,Conjugate Vaccines,False,Conjugate Vaccines,,,,
28455a47-b4a0-4f67-8c41-d8837ede04b9,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"A conjugate vaccine is a type of subunit vaccine that consists of a protein conjugated to a capsule polysaccharide. Conjugate vaccines have been developed to enhance the efficacy of subunit vaccines against pathogens that have protective polysaccharide capsules that help them evade phagocytosis, causing invasive infections that can lead to meningitis and other serious conditions. The subunit vaccines against these pathogens introduce T-independent capsular polysaccharide antigens that result in the production of antibodies that can opsonize the capsule and thus combat the infection; however, children under the age of two years do not respond effectively to these vaccines. Children do respond effectively when vaccinated with the conjugate vaccine, in which a protein with T-dependent antigens is conjugated to the capsule polysaccharide. The conjugated protein-polysaccharide antigen stimulates production of antibodies against both the protein and the capsule polysaccharide. Table 14.3 lists examples of conjugate vaccines.",True,Conjugate Vaccines,,,,
82b28575-bcbd-41e8-a185-64f76be3dac9,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"(Haemophilus influenzae, Streptococcus pneumoniae, Neisseria meningitides)",False,"(Haemophilus influenzae, Streptococcus pneumoniae, Neisseria meningitides)",,,,
1eddc3fb-fbca-4bf8-9bf2-0853cc8702f0,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,Classifications of Adaptive Immunity,False,Classifications of Adaptive Immunity,,,,
21405559-14bb-474c-8a2d-1674d2c4f907,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Natural active immunity is adaptive immunity that develops after natural exposure to a pathogen (Figure 14.24). Examples would include the lifelong immunity that develops after recovery from a chickenpox or measles infection (although an acute infection is not always necessary to activate adaptive immunity). The length of time that an individual is protected can vary substantially depending upon the pathogen and antigens involved. For example, activation of adaptive immunity by protein spike structures during an intracellular viral infection can activate lifelong immunity, whereas activation by carbohydrate capsule antigens during an extracellular bacterial infection may activate shorter-term immunity.",True,Classifications of Adaptive Immunity,Figure 14.24,14.5	Vaccines,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.24.png,"Figure 14.24 The four classifications of immunity. (credit top left photo: modification of work by USDA; credit top right photo: modification of work by “Michaelberry”/Wikimedia; credit bottom left photo: modification of work by Centers for Disease Control and Prevention; credit bottom right photo: modification of work by Friskila Silitonga, Indonesia, Centers for Disease Control and Prevention)"
9e1de1d7-9f04-498f-872c-7f07fc881451,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Natural passive immunity involves the natural passage of antibodies from a mother to her child before and after birth. IgG is the only antibody class that can cross the placenta from mother’s blood to the fetal blood supply. Placental transfer of IgG is an important passive immune defense for the infant, lasting up to six months after birth. Secretory IgA can also be transferred from mother to infant through breast milk.",True,Classifications of Adaptive Immunity,,,,
e5b1463f-6392-4d8e-a8d2-e13a34edef0c,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Artificial passive immunity refers to the transfer of antibodies produced by a donor (human or animal) to another individual. This transfer of antibodies may be done as a prophylactic measure (i.e., to prevent disease after exposure to a pathogen) or as a strategy for treating an active infection. For example, artificial passive immunity is commonly used for post-exposure prophylaxis against rabies, hepatitis A, hepatitis B, and chickenpox (in high risk individuals). Active infections treated by artificial passive immunity include cytomegalovirus infections in immunocompromised patients and Ebola virus infections. In 1995, eight patients in the Democratic Republic of the Congo with active Ebola infections were treated with blood transfusions from patients who were recovering from Ebola. Only one of the eight patients died (a 12.5% mortality rate), which was much lower than the expected 80% mortality rate for Ebola in untreated patients.[1] Artificial passive immunity is also used for the treatment of diseases caused by bacterial toxins, including tetanus, botulism, and diphtheria.",True,Classifications of Adaptive Immunity,,,,
4790a5f4-6860-4c41-b73c-95b04781468c,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Artificial active immunity is the foundation for vaccination. It involves the activation of adaptive immunity through the deliberate exposure of an individual to weakened or inactivated pathogens, or preparations consisting of key pathogen antigens.",True,Classifications of Adaptive Immunity,,,,
21478925-5c9e-4575-9b5c-8845f6e5fce6,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"The four kinds of immunity just described result from an individual’s adaptive immune system. For any given disease, an individual may be considered immune or susceptible depending on his or her ability to mount an effective immune response upon exposure. Thus, any given population is likely to have some individuals who are immune and other individuals who are susceptible. If a population has very few susceptible individuals, even those susceptible individuals will be protected by a phenomenon called herd immunity. Herd immunity has nothing to do with an individual’s ability to mount an effective immune response; rather, it occurs because there are too few susceptible individuals in a population for the disease to spread effectively.",True,Classifications of Adaptive Immunity,,,,
c4ff9c52-b155-4684-be02-bda0e73cb6fc,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Vaccination programs create herd immunity by greatly reducing the number of susceptible individuals in a population. Even if some individuals in the population are not vaccinated, as long as a certain percentage is immune (either naturally or artificially), the few susceptible individuals are unlikely to be exposed to the pathogen. However, because new individuals are constantly entering populations (for example, through birth or relocation), vaccination programs are necessary to maintain herd immunity.",True,Classifications of Adaptive Immunity,,,,
2f82967a-2e08-44d6-bd8d-4981f91b5cba,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"It is believed that this growing number of unvaccinated individuals has led to new outbreaks of whooping cough and measles. We would expect that herd immunity would protect those unvaccinated in our population, but herd immunity can only be maintained if enough individuals are being vaccinated.",True,Classifications of Adaptive Immunity,,,,
7aba00d1-6d01-4983-a3d3-5da0f93374d3,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Vaccination is clearly beneficial for public health. But from the individual parent’s perspective the view can be murkier. Vaccines, like all medical interventions, have associated risks, and while the risks of vaccination may be extremely low compared to the risks of infection, parents may not always understand or accept the consensus of the medical community. Do such parents have a right to withhold vaccination from their children? Should they be allowed to put their children—and society at large—at risk?",True,Classifications of Adaptive Immunity,,,,
2a97c13e-0c2c-40a8-b777-734dcaaed0da,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Many governments insist on childhood vaccinations as a condition for entering public school, but it has become easy in most states to opt out of the requirement or to keep children out of the public system. Since the 1970s, West Virginia and Mississippi have had in place a stringent requirement for childhood vaccination, without exceptions, and neither state has had a case of measles since the early 1990s. California lawmakers recently passed a similar law in response to a measles outbreak in 2015, making it much more difficult for parents to opt out of vaccines if their children are attending public schools. Given this track record and renewed legislative efforts, should other states adopt similarly strict requirements?",True,Classifications of Adaptive Immunity,,,,
b159ca62-8195-4924-b3a6-763b7fc6a717,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"What role should health-care providers play in promoting or enforcing universal vaccination? Studies have shown that many parents’ minds can be changed in response to information delivered by health-care workers, but is it the place of health-care workers to try to persuade parents to have their children vaccinated? Some health-care providers are understandably reluctant to treat unvaccinated patients. Do they have the right to refuse service to patients who decline vaccines? Do insurance companies have the right to deny coverage to antivaxxers? These are all ethical questions that policymakers may be forced to address as more parents skirt vaccination norms.",True,Classifications of Adaptive Immunity,,,,
5d923bf2-af10-4ccf-9665-8f20bc28569f,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,Variolation and Vaccination,False,Variolation and Vaccination,,,,
72394cba-3e4f-458c-83a5-c8c54c439b2e,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Although the majority of individuals treated by variolation developed only mild infections, the practice was not without risks. More serious and sometimes fatal infections did occur, and because smallpox was contagious, infections resulting from variolation could lead to epidemics. Even so, the practice of variolation for smallpox prevention spread to other regions, including India, Africa, and Europe.",True,Variolation and Vaccination,,,,
ca6a4edf-1ff9-4401-88c4-4474f85533a8,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Although variolation had been practiced for centuries, the English physician Edward Jenner (1749–1823) is generally credited with developing the modern process of vaccination. Jenner observed that milkmaids who developed cowpox, a disease similar to smallpox but milder, were immune to the more serious smallpox. This led Jenner to hypothesize that exposure to a less virulent pathogen could provide immune protection against a more virulent pathogen, providing a safer alternative to variolation. In 1796, Jenner tested his hypothesis by obtaining infectious samples from a milkmaid’s active cowpox lesion and injecting the materials into a young boy (Figure 14.25). The boy developed a mild infection that included a low-grade fever, discomfort in his axillae (armpit) and loss of appetite. When the boy was later infected with infectious samples from smallpox lesions, he did not contract smallpox.[3] This new approach was termed vaccination, a name deriving from the use of cowpox (Latin vacca meaning “cow”) to protect against smallpox. Today, we know that Jenner’s vaccine worked because the cowpox virus is genetically and antigenically related to the Variola viruses that caused smallpox. Exposure to cowpox antigens resulted in a primary response and the production of memory cells that identical or related epitopes of Variola virus upon a later exposure to smallpox.",True,Variolation and Vaccination,Figure 14.25,14.5	Vaccines,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.26.png,"Figure 14.25 (a) A painting of Edward Jenner depicts a cow and a milkmaid in the background. (b) Lesions on a patient infected with cowpox, a zoonotic disease caused by a virus closely related to the one that causes smallpox. (credit b: modification of work by the Centers for Disease Control and Prevention)"
a4122a02-aea7-48a7-be98-635d192b6ace,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"The success of Jenner’s smallpox vaccination led other scientists to develop vaccines for other diseases. Perhaps the most notable was Louis Pasteur, who developed vaccines for rabies, cholera, and anthrax. During the 20th and 21st centuries, effective vaccines were developed to prevent a wide range of diseases caused by viruses (e.g., chickenpox and shingles, hepatitis, measles, mumps, polio, and yellow fever) and bacteria (e.g., diphtheria, pneumococcal pneumonia, tetanus, and whooping cough,).",True,Variolation and Vaccination,,,,
2f07fb46-b250-47c5-b78b-f35ac917914f,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,Classes of Vaccines,False,Classes of Vaccines,,,,
b7cc59f4-ccd7-4a4f-9b56-5dc90799e67a,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"For a vaccine to provide protection against a disease, it must expose an individual to pathogen-specific antigens that will stimulate a protective adaptive immune response. By its very nature, this entails some risk. As with any pharmaceutical drug, vaccines have the potential to cause adverse effects. However, the ideal vaccine causes no severe adverse effects and poses no risk of contracting the disease that it is intended to prevent. Various types of vaccines have been developed with these goals in mind. These different classes of vaccines are described in the next section and summarized in Table 14.3.",True,Classes of Vaccines,,,,
631087c2-a60d-4081-98d4-10c6559986fe,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,Live attenuated vaccines expose an individual to a weakened strain of a pathogen with the goal of establishing a subclinical infection that will activate the adaptive immune defenses. Pathogens are attenuated to decrease their virulence using methods such as genetic manipulation (to eliminate key virulence factors) or long-term culturing in an unnatural host or environment (to promote mutations and decrease virulence).,True,Classes of Vaccines,,,,
6b64035f-cd66-4934-97c1-d1e39711e0f9,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"By establishing an active infection, live attenuated vaccines stimulate a more comprehensive immune response than some other types of vaccines. Live attenuated vaccines activate both cellular and humoral immunity and stimulate the development of memory for long-lasting immunity. In some cases, vaccination of one individual with a live attenuated pathogen can even lead to natural transmission of the attenuated pathogen to other individuals. This can cause the other individuals to also develop an active, subclinical infection that activates their adaptive immune defenses.",True,Classes of Vaccines,,,,
2f1eb6fb-f678-4fbc-9e23-be8361cb6751,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,Disadvantages associated with live attenuated vaccines include the challenges associated with long-term storage and transport as well as the potential for a patient to develop signs and symptoms of disease during the active infection (particularly in immunocompromised patients). There is also a risk of the attenuated pathogen reverting back to full virulence. Table 14.3 lists examples live attenuated vaccines.,True,Classes of Vaccines,,,,
f87d1957-1a3a-46cf-8074-aca282bd99bc,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Inactivated vaccines contain whole pathogens that have been killed or inactivated with heat, chemicals, or radiation. For inactivated vaccines to be effective, the inactivation process must not affect the structure of key antigens on the pathogen.",True,Classes of Vaccines,,,,
51d13ad3-c4d1-44b3-96ef-4d79ff848273,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Because the pathogen is killed or inactive, inactivated vaccines do not produce an active infection, and the resulting immune response is weaker and less comprehensive than that provoked by a live attenuated vaccine. Typically the response involves only humoral immunity, and the pathogen cannot be transmitted to other individuals. In addition, inactivated vaccines usually require higher doses and multiple boosters, possibly causing inflammatory reactions at the site of injection.",True,Classes of Vaccines,,,,
c79a58fd-0d34-483c-ab65-f1f442d6686e,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Despite these disadvantages, inactivated vaccines do have the advantages of long-term storage stability and ease of transport. Also, there is no risk of causing severe active infections. However, inactivated vaccines are not without their side effects. Table 14.3 lists examples of inactivated vaccines.",True,Classes of Vaccines,,,,
5808f595-1b9d-4877-ab17-98bcf3e50d18,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Whereas live attenuated and inactive vaccines expose an individual to a weakened or dead pathogen, subunit vaccines only expose the patient to the key antigens of a pathogen—not whole cells or viruses. Subunit vaccines can be produced either by chemically degrading a pathogen and isolating its key antigens or by producing the antigens through genetic engineering. Because these vaccines contain only the essential antigens of a pathogen, the risk of side effects is relatively low. Table 14.3 lists examples of subunit vaccines.",True,Classes of Vaccines,,,,
c00a8a34-3bea-4eea-8b9d-ef6abb0b450b,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"Like subunit vaccines, toxoid vaccines do not introduce a whole pathogen to the patient; they contain inactivated bacterial toxins, called toxoids. Toxoid vaccines are used to prevent diseases in which bacterial toxins play an important role in pathogenesis. These vaccines activate humoral immunity that neutralizes the toxins. Table 14.3 lists examples of toxoid vaccines.",True,Classes of Vaccines,,,,
3b1eaa28-5365-4f4f-a0af-15fef3e62d73,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"A conjugate vaccine is a type of subunit vaccine that consists of a protein conjugated to a capsule polysaccharide. Conjugate vaccines have been developed to enhance the efficacy of subunit vaccines against pathogens that have protective polysaccharide capsules that help them evade phagocytosis, causing invasive infections that can lead to meningitis and other serious conditions. The subunit vaccines against these pathogens introduce T-independent capsular polysaccharide antigens that result in the production of antibodies that can opsonize the capsule and thus combat the infection; however, children under the age of two years do not respond effectively to these vaccines. Children do respond effectively when vaccinated with the conjugate vaccine, in which a protein with T-dependent antigens is conjugated to the capsule polysaccharide. The conjugated protein-polysaccharide antigen stimulates production of antibodies against both the protein and the capsule polysaccharide. Table 14.3 lists examples of conjugate vaccines.",True,Classes of Vaccines,,,,
2c764c49-83eb-43f5-a153-21a1265fd017,https://open.oregonstate.education/microbiology/,14.5	Vaccines,https://open.oregonstate.education/microbiology/chapter/18-5vaccines/,"(Haemophilus influenzae, Streptococcus pneumoniae, Neisseria meningitides)",False,"(Haemophilus influenzae, Streptococcus pneumoniae, Neisseria meningitides)",,,,
e51fe8b1-0b9d-4143-9e86-7d65391b8bd3,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,B Cell Production and Maturation,False,B Cell Production and Maturation,,,,
e9ea5aa9-009e-48bd-adca-82890399cb59,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"Like T cells, B cells are formed from multipotent hematopoietic stem cells (HSCs) in the bone marrow and follow a pathway through lymphoid stem cell and lymphoblast. Unlike T cells, however, lymphoblasts destined to become B cells do not leave the bone marrow and travel to the thymus for maturation. Rather, eventual B cells continue to mature in the bone marrow.",True,B Cell Production and Maturation,,,,
402a4684-3dd0-48c4-a78e-7ed4b3457202,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"The first step of B cell maturation is an assessment of the functionality of their antigen-binding receptors. This occurs through positive selection for B cells with normal functional receptors. A mechanism of negative selection is then used to eliminate self-reacting B cells and minimize the risk of autoimmunity. Negative selection of self-reacting B cells can involve elimination by apoptosis, editing or modification of the receptors so they are no longer self-reactive, or induction of anergy in the B cell. Immature B cells that pass the selection in the bone marrow then travel to the spleen for their final stages of maturation. There they become naïve mature B cells, i.e., mature B cells that have not yet been activated.",True,B Cell Production and Maturation,,,,
82fb4909-8373-46ec-b979-2859a1a3ea0c,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,B-Cell Receptors,False,B-Cell Receptors,,,,
669b1339-98a9-436f-85de-2807e7f1f076,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"Like T cells, B cells possess antigen-specific receptors with diverse specificities. Although they rely on T cells for optimum function, B cells can be activated without help from T cells. B-cell receptors (BCRs) for naïve mature B cells are membrane-bound monomeric forms of IgD and IgM. They have two identical heavy chains and two identical light chains connected by disulfide bonds into a basic “Y” shape (Figure 14.20). The trunk of the Y-shaped molecule, the constant region of the two heavy chains, spans the B cell membrane. The two antigen-binding sites exposed to the exterior of the B cell are involved in the binding of specific pathogen epitopes to initiate the activation process. It is estimated that each naïve mature B cell has upwards of 100,000 BCRs on its membrane, and each of these BCRs has an identical epitope-binding specificity.",True,B-Cell Receptors,Figure 14.20,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.20.png,Figure 14.20 B-cell receptors are embedded in the membranes of B cells. The variable regions of all of the receptors on a single cell bind the same specific antigen.
f2530848-12a0-4d71-801c-d1ed59650aea,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"In order to be prepared to react to a wide range of microbial epitopes, B cells, like T cells, use genetic rearrangement of hundreds of gene segments to provide the necessary diversity of receptor specificities.",True,B-Cell Receptors,,,,
827a9a3a-213b-4c5d-9406-d6b6ac798cb5,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"One important difference between BCRs and TCRs is the way they can interact with antigenic epitopes. Whereas TCRs can only interact with antigenic epitopes that are presented within the antigen-binding cleft of MHC I or MHC II, BCRs do not require antigen presentation with MHC; they can interact with epitopes on free antigens or with epitopes displayed on the surface of intact pathogens. Another important difference is that TCRs only recognize protein epitopes, whereas BCRs can recognize epitopes associated with different molecular classes (e.g., proteins, polysaccharides, lipopolysaccharides).",True,B-Cell Receptors,,,,
4fbc9c19-b6a0-4651-9bba-40d080832d4f,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"Activation of B cells occurs through different mechanisms depending on the molecular class of the antigen. Activation of a B cell by a protein antigen requires the B cell to function as an APC, presenting the protein epitopes with MHC II to helper T cells. Because of their dependence on T cells for activation of B cells, protein antigens are classified as T- dependent antigens. In contrast, polysaccharides, lipopolysaccharides, and other nonprotein antigens are considered T-independent antigens because they can activate B cells without antigen processing and presentation to T cells.",True,B-Cell Receptors,,,,
68b42d87-2a45-4ad8-8dff-d61b7bb85ad3,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"Activation of B cells without the cooperation of helper T cells is referred to as T cell-independent activation and occurs when BCRs interact with T-independent antigens. T-independent antigens (e.g., polysaccharide capsules, lipopolysaccharide) have repetitive epitope units within their structure, and this repetition allows for the cross-linkage of multiple BCRs, providing the first signal for activation (Figure 14.21). Because T cells are not involved, the second signal has to come from other sources, such as interactions of toll-like receptors with PAMPs or interactions with factors from the complement system.",True,B-Cell Receptors,Figure 14.21,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.21.png,"Figure 14.21 T-independent antigens have repeating epitopes that can induce B cell recognition and activation without involvement from T cells. A second signal, such as interaction of TLRs with PAMPs (not shown), is also required for activation of the B cell. Once activated, the B cell proliferates and differentiates into antibody-secreting plasma cells."
636f901d-03a4-4499-8813-e798eeaaf3bc,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"Once a B cell is activated, it undergoes clonal proliferation and daughter cells differentiate into plasma cells. Plasma cells are antibody factories that secrete large quantities of antibodies. After differentiation, the surface BCRs disappear and the plasma cell secretes pentameric IgM molecules that have the same antigen specificity as the BCRs (Figure 14.21).",True,B-Cell Receptors,Figure 14.21,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.21.png,"Figure 14.21 T-independent antigens have repeating epitopes that can induce B cell recognition and activation without involvement from T cells. A second signal, such as interaction of TLRs with PAMPs (not shown), is also required for activation of the B cell. Once activated, the B cell proliferates and differentiates into antibody-secreting plasma cells."
76f99f78-06d2-499c-b2d9-e176b55e436a,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,The T cell-independent response is short-lived and does not result in the production of memory B cells. Thus it will not result in a secondary response to subsequent exposures to T-independent antigens.,True,B-Cell Receptors,,,,
a9504c13-65e2-4422-bfe5-c3fcd2b2e7de,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"T cell-dependent activation of B cells is more complex than T cell-independent activation, but the resulting immune response is stronger and develops memory. T cell-dependent activation can occur either in response to free protein antigens or to protein antigens associated with an intact pathogen. Interaction between the BCRs on a naïve mature B cell and a free protein antigen stimulate internalization of the antigen, whereas interaction with antigens associated with an intact pathogen initiates the extraction of the antigen from the pathogen before internalization. Once internalized inside the B cell, the protein antigen is processed and presented with MHC II. The presented antigen is then recognized by helper T cells specific to the same antigen. The TCR of the helper T cell recognizes the foreign antigen, and the T cell’s CD4 molecule interacts with MHC II on the B cell. The coordination between B cells and helper T cells that are specific to the same antigen is referred to as linked recognition.",True,B-Cell Receptors,,,,
38dee2a1-a44d-4350-b6e6-0e2f77ba6fa5,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"Once activated by linked recognition, TH2 cells produce and secrete cytokines that activate the B cell and cause proliferation into clonal daughter cells. After several rounds of proliferation, additional cytokines provided by the TH2 cells stimulate the differentiation of activated B cell clones into memory B cells, which will quickly respond to subsequent exposures to the same protein epitope, and plasma cells that lose their membrane BCRs and initially secrete pentameric IgM (Figure 14.22).",True,B-Cell Receptors,Figure 14.22,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.22.png,"Figure 14.22 In T cell-dependent activation of B cells, the B cell recognizes and internalizes an antigen and presents it to a helper T cell that is specific to the same antigen. The helper T cell interacts with the antigen presented by the B cell, which activates the T cell and stimulates the release of cytokines that then activate the B cell. Activation of the B cell triggers proliferation and differentiation into B cells and plasma cells."
75e33ec2-8709-43f4-aa0a-3d45ae7d1836,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"After initial secretion of IgM, cytokines secreted by TH2 cells stimulate the plasma cells to switch from IgM production to production of IgG, IgA, or IgE. This process, called class switching or isotype switching, allows plasma cells cloned from the same activated B cell to produce a variety of antibody classes with the same epitope specificity. Class switching is accomplished by genetic rearrangement of gene segments encoding the constant region, which determines an antibody’s class. The variable region is not changed, so the new class of antibody retains the original epitope specificity.",True,B-Cell Receptors,,,,
b8a033d0-cc28-4817-9d4b-0036cf91db09,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,Primary and Secondary Responses,False,Primary and Secondary Responses,,,,
b742c520-7587-4d77-b3da-3ca18602dba9,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"T cell-dependent activation of B cells plays an important role in both the primary and secondary responses associated with adaptive immunity. With the first exposure to a protein antigen, a T cell-dependent primary antibody response occurs. The initial stage of the primary response is a lag period, or latent period, of approximately 10 days, during which no antibody can be detected in serum. This lag period is the time required for all of the steps of the primary response, including naïve mature B cell binding of antigen with BCRs, antigen processing and presentation, helper T cell activation, B cell activation, and clonal proliferation. The end of the lag period is characterized by a rise in IgM levels in the serum, as TH2 cells stimulate B cell differentiation into plasma cells. IgM levels reach their peak around 14 days after primary antigen exposure; at about this same time, TH2 stimulates antibody class switching, and IgM levels in serum begin to decline. Meanwhile, levels of IgG increase until they reach a peak about three weeks into the primary response (Figure 14.23).",True,Primary and Secondary Responses,Figure 14.23,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.23.png,"Figure 14.23 Compared to the primary response, the secondary antibody response occurs more quickly and produces antibody levels that are higher and more sustained. The secondary response mostly involves IgG."
00b901e9-2e9d-4e93-9029-9d20ae6d3d95,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"During the primary response, some of the cloned B cells are differentiated into memory B cells programmed to respond to subsequent exposures. This secondary response occurs more quickly and forcefully than the primary response. The lag period is decreased to only a few days and the production of IgG is significantly higher than observed for the primary response (Figure 14.23). In addition, the antibodies produced during the secondary response are more effective and bind with higher affinity to the targeted epitopes. Plasma cells produced during secondary responses live longer than those produced during the primary response, so levels of specific antibody remain elevated for a longer period of time.",True,Primary and Secondary Responses,Figure 14.23,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.23.png,"Figure 14.23 Compared to the primary response, the secondary antibody response occurs more quickly and produces antibody levels that are higher and more sustained. The secondary response mostly involves IgG."
217d768a-9139-46dc-b7b1-04c6d158304d,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"Activation of B cells without the cooperation of helper T cells is referred to as T cell-independent activation and occurs when BCRs interact with T-independent antigens. T-independent antigens (e.g., polysaccharide capsules, lipopolysaccharide) have repetitive epitope units within their structure, and this repetition allows for the cross-linkage of multiple BCRs, providing the first signal for activation (Figure 14.21). Because T cells are not involved, the second signal has to come from other sources, such as interactions of toll-like receptors with PAMPs or interactions with factors from the complement system.",True,Primary and Secondary Responses,Figure 14.21,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.21.png,"Figure 14.21 T-independent antigens have repeating epitopes that can induce B cell recognition and activation without involvement from T cells. A second signal, such as interaction of TLRs with PAMPs (not shown), is also required for activation of the B cell. Once activated, the B cell proliferates and differentiates into antibody-secreting plasma cells."
ce14383d-82ab-4312-9348-a5a7d4da6ba6,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"Once a B cell is activated, it undergoes clonal proliferation and daughter cells differentiate into plasma cells. Plasma cells are antibody factories that secrete large quantities of antibodies. After differentiation, the surface BCRs disappear and the plasma cell secretes pentameric IgM molecules that have the same antigen specificity as the BCRs (Figure 14.21).",True,Primary and Secondary Responses,Figure 14.21,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.21.png,"Figure 14.21 T-independent antigens have repeating epitopes that can induce B cell recognition and activation without involvement from T cells. A second signal, such as interaction of TLRs with PAMPs (not shown), is also required for activation of the B cell. Once activated, the B cell proliferates and differentiates into antibody-secreting plasma cells."
3e8e4f94-66e3-42d9-a44a-8e220aad201e,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,The T cell-independent response is short-lived and does not result in the production of memory B cells. Thus it will not result in a secondary response to subsequent exposures to T-independent antigens.,True,Primary and Secondary Responses,,,,
b31f03cc-0f64-481b-a01b-b351420d6bbf,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"T cell-dependent activation of B cells is more complex than T cell-independent activation, but the resulting immune response is stronger and develops memory. T cell-dependent activation can occur either in response to free protein antigens or to protein antigens associated with an intact pathogen. Interaction between the BCRs on a naïve mature B cell and a free protein antigen stimulate internalization of the antigen, whereas interaction with antigens associated with an intact pathogen initiates the extraction of the antigen from the pathogen before internalization. Once internalized inside the B cell, the protein antigen is processed and presented with MHC II. The presented antigen is then recognized by helper T cells specific to the same antigen. The TCR of the helper T cell recognizes the foreign antigen, and the T cell’s CD4 molecule interacts with MHC II on the B cell. The coordination between B cells and helper T cells that are specific to the same antigen is referred to as linked recognition.",True,Primary and Secondary Responses,,,,
5933050d-2f11-49bb-8e6c-6c56bfab1574,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"Once activated by linked recognition, TH2 cells produce and secrete cytokines that activate the B cell and cause proliferation into clonal daughter cells. After several rounds of proliferation, additional cytokines provided by the TH2 cells stimulate the differentiation of activated B cell clones into memory B cells, which will quickly respond to subsequent exposures to the same protein epitope, and plasma cells that lose their membrane BCRs and initially secrete pentameric IgM (Figure 14.22).",True,Primary and Secondary Responses,Figure 14.22,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.22.png,"Figure 14.22 In T cell-dependent activation of B cells, the B cell recognizes and internalizes an antigen and presents it to a helper T cell that is specific to the same antigen. The helper T cell interacts with the antigen presented by the B cell, which activates the T cell and stimulates the release of cytokines that then activate the B cell. Activation of the B cell triggers proliferation and differentiation into B cells and plasma cells."
efcd4fb0-fd67-40aa-bb2c-2e4d8d55367e,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"After initial secretion of IgM, cytokines secreted by TH2 cells stimulate the plasma cells to switch from IgM production to production of IgG, IgA, or IgE. This process, called class switching or isotype switching, allows plasma cells cloned from the same activated B cell to produce a variety of antibody classes with the same epitope specificity. Class switching is accomplished by genetic rearrangement of gene segments encoding the constant region, which determines an antibody’s class. The variable region is not changed, so the new class of antibody retains the original epitope specificity.",True,Primary and Secondary Responses,,,,
6131d077-32d8-434e-be0a-f8d4485e6cb2,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,Primary and Secondary Responses,False,Primary and Secondary Responses,,,,
9f8a65f0-49b9-4126-8b76-e1b4368bf741,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"T cell-dependent activation of B cells plays an important role in both the primary and secondary responses associated with adaptive immunity. With the first exposure to a protein antigen, a T cell-dependent primary antibody response occurs. The initial stage of the primary response is a lag period, or latent period, of approximately 10 days, during which no antibody can be detected in serum. This lag period is the time required for all of the steps of the primary response, including naïve mature B cell binding of antigen with BCRs, antigen processing and presentation, helper T cell activation, B cell activation, and clonal proliferation. The end of the lag period is characterized by a rise in IgM levels in the serum, as TH2 cells stimulate B cell differentiation into plasma cells. IgM levels reach their peak around 14 days after primary antigen exposure; at about this same time, TH2 stimulates antibody class switching, and IgM levels in serum begin to decline. Meanwhile, levels of IgG increase until they reach a peak about three weeks into the primary response (Figure 14.23).",True,Primary and Secondary Responses,Figure 14.23,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.23.png,"Figure 14.23 Compared to the primary response, the secondary antibody response occurs more quickly and produces antibody levels that are higher and more sustained. The secondary response mostly involves IgG."
11c0fd49-7f38-40df-975a-6c581e890d7c,https://open.oregonstate.education/microbiology/,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/microbiology/chapter/18-4b-lymphocytes-and-humoral-immunity/,"During the primary response, some of the cloned B cells are differentiated into memory B cells programmed to respond to subsequent exposures. This secondary response occurs more quickly and forcefully than the primary response. The lag period is decreased to only a few days and the production of IgG is significantly higher than observed for the primary response (Figure 14.23). In addition, the antibodies produced during the secondary response are more effective and bind with higher affinity to the targeted epitopes. Plasma cells produced during secondary responses live longer than those produced during the primary response, so levels of specific antibody remain elevated for a longer period of time.",True,Primary and Secondary Responses,Figure 14.23,14.4	B Lymphocytes and Humoral Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.23.png,"Figure 14.23 Compared to the primary response, the secondary antibody response occurs more quickly and produces antibody levels that are higher and more sustained. The secondary response mostly involves IgG."
dd2a3efb-7fab-4ad4-8a55-36bf1a398153,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,Cellular Immunity,False,Cellular Immunity,,,,
a937e968-2051-4a39-bcac-844cd874645a,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,T Cell Production and Maturation,False,T Cell Production and Maturation,,,,
098f5d1e-5db5-49e5-b144-ec07e2fb8cef,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"T cells, like all other white blood cells involved in innate and adaptive immunity, are formed from multipotent hematopoietic stem cells (HSCs) in the bone marrow. However, unlike the white blood cells of innate immunity, eventual T cells differentiate first into lymphoid stem cells that then become small, immature lymphocytes, sometimes called lymphoblasts. The first steps of differentiation occur in the red marrow of bones (Figure 14.14), after which immature T lymphocytes enter the bloodstream and travel to the thymus for the final steps of maturation (Figure 14.15). Once in the thymus, the immature T lymphocytes are referred to as thymocytes.",True,T Cell Production and Maturation,Figure 14.14,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.14.png,"Figure 14.14 (a) Red bone marrow can be found in the head of the femur (thighbone) and is also present in the flat bones of the body, such as the ilium and the scapula. (b) Red bone marrow is the site of production and differentiation of many formed elements of blood, including erythrocytes, leukocytes, and platelets. The yellow bone marrow is populated primarily with adipose cells."
32366d83-7f7d-4cce-913d-17c0a7a8668c,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"The maturation of thymocytes within the thymus can be divided into tree critical steps of positive and negative selection, collectively referred to as thymic selection. The first step of thymic selection occurs in the cortex of the thymus and involves the development of a functional T-cell receptor (TCR) that is required for activation by APCs. Thymocytes with defective TCRs are removed by negative selection through the induction of apoptosis (programmed controlled cell death). The second step of thymic selection also occurs in the cortex and involves the positive selection of thymocytes that will interact appropriately with MHC molecules. Thymocytes that can interact appropriately with MHC molecules receive a positive stimulation that moves them further through the process of maturation, whereas thymocytes that do not interact appropriately are not stimulated and are eliminated by apoptosis. The third and final step of thymic selection occurs in both the cortex and medulla and involves negative selection to remove self- reacting thymocytes, those that react to self-antigens, by apoptosis. This final step is sometimes referred to as central tolerance because it prevents self-reacting T cells from reaching the bloodstream and potentially causing autoimmune disease, which occurs when the immune system attacks healthy “self” cells.",True,T Cell Production and Maturation,,,,
c3ef68e2-d799-497d-8d7f-e3eaf96eeac5,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"Despite central tolerance, some self-reactive T cells generally escape the thymus and enter the peripheral bloodstream. Therefore, a second line of defense called peripheral tolerance is needed to protect against autoimmune disease. Peripheral tolerance involves mechanisms of anergy and inhibition of self-reactive T cells by regulatory T cells. Anergy refers to a state of nonresponsiveness to antigen stimulation. In the case of self-reactive T cells that escape the thymus, lack of an essential co-stimulatory signal required for activation causes anergy and prevents autoimmune activation. Regulatory T cells participate in peripheral tolerance by inhibiting the activation and function of self- reactive T cells and by secreting anti-inflammatory cytokines.",True,T Cell Production and Maturation,,,,
eb17d448-758a-4f1a-a9dc-6ba4732bfb06,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"It is not completely understood what events specifically direct maturation of thymocytes into regulatory T cells. Current theories suggest the critical events may occur during the third step of thymic selection, when most self-reactive T cells are eliminated. Regulatory T cells may receive a unique signal that is below the threshold required to target them for negative selection and apoptosis. Consequently, these cells continue to mature and then exit the thymus, armed to inhibit the activation of self-reactive T cells.",True,T Cell Production and Maturation,,,,
25963559-5d69-423d-8739-5870a5cc56c2,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"It has been estimated that the three steps of thymic selection eliminate 98% of thymocytes. The remaining 2% that exit the thymus migrate through the bloodstream and lymphatic system to sites of secondary lymphoid organs/tissues, such as the lymph nodes, spleen, and tonsils (Figure 14.15), where they await activation through the presentation of specific antigens by APCs. Until they are activated, they are known as mature naïve T cells.",True,T Cell Production and Maturation,Figure 14.15,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.15.png,"Figure 14.15 The thymus is a bi-lobed, H-shaped glandular organ that is located just above the heart. It is surrounded by a fibrous capsule of connective tissue. The darkly staining cortex and the lighter staining medulla of individual lobules are clearly visible in the light micrograph of the thymus of a newborn (top right, LM × 100). (credit micrograph: modification of micrograph provided by the Regents of University of Michigan Medical School © 2012)"
a12af3db-9a80-41d1-85ac-01ebf9c6c9a4,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,Classes of T Cells,False,Classes of T Cells,,,,
0d114f4f-030c-4e0a-a070-a7713ed45d7c,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"T cells can be categorized into three distinct classes: helper T cells, regulatory T cells, and cytotoxic T cells. These classes are differentiated based on their expression of certain surface molecules, their mode of activation, and their functional roles in adaptive immunity (Table 14.1).",True,Classes of T Cells,,,,
c6e43627-ee14-43ad-baf6-bde12b5168f7,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"All T cells produce cluster of differentiation (CD) molecules, cell surface glycoproteins that can be used to identify and distinguish between the various types of white blood cells. Although T cells can produce a variety of CD molecules, CD4 and CD8 are the two most important used for differentiation of the classes. Helper T cells and regulatory T cells are characterized by the expression of CD4 on their surface, whereas cytotoxic T cells are characterized by the expression of CD8.",True,Classes of T Cells,,,,
5d38e254-1546-4a0d-ac94-bf432a8e5e72,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"Classes of T cells can also be distinguished by the specific MHC molecules and APCs with which they interact for activation. Helper T cells and regulatory T cells can only be activated by APCs presenting antigens associated with MHC II. In contrast, cytotoxic T cells recognize antigens presented in association with MHC I, either by APCs or by nucleated cells infected with an intracellular pathogen.",True,Classes of T Cells,,,,
0b8e5262-1378-4a48-bd54-a56faef98bb2,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"The different classes of T cells also play different functional roles in the immune system. Helper T cells serve as the central orchestrators that help activate and direct functions of humoral and cellular immunity. In addition, helper T cells enhance the pathogen-killing functions of macrophages and NK cells of innate immunity. In contrast, the primary role of regulatory T cells is to prevent undesirable and potentially damaging immune responses. Their role in peripheral tolerance, for example, protects against autoimmune disorders, as discussed earlier. Finally, cytotoxic T cells are the primary effector cells for cellular immunity. They recognize and target cells that have been infected by intracellular pathogens, destroying infected cells along with the pathogens inside.",True,Classes of T Cells,,,,
d790f70c-2871-4136-ac90-4c3b9f294f32,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,T-Cell Receptors,False,T-Cell Receptors,,,,
8f6d30de-ea7d-4d59-87ce-63ef8ec0c2ae,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"For both helper T cells and cytotoxic T cells, activation is a complex process that requires the interactions of multiple molecules and exposure to cytokines. The T-cell receptor (TCR) is involved in the first step of pathogen epitope recognition during the activation process.",True,T-Cell Receptors,,,,
0c5f6c10-d129-409e-82e9-5a230ad87f38,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"The TCR comes from the same receptor family as the antibodies IgD and IgM, the antigen receptors on the B cell membrane surface, and thus shares common structural elements. Similar to antibodies, the TCR has a variable region and a constant region, and the variable region provides the antigen-binding site (Figure 14.16). However, the structure of TCR is smaller and less complex than the immunoglobulin molecules (Figure 14.15). Whereas immunoglobulins have four peptide chains and Y-shaped structures, the TCR consists of just two peptide chains (α and β chains), both of which span the cytoplasmic membrane of the T cell.",True,T-Cell Receptors,Figure 14.16,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.16.png,Figure 14.16 A T-cell receptor spans the cytoplasmic membrane and projects variable binding regions into the extracellular space to bind processed antigens associated with MHC I or MHC II molecules.
4c785fd9-7b16-484d-a9f7-edf3a293f9b3,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"TCRs are epitope-specific, and it has been estimated that 25 million T cells with unique epitope-binding TCRs are required to protect an individual against a wide range of microbial pathogens. Because the human genome only contains about 25,000 genes, we know that each specific TCR cannot be encoded by its own set of genes. This raises the question of how such a vast population of T cells with millions of specific TCRs can be achieved. The answer is a process called genetic rearrangement, which occurs in the thymus during the first step of thymic selection, providing the genetic diversity required to produce millions of TCRs with unique epitope-specific variable regions.",True,T-Cell Receptors,,,,
c7c29669-16dc-421d-9bcb-d39363720563,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,Activation and Differentiation of Helper T Cells,False,Activation and Differentiation of Helper T Cells,,,,
08008e45-0cf0-45c9-a50c-8f9df755aeb7,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"Helper T cells can only be activated by APCs presenting processed foreign epitopes in association with MHC II. The first step in the activation process is TCR recognition of the specific foreign epitope presented within the MHC II antigen-binding cleft. The second step involves the interaction of CD4 on the helper T cell with a region of the MHC II molecule separate from the antigen-binding cleft. This second interaction anchors the MHC II-TCR complex and ensures that the helper T cell is recognizing both the foreign (“nonself”) epitope and “self” antigen of the APC; both recognitions are required for activation of the cell. In the third step, the APC and T cell secrete cytokines that activate the helper T cell. The activated helper T cell then proliferates, dividing by mitosis to produce clonal naïve helper T cells that differentiate into subtypes with different functions (Figure 14.17).",True,Activation and Differentiation of Helper T Cells,Figure 14.17,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.17.png,Figure 14.17 This illustration depicts the activation of a naïve (unactivated) helper T cell by an antigen-presenting cell and the subsequent proliferation and differentiation of the activated T cell into different subtypes.
f142c156-0756-44cb-b296-30fb736df03e,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"Activated helper T cells can differentiate into one of four distinct subtypes, summarized in Table 14.2. The differentiation process is directed by APC-secreted cytokines. Depending on which APC-secreted cytokines interact with an activated helper T cell, the cell may differentiate into a T helper 1 (TH1) cell, a T helper 2 (TH2) cell, or a memory helper T cell. The two types of helper T cells are relatively short-lived effector cells, meaning that they perform various functions of the immediate immune response. In contrast, memory helper T cells are relatively long lived; they are programmed to “remember” a specific antigen or epitope in order to mount a rapid, strong, secondary response to subsequent exposures.",True,Activation and Differentiation of Helper T Cells,,,,
74bc519d-dd21-4db0-8eda-e60042ea8ae6,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"TH1 cells secrete their own cytokines that are involved in stimulating and orchestrating other cells involved in adaptive and innate immunity. For example, they stimulate cytotoxic T cells, enhancing their killing of infected cells and promoting differentiation into memory cytotoxic T cells. TH1 cells also stimulate macrophages and neutrophils to become more effective in their killing of intracellular bacteria. They can also stimulate NK cells to become more effective at killing target cells.",True,Activation and Differentiation of Helper T Cells,,,,
bb5acf19-a8aa-4522-980a-833fce4d9f09,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"TH2 cells play an important role in orchestrating the humoral immune response through their secretion of cytokines that activate B cells and direct B cell differentiation and antibody production. Various cytokines produced by TH2 cells orchestrate antibody class switching, which allows B cells to switch between the production of IgM, IgG, IgA, and IgE as needed to carry out specific antibody functions and to provide pathogen-specific humoral immune responses.",True,Activation and Differentiation of Helper T Cells,,,,
0e2e246b-4c18-4531-92db-cb0849281435,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"A third subtype of helper T cells called TH17 cells was discovered through observations that immunity to some infections is not associated with TH1 or TH2 cells. TH17 cells and the cytokines they produce appear to be specifically responsible for the body’s defense against chronic mucocutaneous infections. Patients who lack sufficient TH17 cells in the mucosa (e.g., HIV patients) may be more susceptible to bacteremia and gastrointestinal infections.[1]",True,Activation and Differentiation of Helper T Cells,,,,
d989e86f-9bb4-44de-bbe0-1dc449b4c822,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,Activation and Differentiation of Cytotoxic T Cells,False,Activation and Differentiation of Cytotoxic T Cells,,,,
9bf41f34-caaa-4a0f-bd53-328c0c947fd6,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"Cytotoxic T cells (also referred to as cytotoxic T lymphocytes, or CTLs) are activated by APCs in a three-step process similar to that of helper T cells. The key difference is that the activation of cytotoxic T cells involves recognition of an antigen presented with MHC I (as opposed to MHC II) and interaction of CD8 (as opposed to CD4) with the receptor complex. After the successful co-recognition of foreign epitope and self-antigen, the production of cytokines by the APC and the cytotoxic T cell activate clonal proliferation and differentiation. Activated cytotoxic T cells can differentiate into effector cytotoxic T cells that target pathogens for destruction or memory cells that are ready to respond to subsequent exposures.",True,Activation and Differentiation of Cytotoxic T Cells,,,,
f5640c8d-7289-4f2b-82b8-ae1ef4792cc0,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"As noted, proliferation and differentiation of cytotoxic T cells is also stimulated by cytokines secreted from TH1 cells activated by the same foreign epitope. The co-stimulation that comes from these TH1 cells is provided by secreted cytokines. Although it is possible for activation of cytotoxic T cells to occur without stimulation from TH1 cells, the activation is not as effective or long-lasting.",True,Activation and Differentiation of Cytotoxic T Cells,,,,
75fe97a7-70bf-4727-885f-9711cc2623ed,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"Once activated, cytotoxic T cells serve as the effector cells of cellular immunity, recognizing and kill cells infected with intracellular pathogens through a mechanism very similar to that of NK cells. However, whereas NK cells recognize nonspecific signals of cell stress or abnormality, cytotoxic T cells recognize infected cells through antigen presentation of pathogen-specific epitopes associated with MHC I. Once an infected cell is recognized, the TCR of the cytotoxic T cell binds to the epitope and releases perforin and granzymes that destroy the infected cell (Figure 14.18). Perforin is a protein that creates pores in the target cell, and granzymes are proteases that enter the pores and induce apoptosis. This mechanism of programmed cell death is a controlled and efficient means of destroying and removing infected cells without releasing the pathogens inside to infect neighboring cells, as might occur if the infected cells were simply lysed.",True,Activation and Differentiation of Cytotoxic T Cells,Figure 14.18,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.18.png,"Figure 14.18 This figure illustrates the activation of a naïve (unactivated) cytotoxic T cell (CTL) by an antigen- presenting MHC I molecule on an infected body cell. Once activated, the CTL releases perforin and granzymes that invade the infected cell and induce controlled cell death, or apoptosis."
3dd82f75-2272-434e-9bf3-893ccdf4923d,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,Superantigens and Unregulated Activation of T Cells,False,Superantigens and Unregulated Activation of T Cells,,,,
7d068959-d01a-45de-acae-f1c6e287baa0,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"When T cell activation is controlled and regulated, the result is a protective response that is effective in combating infections. However, if T cell activation is unregulated and excessive, the result can be a life-threatening. Certain bacterial and viral pathogens produce toxins known as superantigens (see Virulence Factors of Bacterial and Viral Pathogens) that can trigger such an unregulated response. Known bacterial superantigens include toxic shock syndrome toxin (TSST), staphylococcal enterotoxins, streptococcal pyrogenic toxins, streptococcal superantigen, and the streptococcal mitogenic exotoxin. Viruses known to produce superantigens include Epstein-Barr virus (human herpesvirus 4), cytomegalovirus (human herpesvirus 5), and others.",True,Superantigens and Unregulated Activation of T Cells,,,,
77afdf1a-4a26-4d6f-8fa7-19b8e0f96b9b,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"The mechanism of T cell activation by superantigens involves their simultaneous binding to MHC II molecules of APCs and the variable region of the TCR β chain. This binding occurs outside of the antigen-binding cleft of MHC II, so the superantigen will bridge together and activate MHC II and TCR without specific foreign epitope recognition (Figure 14.19). The result is an excessive, uncontrolled release of cytokines, often called a cytokine storm, which stimulates an excessive inflammatory response. This can lead to a dangerous decrease in blood pressure, shock, multi- organ failure, and potentially, death.",True,Superantigens and Unregulated Activation of T Cells,Figure 14.19,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.19.png,"Figure 14.19 (a) The macrophage in this figure is presenting a foreign epitope that does not match the TCR of the T cell. Because the T cell does not recognize the epitope, it is not activated. (b) The macrophage in this figure is presenting a superantigen that is not recognized by the TCR of the T cell, yet the superantigen still is able to bridge and bind the MHC II and TCR molecules. This nonspecific, uncontrolled activation of the T cell results in an excessive release of cytokines that activate other T cells and cause excessive inflammation. (credit: modification of work by “Microbiotic”/YouTube)"
7cbd6d54-866d-4663-b0be-296238a0a06e,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,T Cell Production and Maturation,False,T Cell Production and Maturation,,,,
0886d0b4-5055-47ec-afe3-3736789de839,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"The maturation of thymocytes within the thymus can be divided into tree critical steps of positive and negative selection, collectively referred to as thymic selection. The first step of thymic selection occurs in the cortex of the thymus and involves the development of a functional T-cell receptor (TCR) that is required for activation by APCs. Thymocytes with defective TCRs are removed by negative selection through the induction of apoptosis (programmed controlled cell death). The second step of thymic selection also occurs in the cortex and involves the positive selection of thymocytes that will interact appropriately with MHC molecules. Thymocytes that can interact appropriately with MHC molecules receive a positive stimulation that moves them further through the process of maturation, whereas thymocytes that do not interact appropriately are not stimulated and are eliminated by apoptosis. The third and final step of thymic selection occurs in both the cortex and medulla and involves negative selection to remove self- reacting thymocytes, those that react to self-antigens, by apoptosis. This final step is sometimes referred to as central tolerance because it prevents self-reacting T cells from reaching the bloodstream and potentially causing autoimmune disease, which occurs when the immune system attacks healthy “self” cells.",True,T Cell Production and Maturation,,,,
1eaab60b-cc40-41ca-891c-46ac8a4add1e,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"Despite central tolerance, some self-reactive T cells generally escape the thymus and enter the peripheral bloodstream. Therefore, a second line of defense called peripheral tolerance is needed to protect against autoimmune disease. Peripheral tolerance involves mechanisms of anergy and inhibition of self-reactive T cells by regulatory T cells. Anergy refers to a state of nonresponsiveness to antigen stimulation. In the case of self-reactive T cells that escape the thymus, lack of an essential co-stimulatory signal required for activation causes anergy and prevents autoimmune activation. Regulatory T cells participate in peripheral tolerance by inhibiting the activation and function of self- reactive T cells and by secreting anti-inflammatory cytokines.",True,T Cell Production and Maturation,,,,
d321ccae-fca0-44d1-b20b-36285f43be9c,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"It is not completely understood what events specifically direct maturation of thymocytes into regulatory T cells. Current theories suggest the critical events may occur during the third step of thymic selection, when most self-reactive T cells are eliminated. Regulatory T cells may receive a unique signal that is below the threshold required to target them for negative selection and apoptosis. Consequently, these cells continue to mature and then exit the thymus, armed to inhibit the activation of self-reactive T cells.",True,T Cell Production and Maturation,,,,
49b45e72-93ce-4d6f-b1e6-636e3e5325df,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"It has been estimated that the three steps of thymic selection eliminate 98% of thymocytes. The remaining 2% that exit the thymus migrate through the bloodstream and lymphatic system to sites of secondary lymphoid organs/tissues, such as the lymph nodes, spleen, and tonsils (Figure 14.15), where they await activation through the presentation of specific antigens by APCs. Until they are activated, they are known as mature naïve T cells.",True,T Cell Production and Maturation,Figure 14.15,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.15.png,"Figure 14.15 The thymus is a bi-lobed, H-shaped glandular organ that is located just above the heart. It is surrounded by a fibrous capsule of connective tissue. The darkly staining cortex and the lighter staining medulla of individual lobules are clearly visible in the light micrograph of the thymus of a newborn (top right, LM × 100). (credit micrograph: modification of micrograph provided by the Regents of University of Michigan Medical School © 2012)"
ec5bb4c9-5e85-4e1e-9b86-15c6749bd492,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,Classes of T Cells,False,Classes of T Cells,,,,
4e6ebdd5-a167-4681-b02b-52a3682f6ef8,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"T cells can be categorized into three distinct classes: helper T cells, regulatory T cells, and cytotoxic T cells. These classes are differentiated based on their expression of certain surface molecules, their mode of activation, and their functional roles in adaptive immunity (Table 14.1).",True,Classes of T Cells,,,,
fa98eca1-f13c-4276-817d-a680732408be,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"All T cells produce cluster of differentiation (CD) molecules, cell surface glycoproteins that can be used to identify and distinguish between the various types of white blood cells. Although T cells can produce a variety of CD molecules, CD4 and CD8 are the two most important used for differentiation of the classes. Helper T cells and regulatory T cells are characterized by the expression of CD4 on their surface, whereas cytotoxic T cells are characterized by the expression of CD8.",True,Classes of T Cells,,,,
c4e9ed4c-e7b1-4c8f-8b07-31e266807c81,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"Classes of T cells can also be distinguished by the specific MHC molecules and APCs with which they interact for activation. Helper T cells and regulatory T cells can only be activated by APCs presenting antigens associated with MHC II. In contrast, cytotoxic T cells recognize antigens presented in association with MHC I, either by APCs or by nucleated cells infected with an intracellular pathogen.",True,Classes of T Cells,,,,
5faa98c9-7bcb-4ffe-9a33-a6cfc31d86ce,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"The different classes of T cells also play different functional roles in the immune system. Helper T cells serve as the central orchestrators that help activate and direct functions of humoral and cellular immunity. In addition, helper T cells enhance the pathogen-killing functions of macrophages and NK cells of innate immunity. In contrast, the primary role of regulatory T cells is to prevent undesirable and potentially damaging immune responses. Their role in peripheral tolerance, for example, protects against autoimmune disorders, as discussed earlier. Finally, cytotoxic T cells are the primary effector cells for cellular immunity. They recognize and target cells that have been infected by intracellular pathogens, destroying infected cells along with the pathogens inside.",True,Classes of T Cells,,,,
c43f22f0-c9ee-4e45-a593-3bf736e21acd,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,T-Cell Receptors,False,T-Cell Receptors,,,,
bd8dc39a-b851-462f-ad56-e48ada9d248d,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"The TCR comes from the same receptor family as the antibodies IgD and IgM, the antigen receptors on the B cell membrane surface, and thus shares common structural elements. Similar to antibodies, the TCR has a variable region and a constant region, and the variable region provides the antigen-binding site (Figure 14.16). However, the structure of TCR is smaller and less complex than the immunoglobulin molecules (Figure 14.15). Whereas immunoglobulins have four peptide chains and Y-shaped structures, the TCR consists of just two peptide chains (α and β chains), both of which span the cytoplasmic membrane of the T cell.",True,T-Cell Receptors,Figure 14.16,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.16.png,Figure 14.16 A T-cell receptor spans the cytoplasmic membrane and projects variable binding regions into the extracellular space to bind processed antigens associated with MHC I or MHC II molecules.
8f018309-e747-4bec-8ab9-7c7d7f7613b1,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"TCRs are epitope-specific, and it has been estimated that 25 million T cells with unique epitope-binding TCRs are required to protect an individual against a wide range of microbial pathogens. Because the human genome only contains about 25,000 genes, we know that each specific TCR cannot be encoded by its own set of genes. This raises the question of how such a vast population of T cells with millions of specific TCRs can be achieved. The answer is a process called genetic rearrangement, which occurs in the thymus during the first step of thymic selection, providing the genetic diversity required to produce millions of TCRs with unique epitope-specific variable regions.",True,T-Cell Receptors,,,,
b094d740-ed8d-4568-8255-211650b2325a,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,Activation and Differentiation of Helper T Cells,False,Activation and Differentiation of Helper T Cells,,,,
b81fc3a4-3d7a-476c-8a81-b28d7ea5375c,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"Helper T cells can only be activated by APCs presenting processed foreign epitopes in association with MHC II. The first step in the activation process is TCR recognition of the specific foreign epitope presented within the MHC II antigen-binding cleft. The second step involves the interaction of CD4 on the helper T cell with a region of the MHC II molecule separate from the antigen-binding cleft. This second interaction anchors the MHC II-TCR complex and ensures that the helper T cell is recognizing both the foreign (“nonself”) epitope and “self” antigen of the APC; both recognitions are required for activation of the cell. In the third step, the APC and T cell secrete cytokines that activate the helper T cell. The activated helper T cell then proliferates, dividing by mitosis to produce clonal naïve helper T cells that differentiate into subtypes with different functions (Figure 14.17).",True,Activation and Differentiation of Helper T Cells,Figure 14.17,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.17.png,Figure 14.17 This illustration depicts the activation of a naïve (unactivated) helper T cell by an antigen-presenting cell and the subsequent proliferation and differentiation of the activated T cell into different subtypes.
5e5b363b-63e4-4495-b270-0edd45582717,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"TH1 cells secrete their own cytokines that are involved in stimulating and orchestrating other cells involved in adaptive and innate immunity. For example, they stimulate cytotoxic T cells, enhancing their killing of infected cells and promoting differentiation into memory cytotoxic T cells. TH1 cells also stimulate macrophages and neutrophils to become more effective in their killing of intracellular bacteria. They can also stimulate NK cells to become more effective at killing target cells.",True,Activation and Differentiation of Helper T Cells,,,,
ce794603-a798-4126-bf5a-643d563cea37,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"TH2 cells play an important role in orchestrating the humoral immune response through their secretion of cytokines that activate B cells and direct B cell differentiation and antibody production. Various cytokines produced by TH2 cells orchestrate antibody class switching, which allows B cells to switch between the production of IgM, IgG, IgA, and IgE as needed to carry out specific antibody functions and to provide pathogen-specific humoral immune responses.",True,Activation and Differentiation of Helper T Cells,,,,
96f40551-f849-40f1-901b-0e984f16ccfc,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"A third subtype of helper T cells called TH17 cells was discovered through observations that immunity to some infections is not associated with TH1 or TH2 cells. TH17 cells and the cytokines they produce appear to be specifically responsible for the body’s defense against chronic mucocutaneous infections. Patients who lack sufficient TH17 cells in the mucosa (e.g., HIV patients) may be more susceptible to bacteremia and gastrointestinal infections.[1]",True,Activation and Differentiation of Helper T Cells,,,,
418c5f6e-65f8-4261-b647-995a9114855e,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,Activation and Differentiation of Cytotoxic T Cells,False,Activation and Differentiation of Cytotoxic T Cells,,,,
658148c3-93ee-4252-a369-ecd51bde62e7,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"Cytotoxic T cells (also referred to as cytotoxic T lymphocytes, or CTLs) are activated by APCs in a three-step process similar to that of helper T cells. The key difference is that the activation of cytotoxic T cells involves recognition of an antigen presented with MHC I (as opposed to MHC II) and interaction of CD8 (as opposed to CD4) with the receptor complex. After the successful co-recognition of foreign epitope and self-antigen, the production of cytokines by the APC and the cytotoxic T cell activate clonal proliferation and differentiation. Activated cytotoxic T cells can differentiate into effector cytotoxic T cells that target pathogens for destruction or memory cells that are ready to respond to subsequent exposures.",True,Activation and Differentiation of Cytotoxic T Cells,,,,
64193cee-2e5e-4396-a1a2-aeda250b5d9f,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"As noted, proliferation and differentiation of cytotoxic T cells is also stimulated by cytokines secreted from TH1 cells activated by the same foreign epitope. The co-stimulation that comes from these TH1 cells is provided by secreted cytokines. Although it is possible for activation of cytotoxic T cells to occur without stimulation from TH1 cells, the activation is not as effective or long-lasting.",True,Activation and Differentiation of Cytotoxic T Cells,,,,
e46c2675-98d9-40d4-b6ec-aadb89dd7a7b,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"Once activated, cytotoxic T cells serve as the effector cells of cellular immunity, recognizing and kill cells infected with intracellular pathogens through a mechanism very similar to that of NK cells. However, whereas NK cells recognize nonspecific signals of cell stress or abnormality, cytotoxic T cells recognize infected cells through antigen presentation of pathogen-specific epitopes associated with MHC I. Once an infected cell is recognized, the TCR of the cytotoxic T cell binds to the epitope and releases perforin and granzymes that destroy the infected cell (Figure 14.18). Perforin is a protein that creates pores in the target cell, and granzymes are proteases that enter the pores and induce apoptosis. This mechanism of programmed cell death is a controlled and efficient means of destroying and removing infected cells without releasing the pathogens inside to infect neighboring cells, as might occur if the infected cells were simply lysed.",True,Activation and Differentiation of Cytotoxic T Cells,Figure 14.18,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.18.png,"Figure 14.18 This figure illustrates the activation of a naïve (unactivated) cytotoxic T cell (CTL) by an antigen- presenting MHC I molecule on an infected body cell. Once activated, the CTL releases perforin and granzymes that invade the infected cell and induce controlled cell death, or apoptosis."
dacb4cc9-92a6-4a55-bd40-aedada37d9b6,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,Superantigens and Unregulated Activation of T Cells,False,Superantigens and Unregulated Activation of T Cells,,,,
ff7226b0-a073-48e7-a51a-f022ce782bd0,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"When T cell activation is controlled and regulated, the result is a protective response that is effective in combating infections. However, if T cell activation is unregulated and excessive, the result can be a life-threatening. Certain bacterial and viral pathogens produce toxins known as superantigens (see Virulence Factors of Bacterial and Viral Pathogens) that can trigger such an unregulated response. Known bacterial superantigens include toxic shock syndrome toxin (TSST), staphylococcal enterotoxins, streptococcal pyrogenic toxins, streptococcal superantigen, and the streptococcal mitogenic exotoxin. Viruses known to produce superantigens include Epstein-Barr virus (human herpesvirus 4), cytomegalovirus (human herpesvirus 5), and others.",True,Superantigens and Unregulated Activation of T Cells,,,,
a0ed7e4d-8964-47f2-ad9e-5e24c523db7d,https://open.oregonstate.education/microbiology/,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/microbiology/chapter/18-3t-lymphocytes-and-cellular-immunity/,"The mechanism of T cell activation by superantigens involves their simultaneous binding to MHC II molecules of APCs and the variable region of the TCR β chain. This binding occurs outside of the antigen-binding cleft of MHC II, so the superantigen will bridge together and activate MHC II and TCR without specific foreign epitope recognition (Figure 14.19). The result is an excessive, uncontrolled release of cytokines, often called a cytokine storm, which stimulates an excessive inflammatory response. This can lead to a dangerous decrease in blood pressure, shock, multi- organ failure, and potentially, death.",True,Superantigens and Unregulated Activation of T Cells,Figure 14.19,14.3	T Lymphocytes and Cellular Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.19.png,"Figure 14.19 (a) The macrophage in this figure is presenting a foreign epitope that does not match the TCR of the T cell. Because the T cell does not recognize the epitope, it is not activated. (b) The macrophage in this figure is presenting a superantigen that is not recognized by the TCR of the T cell, yet the superantigen still is able to bridge and bind the MHC II and TCR molecules. This nonspecific, uncontrolled activation of the T cell results in an excessive release of cytokines that activate other T cells and cause excessive inflammation. (credit: modification of work by “Microbiotic”/YouTube)"
444db79b-57a6-4a01-865d-c1696cacfd39,https://open.oregonstate.education/microbiology/,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/microbiology/chapter/18-2major-histocompatibility-complexes-and-antigen-presenting-cells/,Major Histocompatibility Complex Molecules,False,Major Histocompatibility Complex Molecules,,,,
a935a7bf-487d-4c69-b5a8-f1781e5ebb3f,https://open.oregonstate.education/microbiology/,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/microbiology/chapter/18-2major-histocompatibility-complexes-and-antigen-presenting-cells/,"The major histocompatibility complex (MHC) is a collection of genes coding for MHC molecules found on the surface of all nucleated cells of the body. In humans, the MHC genes are also referred to as human leukocyte antigen (HLA) genes. Mature red blood cells, which lack a nucleus, are the only cells that do not express MHC molecules on their surface.",True,Major Histocompatibility Complex Molecules,,,,
63fc4e95-865a-47e2-9989-fa3e8ca77d22,https://open.oregonstate.education/microbiology/,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/microbiology/chapter/18-2major-histocompatibility-complexes-and-antigen-presenting-cells/,"There are two classes of MHC molecules involved in adaptive immunity, MHC I and MHC II (Figure 14.11). MHC I molecules are found on all nucleated cells; they present normal self-antigens as well as abnormal or nonself pathogens to the effector T cells involved in cellular immunity. In contrast, MHC II molecules are only found on macrophages, dendritic cells, and B cells; they present abnormal or nonself pathogen antigens for the initial activation of T cells.",True,Major Histocompatibility Complex Molecules,Figure 14.11,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.11.png,"Figure 14.11 MHC I are found on all nucleated body cells, and MHC II are found on macrophages, dendritic cells, and B cells (along with MHC I). The antigen-binding cleft of MHC I is formed by domains α1 and α2. The antigen- binding cleft of MHC II is formed by domains α1 and β1."
96440eda-86f2-4d9c-a066-9b0ddb2ce5ab,https://open.oregonstate.education/microbiology/,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/microbiology/chapter/18-2major-histocompatibility-complexes-and-antigen-presenting-cells/,"Both types of MHC molecules are transmembrane glycoproteins that assemble as dimers in the cytoplasmic membrane of cells, but their structures are quite different. MHC I molecules are composed of a longer α protein chain coupled with a smaller β2 microglobulin protein, and only the α chain spans the cytoplasmic membrane. The α chain of the MHC I molecule folds into three separate domains: α1, α2 and α3. MHC II molecules are composed of two protein chains (an α and a β chain) that are approximately similar in length. Both chains of the MHC II molecule possess portions that span the plasma membrane, and each chain folds into two separate domains: α1 and α2, and β1, and β2. In order to present abnormal or non-self-antigens to T cells, MHC molecules have a cleft that serves as the antigen-binding site near the “top” (or outermost) portion of the MHC-I or MHC-II dimer. For MHC I, the antigen- binding cleft is formed by the α1 and α2 domains, whereas for MHC II, the cleft is formed by the α1 and β1 domains (Figure 14.11).",True,Major Histocompatibility Complex Molecules,Figure 14.11,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.11.png,"Figure 14.11 MHC I are found on all nucleated body cells, and MHC II are found on macrophages, dendritic cells, and B cells (along with MHC I). The antigen-binding cleft of MHC I is formed by domains α1 and α2. The antigen- binding cleft of MHC II is formed by domains α1 and β1."
167b9947-10f7-41fe-9e61-108b92127f89,https://open.oregonstate.education/microbiology/,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/microbiology/chapter/18-2major-histocompatibility-complexes-and-antigen-presenting-cells/,Antigen-Presenting Cells (APCs),False,Antigen-Presenting Cells (APCs),,,,
4e2780ef-6d14-4a83-8b28-e641d15aabd7,https://open.oregonstate.education/microbiology/,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/microbiology/chapter/18-2major-histocompatibility-complexes-and-antigen-presenting-cells/,"All nucleated cells in the body have mechanisms for processing and presenting antigens in association with MHC molecules. This signals the immune system, indicating whether the cell is normal and healthy or infected with an intracellular pathogen. However, only macrophages, dendritic cells, and B cells have the ability to present antigens specifically for the purpose of activating T cells; for this reason, these types of cells are sometimes referred to as antigen-presenting cells (APCs).",True,Antigen-Presenting Cells (APCs),,,,
412d0560-6b88-40ba-8837-c1641c203cd0,https://open.oregonstate.education/microbiology/,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/microbiology/chapter/18-2major-histocompatibility-complexes-and-antigen-presenting-cells/,"While all APCs play a similar role in adaptive immunity, there are some important differences to consider. Macrophages and dendritic cells are phagocytes that ingest and kill pathogens that penetrate the first-line barriers (i.e., skin and mucous membranes). B cells, on the other hand, do not function as phagocytes but play a primary role in the production and secretion of antibodies. In addition, whereas macrophages and dendritic cells recognize pathogens through nonspecific receptor interactions (e.g., PAMPs, toll-like receptors, and receptors for opsonizing complement or antibody), B cells interact with foreign pathogens or their free antigens using antigen-specific immunoglobulin as receptors (monomeric IgD and IgM). When the immunoglobulin receptors bind to an antigen, the B cell internalizes the antigen by endocytosis before processing and presentting the antigen to T cells.",True,Antigen-Presenting Cells (APCs),,,,
b5d83848-0a6d-46cf-a618-9e6cd68f7692,https://open.oregonstate.education/microbiology/,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/microbiology/chapter/18-2major-histocompatibility-complexes-and-antigen-presenting-cells/,"MHC II molecules are only found on the surface of APCs. Macrophages and dendritic cells use similar mechanisms for processing and presentation of antigens and their epitopes in association with MHC II; B cells use somewhat different mechanisms that will be described further in B Lymphocytes and Humoral Immunity. For now, we will focus on the steps of the process as they pertain to dendritic cells.",True,Antigen-Presenting Cells (APCs),,,,
b4d19c74-daea-46aa-bdb4-0b0d62830f21,https://open.oregonstate.education/microbiology/,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/microbiology/chapter/18-2major-histocompatibility-complexes-and-antigen-presenting-cells/,"After a dendritic cell recognizes and attaches to a pathogen cell, the pathogen is internalized by phagocytosis and is initially contained within a phagosome. Lysosomes containing antimicrobial enzymes and chemicals fuse with the phagosome to create a phagolysosome, where degradation of the pathogen for antigen processing begins. Proteases (protein-degrading) are especially important in antigen processing because only protein antigen epitopes are presented to T cells by MHC II (Figure 14.12).",True,Antigen-Presenting Cells (APCs),Figure 14.12,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.12.png,"Figure 14.12 A dendritic cell phagocytoses a bacterial cell and brings it into a phagosome. Lysosomes fuse with the phagosome to create a phagolysosome, where antimicrobial chemicals and enzymes degrade the bacterial cell. Proteases process bacterial antigens, and the most antigenic epitopes are selected and presented on the cell’s surface in conjunction with MHC II molecules. T cells recognize the presented antigens and are thus activated."
7d9c75de-9e31-4ff0-97dd-a18eccbfa518,https://open.oregonstate.education/microbiology/,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/microbiology/chapter/18-2major-histocompatibility-complexes-and-antigen-presenting-cells/,"APCs do not present all possible epitopes to T cells; only a selection of the most antigenic or immunodominant epitopes are presented. The mechanism by which epitopes are selected for processing and presentation by an APC is complicated and not well understood; however, once the most antigenic, immunodominant epitopes have been processed, they associate within the antigen-binding cleft of MHC II molecules and are translocated to the cell surface of the dendritic cell for presentation to T cells.",True,Antigen-Presenting Cells (APCs),,,,
a38769b8-effa-4a1b-980d-ac4f59b7137a,https://open.oregonstate.education/microbiology/,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/microbiology/chapter/18-2major-histocompatibility-complexes-and-antigen-presenting-cells/,"MHC I molecules, found on all normal, healthy, nucleated cells, signal to the immune system that the cell is a normal “self” cell. In a healthy cell, proteins normally found in the cytoplasm are degraded by proteasomes (enzyme complexes responsible for degradation and processing of proteins) and processed into self-antigen epitopes; these self-antigen epitopes bind within the MHC I antigen-binding cleft and are then presented on the cell surface. Immune cells, such as NK cells, recognize these self-antigens and do not target the cell for destruction. However, if a cell becomes infected with an intracellular pathogen (e.g., a virus), protein antigens specific to the pathogen are processed in the proteasomes and bind with MHC I molecules for presentation on the cell surface. This presentation of pathogen-specific antigens with MHC I signals that the infected cell must be targeted for destruction along with the pathogen.",True,Antigen-Presenting Cells (APCs),,,,
b89987d7-3a88-40b4-a9ba-fad56fdef6a1,https://open.oregonstate.education/microbiology/,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/microbiology/chapter/18-2major-histocompatibility-complexes-and-antigen-presenting-cells/,"Before elimination of infected cells can begin, APCs must first activate the T cells involved in cellular immunity. If an intracellular pathogen directly infects the cytoplasm of an APC, then the processing and presentation of antigens can occur as described (in proteasomes and on the cell surface with MHC I). However, if the intracellular pathogen does not directly infect APCs, an alternative strategy called cross-presentation is utilized. In cross-presentation, antigens are brought into the APC by mechanisms normally leading to presentation with MHC II (i.e., through phagocytosis), but the antigen is presented on an MHC I molecule for CD8 T cells. The exact mechanisms by which cross-presentation occur are not yet well understood, but it appears that cross-presentation is primarily a function of dendritic cells and not macrophages or B cells.",True,Antigen-Presenting Cells (APCs),,,,
622f71c8-8e40-4688-9723-76c91b914ce4,https://open.oregonstate.education/microbiology/,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/microbiology/chapter/18-2major-histocompatibility-complexes-and-antigen-presenting-cells/,"After a dendritic cell recognizes and attaches to a pathogen cell, the pathogen is internalized by phagocytosis and is initially contained within a phagosome. Lysosomes containing antimicrobial enzymes and chemicals fuse with the phagosome to create a phagolysosome, where degradation of the pathogen for antigen processing begins. Proteases (protein-degrading) are especially important in antigen processing because only protein antigen epitopes are presented to T cells by MHC II (Figure 14.12).",True,Antigen-Presenting Cells (APCs),Figure 14.12,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.12.png,"Figure 14.12 A dendritic cell phagocytoses a bacterial cell and brings it into a phagosome. Lysosomes fuse with the phagosome to create a phagolysosome, where antimicrobial chemicals and enzymes degrade the bacterial cell. Proteases process bacterial antigens, and the most antigenic epitopes are selected and presented on the cell’s surface in conjunction with MHC II molecules. T cells recognize the presented antigens and are thus activated."
ebe6a92c-5d7f-460c-b72d-5ddead142440,https://open.oregonstate.education/microbiology/,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/microbiology/chapter/18-2major-histocompatibility-complexes-and-antigen-presenting-cells/,"APCs do not present all possible epitopes to T cells; only a selection of the most antigenic or immunodominant epitopes are presented. The mechanism by which epitopes are selected for processing and presentation by an APC is complicated and not well understood; however, once the most antigenic, immunodominant epitopes have been processed, they associate within the antigen-binding cleft of MHC II molecules and are translocated to the cell surface of the dendritic cell for presentation to T cells.",True,Antigen-Presenting Cells (APCs),,,,
d73cca30-8ddd-44cc-8d22-95cf698b007d,https://open.oregonstate.education/microbiology/,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/microbiology/chapter/18-2major-histocompatibility-complexes-and-antigen-presenting-cells/,"MHC I molecules, found on all normal, healthy, nucleated cells, signal to the immune system that the cell is a normal “self” cell. In a healthy cell, proteins normally found in the cytoplasm are degraded by proteasomes (enzyme complexes responsible for degradation and processing of proteins) and processed into self-antigen epitopes; these self-antigen epitopes bind within the MHC I antigen-binding cleft and are then presented on the cell surface. Immune cells, such as NK cells, recognize these self-antigens and do not target the cell for destruction. However, if a cell becomes infected with an intracellular pathogen (e.g., a virus), protein antigens specific to the pathogen are processed in the proteasomes and bind with MHC I molecules for presentation on the cell surface. This presentation of pathogen-specific antigens with MHC I signals that the infected cell must be targeted for destruction along with the pathogen.",True,Antigen-Presenting Cells (APCs),,,,
43995018-8b4f-44a1-a82b-2e2d0b16a992,https://open.oregonstate.education/microbiology/,14.2	Major Histocompatibility Complexes and Antigen-Presenting Cells,https://open.oregonstate.education/microbiology/chapter/18-2major-histocompatibility-complexes-and-antigen-presenting-cells/,"Before elimination of infected cells can begin, APCs must first activate the T cells involved in cellular immunity. If an intracellular pathogen directly infects the cytoplasm of an APC, then the processing and presentation of antigens can occur as described (in proteasomes and on the cell surface with MHC I). However, if the intracellular pathogen does not directly infect APCs, an alternative strategy called cross-presentation is utilized. In cross-presentation, antigens are brought into the APC by mechanisms normally leading to presentation with MHC II (i.e., through phagocytosis), but the antigen is presented on an MHC I molecule for CD8 T cells. The exact mechanisms by which cross-presentation occur are not yet well understood, but it appears that cross-presentation is primarily a function of dendritic cells and not macrophages or B cells.",True,Antigen-Presenting Cells (APCs),,,,
b7a4aae2-c44a-44ed-a2cf-091073765e36,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Specificity and memory are achieved by essentially programming certain cells involved in the immune response to respond rapidly to subsequent exposures of the pathogen. This programming occurs as a result of the first exposure to a pathogen or vaccine, which triggers a primary response. Subsequent exposures result in a secondary response that is faster and stronger as a result of the body’s memory of the first exposure (Figure 14.2). This secondary response, however, is specific to the pathogen in question. For example, exposure to one virus (e.g., varicella-zoster virus) will not provide protection against other viral diseases (e.g., measles, mumps, or polio).",True,Antigen-Presenting Cells (APCs),Figure 14.2,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.2.png,Figure 14.2 This graph illustrates the primary and secondary immune responses related to antibody production after an initial and secondary exposure to an antigen. Notice that the secondary response is faster and provides a much higher concentration of antibody.
56f2ef39-b213-4f3f-b8fc-99d07cf498fa,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Adaptive specific immunity involves the actions of two distinct cell types: B lymphocytes (B cells) and T lymphocytes (T cells). Although B cells and T cells arise from a common hematopoietic stem cell differentiation pathway, their sites of maturation and their roles in adaptive immunity are very different.",True,Antigen-Presenting Cells (APCs),,,,
5f9303ff-984c-4538-972d-a29c2b1ad008,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"B cells mature in the bone marrow and are responsible for the production of glycoproteins called antibodies, or immunoglobulins. Antibodies are involved in the body’s defense against pathogens and toxins in the extracellular environment. Mechanisms of adaptive specific immunity that involve B cells and antibody production are referred to as humoral immunity. The maturation of T cells occurs in the thymus. T cells function as the central orchestrator of both innate and adaptive immune responses. They are also responsible for destruction of cells infected with intracellular pathogens. The targeting and destruction of intracellular pathogens by T cells is called cell-mediated immunity, or cellular immunity.",True,Antigen-Presenting Cells (APCs),,,,
c3ca212c-f64c-411c-80ed-e0e6631ef98e,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,Antigens,False,Antigens,,,,
5ec85868-08e3-4502-9a8c-27087ffac574,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Activation of the adaptive immune defenses is triggered by pathogen-specific molecular structures called antigens. Antigens are similar to the pathogen-associated molecular patterns (PAMPs) discussed in Pathogen Recognition and Phagocytosis; however, whereas PAMPs are molecular structures found on numerous pathogens, antigens are unique to a specific pathogen. The antigens that stimulate adaptive immunity to chickenpox, for example, are unique to the varicella-zoster virus but significantly different from the antigens associated with other viral pathogens.",True,Antigens,,,,
3f1bd982-7d5b-460c-a8be-3b8d3d42633b,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"The term antigen was initially used to describe molecules that stimulate the production of antibodies; in fact, the term comes from a combination of the words antibody and generator, and a molecule that stimulates antibody production is said to be antigenic. However, the role of antigens is not limited to humoral immunity and the production of antibodies; antigens also play an essential role in stimulating cellular immunity, and for this reason antigens are sometimes more accurately referred to as immunogens. In this text, however, we will typically refer to them as antigens.",True,Antigens,,,,
cd163700-0edb-473a-8886-d121a52368e2,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Pathogens possess a variety of structures that may contain antigens. For example, antigens from bacterial cells may be associated with their capsules, cell walls, fimbriae, flagella, or pili. Bacterial antigens may also be associated with extracellular toxins and enzymes that they secrete. Viruses possess a variety of antigens associated with their capsids, envelopes, and the spike structures they use for attachment to cells.",True,Antigens,,,,
181df80e-a955-4c15-ad80-59b3266e5132,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Antigens may belong to any number of molecular classes, including carbohydrates, lipids, nucleic acids, proteins, and combinations of these molecules. Antigens of different classes vary in their ability to stimulate adaptive immune defenses as well as in the type of response they stimulate (humoral or cellular). The structural complexity of an antigenic molecule is an important factor in its antigenic potential. In general, more complex molecules are more effective as antigens. For example, the three-dimensional complex structure of proteins make them the most effective and potent antigens, capable of stimulating both humoral and cellular immunity. In comparison, carbohydrates are less complex in structure and therefore less effective as antigens; they can only stimulate humoral immune defenses. Lipids and nucleic acids are the least antigenic molecules, and in some cases may only become antigenic when combined with proteins or carbohydrates to form glycolipids, lipoproteins, or nucleoproteins.",True,Antigens,,,,
a61cbbaa-a8a7-4489-9fe7-f5dd9652fad1,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"One reason the three-dimensional complexity of antigens is so important is that antibodies and T cells do not recognize and interact with an entire antigen but with smaller exposed regions on the surface of antigens called epitopes. A single antigen may possess several different epitopes (Figure 14.3), and different antibodies may bind to different epitopes on the same antigen (Figure 14.4). For example, the bacterial flagellum is a large, complex protein structure that can possess hundreds or even thousands of epitopes with unique three-dimensional structures. Moreover, flagella from different bacterial species (or even strains of the same species) contain unique epitopes that can only be bound by specific antibodies.",True,Antigens,Figure 14.3,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.3.png,Figure 14.3 An antigen is a macromolecule that reacts with components of the immune system. A given antigen may contain several motifs that are recognized by immune cells.
0816c193-583e-443d-9c21-b3f0f857457c,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,Antibodies,False,Antibodies,,,,
24f14fde-7fca-4dd6-b436-8098d2d09b1d,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Antibodies (also called immunoglobulins) are glycoproteins that are present in both the blood and tissue fluids. The basic structure of an antibody monomer consists of four protein chains held together by disulfide bonds (Figure 14.5). The two largest chains are identical to each other and are called the heavy chains. The two smaller chains are also identical to each other and are called the light chains. Joined together, the heavy and light chains form a basic Y- shaped structure.",True,Antibodies,Figure 14.5,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.5.png,Figure 14.5 (a) The typical four-chain structure of a generic antibody monomer. (b) The corresponding three- dimensional structure of the antibody IgG. (credit b: modification of work by Tim Vickers)
aede298c-57d0-4dea-9185-8e0008956f3a,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"The two ‘arms’ of the Y-shaped antibody molecule are known as the Fab region, for “fragment of antigen binding.” The far end of the Fab region is the variable region, which serves as the site of antigen binding. The amino acid sequence in the variable region dictates the three-dimensional structure, and thus the specific three-dimensional epitope to which the Fab region is capable of binding. Although the epitope specificity of the Fab regions is identical for each arm of a single antibody molecule, this region displays a high degree of variability between antibodies with different epitope specificities. Binding to the Fab region is necessary for neutralization of pathogens, agglutination or aggregation of pathogens, and antibody-dependent cell-mediated cytotoxicity.",True,Antibodies,,,,
2d5e9474-3034-4682-9c06-ddf6a5958dcb,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"The constant region of an antibody molecule determines its class, or isotype. The five classes of antibodies are IgG, IgM, IgA, IgD, and IgE. Each class possesses unique heavy chains designated by Greek letters γ, μ, α, δ, and ε, respectively. Antibody classes also exhibit important differences in abundance in serum, arrangement, body sites of action, functional roles, and size (Figure 14.6).",True,Antibodies,Figure 14.6,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.6.png,Figure 14.6 Details associated with the different human antibodies or immunoglobulin (Ig) classes.
068b7b0e-2a0f-4923-983a-aeea9efe51ea,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"IgG is a monomer that is by far the most abundant antibody in human blood, accounting for about 80% of total serum antibody. IgG penetrates efficiently into tissue spaces, and is the only antibody class with the ability to cross the placental barrier, providing passive immunity to the developing fetus during pregnancy. IgG is also the most versatile antibody class in terms of its role in the body’s defense against pathogens.",True,Antibodies,,,,
c607bed2-57e7-43d2-aa3e-7bfa1a4a643b,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"IgM is initially produced in a monomeric membrane-bound form that serves as an antigen-binding receptor on B cells. The secreted form of IgM assembles into a pentamer with five monomers of IgM bound together by a protein structure called the J chain. Although the location of the J chain relative to the Fc regions of the five monomers prevents IgM from performing some of the functions of IgG, the ten available Fab sites associated with a pentameric IgM make it an important antibody in the body’s arsenal of defenses. IgM is the first antibody produced and secreted by B cells during the primary and secondary immune responses, making pathogen-specific IgM a valuable diagnostic marker during active or recent infections.",True,Antibodies,,,,
a04ff6c4-851f-4c2b-a238-8448b27f9a44,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"IgA accounts for about 13% of total serum antibody, and secretory IgA is the most common and abundant antibody class found in the mucus secretions that protect the mucous membranes. IgA can also be found in other secretions such as breast milk, tears, and saliva. Secretory IgA is assembled into a dimeric form with two monomers joined by a protein structure called the secretory component. One of the important functions of secretory IgA is to trap pathogens in mucus so that they can later be eliminated from the body.",True,Antibodies,,,,
aacca5a9-d2d9-4f08-9e77-c58082a54f1d,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Similar to IgM, IgD is a membrane-bound monomer found on the surface of B cells, where it serves as an antigen- binding receptor. However, IgD is not secreted by B cells, and only trace amounts are detected in serum. These trace amounts most likely come from the degradation of old B cells and the release of IgD molecules from their cytoplasmic membranes.",True,Antibodies,,,,
30eb7b7e-da24-4d85-a3c6-5da653ff3fec,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"IgE is the least abundant antibody class in serum. Like IgG, it is secreted as a monomer, but its role in adaptive immunity is restricted to anti-parasitic defenses. The Fc region of IgE binds to basophils and mast cells. The Fab region of the bound IgE then interacts with specific antigen epitopes, causing the cells to release potent pro- inflammatory mediators. The inflammatory reaction resulting from the activation of mast cells and basophils aids in the defense against parasites, but this reaction is also central to allergic reactions (see Diseases of the Immune System.)",True,Antibodies,,,,
5c11fe80-bd55-49a1-abfe-a190aae1e0a9,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Different classes of antibody play important roles in the body’s defense against pathogens. These functions include neutralization of pathogens, opsonization for phagocytosis, agglutination, complement activation, and antibody- dependent cell-mediated cytotoxicity. For most of these functions, antibodies also provide an important link between adaptive specific immunity and innate nonspecific immunity.",True,Antibodies,,,,
e6739c2c-eb1e-4e66-8e77-d9b40e5deb80,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Neutralization involves the binding of certain antibodies (IgG, IgM, or IgA) to epitopes on the surface of pathogens or toxins, preventing their attachment to cells. For example, Secretory IgA can bind to specific pathogens and block initial attachment to intestinal mucosal cells. Similarly, specific antibodies can bind to certain toxins, blocking them from attaching to target cells and thus neutralizing their toxic effects. Viruses can be neutralized and prevented from infecting a cell by the same mechanism (Figure 14.7).",True,Antibodies,Figure 14.7,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.7.png,"Figure 14.7 Neutralization involves the binding of specific antibodies to antigens found on bacteria, viruses, and toxins, preventing them from attaching to target cells."
f221debb-9706-481b-8378-9614f914e984,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"As described in Chemical Defenses, opsonization is the coating of a pathogen with molecules, such as complement factors, C-reactive protein, and serum amyloid A, to assist in phagocyte binding to facilitate phagocytosis. IgG antibodies also serve as excellent opsonins, binding their Fab sites to specific epitopes on the surface of pathogens. Phagocytic cells such as macrophages, dendritic cells, and neutrophils have receptors on their surfaces that recognize and bind to the Fc portion of the IgG molecules; thus, IgG helps such phagocytes attach to and engulf the pathogens they have bound (Figure 14.8).",True,Antibodies,Figure 14.8,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.8.png,"Figure 14.8 Antibodies serve as opsonins and inhibit infection by tagging pathogens for destruction by macrophages, dendritic cells, and neutrophils. These phagocytic cells use Fc receptors to bind to IgG-opsonized pathogens and initiate the first step of attachment before phagocytosis."
65cf14d4-4286-4ee3-a55b-cfba5e2e27c7,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Agglutination or aggregation involves the cross-linking of pathogens by antibodies to create large aggregates (Figure 14.9). IgG has two Fab antigen-binding sites, which can bind to two separate pathogen cells, clumping them together. When multiple IgG antibodies are involved, large aggregates can develop; these aggregates are easier for the kidneys and spleen to filter from the blood and easier for phagocytes to ingest for destruction. The pentameric structure of IgM provides ten Fab binding sites per molecule, making it the most efficient antibody for agglutination.",True,Antibodies,Figure 14.9,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.9.png,"Figure 14.9 Antibodies, especially IgM antibodies, agglutinate bacteria by binding to epitopes on two or more bacteria simultaneously. When multiple pathogens and antibodies are present, aggregates form when the binding sites of antibodies bind with separate pathogens."
4df3bf51-26f6-410e-8a14-5129b45370e8,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Another important function of antibodies is activation of the complement cascade. As discussed in the previous chapter, the complement system is an important component of the innate defenses, promoting the inflammatory response, recruiting phagocytes to site of infection, enhancing phagocytosis by opsonization, and killing gram- negative bacterial pathogens with the membrane attack complex (MAC). Complement activation can occur through three different pathways, but the most efficient is the classical pathway, which requires the initial binding of IgG or IgM antibodies to the surface of a pathogen cell, allowing for recruitment and activation of the C1 complex.",True,Antibodies,,,,
eee3fdc0-52b9-4bbe-9b36-af4d93f1146e,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Yet another important function of antibodies is antibody-dependent cell-mediated cytotoxicity (ADCC), which enhances killing of pathogens that are too large to be phagocytosed. This process is best characterized for natural killer cells (NK cells), as shown in Figure 14.10, but it can also involve macrophages and eosinophils. ADCC occurs when the Fab region of an IgG antibody binds to a large pathogen; Fc receptors on effector cells (e.g., NK cells) then bind to the Fc region of the antibody, bringing them into close proximity with the target pathogen. The effector cell then secretes powerful cytotoxins (e.g., perforin and granzymes) that kill the pathogen.",True,Antibodies,Figure 14.10,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.10.png,"Figure 14.10 In this example of ADCC, antibodies bind to a large pathogenic cell that is too big for phagocytosis and then bind to Fc receptors on the membrane of a natural killer cell. This interaction brings the NK cell into close proximity, where it can kill the pathogen through release of lethal extracellular cytotoxins."
f25ad130-e1f2-41da-a0cb-5e505e8490e0,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,Antigens,False,Antigens,,,,
1696a012-7ce1-4327-b0e9-46fc45ffa8ed,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Activation of the adaptive immune defenses is triggered by pathogen-specific molecular structures called antigens. Antigens are similar to the pathogen-associated molecular patterns (PAMPs) discussed in Pathogen Recognition and Phagocytosis; however, whereas PAMPs are molecular structures found on numerous pathogens, antigens are unique to a specific pathogen. The antigens that stimulate adaptive immunity to chickenpox, for example, are unique to the varicella-zoster virus but significantly different from the antigens associated with other viral pathogens.",True,Antigens,,,,
46fcca0f-2a9f-4f23-afbb-69f5ae0582c8,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"The term antigen was initially used to describe molecules that stimulate the production of antibodies; in fact, the term comes from a combination of the words antibody and generator, and a molecule that stimulates antibody production is said to be antigenic. However, the role of antigens is not limited to humoral immunity and the production of antibodies; antigens also play an essential role in stimulating cellular immunity, and for this reason antigens are sometimes more accurately referred to as immunogens. In this text, however, we will typically refer to them as antigens.",True,Antigens,,,,
58f6a900-12c5-475b-9d92-15b0e2eb2dae,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Pathogens possess a variety of structures that may contain antigens. For example, antigens from bacterial cells may be associated with their capsules, cell walls, fimbriae, flagella, or pili. Bacterial antigens may also be associated with extracellular toxins and enzymes that they secrete. Viruses possess a variety of antigens associated with their capsids, envelopes, and the spike structures they use for attachment to cells.",True,Antigens,,,,
0431b1e3-3b30-4734-9505-722a964119ef,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Antigens may belong to any number of molecular classes, including carbohydrates, lipids, nucleic acids, proteins, and combinations of these molecules. Antigens of different classes vary in their ability to stimulate adaptive immune defenses as well as in the type of response they stimulate (humoral or cellular). The structural complexity of an antigenic molecule is an important factor in its antigenic potential. In general, more complex molecules are more effective as antigens. For example, the three-dimensional complex structure of proteins make them the most effective and potent antigens, capable of stimulating both humoral and cellular immunity. In comparison, carbohydrates are less complex in structure and therefore less effective as antigens; they can only stimulate humoral immune defenses. Lipids and nucleic acids are the least antigenic molecules, and in some cases may only become antigenic when combined with proteins or carbohydrates to form glycolipids, lipoproteins, or nucleoproteins.",True,Antigens,,,,
1b8363db-df82-4bfd-bb2f-7ba3b35c0d9a,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"One reason the three-dimensional complexity of antigens is so important is that antibodies and T cells do not recognize and interact with an entire antigen but with smaller exposed regions on the surface of antigens called epitopes. A single antigen may possess several different epitopes (Figure 14.3), and different antibodies may bind to different epitopes on the same antigen (Figure 14.4). For example, the bacterial flagellum is a large, complex protein structure that can possess hundreds or even thousands of epitopes with unique three-dimensional structures. Moreover, flagella from different bacterial species (or even strains of the same species) contain unique epitopes that can only be bound by specific antibodies.",True,Antigens,Figure 14.3,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.3.png,Figure 14.3 An antigen is a macromolecule that reacts with components of the immune system. A given antigen may contain several motifs that are recognized by immune cells.
3a490ba7-e1a5-4528-b286-f5db38624c42,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,Antibodies,False,Antibodies,,,,
f2b668ff-7ae2-48b0-9871-77759c617f06,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Antibodies (also called immunoglobulins) are glycoproteins that are present in both the blood and tissue fluids. The basic structure of an antibody monomer consists of four protein chains held together by disulfide bonds (Figure 14.5). The two largest chains are identical to each other and are called the heavy chains. The two smaller chains are also identical to each other and are called the light chains. Joined together, the heavy and light chains form a basic Y- shaped structure.",True,Antibodies,Figure 14.5,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.5.png,Figure 14.5 (a) The typical four-chain structure of a generic antibody monomer. (b) The corresponding three- dimensional structure of the antibody IgG. (credit b: modification of work by Tim Vickers)
40f9e8d6-c664-47ca-b684-fb1083099a26,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"The two ‘arms’ of the Y-shaped antibody molecule are known as the Fab region, for “fragment of antigen binding.” The far end of the Fab region is the variable region, which serves as the site of antigen binding. The amino acid sequence in the variable region dictates the three-dimensional structure, and thus the specific three-dimensional epitope to which the Fab region is capable of binding. Although the epitope specificity of the Fab regions is identical for each arm of a single antibody molecule, this region displays a high degree of variability between antibodies with different epitope specificities. Binding to the Fab region is necessary for neutralization of pathogens, agglutination or aggregation of pathogens, and antibody-dependent cell-mediated cytotoxicity.",True,Antibodies,,,,
ca1ea862-00ac-4a6e-99ae-3d560563ec00,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"The constant region of an antibody molecule determines its class, or isotype. The five classes of antibodies are IgG, IgM, IgA, IgD, and IgE. Each class possesses unique heavy chains designated by Greek letters γ, μ, α, δ, and ε, respectively. Antibody classes also exhibit important differences in abundance in serum, arrangement, body sites of action, functional roles, and size (Figure 14.6).",True,Antibodies,Figure 14.6,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.6.png,Figure 14.6 Details associated with the different human antibodies or immunoglobulin (Ig) classes.
297ee8bc-35c3-419a-b37b-6d9db2f15c65,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"IgG is a monomer that is by far the most abundant antibody in human blood, accounting for about 80% of total serum antibody. IgG penetrates efficiently into tissue spaces, and is the only antibody class with the ability to cross the placental barrier, providing passive immunity to the developing fetus during pregnancy. IgG is also the most versatile antibody class in terms of its role in the body’s defense against pathogens.",True,Antibodies,,,,
3fc70b01-60eb-4528-8c2f-2c84ed8b7f90,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"IgM is initially produced in a monomeric membrane-bound form that serves as an antigen-binding receptor on B cells. The secreted form of IgM assembles into a pentamer with five monomers of IgM bound together by a protein structure called the J chain. Although the location of the J chain relative to the Fc regions of the five monomers prevents IgM from performing some of the functions of IgG, the ten available Fab sites associated with a pentameric IgM make it an important antibody in the body’s arsenal of defenses. IgM is the first antibody produced and secreted by B cells during the primary and secondary immune responses, making pathogen-specific IgM a valuable diagnostic marker during active or recent infections.",True,Antibodies,,,,
b202a698-282e-4693-ac67-94ed46412dff,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"IgA accounts for about 13% of total serum antibody, and secretory IgA is the most common and abundant antibody class found in the mucus secretions that protect the mucous membranes. IgA can also be found in other secretions such as breast milk, tears, and saliva. Secretory IgA is assembled into a dimeric form with two monomers joined by a protein structure called the secretory component. One of the important functions of secretory IgA is to trap pathogens in mucus so that they can later be eliminated from the body.",True,Antibodies,,,,
2f8485b6-e6a9-461d-a7fe-229e5fdbe02c,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Similar to IgM, IgD is a membrane-bound monomer found on the surface of B cells, where it serves as an antigen- binding receptor. However, IgD is not secreted by B cells, and only trace amounts are detected in serum. These trace amounts most likely come from the degradation of old B cells and the release of IgD molecules from their cytoplasmic membranes.",True,Antibodies,,,,
b96aa1e0-da15-4ccf-8491-0c78696652ea,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"IgE is the least abundant antibody class in serum. Like IgG, it is secreted as a monomer, but its role in adaptive immunity is restricted to anti-parasitic defenses. The Fc region of IgE binds to basophils and mast cells. The Fab region of the bound IgE then interacts with specific antigen epitopes, causing the cells to release potent pro- inflammatory mediators. The inflammatory reaction resulting from the activation of mast cells and basophils aids in the defense against parasites, but this reaction is also central to allergic reactions (see Diseases of the Immune System.)",True,Antibodies,,,,
29bb02f5-6902-4e6f-94b7-1534d6bf12f9,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Neutralization involves the binding of certain antibodies (IgG, IgM, or IgA) to epitopes on the surface of pathogens or toxins, preventing their attachment to cells. For example, Secretory IgA can bind to specific pathogens and block initial attachment to intestinal mucosal cells. Similarly, specific antibodies can bind to certain toxins, blocking them from attaching to target cells and thus neutralizing their toxic effects. Viruses can be neutralized and prevented from infecting a cell by the same mechanism (Figure 14.7).",True,Antibodies,Figure 14.7,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.7.png,"Figure 14.7 Neutralization involves the binding of specific antibodies to antigens found on bacteria, viruses, and toxins, preventing them from attaching to target cells."
16cf64b2-5a0d-4d8d-883e-9db98bfee4ed,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"As described in Chemical Defenses, opsonization is the coating of a pathogen with molecules, such as complement factors, C-reactive protein, and serum amyloid A, to assist in phagocyte binding to facilitate phagocytosis. IgG antibodies also serve as excellent opsonins, binding their Fab sites to specific epitopes on the surface of pathogens. Phagocytic cells such as macrophages, dendritic cells, and neutrophils have receptors on their surfaces that recognize and bind to the Fc portion of the IgG molecules; thus, IgG helps such phagocytes attach to and engulf the pathogens they have bound (Figure 14.8).",True,Antibodies,Figure 14.8,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.8.png,"Figure 14.8 Antibodies serve as opsonins and inhibit infection by tagging pathogens for destruction by macrophages, dendritic cells, and neutrophils. These phagocytic cells use Fc receptors to bind to IgG-opsonized pathogens and initiate the first step of attachment before phagocytosis."
42a10b7b-68bc-40ba-9e14-c5df4b056e66,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Agglutination or aggregation involves the cross-linking of pathogens by antibodies to create large aggregates (Figure 14.9). IgG has two Fab antigen-binding sites, which can bind to two separate pathogen cells, clumping them together. When multiple IgG antibodies are involved, large aggregates can develop; these aggregates are easier for the kidneys and spleen to filter from the blood and easier for phagocytes to ingest for destruction. The pentameric structure of IgM provides ten Fab binding sites per molecule, making it the most efficient antibody for agglutination.",True,Antibodies,Figure 14.9,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.9.png,"Figure 14.9 Antibodies, especially IgM antibodies, agglutinate bacteria by binding to epitopes on two or more bacteria simultaneously. When multiple pathogens and antibodies are present, aggregates form when the binding sites of antibodies bind with separate pathogens."
373eb969-3321-4cc7-8d3c-4ef2b4c7b97d,https://open.oregonstate.education/microbiology/,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/microbiology/chapter/18-1overview-of-specific-adaptive-immunity/,"Yet another important function of antibodies is antibody-dependent cell-mediated cytotoxicity (ADCC), which enhances killing of pathogens that are too large to be phagocytosed. This process is best characterized for natural killer cells (NK cells), as shown in Figure 14.10, but it can also involve macrophages and eosinophils. ADCC occurs when the Fab region of an IgG antibody binds to a large pathogen; Fc receptors on effector cells (e.g., NK cells) then bind to the Fc region of the antibody, bringing them into close proximity with the target pathogen. The effector cell then secretes powerful cytotoxins (e.g., perforin and granzymes) that kill the pathogen.",True,Antibodies,Figure 14.10,14.1	Overview of Specific Adaptive Immunity,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-18.10.png,"Figure 14.10 In this example of ADCC, antibodies bind to a large pathogenic cell that is too big for phagocytosis and then bind to Fc receptors on the membrane of a natural killer cell. This interaction brings the NK cell into close proximity, where it can kill the pathogen through release of lethal extracellular cytotoxins."
39563ec6-6d3d-4198-9cad-878285c99f8b,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,Acute Inflammation,False,Acute Inflammation,,,,
4283bd56-56c8-4e3a-ab19-6aefcbced37d,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,"An early, if not immediate, response to tissue injury is acute inflammation. Immediately following an injury, vasoconstriction of blood vessels will occur to minimize blood loss. The amount of vasoconstriction is related to the amount of vascular injury, but it is usually brief. Vasoconstriction is followed by vasodilation and increased vascular permeability, as a direct result of the release of histamine from resident mast cells. Increased blood flow and vascular permeability can dilute toxins and bacterial products at the site of injury or infection. They also contribute to the five observable signs associated with the inflammatory response: erythema (redness), edema (swelling), heat, pain, and altered function. Vasodilation and increased vascular permeability are also associated with an influx of phagocytes at the site of injury and/or infection. This can enhance the inflammatory response because phagocytes may release proinflammatory chemicals when they are activated by cellular distress signals released from damaged cells. Figure 13.15 illustrates a typical case of acute inflammation at the site of a skin wound.",True,Acute Inflammation,Figure 13.15,13.5	Inflammation and Fever,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.23.png,"Figure 13.15 (a) Mast cells detect injury to nearby cells and release histamine, initiating an inflammatory response. Histamine increases blood flow to the wound site, and increased vascular permeability allows fluid, proteins, phagocytes, and other immune cells to enter infected tissue. These events result in the swelling and reddening of the injured site, and the increased blood flow to the injured site causes it to feel warm. Inflammation is also associated with pain due to these events stimulating nerve pain receptors in the tissue. The interaction of phagocyte PRRs with cellular distress signals and PAMPs and opsonins on the surface of pathogens leads to the release of more proinflammatory chemicals, enhancing the inflammatory response."
b841c01c-b78c-48ed-b73c-3c16e1915aad,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,"During the period of inflammation, the release of bradykinin causes capillaries to remain dilated, flooding tissues with fluids and leading to edema. Increasing numbers of neutrophils are recruited to the area to fight pathogens. As the fight rages on, pus forms from the accumulation of neutrophils, dead cells, tissue fluids, and lymph. Typically, after a few days, macrophages will help to clear out this pus. Eventually, tissue repair can begin in the wounded area.",True,Acute Inflammation,,,,
9cf8fbe4-94df-4be5-ac5d-f186ff3878ac,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,Chronic Inflammation,False,Chronic Inflammation,,,,
26e7f9fc-6d98-4730-98d5-e177c66d7b10,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,"When acute inflammation is unable to clear an infectious pathogen, chronic inflammation may occur. This often results in an ongoing (and sometimes futile) lower-level battle between the host organism and the pathogen. The wounded area may heal at a superficial level, but pathogens may still be present in deeper tissues, stimulating ongoing inflammation. Additionally, chronic inflammation may be involved in the progression of degenerative neurological diseases such as Alzheimer’s and Parkinson’s, heart disease, and metastatic cancer.",True,Chronic Inflammation,,,,
7e6afded-d7ca-4c1e-88da-6b9a714fe4e1,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,"Chronic inflammation may lead to the formation of granulomas, pockets of infected tissue walled off and surrounded by WBCs. Macrophages and other phagocytes wage an unsuccessful battle to eliminate the pathogens and dead cellular materials within a granuloma. One example of a disease that produces chronic inflammation is tuberculosis, which results in the formation of granulomas in lung tissues(Figure 13.16).",True,Chronic Inflammation,Figure 13.16,13.5	Inflammation and Fever,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.24.png,"Figure 13.16 A tubercle is a granuloma in the lung tissue of a patient with tuberculosis. In this micrograph, white blood cells (stained purple) have walled off a pocket of tissue infected with Mycobacterium tuberculosis. Granulomas also occur in many other forms of disease. (credit: modification of work by Piotrowski WJ, Górski P, Duda-Szymańska J, Kwiatkowska S)"
aaadfa60-9cb2-46b4-be29-809c76762429,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,Chronic inflammation is not just associated with bacterial infections. Chronic inflammation can be an important cause of tissue damage from viral infections. The extensive scarring observed with hepatitis C infections and liver cirrhosis is the result of chronic inflammation.,True,Chronic Inflammation,,,,
b6cad2a5-1e2b-4cbd-89a1-dc4814041e49,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,Fever,False,Fever,,,,
8c027389-001b-46d3-9584-489df6fa556d,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,"A fever is an inflammatory response that extends beyond the site of infection and affects the entire body, resulting in an overall increase in body temperature. Body temperature is normally regulated and maintained by the hypothalamus, an anatomical section of the brain that functions to maintain homeostasis in the body. However, certain bacterial or viral infections can result in the production of pyrogens, chemicals that effectively alter the “thermostat setting” of the hypothalamus to elevate body temperature and cause fever. Pyrogens may be exogenous or endogenous.",True,Fever,,,,
1039d673-992b-4537-9e09-db78c914062a,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,"Like other forms of inflammation, a fever enhances the innate immune defenses by stimulating leukocytes to kill pathogens. The rise in body temperature also may inhibit the growth of many pathogens since human pathogens are mesophiles with optimum growth occurring around 35 °C (95 °F). In addition, some studies suggest that fever may also stimulate release of iron-sequestering compounds from the liver, thereby starving out microbes that rely on iron for growth.[1]",True,Fever,,,,
93abe98e-77a2-4493-8c0f-612f5f48cecf,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,"During fever, the skin may appear pale due to vasoconstriction of the blood vessels in the skin, which is mediated by the hypothalamus to divert blood flow away from extremities, minimizing the loss of heat and raising the core temperature. The hypothalamus will also stimulate shivering of muscles, another effective mechanism of generating heat and raising the core temperature.",True,Fever,,,,
aa25dc77-824e-4d29-b8da-b089a04dc574,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,"The crisis phase occurs when the fever breaks. The hypothalamus stimulates vasodilation, resulting in a return of blood flow to the skin and a subsequent release of heat from the body. The hypothalamus also stimulates sweating, which cools the skin as the sweat evaporates.",True,Fever,,,,
e8bc6aaa-ce24-4a2a-88a0-35f3198f398d,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,"Although a low-level fever may help an individual overcome an illness, in some instances, this immune response can be too strong, causing tissue and organ damage and, in severe cases, even death. The inflammatory response to bacterial superantigens is one scenario in which a life-threatening fever may develop. Superantigens are bacterial or viral proteins that can cause an excessive activation of T cells from the specific adaptive immune defense, as well as an excessive release of cytokines that overstimulates the inflammatory response. For example, Staphylococcus aureus and Streptococcus pyogenes are capable of producing superantigens that cause toxic shock syndrome and scarlet fever, respectively. Both of these conditions can be associated with very high, life-threatening fevers in excess of 42 °C (108 °F).",True,Fever,,,,
ae769879-3d17-4bcb-9987-f4fa52130408,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,Chronic Inflammation,False,Chronic Inflammation,,,,
5a2d1cd5-4b72-459a-a558-16413fa229e3,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,"Chronic inflammation may lead to the formation of granulomas, pockets of infected tissue walled off and surrounded by WBCs. Macrophages and other phagocytes wage an unsuccessful battle to eliminate the pathogens and dead cellular materials within a granuloma. One example of a disease that produces chronic inflammation is tuberculosis, which results in the formation of granulomas in lung tissues(Figure 13.16).",True,Chronic Inflammation,Figure 13.16,13.5	Inflammation and Fever,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.24.png,"Figure 13.16 A tubercle is a granuloma in the lung tissue of a patient with tuberculosis. In this micrograph, white blood cells (stained purple) have walled off a pocket of tissue infected with Mycobacterium tuberculosis. Granulomas also occur in many other forms of disease. (credit: modification of work by Piotrowski WJ, Górski P, Duda-Szymańska J, Kwiatkowska S)"
057e3dd1-0162-4301-ac46-3d609a238279,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,Chronic inflammation is not just associated with bacterial infections. Chronic inflammation can be an important cause of tissue damage from viral infections. The extensive scarring observed with hepatitis C infections and liver cirrhosis is the result of chronic inflammation.,True,Chronic Inflammation,,,,
77a1b637-25af-45ca-b0dd-9a9940bfc56d,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,Fever,False,Fever,,,,
e472661c-cfe8-4945-8b62-b6fce6abda7e,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,"A fever is an inflammatory response that extends beyond the site of infection and affects the entire body, resulting in an overall increase in body temperature. Body temperature is normally regulated and maintained by the hypothalamus, an anatomical section of the brain that functions to maintain homeostasis in the body. However, certain bacterial or viral infections can result in the production of pyrogens, chemicals that effectively alter the “thermostat setting” of the hypothalamus to elevate body temperature and cause fever. Pyrogens may be exogenous or endogenous.",True,Fever,,,,
1456fe6b-1c07-428a-a109-ab4b1417c522,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,"Like other forms of inflammation, a fever enhances the innate immune defenses by stimulating leukocytes to kill pathogens. The rise in body temperature also may inhibit the growth of many pathogens since human pathogens are mesophiles with optimum growth occurring around 35 °C (95 °F). In addition, some studies suggest that fever may also stimulate release of iron-sequestering compounds from the liver, thereby starving out microbes that rely on iron for growth.[1]",True,Fever,,,,
912f9351-828a-4a2f-8ddc-9e1f5e2c0865,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,"During fever, the skin may appear pale due to vasoconstriction of the blood vessels in the skin, which is mediated by the hypothalamus to divert blood flow away from extremities, minimizing the loss of heat and raising the core temperature. The hypothalamus will also stimulate shivering of muscles, another effective mechanism of generating heat and raising the core temperature.",True,Fever,,,,
05255c60-6afb-42df-86be-c4044b495c8e,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,"The crisis phase occurs when the fever breaks. The hypothalamus stimulates vasodilation, resulting in a return of blood flow to the skin and a subsequent release of heat from the body. The hypothalamus also stimulates sweating, which cools the skin as the sweat evaporates.",True,Fever,,,,
5a1f5b75-eb52-45d4-8c2c-1fa4fb475635,https://open.oregonstate.education/microbiology/,13.5	Inflammation and Fever,https://open.oregonstate.education/microbiology/chapter/17-5inflammation-and-fever/,"Although a low-level fever may help an individual overcome an illness, in some instances, this immune response can be too strong, causing tissue and organ damage and, in severe cases, even death. The inflammatory response to bacterial superantigens is one scenario in which a life-threatening fever may develop. Superantigens are bacterial or viral proteins that can cause an excessive activation of T cells from the specific adaptive immune defense, as well as an excessive release of cytokines that overstimulates the inflammatory response. For example, Staphylococcus aureus and Streptococcus pyogenes are capable of producing superantigens that cause toxic shock syndrome and scarlet fever, respectively. Both of these conditions can be associated with very high, life-threatening fevers in excess of 42 °C (108 °F).",True,Fever,,,,
4898a24d-414c-40da-a111-f3d33dd2c4c5,https://open.oregonstate.education/microbiology/,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/microbiology/chapter/17-4pathogen-recognition-and-phagocytosis/,Pathogen Recognition,False,Pathogen Recognition,,,,
44779d98-88ed-4465-8167-989862969a2c,https://open.oregonstate.education/microbiology/,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/microbiology/chapter/17-4pathogen-recognition-and-phagocytosis/,"As described in the previous section, opsonization of pathogens by antibody; complement factors C1q, C3b, and C4b; and lectins can assist phagocytic cells in recognition of pathogens and attachment to initiate phagocytosis. However, not all pathogen recognition is opsonin dependent. Phagocytes can also recognize molecular structures that are common to many groups of pathogenic microbes. Such structures are called pathogen-associated molecular patterns (PAMPs). Common PAMPs include the following:",True,Pathogen Recognition,,,,
72bee643-85a8-4cdb-8dac-83404f4ea7c3,https://open.oregonstate.education/microbiology/,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/microbiology/chapter/17-4pathogen-recognition-and-phagocytosis/,"Like numerous other PAMPs, these substances are integral to the structure of broad classes of microbes.",True,Pathogen Recognition,,,,
3009aa37-a353-47a9-bc46-7c79262fbd9e,https://open.oregonstate.education/microbiology/,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/microbiology/chapter/17-4pathogen-recognition-and-phagocytosis/,"The structures that allow phagocytic cells to detect PAMPs are called pattern recognition receptors (PRRs). One group of PRRs is the toll-like receptors (TLRs), which bind to various PAMPs and communicate with the nucleus of the phagocyte to elicit a response. Many TLRs (and other PRRs) are located on the surface of a phagocyte, but some can also be found embedded in the membranes of interior compartments and organelles (Figure 13.13). These interior PRRs can be useful for the binding and recognition of intracellular pathogens that may have gained access to the inside of the cell before phagocytosis could take place. Viral nucleic acids, for example, might encounter an interior PRR, triggering production of the antiviral cytokine interferon.",True,Pathogen Recognition,Figure 13.13,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.20.png,"Figure 13.13 Phagocytic cells contain pattern recognition receptors (PRRs) capable of recognizing various pathogen-associated molecular patterns (PAMPs). These PRRs can be found on the plasma membrane or in internal phagosomes. When a PRR recognizes a PAMP, it sends a signal to the nucleus that activates genes involved in phagocytosis, cellular proliferation, production and secretion of antiviral interferons and proinflammatory cytokines, and enhanced intracellular killing."
0fc3cb1d-219c-42d5-8fde-569c224b1cb9,https://open.oregonstate.education/microbiology/,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/microbiology/chapter/17-4pathogen-recognition-and-phagocytosis/,"In addition to providing the first step of pathogen recognition, the interaction between PAMPs and PRRs on macrophages provides an intracellular signal that activates the phagocyte, causing it to transition from a dormant state of readiness and slow proliferation to a state of hyperactivity, proliferation, production/secretion of cytokines, and enhanced intracellular killing. PRRs on macrophages also respond to chemical distress signals from damaged or stressed cells. This allows macrophages to extend their responses beyond protection from infectious diseases to a broader role in the inflammatory response initiated from injuries or other diseases.",True,Pathogen Recognition,,,,
675f1f34-8cdc-43ac-9a44-712fc3e5bb02,https://open.oregonstate.education/microbiology/,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/microbiology/chapter/17-4pathogen-recognition-and-phagocytosis/,Pathogen Degradation,False,Pathogen Degradation,,,,
83bfc170-b40b-4b21-ae4a-e963283189bd,https://open.oregonstate.education/microbiology/,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/microbiology/chapter/17-4pathogen-recognition-and-phagocytosis/,"Once pathogen recognition and attachment occurs, the pathogen is engulfed in a vesicle and brought into the internal compartment of the phagocyte in a process called phagocytosis (Figure 13.14). PRRs can aid in phagocytosis by first binding to the pathogen’s surface, but phagocytes are also capable of engulfing nearby items even if they are not bound to specific receptors. To engulf the pathogen, the phagocyte forms a pseudopod that wraps around the pathogen and then pinches it off into a membrane vesicle called a phagosome. Acidification of the phagosome (pH decreases to the range of 4–5) provides an important early antibacterial mechanism. The phagosome containing the pathogen fuses with one or more lysosomes, forming a phagolysosome. Formation of the phagolysosome enhances the acidification, which is essential for activation of pH-dependent digestive lysosomal enzymes and production of hydrogen peroxide and toxic reactive oxygen species. Lysosomal enzymes such as lysozyme, phospholipase, and proteases digest the pathogen.",True,Pathogen Degradation,Figure 13.14,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.21.png,"Figure 13.14 The stages of phagocytosis include the engulfment of a pathogen, the formation of a phagosome, the digestion of the pathogenic particle in the phagolysosome, and the expulsion of undigested materials from the cell."
729e87e3-3daa-4e3a-88a8-ff5a1e7bf5dd,https://open.oregonstate.education/microbiology/,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/microbiology/chapter/17-4pathogen-recognition-and-phagocytosis/,"Once degradation is complete, leftover waste products are excreted from the cell in an exocytic vesicle. However, it is important to note that not all remains of the pathogen are excreted as waste. Macrophages and dendritic cells are also antigen-presenting cells involved in the specific adaptive immune response. These cells further process the remains of the degraded pathogen and present key antigens (specific pathogen proteins) on their cellular surface. This is an important step for stimulation of some adaptive immune responses, as will be discussed in more detail in the next chapter.",True,Pathogen Degradation,,,,
773298e4-2191-447c-b459-c6b2e6ee2612,https://open.oregonstate.education/microbiology/,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/microbiology/chapter/17-4pathogen-recognition-and-phagocytosis/,Visit this link (https://openstax.org/l/22phagpathvid) to view a phagocyte chasing and engulfing a pathogen.,True,Pathogen Degradation,,,,
fbe75fc8-57d1-436a-abb8-d00294f3ccf6,https://open.oregonstate.education/microbiology/,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/microbiology/chapter/17-4pathogen-recognition-and-phagocytosis/,Pathogen Recognition,False,Pathogen Recognition,,,,
7545dc14-e209-42c5-94b4-b11bbd020279,https://open.oregonstate.education/microbiology/,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/microbiology/chapter/17-4pathogen-recognition-and-phagocytosis/,"Like numerous other PAMPs, these substances are integral to the structure of broad classes of microbes.",True,Pathogen Recognition,,,,
0b6741fa-e8cf-4710-bd58-688c36219495,https://open.oregonstate.education/microbiology/,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/microbiology/chapter/17-4pathogen-recognition-and-phagocytosis/,"The structures that allow phagocytic cells to detect PAMPs are called pattern recognition receptors (PRRs). One group of PRRs is the toll-like receptors (TLRs), which bind to various PAMPs and communicate with the nucleus of the phagocyte to elicit a response. Many TLRs (and other PRRs) are located on the surface of a phagocyte, but some can also be found embedded in the membranes of interior compartments and organelles (Figure 13.13). These interior PRRs can be useful for the binding and recognition of intracellular pathogens that may have gained access to the inside of the cell before phagocytosis could take place. Viral nucleic acids, for example, might encounter an interior PRR, triggering production of the antiviral cytokine interferon.",True,Pathogen Recognition,Figure 13.13,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.20.png,"Figure 13.13 Phagocytic cells contain pattern recognition receptors (PRRs) capable of recognizing various pathogen-associated molecular patterns (PAMPs). These PRRs can be found on the plasma membrane or in internal phagosomes. When a PRR recognizes a PAMP, it sends a signal to the nucleus that activates genes involved in phagocytosis, cellular proliferation, production and secretion of antiviral interferons and proinflammatory cytokines, and enhanced intracellular killing."
c02343e1-e299-4ede-b3d6-3e620aff563d,https://open.oregonstate.education/microbiology/,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/microbiology/chapter/17-4pathogen-recognition-and-phagocytosis/,"In addition to providing the first step of pathogen recognition, the interaction between PAMPs and PRRs on macrophages provides an intracellular signal that activates the phagocyte, causing it to transition from a dormant state of readiness and slow proliferation to a state of hyperactivity, proliferation, production/secretion of cytokines, and enhanced intracellular killing. PRRs on macrophages also respond to chemical distress signals from damaged or stressed cells. This allows macrophages to extend their responses beyond protection from infectious diseases to a broader role in the inflammatory response initiated from injuries or other diseases.",True,Pathogen Recognition,,,,
d4d73ad3-ba95-431b-88ac-833e24780652,https://open.oregonstate.education/microbiology/,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/microbiology/chapter/17-4pathogen-recognition-and-phagocytosis/,Pathogen Degradation,False,Pathogen Degradation,,,,
b92af9c9-a7ba-4df8-88dd-4182d3063343,https://open.oregonstate.education/microbiology/,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/microbiology/chapter/17-4pathogen-recognition-and-phagocytosis/,"Once pathogen recognition and attachment occurs, the pathogen is engulfed in a vesicle and brought into the internal compartment of the phagocyte in a process called phagocytosis (Figure 13.14). PRRs can aid in phagocytosis by first binding to the pathogen’s surface, but phagocytes are also capable of engulfing nearby items even if they are not bound to specific receptors. To engulf the pathogen, the phagocyte forms a pseudopod that wraps around the pathogen and then pinches it off into a membrane vesicle called a phagosome. Acidification of the phagosome (pH decreases to the range of 4–5) provides an important early antibacterial mechanism. The phagosome containing the pathogen fuses with one or more lysosomes, forming a phagolysosome. Formation of the phagolysosome enhances the acidification, which is essential for activation of pH-dependent digestive lysosomal enzymes and production of hydrogen peroxide and toxic reactive oxygen species. Lysosomal enzymes such as lysozyme, phospholipase, and proteases digest the pathogen.",True,Pathogen Degradation,Figure 13.14,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.21.png,"Figure 13.14 The stages of phagocytosis include the engulfment of a pathogen, the formation of a phagosome, the digestion of the pathogenic particle in the phagolysosome, and the expulsion of undigested materials from the cell."
39960d78-66b3-4661-bb54-e83b40e5e339,https://open.oregonstate.education/microbiology/,13.4	Pathogen Recognition and Phagocytosis,https://open.oregonstate.education/microbiology/chapter/17-4pathogen-recognition-and-phagocytosis/,"Once degradation is complete, leftover waste products are excreted from the cell in an exocytic vesicle. However, it is important to note that not all remains of the pathogen are excreted as waste. Macrophages and dendritic cells are also antigen-presenting cells involved in the specific adaptive immune response. These cells further process the remains of the degraded pathogen and present key antigens (specific pathogen proteins) on their cellular surface. This is an important step for stimulation of some adaptive immune responses, as will be discussed in more detail in the next chapter.",True,Pathogen Degradation,,,,
2220333a-cae3-4ef9-ab4b-8b41ff3bf332,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"Red blood cells are primarily responsible for carrying oxygen to tissues. Platelets are cellular fragments that participate in blood clot formation and tissue repair. Several different types of WBCs participate in various nonspecific mechanisms of innate and adaptive immunity. In this section, we will focus primarily on the innate mechanisms of various types of WBCs.",True,Pathogen Degradation,,,,
b889c7e2-d364-4d09-8131-1be169480fc8,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,Hematopoiesis,False,Hematopoiesis,,,,
71b2bf7a-59e0-46c1-8571-66fbbbe3811c,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"All of the formed elements of blood are derived from pluripotent hematopoietic stem cells (HSCs) in the bone marrow. As the HSCs make copies of themselves in the bone marrow, individual cells receive different cues from the body that control how they develop and mature. As a result, the HSCs differentiate into different types of blood cells that, once mature, circulate in peripheral blood. This process of differentiation, called hematopoiesis, is shown in more detail in Figure 13.9.",True,Hematopoiesis,Figure 13.9,13.3	Cellular Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.12.png,Figure 13.9 All the formed elements of the blood arise by differentiation of hematopoietic stem cells in the bone marrow.
5fff6d9b-c4d0-4d0c-ace7-6fbcdad43fb2,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"In terms of sheer numbers, the vast majority of HSCs become erythrocytes. Much smaller numbers become leukocytes and platelets. Leukocytes can be further subdivided into granulocytes, which are characterized by numerous granules visible in the cytoplasm, and agranulocytes, which lack granules.",True,Hematopoiesis,,,,
45f8df2d-e504-49fe-ab3c-9ea089d066f3,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,Granulocytes,False,Granulocytes,,,,
badf5f46-2f05-4353-b83c-825d2a5f47d4,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,Neutrophils (PMNs),False,Neutrophils (PMNs),,,,
f39dd455-cd5e-41f8-ad82-723dfb48d565,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"Neutrophils (PMNs) are frequently involved in the elimination and destruction of extracellular bacteria. They are capable of migrating through the walls of blood vessels to areas of bacterial infection and tissue damage, where they seek out and kill infectious bacteria. PMN granules contain a variety of defensins and hydrolytic enzymes that help them destroy bacteria through phagocytosis (described in more detail in Pathogen Recognition and Phagocytosis) In addition, when many neutrophils are brought into an infected area, they can be stimulated to release toxic molecules into the surrounding tissue to better clear infectious agents. This is called degranulation.",True,Neutrophils (PMNs),,,,
33ec7fe6-bf8a-4056-968a-6316370f2326,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"As neutrophils fight an infection, a visible accumulation of leukocytes, cellular debris, and bacteria at the site of infection can be observed. This buildup is what we call pus (also known as purulent or suppurative discharge or drainage). The presence of pus is a sign that the immune defenses have been activated against an infection; historically, some physicians believed that inducing pus formation could actually promote the healing of wounds. The practice of promoting “laudable pus” (by, for instance, wrapping a wound in greasy wool soaked in wine) dates back to the ancient physician Galen in the 2nd century AD, and was practiced in variant forms until the 17th century (though it was not universally accepted). Today, this method is no longer practiced because we now know that it is not effective. Although a small amount of pus formation can indicate a strong immune response, artificially inducing pus formation does not promote recovery.",True,Neutrophils (PMNs),,,,
1953807f-87d3-47ad-b86b-7d86a4c40df1,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,Eosinophils,False,Eosinophils,,,,
fec3cf99-b7e6-472c-9508-69b79a1882a3,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,Basophils,False,Basophils,,,,
537a22f5-8063-40b1-8d4f-34f116750dc6,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"Basophils have cytoplasmic granules of varied size and are named for their granules’ ability to absorb the basic dye methylene blue (Figure 13.10). Their stimulation and degranulation can result from multiple triggering events. This cell type is important in allergic reactions and other responses that involve inflammation. One of the most abundant components of basophil granules is histamine, which is released along with other chemical factors when the basophil is stimulated. These chemicals can be chemotactic and can help to open the gaps between cells in the blood vessels.",True,Basophils,Figure 13.10,13.3	Cellular Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.14.png,Figure 13.10 Granulocytes can be distinguished by the number of lobes in their nuclei and the staining properties of their granules. (credit “neutrophil” micrograph: modification of work by Ed Uthman)
c5e97724-6cad-48a5-88ce-45b592a9ac8f,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,Mast Cells,False,Mast Cells,,,,
542d10b6-5c71-4340-a3d7-37fa6da00bf9,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"Hematopoiesis also gives rise to mast cells, which appear to be derived from the same common myeloid progenitor cell as neutrophils, eosinophils, and basophils. Functionally, mast cells are very similar to basophils, containing many of the same components in their granules (e.g., histamine) and playing a similar role in allergic responses and other inflammatory reactions. However, unlike basophils, mast cells leave the circulating blood and are most frequently found residing in tissues. They are often associated with blood vessels and nerves or found close to surfaces that interface with the external environment, such as the skin and mucous membranes in various regions of the body (Figure 13.11).",True,Mast Cells,Figure 13.11,13.3	Cellular Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.15.png,"Figure 13.11 Mast cells function similarly to basophils by inducing and promoting inflammatory responses. (a) This figure shows mast cells in blood. In a blood smear, they are difficult to differentiate from basophils (b). Unlike basophils, mast cells migrate from the blood into various tissues. (credit right: modification of work by Greenland JR, Xu X, Sayah DM, Liu FC, Jones KD, Looney MR, Caughey GH)"
0b401db7-b8a0-4848-a00e-57040d02e391,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,Agranulocytes,False,Agranulocytes,,,,
c057cd21-9915-4d3c-98ea-06203333e66e,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"As their name suggests, agranulocytes lack visible granules in the cytoplasm. Agranulocytes can be categorized as lymphocytes or monocytes. Among the lymphocytes are natural killer cells, which play an important role in nonspecific innate immune defenses. Lymphocytes also include the B cells and T cells, which are discussed in the next chapter because they are central players in the specific adaptive immune defenses. The monocytes differentiate into macrophages and dendritic cells, which are collectively referred to as the mononuclear phagocyte system.",True,Agranulocytes,,,,
2d3b2426-6651-4efa-8496-114cbf661042,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,Natural Killer Cells,False,Natural Killer Cells,,,,
f674f952-7595-4042-af7d-aa7dabef33f1,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"Most lymphocytes are primarily involved in the specific adaptive immune response, and thus will be discussed in the following chapter. An exception is the natural killer cells (NK cells); these mononuclear lymphocytes use nonspecific mechanisms to recognize and destroy cells that are abnormal in some way. Cancer cells and cells infected with viruses are two examples of cellular abnormalities that are targeted by NK cells. Recognition of such cells involves a complex process of identifying inhibitory and activating molecular markers on the surface of the target cell.",True,Natural Killer Cells,,,,
c99753a1-59e6-4bff-9d67-3290a675bf75,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,Monocytes,False,Monocytes,,,,
2778ce93-6863-43b2-91d2-a0925fe7c1ed,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"The largest of the white blood cells, monocytes have a nucleus that lacks lobes, and they also lack granules in the cytoplasm (Figure 13.12). Nevertheless, they are effective phagocytes, engulfing pathogens and apoptotic cells to help fight infection.",True,Monocytes,Figure 13.12,13.3	Cellular Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.18.png,"Figure 13.12 Monocytes are large, agranular white blood cells with a nucleus that lacks lobes. When monocytes leave the bloodstream, they differentiate and become macrophages with tissue-specific properties. (credit left: modification of work by Armed Forces Institute of Pathology; credit right: modification of work by Centers for Disease Control and Prevention)"
44e809f7-fea7-4fc0-9b6d-295966d9c6f0,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"When monocytes leave the bloodstream and enter a specific body tissue, they differentiate into tissue-specific phagocytes called macrophages and dendritic cells. Macrophages and dendritic cells can reside in body tissues for significant lengths of time. Macrophages in specific body tissues develop characteristics suited to the particular tissue. Not only do they provide immune protection for the tissue in which they reside but they also support normal function of their neighboring tissue cells through the production of cytokines. Dendritic cells are important sentinels residing in the skin and mucous membranes, which are portals of entry for many pathogens. Monocytes, macrophages, and dendritic cells are all highly phagocytic and important promoters of the immune response through their production and release of cytokines. These cells provide an essential bridge between innate and adaptive immune responses, as discussed in the next section as well as the next chapter.",True,Monocytes,,,,
4dfed4c8-6f5a-48ec-8365-1fb5c28bb412,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,Granulocytes,False,Granulocytes,,,,
1bd0c97e-1407-4c7b-b82f-2f1a984b066b,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"As neutrophils fight an infection, a visible accumulation of leukocytes, cellular debris, and bacteria at the site of infection can be observed. This buildup is what we call pus (also known as purulent or suppurative discharge or drainage). The presence of pus is a sign that the immune defenses have been activated against an infection; historically, some physicians believed that inducing pus formation could actually promote the healing of wounds. The practice of promoting “laudable pus” (by, for instance, wrapping a wound in greasy wool soaked in wine) dates back to the ancient physician Galen in the 2nd century AD, and was practiced in variant forms until the 17th century (though it was not universally accepted). Today, this method is no longer practiced because we now know that it is not effective. Although a small amount of pus formation can indicate a strong immune response, artificially inducing pus formation does not promote recovery.",True,Granulocytes,,,,
f322b3f3-c205-4600-be62-e4fac92ad24d,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"Basophils have cytoplasmic granules of varied size and are named for their granules’ ability to absorb the basic dye methylene blue (Figure 13.10). Their stimulation and degranulation can result from multiple triggering events. This cell type is important in allergic reactions and other responses that involve inflammation. One of the most abundant components of basophil granules is histamine, which is released along with other chemical factors when the basophil is stimulated. These chemicals can be chemotactic and can help to open the gaps between cells in the blood vessels.",True,Granulocytes,Figure 13.10,13.3	Cellular Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.14.png,Figure 13.10 Granulocytes can be distinguished by the number of lobes in their nuclei and the staining properties of their granules. (credit “neutrophil” micrograph: modification of work by Ed Uthman)
e961bce8-ee62-4403-b2d2-0eedf70c8745,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"Hematopoiesis also gives rise to mast cells, which appear to be derived from the same common myeloid progenitor cell as neutrophils, eosinophils, and basophils. Functionally, mast cells are very similar to basophils, containing many of the same components in their granules (e.g., histamine) and playing a similar role in allergic responses and other inflammatory reactions. However, unlike basophils, mast cells leave the circulating blood and are most frequently found residing in tissues. They are often associated with blood vessels and nerves or found close to surfaces that interface with the external environment, such as the skin and mucous membranes in various regions of the body (Figure 13.11).",True,Granulocytes,Figure 13.11,13.3	Cellular Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.15.png,"Figure 13.11 Mast cells function similarly to basophils by inducing and promoting inflammatory responses. (a) This figure shows mast cells in blood. In a blood smear, they are difficult to differentiate from basophils (b). Unlike basophils, mast cells migrate from the blood into various tissues. (credit right: modification of work by Greenland JR, Xu X, Sayah DM, Liu FC, Jones KD, Looney MR, Caughey GH)"
6e6c42a9-593e-416d-9aab-f16bee565173,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,Agranulocytes,False,Agranulocytes,,,,
88af6db4-ac7c-4734-bbc8-d20b370f5979,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"As their name suggests, agranulocytes lack visible granules in the cytoplasm. Agranulocytes can be categorized as lymphocytes or monocytes. Among the lymphocytes are natural killer cells, which play an important role in nonspecific innate immune defenses. Lymphocytes also include the B cells and T cells, which are discussed in the next chapter because they are central players in the specific adaptive immune defenses. The monocytes differentiate into macrophages and dendritic cells, which are collectively referred to as the mononuclear phagocyte system.",True,Agranulocytes,,,,
3c9b7c00-1f3e-4218-8fbc-0e06bde34ae8,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"Most lymphocytes are primarily involved in the specific adaptive immune response, and thus will be discussed in the following chapter. An exception is the natural killer cells (NK cells); these mononuclear lymphocytes use nonspecific mechanisms to recognize and destroy cells that are abnormal in some way. Cancer cells and cells infected with viruses are two examples of cellular abnormalities that are targeted by NK cells. Recognition of such cells involves a complex process of identifying inhibitory and activating molecular markers on the surface of the target cell.",True,Agranulocytes,,,,
11433aa7-7eee-4ee4-84b9-f8e09adc91fd,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"The largest of the white blood cells, monocytes have a nucleus that lacks lobes, and they also lack granules in the cytoplasm (Figure 13.12). Nevertheless, they are effective phagocytes, engulfing pathogens and apoptotic cells to help fight infection.",True,Agranulocytes,Figure 13.12,13.3	Cellular Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.18.png,"Figure 13.12 Monocytes are large, agranular white blood cells with a nucleus that lacks lobes. When monocytes leave the bloodstream, they differentiate and become macrophages with tissue-specific properties. (credit left: modification of work by Armed Forces Institute of Pathology; credit right: modification of work by Centers for Disease Control and Prevention)"
fc9dac64-47cd-47cf-85a2-cfcb13add689,https://open.oregonstate.education/microbiology/,13.3	Cellular Defenses,https://open.oregonstate.education/microbiology/chapter/17-3cellular-defenses/,"When monocytes leave the bloodstream and enter a specific body tissue, they differentiate into tissue-specific phagocytes called macrophages and dendritic cells. Macrophages and dendritic cells can reside in body tissues for significant lengths of time. Macrophages in specific body tissues develop characteristics suited to the particular tissue. Not only do they provide immune protection for the tissue in which they reside but they also support normal function of their neighboring tissue cells through the production of cytokines. Dendritic cells are important sentinels residing in the skin and mucous membranes, which are portals of entry for many pathogens. Monocytes, macrophages, and dendritic cells are all highly phagocytic and important promoters of the immune response through their production and release of cytokines. These cells provide an essential bridge between innate and adaptive immune responses, as discussed in the next section as well as the next chapter.",True,Agranulocytes,,,,
204676af-af69-48ac-988c-667ebe153a13,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Some chemical mediators are endogenously produced, meaning they are produced by human body cells; others are produced exogenously, meaning that they are produced by certain microbes that are part of the microbiome. Some mediators are produced continually, bathing the area in the antimicrobial substance; others are produced or activated primarily in response to some stimulus, such as the presence of microbes.",True,Agranulocytes,,,,
7f02529c-f025-47a7-82a2-eb559688f61f,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,Chemical and Enzymatic Mediators Found in Body Fluids,False,Chemical and Enzymatic Mediators Found in Body Fluids,,,,
a7890eb0-f2ef-4fa9-a700-ab411b3cf6ca,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Fluids produced by the skin include examples of both endogenous and exogenous mediators. Sebaceous glands in the dermis secrete an oil called sebum that is released onto the skin surface through hair follicles. This sebum provides an additional layer of defense by helping seal off the pore of the hair follicle, preventing bacteria on the skin’s surface from invading sweat glands and surrounding tissue (Figure 13.7). Certain members of the microbiome can use lipase enzymes to degrade sebum, using it as a food source. This produces oleic acid, which creates a mildly acidic environment on the surface of the skin that is inhospitable to many pathogenic microbes. Oleic acid is an example of an exogenously produced mediator because it is produced by resident microbes and not directly by body cells.",True,Chemical and Enzymatic Mediators Found in Body Fluids,Figure 13.7,13.2	Chemical Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.8.png,"Figure 13.7 Sebaceous glands secrete sebum, a chemical mediator that lubricates and protect the skin from invading microbes. Sebum is also a food source for resident microbes that produce oleic acid, an exogenously produced mediator. (credit micrograph: Micrograph provided by the Regents of University of Michigan Medical School © 2012)"
feb095a5-c39e-4356-8f76-e7ac904fcc1d,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Environmental factors that affect the microbiota of the skin can have a direct impact on the production of chemical mediators. Low humidity or decreased sebum production, for example, could make the skin less habitable for microbes that produce oleic acid, thus making the skin more susceptible to pathogens normally inhibited by the skin’s low pH. Many skin moisturizers are formulated to counter such effects by restoring moisture and essential oils to the skin.",True,Chemical and Enzymatic Mediators Found in Body Fluids,,,,
53dd74a0-a924-47c5-ab84-ad45c22cd952,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"The digestive tract also produces a large number of chemical mediators that inhibit or kill microbes. In the oral cavity, saliva contains mediators such as lactoperoxidase enzymes, and mucus secreted by the esophagus contains the antibacterial enzyme lysozyme. In the stomach, highly acidic gastric fluid kills most microbes. In the lower digestive tract, the intestines have pancreatic and intestinal enzymes, antibacterial peptides, bile produced from the liver, and specialized Paneth cells that produce lysozyme. Together, these mediators are able to eliminate most pathogens that manage to survive the acidic environment of the stomach.",True,Chemical and Enzymatic Mediators Found in Body Fluids,,,,
27d551fe-8333-4433-8672-f0e1ed8d0d08,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"In the urinary tract, urine flushes microbes out of the body during urination. Furthermore, the slight acidity of urine (the average pH is about 6) inhibits the growth of many microbes and potential pathogens in the urinary tract.",True,Chemical and Enzymatic Mediators Found in Body Fluids,,,,
61482697-cd21-4047-9f7e-b96d1ad33964,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"The female reproductive system employs lactate, an exogenously produced chemical mediator, to inhibit microbial growth. The cells and tissue layers composing the vagina produce glycogen, a branched and more complex polymer of glucose. Lactobacilli in the area ferment glycogen to produce lactate, lowering the pH in the vagina and inhibiting transient microbiota, opportunistic pathogens like Candida (a yeast associated with vaginal infections), and other pathogens responsible for sexually transmitted diseases.",True,Chemical and Enzymatic Mediators Found in Body Fluids,,,,
05627c9d-767b-4b65-8f8b-57defb9fecac,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"In the eyes, tears contain the chemical mediators lysozyme and lactoferrin, both of which are capable of eliminating microbes that have found their way to the surface of the eyes. Lysozyme cleaves the bond between NAG and NAM in peptidoglycan, a component of the cell wall in bacteria. It is more effective against gram-positive bacteria, which lack the protective outer membrane associated with gram-negative bacteria. Lactoferrin inhibits microbial growth by chemically binding and sequestering iron. This effectually starves many microbes that require iron for growth.",True,Chemical and Enzymatic Mediators Found in Body Fluids,,,,
b674ad4b-8795-4cb4-ac76-b36dd7f775f3,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"In the ears, cerumen (earwax) exhibits antimicrobial properties due to the presence of fatty acids, which lower the pH to between 3 and 5.",True,Chemical and Enzymatic Mediators Found in Body Fluids,,,,
24ebf443-fd60-4ccb-80f6-452c0da9a5a1,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"The respiratory tract uses various chemical mediators in the nasal passages, trachea, and lungs. The mucus produced in the nasal passages contains a mix of antimicrobial molecules similar to those found in tears and saliva (e.g., lysozyme, lactoferrin, lactoperoxidase). Secretions in the trachea and lungs also contain lysozyme and lactoferrin, as well as a diverse group of additional chemical mediators, such as the lipoprotein complex called surfactant, which has antibacterial properties.",True,Chemical and Enzymatic Mediators Found in Body Fluids,,,,
ee2c684d-ce1d-480e-a0be-6a5d5b2efb14,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,Antimicrobial Peptides,False,Antimicrobial Peptides,,,,
0e9c7476-0e47-459e-a008-a03dd1a63f95,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"AMPs may induce cell damage in microorganisms in a variety of ways, including by inflicting damage to membranes, destroying DNA and RNA, or interfering with cell-wall synthesis. Depending on the specific antimicrobial mechanism, a particular AMP may inhibit only certain groups of microbes (e.g., gram-positive or gram-negative bacteria) or it may be more broadly effective against bacteria, fungi, protozoa, and viruses. Many AMPs are found on the skin, but they can also be found in other regions of the body.",True,Antimicrobial Peptides,,,,
53983708-7c5a-40f0-86e2-832010ae629d,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,A family of AMPs called defensins can be produced by epithelial cells throughout the body as well as by cellular defenses such as macrophages and neutrophils. Defensins may be secreted or act inside host cells; they combat microorganisms by damaging their plasma membranes. AMPs called bacteriocins are produced exogenously by certain members of the resident microbiota within the gastrointestinal tract.,True,Antimicrobial Peptides,,,,
c7ee4a2c-980d-4600-a3e4-768cdefd778d,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,Plasma Protein Mediators,False,Plasma Protein Mediators,,,,
ef59967f-ca4d-45d1-b1a3-d88188ccad06,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Many nonspecific innate immune factors are found in plasma, the fluid portion of blood. Plasma contains electrolytes, sugars, lipids, and proteins, each of which helps to maintain homeostasis (i.e., stable internal body functioning), and contains the proteins involved in the clotting of blood. Additional proteins found in blood plasma, such as acute-phase proteins, complement proteins, and cytokines, are involved in the nonspecific innate immune response.",True,Plasma Protein Mediators,,,,
6898a4c7-7625-4e41-b6ba-6606ae05330b,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,The acute-phase proteins are another class of antimicrobial mediators. Acute-phase proteins are primarily produced in the liver and secreted into the blood in response to inflammatory molecules from the immune system.,True,Plasma Protein Mediators,,,,
a60a56ad-899f-417d-be2c-2a73630bf315,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,The Complement System,False,The Complement System,,,,
025a017b-2bd6-40f8-b5f4-fa442977ac0c,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"The complement system is a group of plasma protein mediators that can act as an innate nonspecific defense while also serving to connect innate and adaptive immunity (discussed in the next chapter). The complement system is composed of more than 30 proteins that normally circulate as precursor proteins in blood. These precursor proteins become activated when stimulated or triggered by a variety of factors, including the presence of microorganisms. Complement proteins are considered part of innate nonspecific immunity because they are always present in the blood and tissue fluids, allowing them to be activated quickly.",True,The Complement System,,,,
e34ae6b4-460d-4a7b-a2f2-640c00ddc091,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,Cytokines,False,Cytokines,,,,
ed74c85a-e838-439b-9633-31446421a8c8,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Cytokines are soluble proteins that act as communication signals between cells. In a nonspecific innate immune response, various cytokines may be released to stimulate production of chemical mediators or other cell functions, such as cell proliferation, cell differentiation, inhibition of cell division, apoptosis, and chemotaxis.",True,Cytokines,,,,
a0abfc08-7cf1-4dcc-bc1c-894b8230365c,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Three important classes of cytokines are the interleukins, chemokines, and interferons. The interleukins were originally thought to be produced only by leukocytes (white blood cells) and to only stimulate leukocytes, thus the reasons for their name. Although interleukins are involved in modulating almost every function of the immune system, their role in the body is not restricted to immunity. Interleukins are also produced by and stimulate a variety of cells unrelated to immune defenses.",True,Cytokines,,,,
ed8e020a-625c-4b9e-b1a7-f7386f9dc2c8,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"The chemokines are chemotactic factors that recruit leukocytes to sites of infection, tissue damage, and inflammation. In contrast to more general chemotactic factors, like complement factor C5a, chemokines are very specific in the subsets of leukocytes they recruit.",True,Cytokines,,,,
ca6937c5-ec3c-48ad-a22c-4df1c506aa51,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Interferons are a diverse group of immune signaling molecules and are especially important in our defense against viruses. Type I interferons (interferon-α and interferon-β) are produced and released by cells infected with virus. These interferons stimulate nearby cells to stop production of mRNA, destroy RNA already produced, and reduce protein synthesis. These cellular changes inhibit viral replication and production of mature virus, slowing the spread of the virus. Type I interferons also stimulate various immune cells involved in viral clearance to more aggressively attack virus-infected cells. Type II interferon (interferon-γ) is an important activator of immune cells (Figure 13.8).",True,Cytokines,Figure 13.8,13.2	Chemical Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.11.png,"Figure 13.8 Interferons are cytokines released by a cell infected with a virus. Interferon-α and interferon-β signal uninfected neighboring cells to inhibit mRNA synthesis, destroy RNA, and reduce protein synthesis (top arrow).Interferon-α and interferon-β also promote apoptosis in cells infected with the virus (middle arrow). Interferon-γ alerts neighboring immune cells to an attack (bottom arrow). Although interferons do not cure the cell releasing them or other infected cells, which will soon die, their release may prevent additional cells from becoming infected, thus stemming the infection."
52e27347-8616-41d0-85e1-1a1bcf1cbe1b,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,Inflammation-Eliciting Mediators,False,Inflammation-Eliciting Mediators,,,,
18514fda-fde9-4416-b423-d0fdcf0f5b0a,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Many of the chemical mediators discussed in this section contribute in some way to inflammation and fever, which are nonspecific immune responses discussed in more detail in Inflammation and Fever. Cytokines stimulate the production of acute-phase proteins, which act as opsonins, activating complement cascades through the lectin pathway.",True,Inflammation-Eliciting Mediators,,,,
111673f6-b595-4be9-90ea-c5a0e27d059b,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Some cytokines also bind mast cells and basophils, inducing them to release histamine, a proinflammatory compound. Histamine receptors are found on a variety of cells and mediate proinflammatory events, such as bronchoconstriction (tightening of the airways) and smooth muscle contraction.",True,Inflammation-Eliciting Mediators,,,,
54e4ad08-2f63-418c-a7aa-c0e19c95eab7,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Certain cytokines also stimulate the production of prostaglandins, chemical mediators that promote the inflammatory effects of kinins and histamines. Prostaglandins can also help to set the body temperature higher, leading to fever, which promotes the activities of white blood cells and slightly inhibits the growth of pathogenic microbes (see Inflammation and Fever).",True,Inflammation-Eliciting Mediators,,,,
1672bdd9-e29f-42f9-b665-74ec75626065,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Another inflammatory mediator, bradykinin, contributes to edema, which occurs when fluids and leukocytes leak out of the bloodstream and into tissues. It binds to receptors on cells in the capillary walls, causing the capillaries to dilate and become more permeable to fluids.",True,Inflammation-Eliciting Mediators,,,,
9cbf1c5a-2b2e-4bdf-be06-11c45deee038,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,Table 13.3 provides a summary of the chemical defenses discussed in this section.,True,Inflammation-Eliciting Mediators,,,,
e25cf8c9-0e3f-4ec3-99e2-79753e066c8b,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"The digestive tract also produces a large number of chemical mediators that inhibit or kill microbes. In the oral cavity, saliva contains mediators such as lactoperoxidase enzymes, and mucus secreted by the esophagus contains the antibacterial enzyme lysozyme. In the stomach, highly acidic gastric fluid kills most microbes. In the lower digestive tract, the intestines have pancreatic and intestinal enzymes, antibacterial peptides, bile produced from the liver, and specialized Paneth cells that produce lysozyme. Together, these mediators are able to eliminate most pathogens that manage to survive the acidic environment of the stomach.",True,Inflammation-Eliciting Mediators,,,,
c0c77d14-4df7-4741-b2d2-d2098c3a1b15,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"In the urinary tract, urine flushes microbes out of the body during urination. Furthermore, the slight acidity of urine (the average pH is about 6) inhibits the growth of many microbes and potential pathogens in the urinary tract.",True,Inflammation-Eliciting Mediators,,,,
7b7c5dd7-0c76-4681-9642-1897c294d3e0,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"The female reproductive system employs lactate, an exogenously produced chemical mediator, to inhibit microbial growth. The cells and tissue layers composing the vagina produce glycogen, a branched and more complex polymer of glucose. Lactobacilli in the area ferment glycogen to produce lactate, lowering the pH in the vagina and inhibiting transient microbiota, opportunistic pathogens like Candida (a yeast associated with vaginal infections), and other pathogens responsible for sexually transmitted diseases.",True,Inflammation-Eliciting Mediators,,,,
93e8495f-6241-4560-95e4-b4d2b123ad01,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"In the eyes, tears contain the chemical mediators lysozyme and lactoferrin, both of which are capable of eliminating microbes that have found their way to the surface of the eyes. Lysozyme cleaves the bond between NAG and NAM in peptidoglycan, a component of the cell wall in bacteria. It is more effective against gram-positive bacteria, which lack the protective outer membrane associated with gram-negative bacteria. Lactoferrin inhibits microbial growth by chemically binding and sequestering iron. This effectually starves many microbes that require iron for growth.",True,Inflammation-Eliciting Mediators,,,,
121fe068-e538-4c61-8503-e6532c19b81e,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"In the ears, cerumen (earwax) exhibits antimicrobial properties due to the presence of fatty acids, which lower the pH to between 3 and 5.",True,Inflammation-Eliciting Mediators,,,,
3a104543-b6dd-4016-9abf-3ad45478e7f2,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"The respiratory tract uses various chemical mediators in the nasal passages, trachea, and lungs. The mucus produced in the nasal passages contains a mix of antimicrobial molecules similar to those found in tears and saliva (e.g., lysozyme, lactoferrin, lactoperoxidase). Secretions in the trachea and lungs also contain lysozyme and lactoferrin, as well as a diverse group of additional chemical mediators, such as the lipoprotein complex called surfactant, which has antibacterial properties.",True,Inflammation-Eliciting Mediators,,,,
bd94c70a-d0ec-47e9-82ff-e16bea55c193,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,Antimicrobial Peptides,False,Antimicrobial Peptides,,,,
53e3a81a-3d4a-4adb-a7fc-6b5dbe3adf4a,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"AMPs may induce cell damage in microorganisms in a variety of ways, including by inflicting damage to membranes, destroying DNA and RNA, or interfering with cell-wall synthesis. Depending on the specific antimicrobial mechanism, a particular AMP may inhibit only certain groups of microbes (e.g., gram-positive or gram-negative bacteria) or it may be more broadly effective against bacteria, fungi, protozoa, and viruses. Many AMPs are found on the skin, but they can also be found in other regions of the body.",True,Antimicrobial Peptides,,,,
502085a4-cd06-4d02-bca2-5f424e137fde,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,A family of AMPs called defensins can be produced by epithelial cells throughout the body as well as by cellular defenses such as macrophages and neutrophils. Defensins may be secreted or act inside host cells; they combat microorganisms by damaging their plasma membranes. AMPs called bacteriocins are produced exogenously by certain members of the resident microbiota within the gastrointestinal tract.,True,Antimicrobial Peptides,,,,
43b00b84-45ec-46ec-b1af-4d5465d921f1,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,Plasma Protein Mediators,False,Plasma Protein Mediators,,,,
09889ba9-93e9-4ccd-b0f8-16c4041e5d23,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Many nonspecific innate immune factors are found in plasma, the fluid portion of blood. Plasma contains electrolytes, sugars, lipids, and proteins, each of which helps to maintain homeostasis (i.e., stable internal body functioning), and contains the proteins involved in the clotting of blood. Additional proteins found in blood plasma, such as acute-phase proteins, complement proteins, and cytokines, are involved in the nonspecific innate immune response.",True,Plasma Protein Mediators,,,,
ebc14221-1343-4030-91da-5c32328d201f,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,The acute-phase proteins are another class of antimicrobial mediators. Acute-phase proteins are primarily produced in the liver and secreted into the blood in response to inflammatory molecules from the immune system.,True,Plasma Protein Mediators,,,,
55ae0c1f-75d2-4ca8-b5da-03a6f2d97f03,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"The complement system is a group of plasma protein mediators that can act as an innate nonspecific defense while also serving to connect innate and adaptive immunity (discussed in the next chapter). The complement system is composed of more than 30 proteins that normally circulate as precursor proteins in blood. These precursor proteins become activated when stimulated or triggered by a variety of factors, including the presence of microorganisms. Complement proteins are considered part of innate nonspecific immunity because they are always present in the blood and tissue fluids, allowing them to be activated quickly.",True,Plasma Protein Mediators,,,,
158b907f-93a4-4c6b-b82f-5ccd6d330d13,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Cytokines are soluble proteins that act as communication signals between cells. In a nonspecific innate immune response, various cytokines may be released to stimulate production of chemical mediators or other cell functions, such as cell proliferation, cell differentiation, inhibition of cell division, apoptosis, and chemotaxis.",True,Plasma Protein Mediators,,,,
e459e5b9-68cd-41fe-8038-8fd34c919650,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Three important classes of cytokines are the interleukins, chemokines, and interferons. The interleukins were originally thought to be produced only by leukocytes (white blood cells) and to only stimulate leukocytes, thus the reasons for their name. Although interleukins are involved in modulating almost every function of the immune system, their role in the body is not restricted to immunity. Interleukins are also produced by and stimulate a variety of cells unrelated to immune defenses.",True,Plasma Protein Mediators,,,,
7590b2c0-e754-4a4c-9bfe-0dc31d0e27bb,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"The chemokines are chemotactic factors that recruit leukocytes to sites of infection, tissue damage, and inflammation. In contrast to more general chemotactic factors, like complement factor C5a, chemokines are very specific in the subsets of leukocytes they recruit.",True,Plasma Protein Mediators,,,,
5097daa4-055f-4a85-b5d8-8685e011cca3,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Interferons are a diverse group of immune signaling molecules and are especially important in our defense against viruses. Type I interferons (interferon-α and interferon-β) are produced and released by cells infected with virus. These interferons stimulate nearby cells to stop production of mRNA, destroy RNA already produced, and reduce protein synthesis. These cellular changes inhibit viral replication and production of mature virus, slowing the spread of the virus. Type I interferons also stimulate various immune cells involved in viral clearance to more aggressively attack virus-infected cells. Type II interferon (interferon-γ) is an important activator of immune cells (Figure 13.8).",True,Plasma Protein Mediators,Figure 13.8,13.2	Chemical Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.11.png,"Figure 13.8 Interferons are cytokines released by a cell infected with a virus. Interferon-α and interferon-β signal uninfected neighboring cells to inhibit mRNA synthesis, destroy RNA, and reduce protein synthesis (top arrow).Interferon-α and interferon-β also promote apoptosis in cells infected with the virus (middle arrow). Interferon-γ alerts neighboring immune cells to an attack (bottom arrow). Although interferons do not cure the cell releasing them or other infected cells, which will soon die, their release may prevent additional cells from becoming infected, thus stemming the infection."
e47a0100-952f-4473-8cf0-57dab29a2a50,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,Inflammation-Eliciting Mediators,False,Inflammation-Eliciting Mediators,,,,
40014e95-3975-4134-9aaa-25f8824a3b2a,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Some cytokines also bind mast cells and basophils, inducing them to release histamine, a proinflammatory compound. Histamine receptors are found on a variety of cells and mediate proinflammatory events, such as bronchoconstriction (tightening of the airways) and smooth muscle contraction.",True,Inflammation-Eliciting Mediators,,,,
14711187-b392-4d7e-8c3f-e47386843d86,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Certain cytokines also stimulate the production of prostaglandins, chemical mediators that promote the inflammatory effects of kinins and histamines. Prostaglandins can also help to set the body temperature higher, leading to fever, which promotes the activities of white blood cells and slightly inhibits the growth of pathogenic microbes (see Inflammation and Fever).",True,Inflammation-Eliciting Mediators,,,,
bc53da67-8248-4803-9277-afe8942053b3,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,"Another inflammatory mediator, bradykinin, contributes to edema, which occurs when fluids and leukocytes leak out of the bloodstream and into tissues. It binds to receptors on cells in the capillary walls, causing the capillaries to dilate and become more permeable to fluids.",True,Inflammation-Eliciting Mediators,,,,
96d8c6a1-386a-42f1-b3b4-2a08c5f3ea42,https://open.oregonstate.education/microbiology/,13.2	Chemical Defenses,https://open.oregonstate.education/microbiology/chapter/17-2chemical-defenses/,Table 13.3 provides a summary of the chemical defenses discussed in this section.,True,Inflammation-Eliciting Mediators,,,,
e7a21e58-ec49-457e-af36-50a6b87e87a0,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,Physical Barriers,False,Physical Barriers,,,,
135a8b1d-2d95-404b-9a93-b0629e3f9358,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"One of the body’s most important physical barriers is the skin barrier, which is composed of three layers of closely packed cells. The thin upper layer is called the epidermis. A second, thicker layer, called the dermis, contains hair follicles, sweat glands, nerves, and blood vessels. A layer of fatty tissue called the hypodermis lies beneath the dermis and contains blood and lymph vessels (Figure 13.2).",True,Physical Barriers,Figure 13.2,13.1	Physical Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.3.png,"Figure 13.2 Human skin has three layers, the epidermis, the dermis, and the hypodermis, which provide a thick barrier between microbes outside the body and deeper tissues. Dead skin cells on the surface of the epidermis are continually shed, taking with them microbes on the skin’s surface. (credit: modification of work by National Institutes of Health)"
3d6b7f56-efbf-4073-8a18-e1147e5cfaa9,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"The topmost layer of skin, the epidermis, consists of cells that are packed with keratin. These dead cells remain as a tightly connected, dense layer of protein-filled cell husks on the surface of the skin. The keratin makes the skin’s surface mechanically tough and resistant to degradation by bacterial enzymes. Fatty acids on the skin’s surface create a dry, salty, and acidic environment that inhibits the growth of some microbes and is highly resistant to breakdown by bacterial enzymes. In addition, the dead cells of the epidermis are frequently shed, along with any microbes that may be clinging to them. Shed skin cells are continually replaced with new cells from below, providing a new barrier that will soon be shed in the same way.",True,Physical Barriers,,,,
90afa1af-cad5-401f-81ae-8c272cf7763d,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"Infections can occur when the skin barrier is compromised or broken. A wound can serve as a point of entry for opportunistic pathogens, which can infect the skin tissue surrounding the wound and possibly spread to deeper tissues.",True,Physical Barriers,,,,
49a29981-3be1-4837-a09b-896e1664d273,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"Mike, a gardener from southern California, recently noticed a small red bump on his left forearm. Initially, he did not think much of it, but soon it grew larger and then ulcerated (opened up), becoming a painful lesion that extended across a large part of his forearm (Figure 13.3). He went to an urgent care facility, where a physician asked about his occupation. When he said he was a landscaper, the physician immediately suspected a case of sporotrichosis, a type of fungal infection known as rose gardener’s disease because it often afflicts landscapers and gardening enthusiasts.",True,Physical Barriers,Figure 13.3,13.1	Physical Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.4.jpg,"Figure 13.3 Rose gardener’s disease can occur when the fungus Sporothrix schenkii breaches the skin through small cuts, such as might be inflicted by thorns. (credit left: modification of work by Elisa Self; credit right: modification of work by Centers for Disease Control and Prevention)"
beba4a6c-6499-4b3b-a0f8-274dd4366cfd,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"Under most conditions, fungi cannot produce skin infections in healthy individuals. Fungi grow filaments known as hyphae, which are not particularly invasive and can be easily kept at bay by the physical barriers of the skin and mucous membranes. However, small wounds in the skin, such as those caused by thorns, can provide an opening for opportunistic pathogens like Sporothrix schenkii, a soil-dwelling fungus and the causative agent of rose gardener’s disease. Once it breaches the skin barrier, S. schenkii can infect the skin and underlying tissues, producing ulcerated lesions like Mike’s. Compounding matters, other pathogens may enter the infected tissue, causing secondary bacterial infections.",True,Physical Barriers,,,,
6d465368-be60-4da6-a26f-77a686f238d2,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"Luckily, rose gardener’s disease is treatable. Mike’s physician wrote him a prescription for some antifungal drugs as well as a course of antibiotics to combat secondary bacterial infections. His lesions eventually healed, and Mike returned to work with a new appreciation for gloves and protective clothing.",True,Physical Barriers,,,,
7310ddb9-3315-4284-af1a-00aa50a2d6ac,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"The mucous membranes lining the nose, mouth, lungs, and urinary and digestive tracts provide another nonspecific barrier against potential pathogens. Mucous membranes consist of a layer of epithelial cells bound by tight junctions. The epithelial cells secrete a moist, sticky substance called mucus, which covers and protects the more fragile cell layers beneath it and traps debris and particulate matter, including microbes. Mucus secretions also contain antimicrobial peptides.",True,Physical Barriers,,,,
fe746bc1-7e95-4278-a38b-5d834c5f4ab9,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"In many regions of the body, mechanical actions serve to flush mucus (along with trapped or dead microbes) out of the body or away from potential sites of infection. For example, in the respiratory system, inhalation can bring microbes, dust, mold spores, and other small airborne debris into the body. This debris becomes trapped in the mucus lining the respiratory tract, a layer known as the mucociliary blanket. The epithelial cells lining the upper parts of the respiratory tract are called ciliated epithelial cells because they have hair-like appendages known as cilia. Movement of the cilia propels debris-laden mucus out and away from the lungs. The expelled mucus is then swallowed and destroyed in the stomach, or coughed up, or sneezed out (Figure 13.4). This system of removal is often called the mucociliary escalator.",True,Physical Barriers,Figure 13.4,13.1	Physical Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.5.png,"Figure 13.4 This scanning electron micrograph shows ciliated and nonciliated epithelial cells from the human trachea. The mucociliary escalator pushes mucus away from the lungs, along with any debris or microorganisms that may be trapped in the sticky mucus, and the mucus moves up to the esophagus where it can be removed by swallowing."
9e967b48-9a9f-4745-9d67-64451c6d6324,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"The mucociliary escalator is such an effective barrier to microbes that the lungs, the lowermost (and most sensitive) portion of the respiratory tract, were long considered to be a sterile environment in healthy individuals. Only recently has research suggested that healthy lungs may have a small normal microbiota. Disruption of the mucociliary escalator by the damaging effects of smoking or diseases such as cystic fibrosis can lead to increased colonization of bacteria in the lower respiratory tract and frequent infections, which highlights the importance of this physical barrier to host defenses.",True,Physical Barriers,,,,
182380b6-3777-4756-b222-276e06e6d930,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"Like the respiratory tract, the digestive tract is a portal of entry through which microbes enter the body, and the mucous membranes lining the digestive tract provide a nonspecific physical barrier against ingested microbes. The intestinal tract is lined with epithelial cells, interspersed with mucus-secreting goblet cells (Figure 13.5). This mucus mixes with material received from the stomach, trapping foodborne microbes and debris. The mechanical action of peristalsis, a series of muscular contractions in the digestive tract, moves the sloughed mucus and other material through the intestines, rectum, and anus, excreting the material in feces.",True,Physical Barriers,Figure 13.5,13.1	Physical Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.6.png,Figure 13.5 Goblet cells produce and secrete mucus. The arrows in this micrograph point to the mucus-secreting goblet cells (magnification 1600⨯) in the intestinal epithelium. (credit micrograph: Micrograph provided by the Regents of University of Michigan Medical School © 2012)
b2541a42-262b-48ed-8e19-8421142833a7,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"The epithelial cells lining the urogenital tract, blood vessels, lymphatic vessels, and certain other tissues are known as endothelia. These tightly packed cells provide a particularly effective frontline barrier against invaders. The endothelia of the blood-brain barrier, for example, protect the central nervous system (CNS), which consists of the brain and the spinal cord. The CNS is one of the most sensitive and important areas of the body, as microbial infection of the CNS can quickly lead to serious and often fatal inflammation. The cell junctions in the blood vessels traveling through the CNS are some of the tightest and toughest in the body, preventing any transient microbes in the bloodstream from entering the CNS. This keeps the cerebrospinal fluid that surrounds and bathes the brain and spinal cord sterile under normal conditions.",True,Physical Barriers,,,,
4af1628d-2a4f-4ca6-a1f1-efe51becd8c9,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,Mechanical Defenses,False,Mechanical Defenses,,,,
6e707538-4e87-41d3-ace7-eaef14862eee,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"In addition to physical barriers that keep microbes out, the body has a number of mechanical defenses that physically remove pathogens from the body, preventing them from taking up residence. We have already discussed several examples of mechanical defenses, including the shedding of skin cells, the expulsion of mucus via the mucociliary escalator, and the excretion of feces through intestinal peristalsis. Other important examples of mechanical defenses include the flushing action of urine and tears, which both serve to carry microbes away from the body. The flushing action of urine is largely responsible for the normally sterile environment of the urinary tract, which includes the kidneys, ureters, and urinary bladder. Urine passing out of the body washes out transient microorganisms, preventing them from taking up residence. The eyes also have physical barriers and mechanical mechanisms for preventing infections. The eyelashes and eyelids prevent dust and airborne microorganisms from reaching the surface of the eye. Any microbes or debris that make it past these physical barriers may be flushed out by the mechanical action of blinking, which bathes the eye in tears, washing debris away (Figure 13.6).",True,Mechanical Defenses,Figure 13.6,13.1	Physical Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.7.png,"Figure 13.6 Tears flush microbes away from the surface of the eye. Urine washes microbes out of the urinary tract as it passes through; as a result, the urinary system is normally sterile."
67665601-7784-4abc-8b94-d59d722881a3,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,Microbiome,False,Microbiome,,,,
0c3eb42c-e659-48a9-a2b6-cd8b171d5b54,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"In various regions of the body, resident microbiota serve as an important first-line defense against invading pathogens. Through their occupation of cellular binding sites and competition for available nutrients, the resident microbiota prevent the critical early steps of pathogen attachment and proliferation required for the establishment of an infection.",True,Microbiome,,,,
cb8771e2-8ef8-43a0-9cf8-4b50ac15764c,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"For example, in the vagina, members of the resident microbiota compete with opportunistic pathogens like the yeast Candida. This competition prevents infections by limiting the availability of nutrients, thus inhibiting the growth of Candida, keeping its population in check. Similar competitions occur between the microbiota and potential pathogens on the skin, in the upper respiratory tract, and in the gastrointestinal tract. As will be discussed later in this chapter, the resident microbiota also contribute to the chemical defenses of the innate nonspecific host defenses.",True,Microbiome,,,,
261f9da8-5b39-4483-9ac2-d7bb5ca749ff,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"The importance of the normal microbiota in host defenses is highlighted by the increased susceptibility to infectious diseases when the microbiota is disrupted or eliminated. Treatment with antibiotics can significantly deplete the normal microbiota of the gastrointestinal tract, providing an advantage for pathogenic bacteria to colonize and cause diarrheal infection. In the case of diarrhea caused by Clostridium difficile, the infection can be severe and potentially lethal. One strategy for treating C. difficile infections is fecal transplantation, which involves the transfer of fecal material from a donor (screened for potential pathogens) into the intestines of the recipient patient as a method of restoring the normal microbiota and combating C. difficile infections.",True,Microbiome,,,,
4f741864-2c7d-4860-8c3e-b061c4c4f14f,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,Table 13.2 provides a summary of the physical defenses discussed in this section.,True,Microbiome,,,,
de23eb7b-972c-4ea0-ac4a-c20350af9dba,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,Physical Barriers,False,Physical Barriers,,,,
d1665e21-52a9-4572-9952-82bd7b61cb0b,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"One of the body’s most important physical barriers is the skin barrier, which is composed of three layers of closely packed cells. The thin upper layer is called the epidermis. A second, thicker layer, called the dermis, contains hair follicles, sweat glands, nerves, and blood vessels. A layer of fatty tissue called the hypodermis lies beneath the dermis and contains blood and lymph vessels (Figure 13.2).",True,Physical Barriers,Figure 13.2,13.1	Physical Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.3.png,"Figure 13.2 Human skin has three layers, the epidermis, the dermis, and the hypodermis, which provide a thick barrier between microbes outside the body and deeper tissues. Dead skin cells on the surface of the epidermis are continually shed, taking with them microbes on the skin’s surface. (credit: modification of work by National Institutes of Health)"
2f8f7e65-3e2c-4a41-ac76-d3dd9e35ff29,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"Infections can occur when the skin barrier is compromised or broken. A wound can serve as a point of entry for opportunistic pathogens, which can infect the skin tissue surrounding the wound and possibly spread to deeper tissues.",True,Physical Barriers,,,,
c28cc71f-fc8b-4141-b613-472f824b4e94,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"Under most conditions, fungi cannot produce skin infections in healthy individuals. Fungi grow filaments known as hyphae, which are not particularly invasive and can be easily kept at bay by the physical barriers of the skin and mucous membranes. However, small wounds in the skin, such as those caused by thorns, can provide an opening for opportunistic pathogens like Sporothrix schenkii, a soil-dwelling fungus and the causative agent of rose gardener’s disease. Once it breaches the skin barrier, S. schenkii can infect the skin and underlying tissues, producing ulcerated lesions like Mike’s. Compounding matters, other pathogens may enter the infected tissue, causing secondary bacterial infections.",True,Physical Barriers,,,,
03d5d2ac-e118-420e-a879-8167deb6700f,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"Luckily, rose gardener’s disease is treatable. Mike’s physician wrote him a prescription for some antifungal drugs as well as a course of antibiotics to combat secondary bacterial infections. His lesions eventually healed, and Mike returned to work with a new appreciation for gloves and protective clothing.",True,Physical Barriers,,,,
fc044cea-6a6c-4b69-b688-1d34ea887cfa,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"In many regions of the body, mechanical actions serve to flush mucus (along with trapped or dead microbes) out of the body or away from potential sites of infection. For example, in the respiratory system, inhalation can bring microbes, dust, mold spores, and other small airborne debris into the body. This debris becomes trapped in the mucus lining the respiratory tract, a layer known as the mucociliary blanket. The epithelial cells lining the upper parts of the respiratory tract are called ciliated epithelial cells because they have hair-like appendages known as cilia. Movement of the cilia propels debris-laden mucus out and away from the lungs. The expelled mucus is then swallowed and destroyed in the stomach, or coughed up, or sneezed out (Figure 13.4). This system of removal is often called the mucociliary escalator.",True,Physical Barriers,Figure 13.4,13.1	Physical Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.5.png,"Figure 13.4 This scanning electron micrograph shows ciliated and nonciliated epithelial cells from the human trachea. The mucociliary escalator pushes mucus away from the lungs, along with any debris or microorganisms that may be trapped in the sticky mucus, and the mucus moves up to the esophagus where it can be removed by swallowing."
7a1f1765-054e-4445-90a8-cb6718b02997,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"Like the respiratory tract, the digestive tract is a portal of entry through which microbes enter the body, and the mucous membranes lining the digestive tract provide a nonspecific physical barrier against ingested microbes. The intestinal tract is lined with epithelial cells, interspersed with mucus-secreting goblet cells (Figure 13.5). This mucus mixes with material received from the stomach, trapping foodborne microbes and debris. The mechanical action of peristalsis, a series of muscular contractions in the digestive tract, moves the sloughed mucus and other material through the intestines, rectum, and anus, excreting the material in feces.",True,Physical Barriers,Figure 13.5,13.1	Physical Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.6.png,Figure 13.5 Goblet cells produce and secrete mucus. The arrows in this micrograph point to the mucus-secreting goblet cells (magnification 1600⨯) in the intestinal epithelium. (credit micrograph: Micrograph provided by the Regents of University of Michigan Medical School © 2012)
dc029705-dd60-44ae-a926-027378e1abb8,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,Mechanical Defenses,False,Mechanical Defenses,,,,
bc1df08c-a48c-4fc8-be42-1ff4953770e8,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"In addition to physical barriers that keep microbes out, the body has a number of mechanical defenses that physically remove pathogens from the body, preventing them from taking up residence. We have already discussed several examples of mechanical defenses, including the shedding of skin cells, the expulsion of mucus via the mucociliary escalator, and the excretion of feces through intestinal peristalsis. Other important examples of mechanical defenses include the flushing action of urine and tears, which both serve to carry microbes away from the body. The flushing action of urine is largely responsible for the normally sterile environment of the urinary tract, which includes the kidneys, ureters, and urinary bladder. Urine passing out of the body washes out transient microorganisms, preventing them from taking up residence. The eyes also have physical barriers and mechanical mechanisms for preventing infections. The eyelashes and eyelids prevent dust and airborne microorganisms from reaching the surface of the eye. Any microbes or debris that make it past these physical barriers may be flushed out by the mechanical action of blinking, which bathes the eye in tears, washing debris away (Figure 13.6).",True,Mechanical Defenses,Figure 13.6,13.1	Physical Defenses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-17.7.png,"Figure 13.6 Tears flush microbes away from the surface of the eye. Urine washes microbes out of the urinary tract as it passes through; as a result, the urinary system is normally sterile."
0ac0733e-1eb1-4f34-8acf-9d495c2028d0,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,Microbiome,False,Microbiome,,,,
a58156a1-9cb9-4ec3-81c2-a0aa6bd7c556,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"In various regions of the body, resident microbiota serve as an important first-line defense against invading pathogens. Through their occupation of cellular binding sites and competition for available nutrients, the resident microbiota prevent the critical early steps of pathogen attachment and proliferation required for the establishment of an infection.",True,Microbiome,,,,
776281a7-f9a9-45e8-8cdd-45b58e0d9a94,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"For example, in the vagina, members of the resident microbiota compete with opportunistic pathogens like the yeast Candida. This competition prevents infections by limiting the availability of nutrients, thus inhibiting the growth of Candida, keeping its population in check. Similar competitions occur between the microbiota and potential pathogens on the skin, in the upper respiratory tract, and in the gastrointestinal tract. As will be discussed later in this chapter, the resident microbiota also contribute to the chemical defenses of the innate nonspecific host defenses.",True,Microbiome,,,,
b25750d7-d347-4344-9ef9-ccc718c51c91,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,"The importance of the normal microbiota in host defenses is highlighted by the increased susceptibility to infectious diseases when the microbiota is disrupted or eliminated. Treatment with antibiotics can significantly deplete the normal microbiota of the gastrointestinal tract, providing an advantage for pathogenic bacteria to colonize and cause diarrheal infection. In the case of diarrhea caused by Clostridium difficile, the infection can be severe and potentially lethal. One strategy for treating C. difficile infections is fecal transplantation, which involves the transfer of fecal material from a donor (screened for potential pathogens) into the intestines of the recipient patient as a method of restoring the normal microbiota and combating C. difficile infections.",True,Microbiome,,,,
aa8129e5-9dd5-4b49-a9b3-cc5b9f0b06ec,https://open.oregonstate.education/microbiology/,13.1	Physical Defenses,https://open.oregonstate.education/microbiology/chapter/17-1physical-defenses/,Table 13.2 provides a summary of the physical defenses discussed in this section.,True,Microbiome,,,,
cd5904e8-4470-46e1-95ec-705896e063aa,https://open.oregonstate.education/microbiology/,12.4 Global Public Health,https://open.oregonstate.education/microbiology/chapter/16-4global-public-health/,The World Health Organization (WHO),False,The World Health Organization (WHO),,,,
d6cbb37d-f402-441f-8fcf-824fb6d41dc5,https://open.oregonstate.education/microbiology/,12.4 Global Public Health,https://open.oregonstate.education/microbiology/chapter/16-4global-public-health/,"International public health issues are coordinated by the World Health Organization (WHO), an agency of the United Nations. Of its roughly $4 billion budget for 2015–16[1], about $1 billion was funded by member states and the remaining $3 billion by voluntary contributions. In addition to monitoring and reporting on infectious disease, WHO also develops and implements strategies for their control and prevention. WHO has had a number of successful international public health campaigns. For example, its vaccination program against smallpox, begun in the mid-1960s, resulted in the global eradication of the disease by 1980. WHO continues to be involved in infectious disease control, primarily in the developing world, with programs targeting malaria, HIV/AIDS, and tuberculosis, among others. It also runs programs to reduce illness and mortality that occur as a result of violence, accidents, lifestyle-associated illnesses such as diabetes, and poor health-care infrastructure.",True,The World Health Organization (WHO),,,,
d8b66983-fea2-475d-af12-f1d6c9ed60a7,https://open.oregonstate.education/microbiology/,12.4 Global Public Health,https://open.oregonstate.education/microbiology/chapter/16-4global-public-health/,"WHO maintains a global alert and response system that coordinates information from member nations. In the event of a public health emergency or epidemic, it provides logistical support and coordinates international response to the emergency. The United States contributes to this effort through the CDC. The CDC carries out international monitoring and public health efforts, mainly in the service of protecting US public health in an increasingly connected world. Similarly, the European Union maintains a Health Security Committee that monitors disease outbreaks within its member countries and internationally, coordinating with WHO.",True,The World Health Organization (WHO),,,,
a8df491b-e81f-4efe-97b2-3858129bc5ec,https://open.oregonstate.education/microbiology/,12.4 Global Public Health,https://open.oregonstate.education/microbiology/chapter/16-4global-public-health/,Emerging and Reemerging Infectious Diseases,False,Emerging and Reemerging Infectious Diseases,,,,
a79dc3d3-a898-4639-b5f4-4af56a3d76ef,https://open.oregonstate.education/microbiology/,12.4 Global Public Health,https://open.oregonstate.education/microbiology/chapter/16-4global-public-health/,"Both WHO and some national public health agencies such as the CDC monitor and prepare for emerging infectious diseases. An emerging infectious disease is either new to the human population or has shown an increase in prevalence in the previous twenty years. Whether the disease is new or conditions have changed to cause an increase in frequency, its status as emerging implies the need to apply resources to understand and control its growing impact.",True,Emerging and Reemerging Infectious Diseases,,,,
2647164a-ca59-4963-a8dc-e61bfa53f66e,https://open.oregonstate.education/microbiology/,12.4 Global Public Health,https://open.oregonstate.education/microbiology/chapter/16-4global-public-health/,"Emerging diseases may change their frequency gradually over time, or they may experience sudden epidemic growth. The importance of vigilance was made clear during the Ebola hemorrhagic fever epidemic in western Africa through 2014–2015. Although health experts had been aware of the Ebola virus since the 1970s, an outbreak on such a large scale had never happened before (Figure 12.14). Previous human epidemics had been small, isolated, and contained. Indeed, the gorilla and chimpanzee populations of western Africa had suffered far worse from Ebola than the human population. The pattern of small isolated human epidemics changed in 2014. Its high transmission rate, coupled with cultural practices for treatment of the dead and perhaps its emergence in an urban setting, caused the disease to spread rapidly, and thousands of people died. The international public health community responded with a large emergency effort to treat patients and contain the epidemic.",True,Emerging and Reemerging Infectious Diseases,Figure 12.14,12.4 Global Public Health,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.16.png,"Figure 12.14 Even before the Ebola epidemic of 2014–15, Ebola was considered an emerging disease because of several smaller outbreaks between the mid-1990s and 2000s."
1d4c460d-d5fc-403f-9451-95bea28a16a4,https://open.oregonstate.education/microbiology/,12.4 Global Public Health,https://open.oregonstate.education/microbiology/chapter/16-4global-public-health/,"Ebola is not the only disease that needs to be monitored in the global environment. In 2015, WHO set priorities on several emerging diseases that had a high probability of causing epidemics and that were poorly understood (and thus urgently required research and development efforts). Emerging diseases are found in all countries, both developed and developing (Table 12.2).",True,Emerging and Reemerging Infectious Diseases,,,,
25f66cd4-ca42-4a5d-b7d7-ed66c4896a4e,https://open.oregonstate.education/microbiology/,12.4 Global Public Health,https://open.oregonstate.education/microbiology/chapter/16-4global-public-health/,"A reemerging infectious disease is a disease that is increasing in frequency after a previous period of decline. Its reemergence may be a result of changing conditions or old prevention regimes that are no longer working. Examples of such diseases are drug-resistant forms of tuberculosis, bacterial pneumonia, and malaria. Drug-resistant strains of the bacteria causing gonorrhea and syphilis are also becoming more widespread, raising concerns of untreatable infections.",True,Emerging and Reemerging Infectious Diseases,,,,
19a98d36-6b0b-4fcb-b0a9-1071652d3991,https://open.oregonstate.education/microbiology/,12.4 Global Public Health,https://open.oregonstate.education/microbiology/chapter/16-4global-public-health/,Influenza (swine flu),False,Influenza (swine flu),,,,
c98c2839-1cdf-42a9-ba47-6e2ff632c304,https://open.oregonstate.education/microbiology/,12.4 Global Public Health,https://open.oregonstate.education/microbiology/chapter/16-4global-public-health/,Influenza (swine flu),False,Influenza (swine flu),,,,
358cdd9e-16e9-45c8-adff-c2196b604874,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,Reservoirs and Carriers,False,Reservoirs and Carriers,,,,
f6f3f2fb-f9d6-40b9-a213-1be980cc37f9,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"For pathogens to persist over long periods of time they require reservoirs where they normally reside. Reservoirs can be living organisms or nonliving sites. Nonliving reservoirs can include soil and water in the environment. These may naturally harbor the organism because it may grow in that environment. These environments may also become contaminated with pathogens in human feces, pathogens shed by intermediate hosts, or pathogens contained in the remains of intermediate hosts.",True,Reservoirs and Carriers,,,,
4e32e867-2281-4b2f-b4ca-241426376102,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Pathogens may have mechanisms of dormancy or resilience that allow them to survive (but typically not to reproduce) for varying periods of time in nonliving environments. For example, Clostridium tetani survives in the soil and in the presence of oxygen as a resistant endospore. Although many viruses are soon destroyed once in contact with air, water, or other non-physiological conditions, certain types are capable of persisting outside of a living cell for varying amounts of time. For example, a study that looked at the ability of influenza viruses to infect a cell culture after varying amounts of time on a banknote showed survival times from 48 hours to 17 days, depending on how they were deposited on the banknote.[1] On the other hand, cold-causing rhinoviruses are somewhat fragile, typically surviving less than a day outside of physiological fluids.",True,Reservoirs and Carriers,,,,
a1b858bf-1213-4005-8551-80a24c5f771e,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"A human acting as a reservoir of a pathogen may or may not be capable of transmitting the pathogen, depending on the stage of infection and the pathogen. To help prevent the spread of disease among school children, the CDC has developed guidelines based on the risk of transmission during the course of the disease. For example, children with chickenpox are considered contagious for five days from the start of the rash, whereas children with most gastrointestinal illnesses should be kept home for 24 hours after the symptoms disappear.",True,Reservoirs and Carriers,,,,
9f2e62e2-f025-45f1-8cce-57072ace6ede,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"An individual capable of transmitting a pathogen without displaying symptoms is referred to as a carrier. A passive carrier is contaminated with the pathogen and can mechanically transmit it to another host; however, a passive carrier is not infected. For example, a health-care professional who fails to wash his hands after seeing a patient harboring an infectious agent could become a passive carrier, transmitting the pathogen to another patient who becomes infected.",True,Reservoirs and Carriers,,,,
0bed43b8-5a0e-4f4a-93b4-a233eb5c9d76,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"By contrast, an active carrier is an infected individual who can transmit the disease to others. An active carrier may or may not exhibit signs or symptoms of infection. For example, active carriers may transmit the disease during the incubation period (before they show signs and symptoms) or the period of convalescence (after symptoms have subsided). Active carriers who do not present signs or symptoms of disease despite infection are called asymptomatic carriers. Pathogens such as hepatitis B virus, herpes simplex virus, and HIV are frequently transmitted by asymptomatic carriers. Mary Mallon, better known as Typhoid Mary, is a famous historical example of an asymptomatic carrier. An Irish immigrant, Mallon worked as a cook for households in and around New York City between 1900 and 1915. In each household, the residents developed typhoid fever (caused by Salmonella typhi) a few weeks after Mallon started working. Later investigations determined that Mallon was responsible for at least 122 cases of typhoid fever, five of which were fatal.[2]",True,Reservoirs and Carriers,,,,
4665776a-f506-459c-a1a8-a724bbd48d92,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"A pathogen may have more than one living reservoir. In zoonotic diseases, animals act as reservoirs of human disease and transmit the infectious agent to humans through direct or indirect contact. In some cases, the disease also affects the animal, but in other cases the animal is asymptomatic.",True,Reservoirs and Carriers,,,,
6f4ca38f-391c-4cef-b5a1-ae7d54c3a43e,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,Transmission,False,Transmission,,,,
37589b14-1349-47c9-9422-0fb38f964897,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Contact transmission includes direct contact or indirect contact. Person-to-person transmission is a form of direct contact transmission. Here the agent is transmitted by physical contact between two individuals (Figure 12.9) through actions such as touching, kissing, sexual intercourse, or droplet sprays. Direct contact can be categorized as vertical, horizontal, or droplet transmission. Vertical direct contact transmission occurs when pathogens are transmitted from mother to child during pregnancy, birth, or breastfeeding. Other kinds of direct contact transmission are called horizontal direct contact transmission. Often, contact between mucous membranes is required for entry of the pathogen into the new host, although skin-to-skin contact can lead to mucous membrane contact if the new host subsequently touches a mucous membrane. Contact transmission may also be site-specific; for example, some diseases can be transmitted by sexual contact but not by other forms of contact.",True,Transmission,Figure 12.9,12.3	Modes of Disease Transmission,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.9.png,"Figure 12.9 Direct contact transmission of pathogens can occur through physical contact. Many pathogens require contact with a mucous membrane to enter the body, but the host may transfer the pathogen from another point of contact (e.g., hand) to a mucous membrane (e.g., mouth or eye). (credit left: modification of work by Lisa Doehnert)"
27ed9697-577f-4248-b0ec-cc1b5d532d93,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"When an individual coughs or sneezes, small droplets of mucus that may contain pathogens are ejected. This leads to direct droplet transmission, which refers to droplet transmission of a pathogen to a new host over distances of one meter or less. A wide variety of diseases are transmitted by droplets, including influenza and many forms of pneumonia. Transmission over distances greater than one meter is called airborne transmission.",True,Transmission,,,,
9463bb3f-2ee4-4d4d-b999-fd4262c3b336,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Indirect contact transmission involves inanimate objects called fomites that become contaminated by pathogens from an infected individual or reservoir (Figure 12.10). For example, an individual with the common cold may sneeze, causing droplets to land on a fomite such as a tablecloth or carpet, or the individual may wipe her nose and then transfer mucus to a fomite such as a doorknob or towel. Transmission occurs indirectly when a new susceptible host later touches the fomite and transfers the contaminated material to a susceptible portal of entry. Fomites can also include objects used in clinical settings that are not properly sterilized, such as syringes, needles, catheters, and surgical equipment. Pathogens transmitted indirectly via such fomites are a major cause of healthcare-associated infections (see Controlling Microbial Growth).",True,Transmission,Figure 12.10,12.3	Modes of Disease Transmission,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.10.png,"Figure 12.10 Fomites are nonliving objects that facilitate the indirect transmission of pathogens. Contaminated doorknobs, towels, and syringes are all common examples of fomites. (credit left: modification of work by Kate Ter Haar; credit middle: modification of work by Vernon Swanepoel; credit right: modification of work by “Zaldylmg”/Flickr)"
2df776f7-ea6b-4686-a676-07a51a95307a,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"The term vehicle transmission refers to the transmission of pathogens through vehicles such as water, food, and air. Water contamination through poor sanitation methods leads to waterborne transmission of disease. Waterborne disease remains a serious problem in many regions throughout the world. The World Health Organization (WHO) estimates that contaminated drinking water is responsible for more than 500,000 deaths each year.[3] Similarly, food contaminated through poor handling or storage can lead to foodborne transmission of disease (Figure 12.11).",True,Transmission,Figure 12.11,12.3	Modes of Disease Transmission,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.11.png,"Figure 12.11 Food is an important vehicle of transmission for pathogens, especially of the gastrointestinal and upper respiratory systems. Notice the glass shield above the food trays, designed to prevent pathogens ejected in coughs and sneezes from entering the food. (credit: Fort George G. Meade Public Affairs Office)"
0b1cc370-e74e-4380-9e35-ba2386b2d989,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Dust and fine particles known as aerosols, which can float in the air, can carry pathogens and facilitate the airborne transmission of disease. For example, dust particles are the dominant mode of transmission of hantavirus to humans. Hantavirus is found in mouse feces, urine, and saliva, but when these substances dry, they can disintegrate into fine particles that can become airborne when disturbed; inhalation of these particles can lead to a serious and sometimes fatal respiratory infection.",True,Transmission,,,,
52c96dc5-3980-4c6b-8203-df9f6a6dce68,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Although droplet transmission over short distances is considered contact transmission as discussed above, longer distance transmission of droplets through the air is considered vehicle transmission. Unlike larger particles that drop quickly out of the air column, fine mucus droplets produced by coughs or sneezes can remain suspended for long periods of time, traveling considerable distances. In certain conditions, droplets desiccate quickly to produce a droplet nucleus that is capable of transmitting pathogens; air temperature and humidity can have an impact on effectiveness of airborne transmission.",True,Transmission,,,,
a13e923f-91a8-4595-b020-ba8ed9417051,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Diseases can also be transmitted by a mechanical or biological vector, an animal (typically an arthropod) that carries the disease from one host to another. Mechanical transmission is facilitated by a mechanical vector, an animal that carries a pathogen from one host to another without being infected itself. For example, a fly may land on fecal matter and later transmit bacteria from the feces to food that it lands on; a human eating the food may then become infected by the bacteria, resulting in a case of diarrhea or dysentery (Figure 12.12).",True,Transmission,Figure 12.12,12.3	Modes of Disease Transmission,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.12.png,"Figure 12.12 (a) A mechanical vector carries a pathogen on its body from one host to another, not as an infection. (b) A biological vector carries a pathogen from one host to another after becoming infected itself."
b81d18bc-f2bb-411d-a5ec-c0e8527a0f5a,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Biological transmission occurs when the pathogen reproduces within a biological vector that transmits the pathogen from one host to another (Figure 12.12). Arthropods are the main vectors responsible for biological transmission (Figure 12.12). Most arthropod vectors transmit the pathogen by biting the host, creating a wound that serves as a portal of entry. The pathogen may go through part of its reproductive cycle in the gut or salivary glands of the arthropod to facilitate its transmission through the bite. For example, hemipterans (called “kissing bugs” or “assassin bugs”) transmit Chagas disease to humans by defecating when they bite, after which the human scratches or rubs the infected feces into a mucous membrane or break in the skin.",True,Transmission,Figure 12.12,12.3	Modes of Disease Transmission,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.12.png,"Figure 12.12 (a) A mechanical vector carries a pathogen on its body from one host to another, not as an infection. (b) A biological vector carries a pathogen from one host to another after becoming infected itself."
6cfef980-6169-4c41-b804-adb0c051e8d4,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Biological insect vectors include mosquitoes, which transmit malaria and other diseases, and lice, which transmit typhus. Other arthropod vectors can include arachnids, primarily ticks, which transmit Lyme disease and other diseases, and mites, which transmit scrub typhus and rickettsial pox. Biological transmission, because it involves survival and reproduction within a parasitized vector, complicates the biology of the pathogen and its transmission. There are also important non-arthropod vectors of disease, including mammals and birds. Various species of mammals can transmit rabies to humans, usually by means of a bite that transmits the rabies virus. Chickens and other domestic poultry can transmit avian influenza to humans through direct or indirect contact with avian influenza virus A shed in the birds’ saliva, mucous, and feces.",True,Transmission,,,,
d6d221c8-6403-47ac-8056-ef80792a63ae,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,Quarantining,False,Quarantining,,,,
b0cf9f1f-7978-4b40-934c-47173f58f93e,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Individuals suspected or known to have been exposed to certain contagious pathogens may be quarantined, or isolated to prevent transmission of the disease to others. Hospitals and other health-care facilities generally set up special wards to isolate patients with particularly hazardous diseases such as tuberculosis or Ebola (Figure 12.13). Depending on the setting, these wards may be equipped with special air-handling methods, and personnel may implement special protocols to limit the risk of transmission, such as personal protective equipment or the use of chemical disinfectant sprays upon entry and exit of medical personnel.",True,Quarantining,Figure 12.13,12.3	Modes of Disease Transmission,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.15.png,"Figure 12.13 (a) The Aeromedical Biological Containment System (ABCS) is a module designed by the CDC and Department of Defense specifically for transporting highly contagious patients by air. (b) An isolation ward for Ebola patients in Lagos, Nigeria. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by CDC Global)"
47ffffcf-83cb-40dc-a3cc-c7ba5b7a1260,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"The duration of the quarantine depends on factors such as the incubation period of the disease and the evidence suggestive of an infection. The patient may be released if signs and symptoms fail to materialize when expected or if preventive treatment can be administered in order to limit the risk of transmission. If the infection is confirmed, the patient may be compelled to remain in isolation until the disease is no longer considered contagious.",True,Quarantining,,,,
f0d7232d-37c2-4160-94a0-07942d71fb44,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"In the United States, public health authorities may only quarantine patients for certain diseases, such as cholera, diphtheria, infectious tuberculosis, and strains of influenza capable of causing a pandemic. Individuals entering the United States or moving between states may be quarantined by the CDC if they are suspected of having been exposed to one of these diseases. Although the CDC routinely monitors entry points to the United States for crew or passengers displaying illness, quarantine is rarely implemented.",True,Quarantining,,,,
ea406e77-f544-43f4-9048-9fef198dc282,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,Healthcare-Associated (Nosocomial) Infections,False,Healthcare-Associated (Nosocomial) Infections,,,,
8642871f-bc05-4690-989f-37058a28310c,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Hospitals, retirement homes, and prisons attract the attention of epidemiologists because these settings are associated with increased incidence of certain diseases. Higher rates of transmission may be caused by characteristics of the environment itself, characteristics of the population, or both. Consequently, special efforts must be taken to limit the risks of infection in these settings.",True,Healthcare-Associated (Nosocomial) Infections,,,,
3d641684-b675-4576-8ef0-0c895dbd4df1,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Infections acquired in health-care facilities, including hospitals, are called nosocomial infections or healthcare- associated infections (HAI). HAIs are often connected with surgery or other invasive procedures that provide the pathogen with access to the portal of infection. For an infection to be classified as an HAI, the patient must have been admitted to the health-care facility for a reason other than the infection. In these settings, patients suffering from primary disease are often afflicted with compromised immunity and are more susceptible to secondary infection and opportunistic pathogens.",True,Healthcare-Associated (Nosocomial) Infections,,,,
6fd7f2c8-582e-41bb-9c33-5146c8fab7fa,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"In 2011, more than 720,000 HAIs occurred in hospitals in the United States, according to the CDC. About 22% of these HAIs occurred at a surgical site, and cases of pneumonia accounted for another 22%; urinary tract infections accounted for an additional 13%, and primary bloodstream infections 10%.[4] Such HAIs often occur when pathogens are introduced to patients’ bodies through contaminated surgical or medical equipment, such as catheters and respiratory ventilators. Health-care facilities seek to limit nosocomial infections through training and hygiene protocols such as those described in Control of Microbial Growth.",True,Healthcare-Associated (Nosocomial) Infections,,,,
931a95c9-72b7-4d56-b36a-e9989a6f6472,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,Transmission,False,Transmission,,,,
0050612c-3466-40a2-aec0-5ba3ce87e560,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Contact transmission includes direct contact or indirect contact. Person-to-person transmission is a form of direct contact transmission. Here the agent is transmitted by physical contact between two individuals (Figure 12.9) through actions such as touching, kissing, sexual intercourse, or droplet sprays. Direct contact can be categorized as vertical, horizontal, or droplet transmission. Vertical direct contact transmission occurs when pathogens are transmitted from mother to child during pregnancy, birth, or breastfeeding. Other kinds of direct contact transmission are called horizontal direct contact transmission. Often, contact between mucous membranes is required for entry of the pathogen into the new host, although skin-to-skin contact can lead to mucous membrane contact if the new host subsequently touches a mucous membrane. Contact transmission may also be site-specific; for example, some diseases can be transmitted by sexual contact but not by other forms of contact.",True,Transmission,Figure 12.9,12.3	Modes of Disease Transmission,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.9.png,"Figure 12.9 Direct contact transmission of pathogens can occur through physical contact. Many pathogens require contact with a mucous membrane to enter the body, but the host may transfer the pathogen from another point of contact (e.g., hand) to a mucous membrane (e.g., mouth or eye). (credit left: modification of work by Lisa Doehnert)"
fc80bab7-6108-4757-b1e4-aa7297d03a52,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"When an individual coughs or sneezes, small droplets of mucus that may contain pathogens are ejected. This leads to direct droplet transmission, which refers to droplet transmission of a pathogen to a new host over distances of one meter or less. A wide variety of diseases are transmitted by droplets, including influenza and many forms of pneumonia. Transmission over distances greater than one meter is called airborne transmission.",True,Transmission,,,,
68e2bce2-9598-4a09-82bb-4bfa1c6cc5ce,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Indirect contact transmission involves inanimate objects called fomites that become contaminated by pathogens from an infected individual or reservoir (Figure 12.10). For example, an individual with the common cold may sneeze, causing droplets to land on a fomite such as a tablecloth or carpet, or the individual may wipe her nose and then transfer mucus to a fomite such as a doorknob or towel. Transmission occurs indirectly when a new susceptible host later touches the fomite and transfers the contaminated material to a susceptible portal of entry. Fomites can also include objects used in clinical settings that are not properly sterilized, such as syringes, needles, catheters, and surgical equipment. Pathogens transmitted indirectly via such fomites are a major cause of healthcare-associated infections (see Controlling Microbial Growth).",True,Transmission,Figure 12.10,12.3	Modes of Disease Transmission,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.10.png,"Figure 12.10 Fomites are nonliving objects that facilitate the indirect transmission of pathogens. Contaminated doorknobs, towels, and syringes are all common examples of fomites. (credit left: modification of work by Kate Ter Haar; credit middle: modification of work by Vernon Swanepoel; credit right: modification of work by “Zaldylmg”/Flickr)"
259aac5b-6eda-460b-af5e-585c7cbb7d79,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"The term vehicle transmission refers to the transmission of pathogens through vehicles such as water, food, and air. Water contamination through poor sanitation methods leads to waterborne transmission of disease. Waterborne disease remains a serious problem in many regions throughout the world. The World Health Organization (WHO) estimates that contaminated drinking water is responsible for more than 500,000 deaths each year.[3] Similarly, food contaminated through poor handling or storage can lead to foodborne transmission of disease (Figure 12.11).",True,Transmission,Figure 12.11,12.3	Modes of Disease Transmission,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.11.png,"Figure 12.11 Food is an important vehicle of transmission for pathogens, especially of the gastrointestinal and upper respiratory systems. Notice the glass shield above the food trays, designed to prevent pathogens ejected in coughs and sneezes from entering the food. (credit: Fort George G. Meade Public Affairs Office)"
bc296f36-f6da-4028-b3c2-d4946b490ee3,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Dust and fine particles known as aerosols, which can float in the air, can carry pathogens and facilitate the airborne transmission of disease. For example, dust particles are the dominant mode of transmission of hantavirus to humans. Hantavirus is found in mouse feces, urine, and saliva, but when these substances dry, they can disintegrate into fine particles that can become airborne when disturbed; inhalation of these particles can lead to a serious and sometimes fatal respiratory infection.",True,Transmission,,,,
b752c8b8-f0e0-4151-8ac1-ca84728599d1,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Although droplet transmission over short distances is considered contact transmission as discussed above, longer distance transmission of droplets through the air is considered vehicle transmission. Unlike larger particles that drop quickly out of the air column, fine mucus droplets produced by coughs or sneezes can remain suspended for long periods of time, traveling considerable distances. In certain conditions, droplets desiccate quickly to produce a droplet nucleus that is capable of transmitting pathogens; air temperature and humidity can have an impact on effectiveness of airborne transmission.",True,Transmission,,,,
628e2062-7975-48bf-b818-02d1ddeace51,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Diseases can also be transmitted by a mechanical or biological vector, an animal (typically an arthropod) that carries the disease from one host to another. Mechanical transmission is facilitated by a mechanical vector, an animal that carries a pathogen from one host to another without being infected itself. For example, a fly may land on fecal matter and later transmit bacteria from the feces to food that it lands on; a human eating the food may then become infected by the bacteria, resulting in a case of diarrhea or dysentery (Figure 12.12).",True,Transmission,Figure 12.12,12.3	Modes of Disease Transmission,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.12.png,"Figure 12.12 (a) A mechanical vector carries a pathogen on its body from one host to another, not as an infection. (b) A biological vector carries a pathogen from one host to another after becoming infected itself."
48091082-4cab-476e-8d4e-b57d0b841922,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Biological transmission occurs when the pathogen reproduces within a biological vector that transmits the pathogen from one host to another (Figure 12.12). Arthropods are the main vectors responsible for biological transmission (Figure 12.12). Most arthropod vectors transmit the pathogen by biting the host, creating a wound that serves as a portal of entry. The pathogen may go through part of its reproductive cycle in the gut or salivary glands of the arthropod to facilitate its transmission through the bite. For example, hemipterans (called “kissing bugs” or “assassin bugs”) transmit Chagas disease to humans by defecating when they bite, after which the human scratches or rubs the infected feces into a mucous membrane or break in the skin.",True,Transmission,Figure 12.12,12.3	Modes of Disease Transmission,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.12.png,"Figure 12.12 (a) A mechanical vector carries a pathogen on its body from one host to another, not as an infection. (b) A biological vector carries a pathogen from one host to another after becoming infected itself."
57281b19-c6a6-43a0-9cfd-28d28fbbf7db,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Biological insect vectors include mosquitoes, which transmit malaria and other diseases, and lice, which transmit typhus. Other arthropod vectors can include arachnids, primarily ticks, which transmit Lyme disease and other diseases, and mites, which transmit scrub typhus and rickettsial pox. Biological transmission, because it involves survival and reproduction within a parasitized vector, complicates the biology of the pathogen and its transmission. There are also important non-arthropod vectors of disease, including mammals and birds. Various species of mammals can transmit rabies to humans, usually by means of a bite that transmits the rabies virus. Chickens and other domestic poultry can transmit avian influenza to humans through direct or indirect contact with avian influenza virus A shed in the birds’ saliva, mucous, and feces.",True,Transmission,,,,
7ce97669-7141-4912-b06c-ed2eb6be10cd,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,Quarantining,False,Quarantining,,,,
b3aefc2e-5536-40e2-ba27-2b57bd78c84a,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Individuals suspected or known to have been exposed to certain contagious pathogens may be quarantined, or isolated to prevent transmission of the disease to others. Hospitals and other health-care facilities generally set up special wards to isolate patients with particularly hazardous diseases such as tuberculosis or Ebola (Figure 12.13). Depending on the setting, these wards may be equipped with special air-handling methods, and personnel may implement special protocols to limit the risk of transmission, such as personal protective equipment or the use of chemical disinfectant sprays upon entry and exit of medical personnel.",True,Quarantining,Figure 12.13,12.3	Modes of Disease Transmission,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.15.png,"Figure 12.13 (a) The Aeromedical Biological Containment System (ABCS) is a module designed by the CDC and Department of Defense specifically for transporting highly contagious patients by air. (b) An isolation ward for Ebola patients in Lagos, Nigeria. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by CDC Global)"
6e68ad0b-0a76-494e-9f45-71cebc8eb758,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"The duration of the quarantine depends on factors such as the incubation period of the disease and the evidence suggestive of an infection. The patient may be released if signs and symptoms fail to materialize when expected or if preventive treatment can be administered in order to limit the risk of transmission. If the infection is confirmed, the patient may be compelled to remain in isolation until the disease is no longer considered contagious.",True,Quarantining,,,,
3187472d-9c58-42ff-8255-5d8cc605efe9,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"In the United States, public health authorities may only quarantine patients for certain diseases, such as cholera, diphtheria, infectious tuberculosis, and strains of influenza capable of causing a pandemic. Individuals entering the United States or moving between states may be quarantined by the CDC if they are suspected of having been exposed to one of these diseases. Although the CDC routinely monitors entry points to the United States for crew or passengers displaying illness, quarantine is rarely implemented.",True,Quarantining,,,,
425f546d-233a-43ce-8cd8-2b20f801728c,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,Healthcare-Associated (Nosocomial) Infections,False,Healthcare-Associated (Nosocomial) Infections,,,,
716fa755-5184-4daa-a987-5ef28e44e3b0,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Hospitals, retirement homes, and prisons attract the attention of epidemiologists because these settings are associated with increased incidence of certain diseases. Higher rates of transmission may be caused by characteristics of the environment itself, characteristics of the population, or both. Consequently, special efforts must be taken to limit the risks of infection in these settings.",True,Healthcare-Associated (Nosocomial) Infections,,,,
0a176ba9-bc42-4415-9f7b-018a31ec95d5,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"Infections acquired in health-care facilities, including hospitals, are called nosocomial infections or healthcare- associated infections (HAI). HAIs are often connected with surgery or other invasive procedures that provide the pathogen with access to the portal of infection. For an infection to be classified as an HAI, the patient must have been admitted to the health-care facility for a reason other than the infection. In these settings, patients suffering from primary disease are often afflicted with compromised immunity and are more susceptible to secondary infection and opportunistic pathogens.",True,Healthcare-Associated (Nosocomial) Infections,,,,
9a0459fd-1ef8-46d7-8976-9bbfdaa9b036,https://open.oregonstate.education/microbiology/,12.3	Modes of Disease Transmission,https://open.oregonstate.education/microbiology/chapter/16-3modes-of-disease-transmission/,"In 2011, more than 720,000 HAIs occurred in hospitals in the United States, according to the CDC. About 22% of these HAIs occurred at a surgical site, and cases of pneumonia accounted for another 22%; urinary tract infections accounted for an additional 13%, and primary bloodstream infections 10%.[4] Such HAIs often occur when pathogens are introduced to patients’ bodies through contaminated surgical or medical equipment, such as catheters and respiratory ventilators. Health-care facilities seek to limit nosocomial infections through training and hygiene protocols such as those described in Control of Microbial Growth.",True,Healthcare-Associated (Nosocomial) Infections,,,,
8983c1b7-4b94-45e7-9658-0b5355502dea,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,Learning Objectives,False,Learning Objectives,,,,
8bca3785-359e-429c-8a6e-9944e579b5df,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,Pioneers of Epidemiology,False,Pioneers of Epidemiology,,,,
55b45bb0-ad1f-416f-b1d1-d87b0098dacb,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"John Snow (Figure 12.5) was a British physician known as the father of epidemiology for determining the source of the 1854 Broad Street cholera epidemic in London. Based on observations he had made during an earlier cholera outbreak (1848–1849), Snow proposed that cholera was spread through a fecal-oral route of transmission and that a microbe was the infectious agent. He investigated the 1854 cholera epidemic in two ways. First, suspecting that contaminated water was the source of the epidemic, Snow identified the source of water for those infected. He found a high frequency of cholera cases among individuals who obtained their water from the River Thames downstream from London. This water contained the refuse and sewage from London and settlements upstream. He also noted that brewery workers did not contract cholera and on investigation found the owners provided the workers with beer to drink and stated that they likely did not drink water.[1] Second, he also painstakingly mapped the incidence of cholera and found a high frequency among those individuals using a particular water pump located on Broad Street. In response to Snow’s advice, local officials removed the pump’s handle,[2] resulting in the containment of the Broad Street cholera epidemic.",True,Pioneers of Epidemiology,Figure 12.5,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.5.png,"Figure 12.5 (a) John Snow (1813–1858), British physician and father of epidemiology. (b) Snow’s detailed mapping of cholera incidence led to the discovery of the contaminated water pump on Broad street (red square) responsible for the 1854 cholera epidemic. (credit a: modification of work by “Rsabbatini”/Wikimedia Commons)"
06adf442-3778-4030-80ad-aab45e05124b,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Snow’s work represents an early epidemiological study and it resulted in the first known public health response to an epidemic. Snow’s meticulous case-tracking methods are now common practice in studying disease outbreaks and in associating new diseases with their causes. His work further shed light on unsanitary sewage practices and the effects of waste dumping in the Thames. Additionally, his work supported the germ theory of disease, which argued disease could be transmitted through contaminated items, including water contaminated with fecal matter.",True,Pioneers of Epidemiology,,,,
818565b5-7b1a-44ed-8825-5afd5901e1f4,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Snow’s work illustrated what is referred to today as a common source spread of infectious disease, in which there is a single source for all of the individuals infected. In this case, the single source was the contaminated well below the Broad Street pump. Types of common source spread include point source spread, continuous common source spread, and intermittent common source spread. In point source spread of infectious disease, the common source operates for a short time period—less than the incubation period of the pathogen. An example of point source spread is a single contaminated potato salad at a group picnic. In continuous common source spread, the infection occurs for an extended period of time, longer than the incubation period. An example of continuous common source spread would be the source of London water taken downstream of the city, which was continuously contaminated with sewage from upstream. Finally, with intermittent common source spread, infections occur for a period, stop, and then begin again. This might be seen in infections from a well that was contaminated only after large rainfalls and that cleared itself of contamination after a short period.",True,Pioneers of Epidemiology,,,,
23adecaf-b4e4-41df-a8da-ce04fdb03b5d,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"In contrast to common source spread, propagated spread occurs through direct or indirect person-to-person contact. With propagated spread, there is no single source for infection; each infected individual becomes a source for one or more subsequent infections. With propagated spread, unless the spread is stopped immediately, infections occur for longer than the incubation period. Although point sources often lead to large-scale but localized outbreaks of short duration, propagated spread typically results in longer duration outbreaks that can vary from small to large, depending on the population and the disease (Figure 12.6). In addition, because of person-to-person transmission, propagated spread cannot be easily stopped at a single source like point source spread.",True,Pioneers of Epidemiology,Figure 12.6,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.6.png,"Figure 12.6 (a) Outbreaks that can be attributed to point source spread often have a short duration. (b) Outbreaks attributed to propagated spread can have a more extended duration. (credit a, b: modification of work by Centers for Disease Control and Prevention)"
f4d1671a-051b-45b9-b7e3-2c0e54569657,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Florence Nightingale’s work is another example of an early epidemiological study. In 1854, Nightingale was part of a contingent of nurses dispatched by the British military to care for wounded soldiers during the Crimean War. Nightingale kept meticulous records regarding the causes of illness and death during the war. Her recordkeeping was a fundamental task of what would later become the science of epidemiology. Her analysis of the data she collected was published in 1858. In this book, she presented monthly frequency data on causes of death in a wedge chart histogram (Figure 12.7). This graphical presentation of data, unusual at the time, powerfully illustrated that the vast majority of casualties during the war occurred not due to wounds sustained in action but to what Nightingale deemed preventable infectious diseases. Often these diseases occurred because of poor sanitation and lack of access to hospital facilities. Nightingale’s findings led to many reforms in the British military’s system of medical care.",True,Pioneers of Epidemiology,Figure 12.7,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.7.png,"Figure 12.7 (a) Florence Nightingale reported on the data she collected as a nurse in the Crimean War. (b) Nightingale’s diagram shows the number of fatalities in soldiers by month of the conflict from various causes. The total number dead in a particular month is equal to the area of the wedge for that month. The colored sections of the wedge represent different causes of death: wounds (pink), preventable infectious diseases (gray), and all other causes (brown)."
f0a26d02-2e86-49ff-924c-bcacf2652db5,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Joseph Lister provided early epidemiological evidence leading to good public health practices in clinics and hospitals. These settings were notorious in the mid-1800s for fatal infections of surgical wounds at a time when the germ theory of disease was not yet widely accepted (see Foundations of Modern Cell Theory). Most physicians did not wash their hands between patient visits or clean and sterilize their surgical tools. Lister, however, discovered the disinfecting properties of carbolic acid, also known as phenol. He introduced several disinfection protocols that dramatically lowered post-surgical infection rates.[3] He demanded that surgeons who worked for him use a 5% carbolic acid solution to clean their surgical tools between patients, and even went so far as to spray the solution onto bandages and over the surgical site during operations (Figure 12.8). He also took precautions not to introduce sources of infection from his skin or clothing by removing his coat, rolling up his sleeves, and washing his hands in a dilute solution of carbolic acid before and during the surgery.",True,Pioneers of Epidemiology,Figure 12.8,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.8.png,Figure 12.8 Joseph Lister initiated the use of a carbolic acid (phenol) during surgeries. This illustration of a surgery shows a pressurized canister of carbolic acid being sprayed over the surgical site.
f6d83e44-a571-4198-a507-d142622979ce,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,John Snow’s own account of his work (https://openstax.org/l/22JohnSnowacco) has additional links and information.,True,Pioneers of Epidemiology,,,,
d03604ed-8dbe-46b2-8a7e-e632090c3116,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,This CDC resource (https://openstax.org/l/22CDCpointsourc) further breaks down the pattern expected from a point-source outbreak.,True,Pioneers of Epidemiology,,,,
ff04a4e1-7525-468c-a1a4-3f0fff9a6bf5,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,Learn more about Nightingale’s wedge chart (https://openstax.org/l/22nightwedgecha) here.,True,Pioneers of Epidemiology,,,,
191d04bb-8126-4420-83d4-b88597f382b1,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,Types of Epidemiological Studies,False,Types of Epidemiological Studies,,,,
74fc5017-4eb7-4b82-a77e-80ec4f482446,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Today, epidemiologists make use of study designs, the manner in which data are gathered to test a hypothesis, similar to those of researchers studying other phenomena that occur in populations. These approaches can be divided into observational studies (in which subjects are not manipulated) and experimental studies (in which subjects are manipulated). Collectively, these studies give modern-day epidemiologists multiple tools for exploring the connections between infectious diseases and the populations of susceptible individuals they might infect.",True,Types of Epidemiological Studies,,,,
d9346654-3268-4d55-aed1-0bdbb6ce1179,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,Observational Studies,False,Observational Studies,,,,
82ca1261-3863-4fb0-bec3-ad19ffb1a896,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"In an observational study, data are gathered from study participants through measurements (such as physiological variables like white blood cell count), or answers to questions in interviews (such as recent travel or exercise frequency). The subjects in an observational study are typically chosen at random from a population of affected or unaffected individuals. However, the subjects in an observational study are in no way manipulated by the researcher. Observational studies are typically easier to carry out than experimental studies, and in certain situations they may be the only studies possible for ethical reasons.",True,Observational Studies,,,,
ae3e5fc1-a729-44c5-be73-4483b2d82f18,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Observational studies are only able to measure associations between disease occurrence and possible causative agents; they do not necessarily prove a causal relationship. For example, suppose a study finds an association between heavy coffee drinking and lower incidence of skin cancer. This might suggest that coffee prevents skin cancer, but there may be another unmeasured factor involved, such as the amount of sun exposure the participants receive. If it turns out that coffee drinkers work more in offices and spend less time outside in the sun than those who drink less coffee, then it may be possible that the lower rate of skin cancer is due to less sun exposure, not to coffee consumption. The observational study cannot distinguish between these two potential causes.",True,Observational Studies,,,,
ceb04510-754d-4146-9dff-d147a296749b,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"There are several useful approaches in observational studies. These include methods classified as descriptive epidemiology and analytical epidemiology. Descriptive epidemiology gathers information about a disease outbreak, the affected individuals, and how the disease has spread over time in an exploratory stage of study. This type of study will involve interviews with patients, their contacts, and their family members; examination of samples and medical records; and even histories of food and beverages consumed. Such a study might be conducted while the outbreak is still occurring. Descriptive studies might form the basis for developing a hypothesis of causation that could be tested by more rigorous observational and experimental studies.",True,Observational Studies,,,,
e8c770d7-985e-43aa-9095-ccd34a6e6a12,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Analytical epidemiology employs carefully selected groups of individuals in an attempt to more convincingly evaluate hypotheses about potential causes for a disease outbreak. The selection of cases is generally made at random, so the results are not biased because of some common characteristic of the study participants. Analytical studies may gather their data by going back in time (retrospective studies), or as events unfold forward in time (prospective studies).",True,Observational Studies,,,,
ed40be12-e24c-45db-ae7f-1ef6bc87656b,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,Experimental Studies,False,Experimental Studies,,,,
fd714152-6b30-476c-88fd-201d81f96ff9,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Experimental epidemiology uses laboratory or clinical studies in which the investigator manipulates the study subjects to study the connections between diseases and potential causative agents or to assess treatments. Examples of treatments might be the administration of a drug, the inclusion or exclusion of different dietary items, physical exercise, or a particular surgical procedure. Animals or humans are used as test subjects. Because experimental studies involve manipulation of subjects, they are typically more difficult and sometimes impossible for ethical reasons.",True,Experimental Studies,,,,
e3adf064-52a0-4f87-8cdc-fbc1eb9ae62a,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Koch’s postulates require experimental interventions to determine the causative agent for a disease. Unlike observational studies, experimental studies can provide strong evidence supporting cause because other factors are typically held constant when the researcher manipulates the subject. The outcomes for one group receiving the treatment are compared to outcomes for a group that does not receive the treatment but is treated the same in every other way. For example, one group might receive a regimen of a drug administered as a pill, while the untreated group receives a placebo (a pill that looks the same but has no active ingredient). Both groups are treated as similarly as possible except for the administration of the drug. Because other variables are held constant in both the treated and the untreated groups, the researcher is more certain that any change in the treated group is a result of the specific manipulation.",True,Experimental Studies,,,,
48017b7f-090c-44b7-8ec2-13050f586ab3,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Experimental studies provide the strongest evidence for the etiology of disease, but they must also be designed carefully to eliminate subtle effects of bias. Typically, experimental studies with humans are conducted as double- blind studies, meaning neither the subjects nor the researchers know who is a treatment case and who is not. This design removes a well-known cause of bias in research called the placebo effect, in which knowledge of the treatment by either the subject or the researcher can influence the outcomes.",True,Experimental Studies,,,,
3344603f-1fdb-40b0-aa92-f4105106b2fe,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,Learning Objectives,False,Learning Objectives,,,,
8a598f59-0e86-4476-a567-b3d84dbadd0f,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,Pioneers of Epidemiology,False,Pioneers of Epidemiology,,,,
210392bb-a84b-4202-83cc-332a83b3b436,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"John Snow (Figure 12.5) was a British physician known as the father of epidemiology for determining the source of the 1854 Broad Street cholera epidemic in London. Based on observations he had made during an earlier cholera outbreak (1848–1849), Snow proposed that cholera was spread through a fecal-oral route of transmission and that a microbe was the infectious agent. He investigated the 1854 cholera epidemic in two ways. First, suspecting that contaminated water was the source of the epidemic, Snow identified the source of water for those infected. He found a high frequency of cholera cases among individuals who obtained their water from the River Thames downstream from London. This water contained the refuse and sewage from London and settlements upstream. He also noted that brewery workers did not contract cholera and on investigation found the owners provided the workers with beer to drink and stated that they likely did not drink water.[1] Second, he also painstakingly mapped the incidence of cholera and found a high frequency among those individuals using a particular water pump located on Broad Street. In response to Snow’s advice, local officials removed the pump’s handle,[2] resulting in the containment of the Broad Street cholera epidemic.",True,Pioneers of Epidemiology,Figure 12.5,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.5.png,"Figure 12.5 (a) John Snow (1813–1858), British physician and father of epidemiology. (b) Snow’s detailed mapping of cholera incidence led to the discovery of the contaminated water pump on Broad street (red square) responsible for the 1854 cholera epidemic. (credit a: modification of work by “Rsabbatini”/Wikimedia Commons)"
d14f2978-800e-465b-ba5e-68de9dfb7a23,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Snow’s work represents an early epidemiological study and it resulted in the first known public health response to an epidemic. Snow’s meticulous case-tracking methods are now common practice in studying disease outbreaks and in associating new diseases with their causes. His work further shed light on unsanitary sewage practices and the effects of waste dumping in the Thames. Additionally, his work supported the germ theory of disease, which argued disease could be transmitted through contaminated items, including water contaminated with fecal matter.",True,Pioneers of Epidemiology,,,,
ccd44201-50dd-4e56-94d0-4ee0ba18f5fd,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Snow’s work illustrated what is referred to today as a common source spread of infectious disease, in which there is a single source for all of the individuals infected. In this case, the single source was the contaminated well below the Broad Street pump. Types of common source spread include point source spread, continuous common source spread, and intermittent common source spread. In point source spread of infectious disease, the common source operates for a short time period—less than the incubation period of the pathogen. An example of point source spread is a single contaminated potato salad at a group picnic. In continuous common source spread, the infection occurs for an extended period of time, longer than the incubation period. An example of continuous common source spread would be the source of London water taken downstream of the city, which was continuously contaminated with sewage from upstream. Finally, with intermittent common source spread, infections occur for a period, stop, and then begin again. This might be seen in infections from a well that was contaminated only after large rainfalls and that cleared itself of contamination after a short period.",True,Pioneers of Epidemiology,,,,
22c98dd3-04bf-4938-a826-2a7b0164f944,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"In contrast to common source spread, propagated spread occurs through direct or indirect person-to-person contact. With propagated spread, there is no single source for infection; each infected individual becomes a source for one or more subsequent infections. With propagated spread, unless the spread is stopped immediately, infections occur for longer than the incubation period. Although point sources often lead to large-scale but localized outbreaks of short duration, propagated spread typically results in longer duration outbreaks that can vary from small to large, depending on the population and the disease (Figure 12.6). In addition, because of person-to-person transmission, propagated spread cannot be easily stopped at a single source like point source spread.",True,Pioneers of Epidemiology,Figure 12.6,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.6.png,"Figure 12.6 (a) Outbreaks that can be attributed to point source spread often have a short duration. (b) Outbreaks attributed to propagated spread can have a more extended duration. (credit a, b: modification of work by Centers for Disease Control and Prevention)"
1b5b6f3f-d1bd-4298-b791-ca5dff9115fb,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Florence Nightingale’s work is another example of an early epidemiological study. In 1854, Nightingale was part of a contingent of nurses dispatched by the British military to care for wounded soldiers during the Crimean War. Nightingale kept meticulous records regarding the causes of illness and death during the war. Her recordkeeping was a fundamental task of what would later become the science of epidemiology. Her analysis of the data she collected was published in 1858. In this book, she presented monthly frequency data on causes of death in a wedge chart histogram (Figure 12.7). This graphical presentation of data, unusual at the time, powerfully illustrated that the vast majority of casualties during the war occurred not due to wounds sustained in action but to what Nightingale deemed preventable infectious diseases. Often these diseases occurred because of poor sanitation and lack of access to hospital facilities. Nightingale’s findings led to many reforms in the British military’s system of medical care.",True,Pioneers of Epidemiology,Figure 12.7,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.7.png,"Figure 12.7 (a) Florence Nightingale reported on the data she collected as a nurse in the Crimean War. (b) Nightingale’s diagram shows the number of fatalities in soldiers by month of the conflict from various causes. The total number dead in a particular month is equal to the area of the wedge for that month. The colored sections of the wedge represent different causes of death: wounds (pink), preventable infectious diseases (gray), and all other causes (brown)."
a07b17f7-193e-48db-9ce4-b110ffaf5b28,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Joseph Lister provided early epidemiological evidence leading to good public health practices in clinics and hospitals. These settings were notorious in the mid-1800s for fatal infections of surgical wounds at a time when the germ theory of disease was not yet widely accepted (see Foundations of Modern Cell Theory). Most physicians did not wash their hands between patient visits or clean and sterilize their surgical tools. Lister, however, discovered the disinfecting properties of carbolic acid, also known as phenol. He introduced several disinfection protocols that dramatically lowered post-surgical infection rates.[3] He demanded that surgeons who worked for him use a 5% carbolic acid solution to clean their surgical tools between patients, and even went so far as to spray the solution onto bandages and over the surgical site during operations (Figure 12.8). He also took precautions not to introduce sources of infection from his skin or clothing by removing his coat, rolling up his sleeves, and washing his hands in a dilute solution of carbolic acid before and during the surgery.",True,Pioneers of Epidemiology,Figure 12.8,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.8.png,Figure 12.8 Joseph Lister initiated the use of a carbolic acid (phenol) during surgeries. This illustration of a surgery shows a pressurized canister of carbolic acid being sprayed over the surgical site.
7c02e4b7-5fe4-4fe1-8382-d5b67e2e283d,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,Types of Epidemiological Studies,False,Types of Epidemiological Studies,,,,
fa15dd98-520d-4bd4-b81c-121785be7f43,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Today, epidemiologists make use of study designs, the manner in which data are gathered to test a hypothesis, similar to those of researchers studying other phenomena that occur in populations. These approaches can be divided into observational studies (in which subjects are not manipulated) and experimental studies (in which subjects are manipulated). Collectively, these studies give modern-day epidemiologists multiple tools for exploring the connections between infectious diseases and the populations of susceptible individuals they might infect.",True,Types of Epidemiological Studies,,,,
025e5601-01ed-4485-a9c8-bb544badacc4,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"In an observational study, data are gathered from study participants through measurements (such as physiological variables like white blood cell count), or answers to questions in interviews (such as recent travel or exercise frequency). The subjects in an observational study are typically chosen at random from a population of affected or unaffected individuals. However, the subjects in an observational study are in no way manipulated by the researcher. Observational studies are typically easier to carry out than experimental studies, and in certain situations they may be the only studies possible for ethical reasons.",True,Types of Epidemiological Studies,,,,
aab888f3-fa8a-4d58-b027-7c7382e0656b,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Observational studies are only able to measure associations between disease occurrence and possible causative agents; they do not necessarily prove a causal relationship. For example, suppose a study finds an association between heavy coffee drinking and lower incidence of skin cancer. This might suggest that coffee prevents skin cancer, but there may be another unmeasured factor involved, such as the amount of sun exposure the participants receive. If it turns out that coffee drinkers work more in offices and spend less time outside in the sun than those who drink less coffee, then it may be possible that the lower rate of skin cancer is due to less sun exposure, not to coffee consumption. The observational study cannot distinguish between these two potential causes.",True,Types of Epidemiological Studies,,,,
9981e771-c460-47fa-b8d6-fb751e8fde0d,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"There are several useful approaches in observational studies. These include methods classified as descriptive epidemiology and analytical epidemiology. Descriptive epidemiology gathers information about a disease outbreak, the affected individuals, and how the disease has spread over time in an exploratory stage of study. This type of study will involve interviews with patients, their contacts, and their family members; examination of samples and medical records; and even histories of food and beverages consumed. Such a study might be conducted while the outbreak is still occurring. Descriptive studies might form the basis for developing a hypothesis of causation that could be tested by more rigorous observational and experimental studies.",True,Types of Epidemiological Studies,,,,
74f19352-97ab-4cb4-8d00-aad80e11a00a,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Analytical epidemiology employs carefully selected groups of individuals in an attempt to more convincingly evaluate hypotheses about potential causes for a disease outbreak. The selection of cases is generally made at random, so the results are not biased because of some common characteristic of the study participants. Analytical studies may gather their data by going back in time (retrospective studies), or as events unfold forward in time (prospective studies).",True,Types of Epidemiological Studies,,,,
bc56c79c-7790-47d1-8c00-282016dc0ebe,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Experimental epidemiology uses laboratory or clinical studies in which the investigator manipulates the study subjects to study the connections between diseases and potential causative agents or to assess treatments. Examples of treatments might be the administration of a drug, the inclusion or exclusion of different dietary items, physical exercise, or a particular surgical procedure. Animals or humans are used as test subjects. Because experimental studies involve manipulation of subjects, they are typically more difficult and sometimes impossible for ethical reasons.",True,Types of Epidemiological Studies,,,,
31b89c5f-c8ce-4d4b-a9c3-00ac8c10e692,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Koch’s postulates require experimental interventions to determine the causative agent for a disease. Unlike observational studies, experimental studies can provide strong evidence supporting cause because other factors are typically held constant when the researcher manipulates the subject. The outcomes for one group receiving the treatment are compared to outcomes for a group that does not receive the treatment but is treated the same in every other way. For example, one group might receive a regimen of a drug administered as a pill, while the untreated group receives a placebo (a pill that looks the same but has no active ingredient). Both groups are treated as similarly as possible except for the administration of the drug. Because other variables are held constant in both the treated and the untreated groups, the researcher is more certain that any change in the treated group is a result of the specific manipulation.",True,Types of Epidemiological Studies,,,,
62458961-cfca-4e09-abf7-ff639f73a52c,https://open.oregonstate.education/microbiology/,12.2	Tracking Infectious Diseases,https://open.oregonstate.education/microbiology/chapter/16-2tracking-infectious-diseases/,"Experimental studies provide the strongest evidence for the etiology of disease, but they must also be designed carefully to eliminate subtle effects of bias. Typically, experimental studies with humans are conducted as double- blind studies, meaning neither the subjects nor the researchers know who is a treatment case and who is not. This design removes a well-known cause of bias in research called the placebo effect, in which knowledge of the treatment by either the subject or the researcher can influence the outcomes.",True,Types of Epidemiological Studies,,,,
f09ef652-4470-4a60-9205-cdb9b89c84d7,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,Analyzing Disease in a Population,False,Analyzing Disease in a Population,,,,
dd03e1a5-7390-4e2f-9370-fbe44d131c09,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"Epidemiological analyses are always carried out with reference to a population, which is the group of individuals that are at risk for the disease or condition. The population can be defined geographically, but if only a portion of the individuals in that area are susceptible, additional criteria may be required. Susceptible individuals may be defined by particular behaviors, such as intravenous drug use, owning particular pets, or membership in an institution, such as a college. Being able to define the population is important because most measures of interest in epidemiology are made with reference to the size of the population.",True,Analyzing Disease in a Population,,,,
82cda98a-ac8e-4499-8d2d-bffd3a7b5986,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"The state of being diseased is called morbidity. Morbidity in a population can be expressed in a few different ways. Morbidity or total morbidity is expressed in numbers of individuals without reference to the size of the population. The morbidity rate can be expressed as the number of diseased individuals out of a standard number of individuals in the population, such as 100,000, or as a percent of the population.",True,Analyzing Disease in a Population,,,,
3a1b9ce9-3453-4707-82c8-1cccb5338ce8,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"There are two aspects of morbidity that are relevant to an epidemiologist: a disease’s prevalence and its incidence. Prevalence is the number, or proportion, of individuals with a particular illness in a given population at a point in time. For example, the Centers for Disease Control and Prevention (CDC) estimated that in 2012, there were about 1.2 million people 13 years and older with an active human immunodeficiency virus (HIV) infection. Expressed as a proportion, or rate, this is a prevalence of 467 infected persons per 100,000 in the population.[1] On the other hand, incidence is the number or proportion of new cases in a period of time. For the same year and population, the CDC estimates that there were 43,165 newly diagnosed cases of HIV infection, which is an incidence of 13.7 new cases per 100,000 in the population.[2] The relationship between incidence and prevalence can be seen in Figure 12.2. For a chronic disease like HIV infection, prevalence will generally be higher than incidence because it represents the cumulative number of new cases over many years minus the number of cases that are no longer active (e.g., because the patient died or was cured).",True,Analyzing Disease in a Population,Figure 12.2,12.1	The Language of Epidemiologists,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.2.png,Figure 12.2 This graph compares the incidence of HIV (the number of new cases reported each year) with the prevalence (the total number of cases each year). Prevalence and incidence can also be expressed as a rate or proportion for a given population.
ac2626ab-6a6a-4f80-93f5-c73ab62eb9d2,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"In addition to morbidity rates, the incidence and prevalence of mortality (death) may also be reported. A mortality rate can be expressed as the percentage of the population that has died from a disease or as the number of deaths per 100,000 persons (or other suitable standard number).",True,Analyzing Disease in a Population,,,,
44aba4e7-aebb-439e-8d51-345652f72dd2,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,Patterns of Incidence,False,Patterns of Incidence,,,,
11d367d4-d895-4278-bc4e-50f790ebdf49,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"Diseases that are seen only occasionally, and usually without geographic concentration, are called sporadic diseases. Examples of sporadic diseases include tetanus, rabies, and plague. In the United States, Clostridium tetani, the bacterium that causes tetanus, is ubiquitous in the soil environment, but incidences of infection occur only rarely and in scattered locations because most individuals are vaccinated, clean wounds appropriately, or are only rarely in a situation that would cause infection.[3] Likewise in the United States there are a few scattered cases of plague each year, usually contracted from rodents in rural areas in the western states.[4]",True,Patterns of Incidence,,,,
4719b967-f392-4628-87a6-e6ade2d0dfcd,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"Diseases that are constantly present (often at a low level) in a population within a particular geographic region are called endemic diseases. For example, malaria is endemic to some regions of Brazil, but is not endemic to the United States.",True,Patterns of Incidence,,,,
e39b8ad5-3a43-4d43-8aa8-20e8cbb58516,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"Diseases for which a larger than expected number of cases occurs in a short time within a geographic region are called epidemic diseases. Influenza is a good example of a commonly epidemic disease. Incidence patterns of influenza tend to rise each winter in the northern hemisphere. These seasonal increases are expected, so it would not be accurate to say that influenza is epidemic every winter; however, some winters have an usually large number of seasonal influenza cases in particular regions, and such situations would qualify as epidemics (Figure 12.3 and Figure 12.4).",True,Patterns of Incidence,Figure 12.3,12.1	The Language of Epidemiologists,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.3.png,Figure 12.3 The 2007–2008 influenza season in the United States saw much higher than normal numbers of visits to emergency departments for influenza-like symptoms as compared to the previous and the following years. (credit: modification of work by Centers for Disease Control and Prevention)
958ba683-3db7-40da-91f6-fdec1a6d7356,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"An epidemic disease signals the breakdown of an equilibrium in disease frequency, often resulting from some change in environmental conditions or in the population. In the case of influenza, the disruption can be due to antigenic shift or drift (see Virulence Factors of Bacterial and Viral Pathogens), which allows influenza virus strains to circumvent the acquired immunity of their human hosts.",True,Patterns of Incidence,,,,
b3a7227b-8046-42fd-adf0-2ac1181428dc,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"An epidemic that occurs on a worldwide scale is called a pandemic disease. For example, HIV/AIDS is a pandemic disease and novel influenza virus strains often become pandemic.",True,Patterns of Incidence,,,,
0cf20c5b-4587-4d71-899d-d2a22dfc5979,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,Etiology,False,Etiology,,,,
1ee6d724-f6ce-4610-ab31-4c0a30859ca5,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,The Role of Public Health Organizations,False,The Role of Public Health Organizations,,,,
06c692ba-2c55-4c97-ae75-1ad5463fafc9,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"The main national public health agency in the United States is the Centers for Disease Control and Prevention (CDC), an agency of the Department of Health and Human Services. The CDC is charged with protecting the public from disease and injury. One way that the CDC carries out this mission is by overseeing the National Notifiable Disease Surveillance System (NNDSS) in cooperation with regional, state, and territorial public health departments. The NNDSS monitors diseases considered to be of public health importance on a national scale. Such diseases are called notifiable diseases or reportable diseases because all cases must be reported to the CDC. A physician treating a patient with a notifiable disease is legally required to submit a report on the case. Notifiable diseases include HIV infection, measles, West Nile virus infections, and many others. Some states have their own lists of notifiable diseases that include diseases beyond those on the CDC’s list.",True,The Role of Public Health Organizations,,,,
c5aef607-ed1e-43df-aef0-9f7d765401b6,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"Notifiable diseases are tracked by epidemiological studies and the data is used to inform health-care providers and the public about possible risks. The CDC publishes the Morbidity and Mortality Weekly Report (MMWR), which provides physicians and health-care workers with updates on public health issues and the latest data pertaining to notifiable diseases. Table 12.1 is an example of the kind of data contained in the MMWR.",True,The Role of Public Health Organizations,,,,
1b1c0129-61a9-4d61-b09c-25f4d6463284,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,The current Morbidity and Mortality Weekly Report is available online (https://openstax.org/l/22mortweekrep).,True,The Role of Public Health Organizations,,,,
f9477474-6f08-4f3b-86d9-bdaccce919c5,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,Patterns of Incidence,False,Patterns of Incidence,,,,
ffaf8b4d-214a-4199-9f92-9a4f51ed4699,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"Diseases that are seen only occasionally, and usually without geographic concentration, are called sporadic diseases. Examples of sporadic diseases include tetanus, rabies, and plague. In the United States, Clostridium tetani, the bacterium that causes tetanus, is ubiquitous in the soil environment, but incidences of infection occur only rarely and in scattered locations because most individuals are vaccinated, clean wounds appropriately, or are only rarely in a situation that would cause infection.[3] Likewise in the United States there are a few scattered cases of plague each year, usually contracted from rodents in rural areas in the western states.[4]",True,Patterns of Incidence,,,,
e63e3b26-890b-406c-810e-bc90ab5419af,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"Diseases that are constantly present (often at a low level) in a population within a particular geographic region are called endemic diseases. For example, malaria is endemic to some regions of Brazil, but is not endemic to the United States.",True,Patterns of Incidence,,,,
64f4bd8a-32ae-4088-842d-1ec49891e3cb,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"Diseases for which a larger than expected number of cases occurs in a short time within a geographic region are called epidemic diseases. Influenza is a good example of a commonly epidemic disease. Incidence patterns of influenza tend to rise each winter in the northern hemisphere. These seasonal increases are expected, so it would not be accurate to say that influenza is epidemic every winter; however, some winters have an usually large number of seasonal influenza cases in particular regions, and such situations would qualify as epidemics (Figure 12.3 and Figure 12.4).",True,Patterns of Incidence,Figure 12.3,12.1	The Language of Epidemiologists,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-16.3.png,Figure 12.3 The 2007–2008 influenza season in the United States saw much higher than normal numbers of visits to emergency departments for influenza-like symptoms as compared to the previous and the following years. (credit: modification of work by Centers for Disease Control and Prevention)
dc827fc1-4ac6-422f-bf32-0e5d480f4340,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"An epidemic disease signals the breakdown of an equilibrium in disease frequency, often resulting from some change in environmental conditions or in the population. In the case of influenza, the disruption can be due to antigenic shift or drift (see Virulence Factors of Bacterial and Viral Pathogens), which allows influenza virus strains to circumvent the acquired immunity of their human hosts.",True,Patterns of Incidence,,,,
3d8f48bd-cb2e-433b-93fa-60c81644f2d4,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"An epidemic that occurs on a worldwide scale is called a pandemic disease. For example, HIV/AIDS is a pandemic disease and novel influenza virus strains often become pandemic.",True,Patterns of Incidence,,,,
4fea0c2d-72f2-4ae7-8b59-36721224068d,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,Etiology,False,Etiology,,,,
51b70ab0-7b0b-44a5-9289-144dab5c53dc,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,The Role of Public Health Organizations,False,The Role of Public Health Organizations,,,,
ed2f7d04-f27a-4fc9-bfd5-437102d99465,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"The main national public health agency in the United States is the Centers for Disease Control and Prevention (CDC), an agency of the Department of Health and Human Services. The CDC is charged with protecting the public from disease and injury. One way that the CDC carries out this mission is by overseeing the National Notifiable Disease Surveillance System (NNDSS) in cooperation with regional, state, and territorial public health departments. The NNDSS monitors diseases considered to be of public health importance on a national scale. Such diseases are called notifiable diseases or reportable diseases because all cases must be reported to the CDC. A physician treating a patient with a notifiable disease is legally required to submit a report on the case. Notifiable diseases include HIV infection, measles, West Nile virus infections, and many others. Some states have their own lists of notifiable diseases that include diseases beyond those on the CDC’s list.",True,The Role of Public Health Organizations,,,,
2a020eed-9e30-4cdb-b925-45fc8edf42fd,https://open.oregonstate.education/microbiology/,12.1	The Language of Epidemiologists,https://open.oregonstate.education/microbiology/chapter/16-1the-language-of-epidemiologists/,"Notifiable diseases are tracked by epidemiological studies and the data is used to inform health-care providers and the public about possible risks. The CDC publishes the Morbidity and Mortality Weekly Report (MMWR), which provides physicians and health-care workers with updates on public health issues and the latest data pertaining to notifiable diseases. Table 12.1 is an example of the kind of data contained in the MMWR.",True,The Role of Public Health Organizations,,,,
addcfa83-5159-4f64-ac4a-e01bca51ce06,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,Learning Objectives,False,Learning Objectives,,,,
3dc96f2b-b5a3-4d9a-8a31-0d4a337555d3,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,Bacterial Exoenzymes and Toxins as Virulence Factors,False,Bacterial Exoenzymes and Toxins as Virulence Factors,,,,
fc23df86-bac8-4f47-9d92-573763419e21,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"After exposure and adhesion, the next step in pathogenesis is invasion, which can involve enzymes and toxins. Many pathogens achieve invasion by entering the bloodstream, an effective means of dissemination because blood vessels pass close to every cell in the body. The downside of this mechanism of dispersal is that the blood also includes numerous elements of the immune system. Various terms ending in –emia are used to describe the presence of pathogens in the bloodstream. The presence of bacteria in blood is called bacteremia. When viruses are found in the blood, it is called viremia. The term toxemia describes the condition when toxins are found in the blood. If bacteria are both present and multiplying in the blood, this condition is called septicemia. Patients with septicemia are described as septic.",True,Bacterial Exoenzymes and Toxins as Virulence Factors,,,,
06983346-92e8-4453-9b69-c8aa91802b5b,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,Exoenzymes,False,Exoenzymes,,,,
a19feef6-bbe5-4b12-b3a7-7cc119e83c90,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Some pathogens produce extracellular enzymes, or exoenzymes, that enable them to invade host cells and deeper tissues. Exoenzymes have a wide variety of targets. Each exoenzyme functions in the context of a particular tissue structure to facilitate invasion or support its own growth and defend against the immune system. For example, hyaluronidase S, an enzyme produced by pathogens like Staphylococcus aureus, degrades the glycoside hyaluronan (hyaluronic acid), which acts as an intercellular cement between adjacent cells in connective tissue (Figure 11.8). This allows the pathogen to pass through the tissue layers at the portal of entry and disseminate elsewhere in the body. Other exoenzymes break down the phospholipid bilyer of host cells, collagen in connective tissue, or DNA released by dying cells.",True,Exoenzymes,Figure 11.8,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.11.png,"Figure 11.8 (a) Hyaluronan is a polymer found in the layers of epidermis that connect adjacent cells. (b) Hyaluronidase produced by bacteria degrades this adhesive polymer in the extracellular matrix, allowing passage between cells that would otherwise be blocked."
b23ff127-1597-4e5a-8e27-47e677c5c93a,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,Toxins,False,Toxins,,,,
38f28919-4db3-4959-b019-67413fffc061,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"In addition to exoenzymes, certain pathogens are able to produce toxins, biological poisons that assist in their ability to invade and cause damage to tissues. The ability of a pathogen to produce toxins to cause damage to host cells is called toxigenicity.",True,Toxins,,,,
69603038-4d2a-4d08-a5be-9ac81558cc8e,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Toxins can be categorized as endotoxins or exotoxins. The lipopolysaccharide (LPS) found on the outer membrane of gram-negative bacteria is called endotoxin (Figure 11.9). During infection and disease, gram-negative bacterial pathogens release endotoxin either when the cell dies, resulting in the disintegration of the membrane, or when the bacterium undergoes binary fission. The lipid component of endotoxin, lipid A, is responsible for the toxic properties of the LPS molecule. Lipid A is relatively conserved across different genera of gram-negative bacteria; therefore, the toxic properties of lipid A are similar regardless of the gram-negative pathogen. Lipid A triggers the immune system’s inflammatory response (see Inflammation and Fever). If the concentration of endotoxin in the body is low, the inflammatory response may provide the host an effective defense against infection; on the other hand, high concentrations of endotoxin in the blood can cause an excessive inflammatory response, leading to a severe drop in blood pressure, multi-organ failure, and death.",True,Toxins,Figure 11.9,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.13.png,"Figure 11.9. Lipopolysaccharide is composed of lipid A, a core glycolipid, and an O-specific polysaccharide side chain. Lipid A is the toxic component that promotes inflammation and fever."
8578ee0f-d3bd-4bab-ba50-8ba6164e8226,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Unlike the toxic lipid A of endotoxin, exotoxins are protein molecules that are produced by a wide variety of living pathogenic bacteria. Although some gram-negative pathogens produce exotoxins, the majority are produced by gram- positive pathogens. Exotoxins differ from endotoxin in several other key characteristics, summarized in Table 11.2. In contrast to endotoxin, which stimulates a general systemic inflammatory response when released, exotoxins are much more specific in their action and the cells they interact with. Each exotoxin targets specific receptors on specific cells and damages those cells through unique molecular mechanisms. Endotoxin remains stable at high temperatures, and requires heating at 121 °C (250 °F) for 45 minutes to inactivate. By contrast, most exotoxins are heat labile because of their protein structure, and many are denatured (inactivated) at temperatures above 41 °C (106 °F). As discussed earlier, endotoxin can stimulate a lethal inflammatory response at very high concentrations and has  a measured LD50 of 0.24 mg/kg. By contrast, very small concentrations of exotoxins can be lethal. For example, botulinum toxin, which causes botulism, has an LD50 of 0.000001 mg/kg (240,000 times more lethal than endotoxin).",True,Toxins,,,,
0583a0f8-2b67-448f-a8d6-e5b57dc37855,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"The exotoxins can be grouped into three categories based on their target: intracellular targeting, membrane disrupting, and superantigens.",True,Toxins,,,,
5c339218-a40c-4ef5-968b-6c27005ec863,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"The intracellular targeting toxins comprise two components: A for activity and B for binding. Thus, these types of toxins are known as A-B exotoxins (Figure 11.10). The B component is responsible for the cellular specificity of the toxin and mediates the initial attachment of the toxin to specific cell surface receptors. Once the A-B toxin binds to the host cell, it is brought into the cell by endocytosis and entrapped in a vacuole. The A and B subunits separate as the vacuole acidifies. The A subunit then enters the cell cytoplasm and interferes with the specific internal cellular function that it targets. Four unique examples of A-B toxins are the diphtheria, cholera, botulinum, and tetanus toxins.",True,Toxins,Figure 11.10,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.14.png,"Figure 11.10 (a) In A-B toxins, the B component binds to the host cell through its interaction with specific cell surface receptors. (b) The toxin is brought in through endocytosis. (c) Once inside the vacuole, the A component (active component) separates from the B component and the A component gains access to the cytoplasm. (credit: modification of work by “Biology Discussion Forum”/YouTube)"
4a126e81-3f66-4043-b1b0-2f5a177c33ad,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,Click this link (https://openstax.org/l/22Botulin) to see an animation of how the botulinum toxin functions.,True,Toxins,,,,
7b6eeef1-d5f3-4bf5-8a72-d1dfd25ee3a5,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Membrane-disrupting toxins affect cell membrane function either by forming pores or by disrupting the phospholipid bilayer in host cell membranes. Two types of membrane-disrupting exotoxins are hemolysins and leukocidins, which form pores in cell membranes, causing leakage of the cytoplasmic contents and cell lysis. These toxins were originally thought to target red blood cells (erythrocytes) and white blood cells (leukocytes), respectively, but we now know they can affect other cells as well.",True,Toxins,,,,
9da9f1c7-2113-4dc3-acbf-c8bc0b1267cf,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"The third class of exotoxins is the superantigens. These are exotoxins that trigger an excessive, nonspecific stimulation of immune cells to secrete cytokines (chemical messengers). The excessive production of cytokines, often called a cytokine storm, elicits a strong immune and inflammatory response that can cause life-threatening high fevers, low blood pressure, multi-organ failure, shock, and death. The prototype superantigen is the toxic shock syndrome toxin of S. aureus. Most toxic shock syndrome cases are associated with vaginal colonization by toxin- producing S. aureus in menstruating women; however, colonization of other body sites can also occur. Some strains of Streptococcus pyogenes also produce superantigens; they are referred to as the streptococcal mitogenic exotoxins and the streptococcal pyrogenic toxins.",True,Toxins,,,,
8b4be7f5-2c47-4f28-90f4-a8b3634cd285,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,Virulence Factors for Survival in the Host and Immune Evasion,False,Virulence Factors for Survival in the Host and Immune Evasion,,,,
9aa68723-c0e5-4076-b0a0-bd5d685fc1d2,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Evading the immune system is also important to invasiveness. Bacteria use a variety of virulence factors to evade phagocytosis by cells of the immune system. For example, many bacteria produce capsules, which are used in adhesion but also aid in immune evasion by preventing ingestion by phagocytes. The composition of the capsule prevents immune cells from being able to adhere and then phagocytose the cell. In addition, the capsule makes the bacterial cell much larger, making it harder for immune cells to engulf the pathogen (Figure 11.11). Some pathogens can also produce proteases to protect themselves against phagocytosis.",True,Virulence Factors for Survival in the Host and Immune Evasion,Figure 11.11,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.17.png,"Figure 11.11 (a) A micrograph of capsules around bacterial cells. (b) Antibodies normally function by binding to antigens, molecules on the surface of pathogenic bacteria. Phagocytes then bind to the antibody, initiating phagocytosis. (c) Some bacteria also produce proteases, virulence factors that break down host antibodies to evade phagocytosis. (credit a: modification of work by Centers for Disease Control and Prevention)"
6e579bc6-3330-47aa-8497-e2a099faea5a,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"In addition to capsules and proteases, some bacterial pathogens produce other virulence factors that allow them to evade the immune system, such as fimbriae to inhibit phagocytosis or mycolic acid to resist some of the killing mechanisms within the phagolysosome.",True,Virulence Factors for Survival in the Host and Immune Evasion,,,,
2aaa3cb6-4790-4b3c-80a6-b5198afa8f8a,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Some bacteria produce virulence factors that promote infection by exploiting molecules naturally produced by the host. For example, most strains of Staphylococcus aureus produce the exoenzyme coagulase, which exploits the natural mechanism of blood clotting to evade the immune system. Normally, blood clotting is triggered in response to blood vessel damage; platelets begin to plug the clot, and a cascade of reactions occurs in which fibrinogen, a soluble protein made by the liver, is cleaved into fibrin. Fibrin is an insoluble, thread-like protein that binds to blood platelets, cross-links, and contracts to form a mesh of clumped platelets and red blood cells. The resulting clot prevents further loss of blood from the damaged blood vessels. However, if bacteria release coagulase into the bloodstream, the fibrinogen-to-fibrin cascade is triggered in the absence of blood vessel damage. The resulting clot coats the bacteria in fibrin, protecting the bacteria from exposure to phagocytic immune cells circulating in the bloodstream.",True,Virulence Factors for Survival in the Host and Immune Evasion,,,,
731b3117-9947-4c5d-a2b1-6592897c34be,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Whereas coagulase causes blood to clot, kinases have the opposite effect by triggering the conversion of plasminogen to plasmin, which is involved in the digestion of fibrin clots. By digesting a clot, kinases allow pathogens trapped in the clot to escape and spread. Examples of kinases include staphylokinases and streptokinases, produced by Staphylococcus aureus and Streptococcus pyogenes, respectively. It is intriguing that S. aureus can produce both coagulase to promote clotting and staphylokinase to stimulate the digestion of clots. The action of the coagulase provides an important protective barrier from the immune system, but when nutrient supplies are diminished or other conditions signal a need for the pathogen to escape and spread, the production of staphylokinase can initiate this process.",True,Virulence Factors for Survival in the Host and Immune Evasion,,,,
bfa82d94-193e-41a4-a48b-6f09c3790621,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"A final mechanism that pathogens can use to protect themselves against the immune system is called antigenic variation, which is the alteration of surface proteins so that a pathogen is no longer recognized by the host’s immune system.",True,Virulence Factors for Survival in the Host and Immune Evasion,,,,
2d6141c8-5b39-424f-af4e-5b335fa3730f,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,Viral Virulence,False,Viral Virulence,,,,
02ffa079-aa95-4e12-819f-7b0e990e3daa,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Although viral pathogens are not similar to bacterial pathogens in terms of structure, some of the properties that contribute to their virulence are similar. Viruses use adhesins to facilitate adhesion to host cells, and certain enveloped viruses rely on antigenic variation to avoid the host immune defenses. These virulence factors are discussed in more detail in the following sections.",True,Viral Virulence,,,,
13b62b28-0839-42f6-810f-10fcdd92d78b,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,Viral Adhesins,False,Viral Adhesins,,,,
3ce75ed1-e963-49cb-a835-0cb805e938ec,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"One of the first steps in any viral infection is adhesion of the virus to specific receptors on the surface of cells. This process is mediated by adhesins that are part of the viral capsid or membrane envelope. The interaction of viral adhesins with specific cell receptors defines the tropism (preferential targeting) of viruses for specific cells, tissues, and organs in the body. The spike protein hemagglutinin found on Influenzavirus is an example of a viral adhesin; it allows the virus to bind to the sialic acid on the membrane of host respiratory and intestinal cells.",True,Viral Adhesins,,,,
6163f154-ca22-45b2-856f-30a40a070ed5,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,Antigenic Variation in Viruses,False,Antigenic Variation in Viruses,,,,
1124e146-ff12-424d-9116-d2daf81ab86f,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Antigenic variation also occurs in certain types of enveloped viruses, including influenza viruses, which exhibit two forms of antigenic variation: antigenic drift and antigenic shift (Figure 11.12). Antigenic drift is the result of point mutations causing slight changes in the spike proteins hemagglutinin (H) and neuraminidase (N). On the other hand, antigenic shift is a major change in spike proteins due to gene reassortment. This reassortment for antigenic shift occurs typically when two different influenza viruses infect the same host.",True,Antigenic Variation in Viruses,Figure 11.12,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.18.png,"Figure 11.12 Antigenic drift and antigenic shift in influenza viruses. (a) In antigenic drift, mutations in the genes for the surface proteins neuraminidase and/or hemagglutinin result in small antigenic changes over time. (b) In antigenic shift, simultaneous infection of a cell with two different influenza viruses results in mixing of the genes. The resultant virus possesses a mixture of the proteins of the original viruses. Influenza pandemics can often be traced to antigenic shifts."
86214247-d350-4db2-ae34-c65ba49e0f02,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"The rate of antigenic variation in influenza viruses is very high, making it difficult for the immune system to recognize the many different strains of Influenzavirus. Although the body may develop immunity to one strain through natural exposure or vaccination, antigenic variation results in the continual emergence of new strains that the immune system will not recognize. This is the main reason that vaccines against Influenzavirus must be given annually. Each year’s influenza vaccine provides protection against the most prevalent strains for that year, but new or different strains may be more prevalent the following year.",True,Antigenic Variation in Viruses,,,,
a7b1e6fe-6231-48c5-a0b2-8427b2213ed4,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,Learning Objectives,False,Learning Objectives,,,,
0040e185-486a-440d-9fe8-20a84c737096,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,Bacterial Exoenzymes and Toxins as Virulence Factors,False,Bacterial Exoenzymes and Toxins as Virulence Factors,,,,
193cf1e6-ce82-4073-b6f3-d2e7e4a258ac,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"After exposure and adhesion, the next step in pathogenesis is invasion, which can involve enzymes and toxins. Many pathogens achieve invasion by entering the bloodstream, an effective means of dissemination because blood vessels pass close to every cell in the body. The downside of this mechanism of dispersal is that the blood also includes numerous elements of the immune system. Various terms ending in –emia are used to describe the presence of pathogens in the bloodstream. The presence of bacteria in blood is called bacteremia. When viruses are found in the blood, it is called viremia. The term toxemia describes the condition when toxins are found in the blood. If bacteria are both present and multiplying in the blood, this condition is called septicemia. Patients with septicemia are described as septic.",True,Bacterial Exoenzymes and Toxins as Virulence Factors,,,,
1739ad31-ce8a-44f7-8c2e-2925f2216e4c,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Some pathogens produce extracellular enzymes, or exoenzymes, that enable them to invade host cells and deeper tissues. Exoenzymes have a wide variety of targets. Each exoenzyme functions in the context of a particular tissue structure to facilitate invasion or support its own growth and defend against the immune system. For example, hyaluronidase S, an enzyme produced by pathogens like Staphylococcus aureus, degrades the glycoside hyaluronan (hyaluronic acid), which acts as an intercellular cement between adjacent cells in connective tissue (Figure 11.8). This allows the pathogen to pass through the tissue layers at the portal of entry and disseminate elsewhere in the body. Other exoenzymes break down the phospholipid bilyer of host cells, collagen in connective tissue, or DNA released by dying cells.",True,Bacterial Exoenzymes and Toxins as Virulence Factors,Figure 11.8,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.11.png,"Figure 11.8 (a) Hyaluronan is a polymer found in the layers of epidermis that connect adjacent cells. (b) Hyaluronidase produced by bacteria degrades this adhesive polymer in the extracellular matrix, allowing passage between cells that would otherwise be blocked."
91d4a915-5655-4f15-8e4d-1c9a5bbe7dbc,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"In addition to exoenzymes, certain pathogens are able to produce toxins, biological poisons that assist in their ability to invade and cause damage to tissues. The ability of a pathogen to produce toxins to cause damage to host cells is called toxigenicity.",True,Bacterial Exoenzymes and Toxins as Virulence Factors,,,,
7979cc35-c434-4d56-b2d6-0182cf8bf349,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Toxins can be categorized as endotoxins or exotoxins. The lipopolysaccharide (LPS) found on the outer membrane of gram-negative bacteria is called endotoxin (Figure 11.9). During infection and disease, gram-negative bacterial pathogens release endotoxin either when the cell dies, resulting in the disintegration of the membrane, or when the bacterium undergoes binary fission. The lipid component of endotoxin, lipid A, is responsible for the toxic properties of the LPS molecule. Lipid A is relatively conserved across different genera of gram-negative bacteria; therefore, the toxic properties of lipid A are similar regardless of the gram-negative pathogen. Lipid A triggers the immune system’s inflammatory response (see Inflammation and Fever). If the concentration of endotoxin in the body is low, the inflammatory response may provide the host an effective defense against infection; on the other hand, high concentrations of endotoxin in the blood can cause an excessive inflammatory response, leading to a severe drop in blood pressure, multi-organ failure, and death.",True,Bacterial Exoenzymes and Toxins as Virulence Factors,Figure 11.9,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.13.png,"Figure 11.9. Lipopolysaccharide is composed of lipid A, a core glycolipid, and an O-specific polysaccharide side chain. Lipid A is the toxic component that promotes inflammation and fever."
962d5393-ca7a-4ad7-a6f6-2e16e7a2a738,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Unlike the toxic lipid A of endotoxin, exotoxins are protein molecules that are produced by a wide variety of living pathogenic bacteria. Although some gram-negative pathogens produce exotoxins, the majority are produced by gram- positive pathogens. Exotoxins differ from endotoxin in several other key characteristics, summarized in Table 11.2. In contrast to endotoxin, which stimulates a general systemic inflammatory response when released, exotoxins are much more specific in their action and the cells they interact with. Each exotoxin targets specific receptors on specific cells and damages those cells through unique molecular mechanisms. Endotoxin remains stable at high temperatures, and requires heating at 121 °C (250 °F) for 45 minutes to inactivate. By contrast, most exotoxins are heat labile because of their protein structure, and many are denatured (inactivated) at temperatures above 41 °C (106 °F). As discussed earlier, endotoxin can stimulate a lethal inflammatory response at very high concentrations and has  a measured LD50 of 0.24 mg/kg. By contrast, very small concentrations of exotoxins can be lethal. For example, botulinum toxin, which causes botulism, has an LD50 of 0.000001 mg/kg (240,000 times more lethal than endotoxin).",True,Bacterial Exoenzymes and Toxins as Virulence Factors,,,,
8374aefa-3513-402c-95f4-68e2723c5843,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"The exotoxins can be grouped into three categories based on their target: intracellular targeting, membrane disrupting, and superantigens.",True,Bacterial Exoenzymes and Toxins as Virulence Factors,,,,
692f9a4b-bd58-4b69-9cd2-fa3f9957ca5c,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"The intracellular targeting toxins comprise two components: A for activity and B for binding. Thus, these types of toxins are known as A-B exotoxins (Figure 11.10). The B component is responsible for the cellular specificity of the toxin and mediates the initial attachment of the toxin to specific cell surface receptors. Once the A-B toxin binds to the host cell, it is brought into the cell by endocytosis and entrapped in a vacuole. The A and B subunits separate as the vacuole acidifies. The A subunit then enters the cell cytoplasm and interferes with the specific internal cellular function that it targets. Four unique examples of A-B toxins are the diphtheria, cholera, botulinum, and tetanus toxins.",True,Bacterial Exoenzymes and Toxins as Virulence Factors,Figure 11.10,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.14.png,"Figure 11.10 (a) In A-B toxins, the B component binds to the host cell through its interaction with specific cell surface receptors. (b) The toxin is brought in through endocytosis. (c) Once inside the vacuole, the A component (active component) separates from the B component and the A component gains access to the cytoplasm. (credit: modification of work by “Biology Discussion Forum”/YouTube)"
b07d9fe9-c138-4e49-8522-6e9d74e88f62,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Membrane-disrupting toxins affect cell membrane function either by forming pores or by disrupting the phospholipid bilayer in host cell membranes. Two types of membrane-disrupting exotoxins are hemolysins and leukocidins, which form pores in cell membranes, causing leakage of the cytoplasmic contents and cell lysis. These toxins were originally thought to target red blood cells (erythrocytes) and white blood cells (leukocytes), respectively, but we now know they can affect other cells as well.",True,Bacterial Exoenzymes and Toxins as Virulence Factors,,,,
1604737f-ee38-4861-a6ac-a3a1cab996c0,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"The third class of exotoxins is the superantigens. These are exotoxins that trigger an excessive, nonspecific stimulation of immune cells to secrete cytokines (chemical messengers). The excessive production of cytokines, often called a cytokine storm, elicits a strong immune and inflammatory response that can cause life-threatening high fevers, low blood pressure, multi-organ failure, shock, and death. The prototype superantigen is the toxic shock syndrome toxin of S. aureus. Most toxic shock syndrome cases are associated with vaginal colonization by toxin- producing S. aureus in menstruating women; however, colonization of other body sites can also occur. Some strains of Streptococcus pyogenes also produce superantigens; they are referred to as the streptococcal mitogenic exotoxins and the streptococcal pyrogenic toxins.",True,Bacterial Exoenzymes and Toxins as Virulence Factors,,,,
2510429c-4bee-47cb-aa36-d16f26830d00,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,Virulence Factors for Survival in the Host and Immune Evasion,False,Virulence Factors for Survival in the Host and Immune Evasion,,,,
7bf9e239-b2e4-416b-9c7c-28a25a878510,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Evading the immune system is also important to invasiveness. Bacteria use a variety of virulence factors to evade phagocytosis by cells of the immune system. For example, many bacteria produce capsules, which are used in adhesion but also aid in immune evasion by preventing ingestion by phagocytes. The composition of the capsule prevents immune cells from being able to adhere and then phagocytose the cell. In addition, the capsule makes the bacterial cell much larger, making it harder for immune cells to engulf the pathogen (Figure 11.11). Some pathogens can also produce proteases to protect themselves against phagocytosis.",True,Virulence Factors for Survival in the Host and Immune Evasion,Figure 11.11,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.17.png,"Figure 11.11 (a) A micrograph of capsules around bacterial cells. (b) Antibodies normally function by binding to antigens, molecules on the surface of pathogenic bacteria. Phagocytes then bind to the antibody, initiating phagocytosis. (c) Some bacteria also produce proteases, virulence factors that break down host antibodies to evade phagocytosis. (credit a: modification of work by Centers for Disease Control and Prevention)"
772712c3-96f5-4bcb-b6be-238acc7e71d5,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"In addition to capsules and proteases, some bacterial pathogens produce other virulence factors that allow them to evade the immune system, such as fimbriae to inhibit phagocytosis or mycolic acid to resist some of the killing mechanisms within the phagolysosome.",True,Virulence Factors for Survival in the Host and Immune Evasion,,,,
8565f2d7-c89b-4a76-8f0a-fe4a4d714ea9,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Some bacteria produce virulence factors that promote infection by exploiting molecules naturally produced by the host. For example, most strains of Staphylococcus aureus produce the exoenzyme coagulase, which exploits the natural mechanism of blood clotting to evade the immune system. Normally, blood clotting is triggered in response to blood vessel damage; platelets begin to plug the clot, and a cascade of reactions occurs in which fibrinogen, a soluble protein made by the liver, is cleaved into fibrin. Fibrin is an insoluble, thread-like protein that binds to blood platelets, cross-links, and contracts to form a mesh of clumped platelets and red blood cells. The resulting clot prevents further loss of blood from the damaged blood vessels. However, if bacteria release coagulase into the bloodstream, the fibrinogen-to-fibrin cascade is triggered in the absence of blood vessel damage. The resulting clot coats the bacteria in fibrin, protecting the bacteria from exposure to phagocytic immune cells circulating in the bloodstream.",True,Virulence Factors for Survival in the Host and Immune Evasion,,,,
b2403f40-8d14-41b8-98a5-8cd039fda52f,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Whereas coagulase causes blood to clot, kinases have the opposite effect by triggering the conversion of plasminogen to plasmin, which is involved in the digestion of fibrin clots. By digesting a clot, kinases allow pathogens trapped in the clot to escape and spread. Examples of kinases include staphylokinases and streptokinases, produced by Staphylococcus aureus and Streptococcus pyogenes, respectively. It is intriguing that S. aureus can produce both coagulase to promote clotting and staphylokinase to stimulate the digestion of clots. The action of the coagulase provides an important protective barrier from the immune system, but when nutrient supplies are diminished or other conditions signal a need for the pathogen to escape and spread, the production of staphylokinase can initiate this process.",True,Virulence Factors for Survival in the Host and Immune Evasion,,,,
effb0621-9feb-4e05-9451-6cd9b244adff,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"A final mechanism that pathogens can use to protect themselves against the immune system is called antigenic variation, which is the alteration of surface proteins so that a pathogen is no longer recognized by the host’s immune system.",True,Virulence Factors for Survival in the Host and Immune Evasion,,,,
c898aa3f-672a-48b7-bad0-d376af1ecca1,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Although viral pathogens are not similar to bacterial pathogens in terms of structure, some of the properties that contribute to their virulence are similar. Viruses use adhesins to facilitate adhesion to host cells, and certain enveloped viruses rely on antigenic variation to avoid the host immune defenses. These virulence factors are discussed in more detail in the following sections.",True,Virulence Factors for Survival in the Host and Immune Evasion,,,,
f3c07f83-db0e-4b2f-ab1d-9ab53e47202d,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"One of the first steps in any viral infection is adhesion of the virus to specific receptors on the surface of cells. This process is mediated by adhesins that are part of the viral capsid or membrane envelope. The interaction of viral adhesins with specific cell receptors defines the tropism (preferential targeting) of viruses for specific cells, tissues, and organs in the body. The spike protein hemagglutinin found on Influenzavirus is an example of a viral adhesin; it allows the virus to bind to the sialic acid on the membrane of host respiratory and intestinal cells.",True,Virulence Factors for Survival in the Host and Immune Evasion,,,,
6a978377-3310-4204-af2f-715bf9c3475c,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"Antigenic variation also occurs in certain types of enveloped viruses, including influenza viruses, which exhibit two forms of antigenic variation: antigenic drift and antigenic shift (Figure 11.12). Antigenic drift is the result of point mutations causing slight changes in the spike proteins hemagglutinin (H) and neuraminidase (N). On the other hand, antigenic shift is a major change in spike proteins due to gene reassortment. This reassortment for antigenic shift occurs typically when two different influenza viruses infect the same host.",True,Virulence Factors for Survival in the Host and Immune Evasion,Figure 11.12,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.18.png,"Figure 11.12 Antigenic drift and antigenic shift in influenza viruses. (a) In antigenic drift, mutations in the genes for the surface proteins neuraminidase and/or hemagglutinin result in small antigenic changes over time. (b) In antigenic shift, simultaneous infection of a cell with two different influenza viruses results in mixing of the genes. The resultant virus possesses a mixture of the proteins of the original viruses. Influenza pandemics can often be traced to antigenic shifts."
7bcab2e0-676d-4ac8-80af-b3285e3038f0,https://open.oregonstate.education/microbiology/,11.3	Virulence Factors of Bacterial and Viral Pathogens,https://open.oregonstate.education/microbiology/chapter/15-3virulence-factors-of-bacterial-and-viral-pathogens/,"The rate of antigenic variation in influenza viruses is very high, making it difficult for the immune system to recognize the many different strains of Influenzavirus. Although the body may develop immunity to one strain through natural exposure or vaccination, antigenic variation results in the continual emergence of new strains that the immune system will not recognize. This is the main reason that vaccines against Influenzavirus must be given annually. Each year’s influenza vaccine provides protection against the most prevalent strains for that year, but new or different strains may be more prevalent the following year.",True,Virulence Factors for Survival in the Host and Immune Evasion,,,,
f5ff2bf1-93e4-46c3-9265-2f2dc9d76040,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,Pathogenicity and Virulence,False,Pathogenicity and Virulence,,,,
4e772d63-f2d7-4268-bb11-37d4a8693fda,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"The ability of a microbial agent to cause disease is called pathogenicity, and the degree to which an organism is pathogenic is called virulence. Virulence is a continuum. On one end of the spectrum are organisms that are avirulent (not harmful) and on the other are organisms that are highly virulent. Highly virulent pathogens will almost always lead to a disease state when introduced to the body, and some may even cause multi-organ and body system failure in healthy individuals. Less virulent pathogens may cause an initial infection, but may not always cause severe illness. Pathogens with low virulence would more likely result in mild signs and symptoms of disease, such as low-grade fever, headache, or muscle aches. Some individuals might even be asymptomatic.",True,Pathogenicity and Virulence,,,,
721609dc-8f92-4275-8b05-5d552fa71138,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Virulence of a pathogen can be quantified using controlled experiments with laboratory animals. Two important indicators of virulence are the median infectious dose (ID50) and the median lethal dose (LD50), both of which are typically determined experimentally using animal models. The ID50 is the number of pathogen cells or virions required to cause active infection in 50% of inoculated animals. The LD50 is the number of pathogenic cells, virions, or amount of toxin required to kill 50% of infected animals. To calculate these values, each group of animals is inoculated with one of a range of known numbers of pathogen cells or virions. In graphs like the one shown in Figure 11.3, the percentage of animals that have been infected (for ID50) or killed (for LD50) is plotted against the concentration of pathogen inoculated. Interpretation of the data from this graph indicates that the LD50 of the pathogen for the test animals is 104 pathogen cells or virions (depending upon the pathogen studied).",True,Pathogenicity and Virulence,Figure 11.3,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.5.png,"Figure 11.3 A graph like this is used to determine LD50 by plotting pathogen concentration against the percent of infected test animals that have died. In this example, the LD50 = 104 pathogenic particles."
721609dc-8f92-4275-8b05-5d552fa71138,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Virulence of a pathogen can be quantified using controlled experiments with laboratory animals. Two important indicators of virulence are the median infectious dose (ID50) and the median lethal dose (LD50), both of which are typically determined experimentally using animal models. The ID50 is the number of pathogen cells or virions required to cause active infection in 50% of inoculated animals. The LD50 is the number of pathogenic cells, virions, or amount of toxin required to kill 50% of infected animals. To calculate these values, each group of animals is inoculated with one of a range of known numbers of pathogen cells or virions. In graphs like the one shown in Figure 11.3, the percentage of animals that have been infected (for ID50) or killed (for LD50) is plotted against the concentration of pathogen inoculated. Interpretation of the data from this graph indicates that the LD50 of the pathogen for the test animals is 104 pathogen cells or virions (depending upon the pathogen studied).",True,Pathogenicity and Virulence,Figure 11.3,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.3.png,"Figure 11.3 The progression of an infectious disease can be divided into five periods, which are related to the number of pathogen particles (red) and the severity of signs and symptoms (blue)."
552af51a-60b2-4489-b195-2ab62a5c91ae,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,Primary Pathogens versus Opportunistic Pathogens,False,Primary Pathogens versus Opportunistic Pathogens,,,,
f4712ae8-3365-4e55-94b9-4f1aad9dcb7d,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Pathogens can be classified as either primary pathogens or opportunistic pathogens. A primary pathogen can cause disease in a host regardless of the host’s resident microbiota or immune system. An opportunistic pathogen, by contrast, can only cause disease in situations that compromise the host’s defenses, such as the body’s protective barriers, immune system, or normal microbiota. Individuals susceptible to opportunistic infections include the very young, the elderly, women who are pregnant, patients undergoing chemotherapy, people with immunodeficiencies (such as acquired immunodeficiency syndrome [AIDS]), patients who are recovering from surgery, and those who have had a breach of protective barriers (such as a severe wound or burn).",True,Primary Pathogens versus Opportunistic Pathogens,,,,
66d16592-7025-445e-9a3d-b04dbd2b7a49,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"An example of a primary pathogen is enterohemorrhagic E. coli (EHEC), which produces a virulence factor known as Shiga toxin. This toxin inhibits protein synthesis, leading to severe and bloody diarrhea, inflammation, and renal failure, even in patients with healthy immune systems. Staphylococcus epidermidis, on the other hand, is an opportunistic pathogen that is among the most frequent causes of nosocomial disease.[1] S. epidermidis is a member of the normal microbiota of the skin, where it is generally avirulent. However, in hospitals, it can also grow in biofilms that form on catheters, implants, or other devices that are inserted into the body during surgical procedures. Once inside the body, S. epidermidis can cause serious infections such as endocarditis, and it produces virulence factors that promote the persistence of such infections.",True,Primary Pathogens versus Opportunistic Pathogens,,,,
d339db82-20ed-450a-bd23-1e4df1086689,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Other members of the normal microbiota can also cause opportunistic infections under certain conditions. This often occurs when microbes that reside harmlessly in one body location end up in a different body system, where they cause disease. For example, E. coli normally found in the large intestine can cause a urinary tract infection if it enters the bladder. This is the leading cause of urinary tract infections among women.",True,Primary Pathogens versus Opportunistic Pathogens,,,,
55e05747-36fe-4024-bbbd-ac0ae341e019,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Members of the normal microbiota may also cause disease when a shift in the environment of the body leads to overgrowth of a particular microorganism. For example, the yeast Candida is part of the normal microbiota of the skin, mouth, intestine, and vagina, but its population is kept in check by other organisms of the microbiota. If an individual is taking antibacterial medications, however, bacteria that would normally inhibit the growth of Candida can be killed off, leading to a sudden growth in the population of Candida, which is not affected by antibacterial medications because it is a fungus. An overgrowth of Candida can manifest as oral thrush (growth on mouth, throat, and tongue), a vaginal yeast infection, or cutaneous candidiasis. Other scenarios can also provide opportunities for Candida infections. Untreated diabetes can result in a high concentration of glucose in the saliva, which provides an optimal environment for the growth of Candida, resulting in thrush. Immunodeficiencies such as those seen in patients with HIV, AIDS, and cancer also lead to higher incidence of thrush. Vaginal yeast infections can result from decreases in estrogen levels during the menstruation or menopause. The amount of glycogen available to lactobacilli in the vagina is controlled by levels of estrogen; when estrogen levels are low, lactobacilli produce less lactic acid. The resultant increase in vaginal pH allows overgrowth of Candida in the vagina.",True,Primary Pathogens versus Opportunistic Pathogens,,,,
32952279-3a4a-4209-9673-255008c096e5,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,Stages of Pathogenesis,False,Stages of Pathogenesis,,,,
25cc0d15-a5db-4eb1-a69c-f394fcda8973,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"To cause disease, a pathogen must successfully achieve four steps or stages of pathogenesis: exposure (contact), adhesion (colonization), invasion, and infection. The pathogen must be able to gain entry to the host, travel to the location where it can establish an infection, evade or overcome the host’s immune response, and cause damage (i.e., disease) to the host. In many cases, the cycle is completed when the pathogen exits the host and is transmitted to a new host.",True,Stages of Pathogenesis,,,,
963a16b1-8e6b-4e72-a9a1-e370261a23ad,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,Exposure,False,Exposure,,,,
40f3e932-50c4-4d75-b680-c793cd96fab1,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"An encounter with a potential pathogen is known as exposure or contact. The food we eat and the objects we handle are all ways that we can come into contact with potential pathogens. Yet, not all contacts result in infection and disease. For a pathogen to cause disease, it needs to be able to gain access into host tissue. An anatomic site through which pathogens can pass into host tissue is called a portal of entry. These are locations where the host cells are in direct contact with the external environment. Major portals of entry are identified in Figure 11.4 and include the skin, mucous membranes, and parenteral routes.",True,Exposure,Figure 11.4,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.6.png,"Figure 11.4 Shown are different portals of entry where pathogens can gain access into the body. With the exception of the placenta, many of these locations are directly exposed to the external environment."
fdfa6d27-ad12-422f-b076-2635a1e8798e,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Mucosal surfaces are the most important portals of entry for microbes; these include the mucous membranes of the respiratory tract, the gastrointestinal tract, and the genitourinary tract. Although most mucosal surfaces are in the interior of the body, some are contiguous with the external skin at various body openings, including the eyes, nose, mouth, urethra, and anus.",True,Exposure,,,,
a5ad2872-58f4-419f-8138-43e5f9d72a71,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Most pathogens are suited to a particular portal of entry. A pathogen’s portal specificity is determined by the organism’s environmental adaptions and by the enzymes and toxins they secrete. The respiratory and gastrointestinal tracts are particularly vulnerable portals of entry because particles that include microorganisms are constantly inhaled or ingested, respectively.",True,Exposure,,,,
221b5604-2b66-4773-91fa-c989d6103342,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Pathogens can also enter through a breach in the protective barriers of the skin and mucous membranes. Pathogens that enter the body in this way are said to enter by the parenteral route. For example, the skin is a good natural barrier to pathogens, but breaks in the skin (e.g., wounds, insect bites, animal bites, needle pricks) can provide a parenteral portal of entry for microorganisms.",True,Exposure,,,,
458f159f-69a2-4590-ad86-277606232795,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"In pregnant women, the placenta normally prevents microorganisms from passing from the mother to the fetus. However, a few pathogens are capable of crossing the blood-placental barrier. Transmission of infectious diseases from mother to baby is also a concern at the time of birth when the baby passes through the birth canal. Babies whose mothers have active chlamydia or gonorrhea infections may be exposed to the causative pathogens in the vagina, which can result in eye infections that lead to blindness. To prevent this, it is standard practice to administer antibiotic drops to infants’ eyes shortly after birth.",True,Exposure,,,,
4548ad34-6100-4363-bb5e-969e0cc1ed9c,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,Adhesion,False,Adhesion,,,,
a8b95205-8c38-4028-9560-399ebf7e000e,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Following the initial exposure, the pathogen adheres at the portal of entry. The term adhesion refers to the capability of pathogenic microbes to attach to the cells of the body using adhesion factors, and different pathogens use various mechanisms to adhere to the cells of host tissues.",True,Adhesion,,,,
6069966b-38a7-4b9d-b7aa-2aa30f390eb7,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Molecules (either proteins or carbohydrates) called adhesins are found on the surface of certain pathogens and bind to specific receptors (glycoproteins) on host cells. Adhesins are present on the fimbriae and flagella of bacteria, the cilia of protozoa, and the capsids or membranes of viruses. Protozoans can also use hooks and barbs for adhesion; spike proteins on viruses also enhance viral adhesion. The production of glycocalyces (slime layers and capsules) (Figure 11.5), with their high sugar and protein content, can also allow certain bacterial pathogens to attach to cells.",True,Adhesion,Figure 11.5,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.7.png,Figure 11.5 Glycocalyx produced by bacteria in a biofilm allows the cells to adhere to host tissues and to medical devices such as the catheter surface shown here. (credit: modification of work by Centers for Disease Control and Prevention)
328d4d06-a3df-4796-89a5-5ab6c68e7110,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Biofilm growth can also act as an adhesion factor. A biofilm is a community of bacteria that produce a glycocalyx, known as extrapolymeric substance (EPS), that allows the biofilm to attach to a surface. Persistent Pseudomonas aeruginosa infections are common in patients suffering from cystic fibrosis, burn wounds, and middle-ear infections (otitis media) because P. aeruginosa produces a biofilm. The EPS allows the bacteria to adhere to the host cells and makes it harder for the host to physically remove the pathogen. The EPS not only allows for attachment but provides protection against the immune system and antibiotic treatments, preventing antibiotics from reaching the bacterial cells within the biofilm. In addition, not all bacteria in a biofilm are rapidly growing; some are in stationary phase. Since antibiotics are most effective against rapidly growing bacteria, portions of bacteria in a biofilm are protected against antibiotics.[2]",True,Adhesion,,,,
efc383db-95b6-446c-82ee-72ab3fcb31e0,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Entry to a cell can occur by endocytosis., a cellular process where the pathogen is surrounded by the cell’s plasma membrane. Some host cells, such as white blood cells and other phagocytes of the immune system, actively endocytose pathogens in a process called phagocytosis. Although phagocytosis allows the pathogen to gain entry to the host cell, in most cases, the host cell kills and degrades the pathogen by using digestive enzymes. Normally, when a pathogen is ingested by a phagocyte, it is enclosed within a phagosome in the cytoplasm; the phagosome fuses with a lysosome to form a phagolysosome, where digestive enzymes kill the pathogen (see Pathogen Recognition and Phagocytosis). However, some intracellular pathogens have the ability to survive and multiply within phagocytes.",True,Adhesion,,,,
b7b5d6d2-515f-4ca8-9a21-04f8ce5bbbc6,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,Infection,False,Infection,,,,
c94989e0-be35-47fa-959f-8118b3f4af0f,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Following invasion, successful multiplication of the pathogen leads to infection. Infections can be described as local, focal, or systemic, depending on the extent of the infection. A local infection is confined to a small area of the body, typically near the portal of entry. For example, a hair follicle infected by Staphylococcus aureus infection may result in a boil around the site of infection, but the bacterium is largely contained to this small location. Other examples of local infections that involve more extensive tissue involvement include urinary tract infections confined to the bladder or pneumonia confined to the lungs.",True,Infection,,,,
f2a0a1b3-0fc9-4f93-85c6-87fcb7d03294,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"In a focal infection, a localized pathogen, or the toxins it produces, can spread to a secondary location. For example, a dental hygienist nicking the gum with a sharp tool can lead to a local infection in the gum by Streptococcus bacteria of the normal oral microbiota. These Streptococcus spp. may then gain access to the bloodstream and make their way to other locations in the body, resulting in a secondary infection.",True,Infection,,,,
a99a4df7-e8b6-46f3-99a3-5b7402cb3348,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"When an infection becomes disseminated throughout the body, we call it a systemic infection. For example, infection by the varicella-zoster virus typically gains entry through a mucous membrane of the upper respiratory system. It then spreads throughout the body, resulting in the classic red skin lesions associated with chickenpox. Since these lesions are not sites of initial infection, they are signs of a systemic infection.",True,Infection,,,,
95feba63-7b3d-4759-9ba1-1c9d97f2322e,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Sometimes a primary infection, the initial infection caused by one pathogen, can lead to a secondary infection by another pathogen. For example, the immune system of a patient with a primary infection by HIV becomes compromised, making the patient more susceptible to secondary diseases like oral thrush and others caused by opportunistic pathogens. Some secondary infections can even develop as a result of treatment for a primary infection. Antibiotic therapy targeting the primary pathogen can cause collateral damage to the normal microbiota, creating an opening for opportunistic pathogens (see Case in Point: A Secondary Yeast Infection).",True,Infection,,,,
4b971ba7-122f-4df9-9397-96c78705889a,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Anita, a 36-year-old mother of three, goes to an urgent care center complaining of pelvic pressure, frequent and painful urination, abdominal cramps, and occasional blood-tinged urine. Suspecting a urinary tract infection (UTI), the physician requests a urine sample and sends it to the lab for a urinalysis. Since it will take approximately 24 hours to get the results of the culturing, the physician immediately starts Anita on the antibiotic ciprofloxacin. The next day, the microbiology lab confirms the presence of E. coli in Anita’s urine, which is consistent with the presumptive diagnosis. However, the antimicrobial susceptibility test indicates that ciprofloxacin would not effectively treat Anita’s UTI, so the physician prescribes a different antibiotic.",True,Infection,,,,
95ec4dae-6ce5-4ba5-9a69-6b181f30d7bb,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"After taking her antibiotics for 1 week, Anita returns to the clinic complaining that the prescription is not working. Although the painful urination has subsided, she is now experiencing vaginal itching, burning, and discharge. After a brief examination, the physician explains to Anita that the antibiotics were likely successful in killing the E. coli responsible for her UTI; however, in the process, they also wiped out many of the “good” bacteria in Anita’s normal microbiota. The new symptoms that Anita has reported are consistent with a secondary yeast infection by Candida albicans, an opportunistic fungus that normally resides in the vagina but is inhibited by the bacteria that normally reside in the same environment.",True,Infection,,,,
e5fbcbf2-27a0-44d4-9b7f-1ad46a5afa26,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"To confirm this diagnosis, a microscope slide of a direct vaginal smear is prepared from the discharge to check for the presence of yeast. A sample of the discharge accompanies this slide to the microbiology lab to determine if there has been an increase in the population of yeast causing vaginitis. After the microbiology lab confirms the diagnosis, the physician prescribes an antifungal drug for Anita to use to eliminate her secondary yeast infection.",True,Infection,,,,
f4f02226-5c4e-49a8-bc7d-abb639564ef9,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,Transmission of Disease,False,Transmission of Disease,,,,
5955a657-7701-48d7-b4ae-82b321d56e2f,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Entry to a cell can occur by endocytosis., a cellular process where the pathogen is surrounded by the cell’s plasma membrane. Some host cells, such as white blood cells and other phagocytes of the immune system, actively endocytose pathogens in a process called phagocytosis. Although phagocytosis allows the pathogen to gain entry to the host cell, in most cases, the host cell kills and degrades the pathogen by using digestive enzymes. Normally, when a pathogen is ingested by a phagocyte, it is enclosed within a phagosome in the cytoplasm; the phagosome fuses with a lysosome to form a phagolysosome, where digestive enzymes kill the pathogen (see Pathogen Recognition and Phagocytosis). However, some intracellular pathogens have the ability to survive and multiply within phagocytes.",True,Transmission of Disease,,,,
427f06ad-cb91-4fc0-91ed-46d6442163d2,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Following invasion, successful multiplication of the pathogen leads to infection. Infections can be described as local, focal, or systemic, depending on the extent of the infection. A local infection is confined to a small area of the body, typically near the portal of entry. For example, a hair follicle infected by Staphylococcus aureus infection may result in a boil around the site of infection, but the bacterium is largely contained to this small location. Other examples of local infections that involve more extensive tissue involvement include urinary tract infections confined to the bladder or pneumonia confined to the lungs.",True,Transmission of Disease,,,,
ac4f8fcb-6f2d-4503-b9fa-c62d8835710a,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"In a focal infection, a localized pathogen, or the toxins it produces, can spread to a secondary location. For example, a dental hygienist nicking the gum with a sharp tool can lead to a local infection in the gum by Streptococcus bacteria of the normal oral microbiota. These Streptococcus spp. may then gain access to the bloodstream and make their way to other locations in the body, resulting in a secondary infection.",True,Transmission of Disease,,,,
aaf5d69e-a22a-4888-9fff-2a4ac871fa71,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"When an infection becomes disseminated throughout the body, we call it a systemic infection. For example, infection by the varicella-zoster virus typically gains entry through a mucous membrane of the upper respiratory system. It then spreads throughout the body, resulting in the classic red skin lesions associated with chickenpox. Since these lesions are not sites of initial infection, they are signs of a systemic infection.",True,Transmission of Disease,,,,
617b7024-04b2-4b8d-ab73-62d3a8bfc51a,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"Sometimes a primary infection, the initial infection caused by one pathogen, can lead to a secondary infection by another pathogen. For example, the immune system of a patient with a primary infection by HIV becomes compromised, making the patient more susceptible to secondary diseases like oral thrush and others caused by opportunistic pathogens. Some secondary infections can even develop as a result of treatment for a primary infection. Antibiotic therapy targeting the primary pathogen can cause collateral damage to the normal microbiota, creating an opening for opportunistic pathogens (see Case in Point: A Secondary Yeast Infection).",True,Transmission of Disease,,,,
922c172b-2b17-48fc-a40b-48733c07aa4d,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"After taking her antibiotics for 1 week, Anita returns to the clinic complaining that the prescription is not working. Although the painful urination has subsided, she is now experiencing vaginal itching, burning, and discharge. After a brief examination, the physician explains to Anita that the antibiotics were likely successful in killing the E. coli responsible for her UTI; however, in the process, they also wiped out many of the “good” bacteria in Anita’s normal microbiota. The new symptoms that Anita has reported are consistent with a secondary yeast infection by Candida albicans, an opportunistic fungus that normally resides in the vagina but is inhibited by the bacteria that normally reside in the same environment.",True,Transmission of Disease,,,,
e75b83c6-2863-40d5-8403-3799740f0d0c,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,"To confirm this diagnosis, a microscope slide of a direct vaginal smear is prepared from the discharge to check for the presence of yeast. A sample of the discharge accompanies this slide to the microbiology lab to determine if there has been an increase in the population of yeast causing vaginitis. After the microbiology lab confirms the diagnosis, the physician prescribes an antifungal drug for Anita to use to eliminate her secondary yeast infection.",True,Transmission of Disease,,,,
742f3530-9685-4f69-afed-f4f6e3cdc0f4,https://open.oregonstate.education/microbiology/,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/microbiology/chapter/15-2how-pathogens-cause-disease/,Transmission of Disease,False,Transmission of Disease,,,,
1af92f0e-caaa-4e85-8107-6b4166db2d9d,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,Signs and Symptoms of Disease,False,Signs and Symptoms of Disease,,,,
6abea2ce-cb77-460f-96bb-b94b839533c9,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"An infection is the successful colonization of a host by a microorganism. Infections can lead to disease, which causes signs and symptoms resulting in a deviation from the normal structure or functioning of the host. Microorganisms that can cause disease are known as pathogens.",True,Signs and Symptoms of Disease,,,,
1a8bf946-93cd-4742-9b02-ed32e4d4136f,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"The signs of disease are objective and measurable, and can be directly observed by a clinician. Vital signs, which are used to measure the body’s basic functions, include body temperature (normally 37 °C [98.6 °F]), heart rate (normally 60–100 beats per minute), breathing rate (normally 12–18 breaths per minute), and blood pressure (normally between 90/60 and 120/80 mm Hg). Changes in any of the body’s vital signs may be indicative of disease. For example, having a fever (a body temperature significantly higher than 37 °C or 98.6 °F) is a sign of disease because it can be measured.",True,Signs and Symptoms of Disease,,,,
d24d83f4-3dc5-411d-9eb1-98d0aa02c0f3,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"In addition to changes in vital signs, other observable conditions may be considered signs of disease. For example, the presence of antibodies in a patient’s serum (the liquid portion of blood that lacks clotting factors) can be observed and measured through blood tests and, therefore, can be considered a sign. However, it is important to note that the presence of antibodies is not always a sign of an active disease. Antibodies can remain in the body long after an infection has resolved; also, they may develop in response to a pathogen that is in the body but not currently causing disease.",True,Signs and Symptoms of Disease,,,,
ac9f5b68-c34d-4d19-8f59-50155f2ddcd8,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"Unlike signs, symptoms of disease are subjective. Symptoms are felt or experienced by the patient, but they cannot be clinically confirmed or objectively measured. Examples of symptoms include nausea, loss of appetite, and pain. Such symptoms are important to consider when diagnosing disease, but they are subject to memory bias and are difficult to measure precisely. Some clinicians attempt to quantify symptoms by asking patients to assign a numerical value to their symptoms. For example, the Wong-Baker Faces pain-rating scale asks patients to rate their pain on a scale of 0–10. An alternative method of quantifying pain is measuring skin conductance fluctuations. These fluctuations reflect sweating due to skin sympathetic nerve activity resulting from the stressor of pain.[1]",True,Signs and Symptoms of Disease,,,,
932159b7-961a-49fd-ad84-2cafdc7424e7,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,A specific group of signs and symptoms characteristic of a particular disease is called a syndrome. Many syndromes are named using a nomenclature based on signs and symptoms or the location of the disease. Table 11.1 lists some of the prefixes and suffixes commonly used in naming syndromes.,True,Signs and Symptoms of Disease,,,,
bf94873d-18ab-40ef-990d-5864226d1ffe,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"Clinicians must rely on signs and on asking questions about symptoms, medical history, and the patient’s recent activities to identify a particular disease and the potential causative agent. Diagnosis is complicated by the fact that different microorganisms can cause similar signs and symptoms in a patient. For example, an individual presenting with symptoms of diarrhea may have been infected by one of a wide variety of pathogenic microorganisms, such as bacteria, viruses, or protozoa.. Likewise, fever is indicative of many types of infection, from the common cold to the deadly Ebola hemorrhagic fever.",True,Signs and Symptoms of Disease,,,,
b277ff48-e189-4300-b82b-7a3d04e247ee,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"Finally, some diseases may be asymptomatic or subclinical, meaning they do not present any noticeable signs or symptoms. For example, most individual infected with herpes simplex virus remain asymptomatic and are unaware that they have been infected.",True,Signs and Symptoms of Disease,,,,
1a1efb19-f315-49a6-acff-7969dae441e0,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,Classifications of Disease,False,Classifications of Disease,,,,
50b5f116-5bec-4728-8691-6986b9fedd72,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"An infectious disease is any disease caused by the direct effect of a pathogen. A pathogen may be cellular (bacteria, parasites, and fungi) or acellular (viruses, viroids, and prions). Some infectious diseases are also communicable, meaning they are capable of being spread from person to person through either direct or indirect mechanisms. Some infectious communicable diseases are also considered contagious diseases, meaning they are easily spread from person to person. Not all contagious diseases are equally so; the degree to which a disease is contagious usually depends on how the pathogen is transmitted. For example, measles is a highly contagious viral disease that can be transmitted when an infected person coughs or sneezes and an uninfected person breathes in droplets containing the virus. Gonorrhea is not as contagious as measles because transmission of the pathogen (Neisseria gonorrhoeae) requires close intimate contact (usually sexual) between an infected person and an uninfected person.",True,Classifications of Disease,,,,
3765de5b-cec7-43ac-b999-71366e57d46e,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"Diseases that are contracted as the result of a medical procedure are known as iatrogenic diseases. Iatrogenic diseases can occur after procedures involving wound treatments, catheterization, or surgery if the wound or surgical site becomes contaminated.",True,Classifications of Disease,,,,
97216db7-dc4d-4ea8-bf0a-99a863be5c32,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"Diseases acquired in hospital settings are known as nosocomial diseases. Several factors contribute to the prevalence and severity of nosocomial diseases. First, sick patients bring numerous pathogens into hospitals, and some of these pathogens can be transmitted easily via improperly sterilized medical equipment, bed sheets, call buttons, door handles, or by clinicians, nurses, or therapists who do not wash their hands before touching a patient. Second, many hospital patients have weakened immune systems, making them more susceptible to infections. Compounding this, the prevalence of antibiotics in hospital settings can select for drug-resistant bacteria that can cause very serious infections that are difficult to treat.",True,Classifications of Disease,,,,
cc6064e6-d118-4a47-84e2-20fa8d338c6c,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"Certain infectious diseases are not transmitted between humans directly but can be transmitted from animals to humans. Such a disease is called zoonotic disease (or zoonosis). According to WHO, a zoonosis is a disease that occurs when a pathogen is transferred from a vertebrate animal to a human; however, sometimes the term is defined more broadly to include diseases transmitted by all animals (including invertebrates). For example, rabies is a viral zoonotic disease spread from animals to humans through bites and contact with infected saliva. Many other zoonotic diseases rely on insects or other arthropods for transmission. An example is Rocky Mountain spotted fever (transmitted through the bite of ticks infected with Rickettsia rickettsii).",True,Classifications of Disease,,,,
c1f53324-8fb8-4539-b3ad-1d917ec5a018,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"In contrast to communicable infectious diseases, a noncommunicable infectious disease is not spread from one  person to another. One example is tetanus, caused by Clostridium tetani, a bacterium that produces endospores that can survive in the soil for many years. This disease is typically only transmitted through contact with a skin wound; it cannot be passed from an infected person to another person. Similarly, Legionnaires disease is caused by Legionella pneumophila, a bacterium that lives within amoebae in moist locations like water-cooling towers. An individual may contract Legionnaires disease via contact with the contaminated water, but once infected, the individual cannot pass the pathogen to other individuals.",True,Classifications of Disease,,,,
ef630739-b0e2-4c68-b6d7-ee94d065fee5,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"In addition to the wide variety of noncommunicable infectious diseases, noninfectious diseases (those not caused by pathogens) are an important cause of morbidity and mortality worldwide. Noninfectious diseases can be caused by a wide variety factors, including genetics, the environment, or immune system dysfunction, to name a few. For example, sickle cell anemia is an inherited disease caused by a genetic mutation that can be passed from parent to offspring (Figure 11.2).",True,Classifications of Disease,Figure 11.2,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.2.png,"Figure 11.2 Blood smears showing two diseases of the blood. (a) Malaria is an infectious, zoonotic disease caused by the protozoan pathogen Plasmodium falciparum (shown here) and several other species of the genus Plasmodium. It is transmitted by mosquitoes to humans. (b) Sickle cell disease is a noninfectious genetic disorder that results in abnormally shaped red blood cells, which can stick together and obstruct the flow of blood through the circulatory system. It is not caused by a pathogen, but rather a genetic mutation. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by Ed Uthman)"
e2fb95f0-c0d6-4a2e-81f5-234095d676ba,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,Periods of Disease,False,Periods of Disease,,,,
8bf133f8-1b86-486c-bf71-ae2fb881f942,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"The five periods of disease (sometimes referred to as stages or phases) include the incubation, prodromal, illness, decline, and convalescence periods (Figure 11.3). The incubation period occurs in an acute disease after the initial entry of the pathogen into the host (patient). It is during this time the pathogen begins multiplying in the host. However, there are insufficient numbers of pathogen particles (cells or viruses) present to cause signs and symptoms of disease. Incubation periods can vary from a day or two in acute disease to months or years in chronic disease, depending upon the pathogen. Factors involved in determining the length of the incubation period are diverse, and can include strength of the pathogen, strength of the host immune defenses, site of infection, type of infection, and the size infectious dose received. During this incubation period, the patient is unaware that a disease is beginning to develop.",True,Periods of Disease,Figure 11.3,11.2	How Pathogens Cause Disease,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.5.png,"Figure 11.3 A graph like this is used to determine LD50 by plotting pathogen concentration against the percent of infected test animals that have died. In this example, the LD50 = 104 pathogenic particles."
8bf133f8-1b86-486c-bf71-ae2fb881f942,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"The five periods of disease (sometimes referred to as stages or phases) include the incubation, prodromal, illness, decline, and convalescence periods (Figure 11.3). The incubation period occurs in an acute disease after the initial entry of the pathogen into the host (patient). It is during this time the pathogen begins multiplying in the host. However, there are insufficient numbers of pathogen particles (cells or viruses) present to cause signs and symptoms of disease. Incubation periods can vary from a day or two in acute disease to months or years in chronic disease, depending upon the pathogen. Factors involved in determining the length of the incubation period are diverse, and can include strength of the pathogen, strength of the host immune defenses, site of infection, type of infection, and the size infectious dose received. During this incubation period, the patient is unaware that a disease is beginning to develop.",True,Periods of Disease,Figure 11.3,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.3.png,"Figure 11.3 The progression of an infectious disease can be divided into five periods, which are related to the number of pathogen particles (red) and the severity of signs and symptoms (blue)."
c4157fdc-a5df-4899-8775-6c1e229ccbd0,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"The prodromal period occurs after the incubation period. During this phase, the pathogen continues to multiply and the host begins to experience general signs and symptoms of illness, which typically result from activation of the immune system, such as fever, pain, soreness, swelling, or inflammation. Usually, such signs and symptoms are too general to indicate a particular disease. Following the prodromal period is the period of illness, during which the signs and symptoms of disease are most obvious and severe.",True,Periods of Disease,,,,
a1cbfc1b-8cb8-47ab-983a-c17d656de113,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"The period of illness is followed by the period of decline, during which the number of pathogen particles begins to decrease, and the signs and symptoms of illness begin to decline. However, during the decline period, patients may become susceptible to developing secondary infections because their immune systems have been weakened by the primary infection. The final period is known as the period of convalescence. During this stage, the patient generally returns to normal functions, although some diseases may inflict permanent damage that the body cannot fully repair.",True,Periods of Disease,,,,
74a29677-8fe4-401a-9ef3-611218c802d5,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"Infectious diseases can be contagious during all five of the periods of disease. Which periods of disease are more likely to associated with transmissibility of an infection depends upon the disease, the pathogen, and the mechanisms by which the disease develops and progresses. For example, with meningitis (infection of the lining of brain), the periods of infectivity depend on the type of pathogen causing the infection. Patients with bacterial meningitis are contagious during the incubation period for up to a week before the onset of the prodromal period, whereas patients with viral meningitis become contagious when the first signs and symptoms of the prodromal period appear. With many viral diseases associated with rashes (e.g., chickenpox, measles, rubella, roseola), patients are contagious during the incubation period up to a week before the rash develops. In contrast, with many respiratory infections (e.g., colds, influenza, diphtheria, strep throat, and pertussis) the patient becomes contagious with the onset of the prodromal period. Depending upon the pathogen, the disease, and the individual infected, transmission can still occur during the periods of decline, convalescence, and even long after signs and symptoms of the disease disappear.",True,Periods of Disease,,,,
8b22ddce-875c-41af-8c7a-513f6c25dcf4,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,Acute and Chronic Diseases,False,Acute and Chronic Diseases,,,,
baec97a6-5231-4475-bdb1-d5ea3f1fd347,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"The duration of the period of illness can vary greatly, depending on the pathogen, effectiveness of the immune response in the host, and any medical treatment received. For an acute disease, pathologic changes occur over a relatively short time (e.g., hours, days, or a few weeks) and involve a rapid onset of disease conditions. For example, influenza (caused by Influenzavirus) is considered an acute disease because the incubation period is approximately 1–2 days. Infected individuals can spread influenza to others for approximately 5 days after becoming ill. After approximately 1 week, individuals enter the period of decline.",True,Acute and Chronic Diseases,,,,
5e334150-7c19-4a0d-ac4a-bef750aae788,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"For a chronic disease, pathologic changes can occur over longer time spans (e.g., months, years, or a lifetime). For example, chronic gastritis (inflammation of the lining of the stomach) is caused by the gram-negative bacterium Helicobacter pylori. H. pylori is able to colonize the stomach and persist in its highly acidic environment by producing the enzyme urease, which modifies the local acidity, allowing the bacteria to survive indefinitely.[2] Consequently, H. pylori infections can recur indefinitely unless the infection is cleared using antibiotics.[3]",True,Acute and Chronic Diseases,,,,
9ebc5b3f-9d06-45d7-b11c-531d333c0ded,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"In latent diseases, as opposed to chronic infections, the causal pathogen goes dormant for extended periods of time with no active replication. An example of a disease that goes into a latent state after the acute infection is chickenpox (varicella-zoster virus [VZV]). VZV evade the host immune system by residing in a latent form within cells of the nervous system for long periods of time, but they can reactivate to become active infections during times of stress and immunosuppression. For example, an initial infection by VZV may result in a case of childhood chickenpox, followed by a long period of latency. The virus may reactivate decades later, causing episodes of shingles in adulthood.",True,Acute and Chronic Diseases,,,,
b6a12ea0-93b8-49a9-b77b-bade6ac01f00,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"Finally, some diseases may be asymptomatic or subclinical, meaning they do not present any noticeable signs or symptoms. For example, most individual infected with herpes simplex virus remain asymptomatic and are unaware that they have been infected.",True,Acute and Chronic Diseases,,,,
eda79c8a-ece7-4be1-937a-96ecf275b690,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,Classifications of Disease,False,Classifications of Disease,,,,
683e4d6d-f06b-4df6-a9f4-5f2d663160ea,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"An infectious disease is any disease caused by the direct effect of a pathogen. A pathogen may be cellular (bacteria, parasites, and fungi) or acellular (viruses, viroids, and prions). Some infectious diseases are also communicable, meaning they are capable of being spread from person to person through either direct or indirect mechanisms. Some infectious communicable diseases are also considered contagious diseases, meaning they are easily spread from person to person. Not all contagious diseases are equally so; the degree to which a disease is contagious usually depends on how the pathogen is transmitted. For example, measles is a highly contagious viral disease that can be transmitted when an infected person coughs or sneezes and an uninfected person breathes in droplets containing the virus. Gonorrhea is not as contagious as measles because transmission of the pathogen (Neisseria gonorrhoeae) requires close intimate contact (usually sexual) between an infected person and an uninfected person.",True,Classifications of Disease,,,,
470878a4-f41a-4f2f-81ca-df4771751450,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"Diseases that are contracted as the result of a medical procedure are known as iatrogenic diseases. Iatrogenic diseases can occur after procedures involving wound treatments, catheterization, or surgery if the wound or surgical site becomes contaminated.",True,Classifications of Disease,,,,
153ea28b-b153-4e01-9d52-f2998fc3c722,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"Diseases acquired in hospital settings are known as nosocomial diseases. Several factors contribute to the prevalence and severity of nosocomial diseases. First, sick patients bring numerous pathogens into hospitals, and some of these pathogens can be transmitted easily via improperly sterilized medical equipment, bed sheets, call buttons, door handles, or by clinicians, nurses, or therapists who do not wash their hands before touching a patient. Second, many hospital patients have weakened immune systems, making them more susceptible to infections. Compounding this, the prevalence of antibiotics in hospital settings can select for drug-resistant bacteria that can cause very serious infections that are difficult to treat.",True,Classifications of Disease,,,,
b137ed9c-cc56-44cc-b06a-ed8bac67f1b2,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"Certain infectious diseases are not transmitted between humans directly but can be transmitted from animals to humans. Such a disease is called zoonotic disease (or zoonosis). According to WHO, a zoonosis is a disease that occurs when a pathogen is transferred from a vertebrate animal to a human; however, sometimes the term is defined more broadly to include diseases transmitted by all animals (including invertebrates). For example, rabies is a viral zoonotic disease spread from animals to humans through bites and contact with infected saliva. Many other zoonotic diseases rely on insects or other arthropods for transmission. An example is Rocky Mountain spotted fever (transmitted through the bite of ticks infected with Rickettsia rickettsii).",True,Classifications of Disease,,,,
14ecec2d-c532-4d69-8f24-4b1dc862b6b5,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"In contrast to communicable infectious diseases, a noncommunicable infectious disease is not spread from one  person to another. One example is tetanus, caused by Clostridium tetani, a bacterium that produces endospores that can survive in the soil for many years. This disease is typically only transmitted through contact with a skin wound; it cannot be passed from an infected person to another person. Similarly, Legionnaires disease is caused by Legionella pneumophila, a bacterium that lives within amoebae in moist locations like water-cooling towers. An individual may contract Legionnaires disease via contact with the contaminated water, but once infected, the individual cannot pass the pathogen to other individuals.",True,Classifications of Disease,,,,
2eb83c91-641d-4284-b4ba-cf9936c6cf06,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"In addition to the wide variety of noncommunicable infectious diseases, noninfectious diseases (those not caused by pathogens) are an important cause of morbidity and mortality worldwide. Noninfectious diseases can be caused by a wide variety factors, including genetics, the environment, or immune system dysfunction, to name a few. For example, sickle cell anemia is an inherited disease caused by a genetic mutation that can be passed from parent to offspring (Figure 11.2).",True,Classifications of Disease,Figure 11.2,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-15.2.png,"Figure 11.2 Blood smears showing two diseases of the blood. (a) Malaria is an infectious, zoonotic disease caused by the protozoan pathogen Plasmodium falciparum (shown here) and several other species of the genus Plasmodium. It is transmitted by mosquitoes to humans. (b) Sickle cell disease is a noninfectious genetic disorder that results in abnormally shaped red blood cells, which can stick together and obstruct the flow of blood through the circulatory system. It is not caused by a pathogen, but rather a genetic mutation. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by Ed Uthman)"
337859b4-000f-4a0d-948b-ce6f406cccd3,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,Periods of Disease,False,Periods of Disease,,,,
9c424cd3-3fe5-4a5b-b6c3-61b2176d9638,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"The period of illness is followed by the period of decline, during which the number of pathogen particles begins to decrease, and the signs and symptoms of illness begin to decline. However, during the decline period, patients may become susceptible to developing secondary infections because their immune systems have been weakened by the primary infection. The final period is known as the period of convalescence. During this stage, the patient generally returns to normal functions, although some diseases may inflict permanent damage that the body cannot fully repair.",True,Periods of Disease,,,,
df5b047b-3809-48ab-9106-3ddcede226e5,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"Infectious diseases can be contagious during all five of the periods of disease. Which periods of disease are more likely to associated with transmissibility of an infection depends upon the disease, the pathogen, and the mechanisms by which the disease develops and progresses. For example, with meningitis (infection of the lining of brain), the periods of infectivity depend on the type of pathogen causing the infection. Patients with bacterial meningitis are contagious during the incubation period for up to a week before the onset of the prodromal period, whereas patients with viral meningitis become contagious when the first signs and symptoms of the prodromal period appear. With many viral diseases associated with rashes (e.g., chickenpox, measles, rubella, roseola), patients are contagious during the incubation period up to a week before the rash develops. In contrast, with many respiratory infections (e.g., colds, influenza, diphtheria, strep throat, and pertussis) the patient becomes contagious with the onset of the prodromal period. Depending upon the pathogen, the disease, and the individual infected, transmission can still occur during the periods of decline, convalescence, and even long after signs and symptoms of the disease disappear.",True,Periods of Disease,,,,
04c5b70b-f2b8-4e02-8849-e920b3d334b9,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,Acute and Chronic Diseases,False,Acute and Chronic Diseases,,,,
4d8f6bb9-18db-4a4a-93d4-1dcc14ad3a51,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"The duration of the period of illness can vary greatly, depending on the pathogen, effectiveness of the immune response in the host, and any medical treatment received. For an acute disease, pathologic changes occur over a relatively short time (e.g., hours, days, or a few weeks) and involve a rapid onset of disease conditions. For example, influenza (caused by Influenzavirus) is considered an acute disease because the incubation period is approximately 1–2 days. Infected individuals can spread influenza to others for approximately 5 days after becoming ill. After approximately 1 week, individuals enter the period of decline.",True,Acute and Chronic Diseases,,,,
499fcb6d-d468-4e3c-afee-087792ab0852,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"For a chronic disease, pathologic changes can occur over longer time spans (e.g., months, years, or a lifetime). For example, chronic gastritis (inflammation of the lining of the stomach) is caused by the gram-negative bacterium Helicobacter pylori. H. pylori is able to colonize the stomach and persist in its highly acidic environment by producing the enzyme urease, which modifies the local acidity, allowing the bacteria to survive indefinitely.[2] Consequently, H. pylori infections can recur indefinitely unless the infection is cleared using antibiotics.[3]",True,Acute and Chronic Diseases,,,,
5b6b9403-e764-4baf-8a6e-b398c4e5edfc,https://open.oregonstate.education/microbiology/,11.1	Characteristics of Infectious Disease,https://open.oregonstate.education/microbiology/chapter/15-1characteristics-of-infectious-disease/,"In latent diseases, as opposed to chronic infections, the causal pathogen goes dormant for extended periods of time with no active replication. An example of a disease that goes into a latent state after the acute infection is chickenpox (varicella-zoster virus [VZV]). VZV evade the host immune system by residing in a latent form within cells of the nervous system for long periods of time, but they can reactivate to become active infections during times of stress and immunosuppression. For example, an initial infection by VZV may result in a case of childhood chickenpox, followed by a long period of latency. The virus may reactivate decades later, causing episodes of shingles in adulthood.",True,Acute and Chronic Diseases,,,,
2eb099fc-bef1-454e-a866-27bf83fd8262,https://open.oregonstate.education/microbiology/,10.6	Current Strategies for Antimicrobial Discovery,https://open.oregonstate.education/microbiology/chapter/14-6current-strategies-for-antimicrobial-discovery/,"Although soils have been widely examined, other environmental niches have not been tested as fully. Since 70% of the earth is covered with water, marine environments could be mined more fully for the presence of antimicrobial- producing microbes. In addition, researchers are using combinatorial chemistry, a method for making a very large number of related compounds from simple precursors, and testing them for antimicrobial activity. An additional strategy that needs to be explored further is the development of compounds that inhibit resistance mechanisms and restore the activity of older drugs. Finally, developing inhibitors of virulence factor production and function could be a very important avenue. Although this strategy would not be directly antibacterial, drugs that slow the progression of an infection could provide an advantage for the immune system and could be used successfully in combination with antimicrobial drugs.",True,Acute and Chronic Diseases,,,,
33a99720-d6bd-41ea-b3c3-d1978dad817a,https://open.oregonstate.education/microbiology/,10.6	Current Strategies for Antimicrobial Discovery,https://open.oregonstate.education/microbiology/chapter/14-6current-strategies-for-antimicrobial-discovery/,"Given that demand usually encourages supply, one might expect pharmaceutical companies to be rushing to get back in the business of developing new antibiotics. But developing new drugs is a lengthy process and requires large investments in research and development. Pharmaceutical companies can typically get a higher return on their investment by developing products for chronic, nonmicrobial diseases like diabetes; such drugs must be taken for life, and therefore generate more long-term revenue than an antibiotic that does its job in a week or two. But what will happen when drugs like vancomycin, a superantimicrobial reserved for use as a last resort, begin to lose their effectiveness against ever more drug-resistant superbugs? Will drug companies wait until all antibiotics have become useless before beginning to look for new ones?",True,Acute and Chronic Diseases,,,,
72c5eb18-33d9-49af-b70b-ea56917e25d8,https://open.oregonstate.education/microbiology/,10.6	Current Strategies for Antimicrobial Discovery,https://open.oregonstate.education/microbiology/chapter/14-6current-strategies-for-antimicrobial-discovery/,"Recently, it has been suggested that large pharmaceutical companies should be given financial incentives to pursue such research. In September 2014, the White House released an executive order entitled “Combating Antibiotic Resistant Bacteria,” calling upon various government agencies and the private sector to work together to “accelerate basic and applied research and development for new antimicrobials, other therapeutics, and vaccines.”[2] As a result, as of March 2015, President Obama’s proposed fiscal year 2016 budget doubled the amount of federal funding to $1.2 billion for “combating and preventing antibiotic resistance,” which includes money for antimicrobial research and development.[3] Similar suggestions have also been made on a global scale. In December 2014, a report chaired by former Goldman Sachs economist Jim O’Neill was published in The Review on Antimicrobial Resistance.[4]",True,Acute and Chronic Diseases,,,,
d6b895a0-0ec2-4330-ae06-ebf5c662b770,https://open.oregonstate.education/microbiology/,10.6	Current Strategies for Antimicrobial Discovery,https://open.oregonstate.education/microbiology/chapter/14-6current-strategies-for-antimicrobial-discovery/,"These developments reflect the growing belief that for-profit pharmaceutical companies must be subsidized to encourage development of new antimicrobials. But some ask whether pharmaceutical development should be motivated by profit at all. Given that millions of lives may hang in the balance, some might argue that drug companies have an ethical obligation to devote their research and development efforts to high-utility drugs, as opposed to highly profitable ones. Yet this obligation conflicts with the fundamental goals of a for-profit company. Are government subsidies enough to ensure that drug companies make the public interest a priority, or should government agencies assume responsibility for developing critical drugs that may have little or no return on investment?",True,Acute and Chronic Diseases,,,,
f39cc933-1f0e-4ae8-8a75-862350abb2eb,https://open.oregonstate.education/microbiology/,10.6	Current Strategies for Antimicrobial Discovery,https://open.oregonstate.education/microbiology/chapter/14-6current-strategies-for-antimicrobial-discovery/,"Given that demand usually encourages supply, one might expect pharmaceutical companies to be rushing to get back in the business of developing new antibiotics. But developing new drugs is a lengthy process and requires large investments in research and development. Pharmaceutical companies can typically get a higher return on their investment by developing products for chronic, nonmicrobial diseases like diabetes; such drugs must be taken for life, and therefore generate more long-term revenue than an antibiotic that does its job in a week or two. But what will happen when drugs like vancomycin, a superantimicrobial reserved for use as a last resort, begin to lose their effectiveness against ever more drug-resistant superbugs? Will drug companies wait until all antibiotics have become useless before beginning to look for new ones?",True,Acute and Chronic Diseases,,,,
90603e65-a365-4c8f-824c-861cb392779b,https://open.oregonstate.education/microbiology/,10.6	Current Strategies for Antimicrobial Discovery,https://open.oregonstate.education/microbiology/chapter/14-6current-strategies-for-antimicrobial-discovery/,"Recently, it has been suggested that large pharmaceutical companies should be given financial incentives to pursue such research. In September 2014, the White House released an executive order entitled “Combating Antibiotic Resistant Bacteria,” calling upon various government agencies and the private sector to work together to “accelerate basic and applied research and development for new antimicrobials, other therapeutics, and vaccines.”[2] As a result, as of March 2015, President Obama’s proposed fiscal year 2016 budget doubled the amount of federal funding to $1.2 billion for “combating and preventing antibiotic resistance,” which includes money for antimicrobial research and development.[3] Similar suggestions have also been made on a global scale. In December 2014, a report chaired by former Goldman Sachs economist Jim O’Neill was published in The Review on Antimicrobial Resistance.[4]",True,Acute and Chronic Diseases,,,,
b9412254-82e7-437f-9e5a-81fb5644a427,https://open.oregonstate.education/microbiology/,10.6	Current Strategies for Antimicrobial Discovery,https://open.oregonstate.education/microbiology/chapter/14-6current-strategies-for-antimicrobial-discovery/,"These developments reflect the growing belief that for-profit pharmaceutical companies must be subsidized to encourage development of new antimicrobials. But some ask whether pharmaceutical development should be motivated by profit at all. Given that millions of lives may hang in the balance, some might argue that drug companies have an ethical obligation to devote their research and development efforts to high-utility drugs, as opposed to highly profitable ones. Yet this obligation conflicts with the fundamental goals of a for-profit company. Are government subsidies enough to ensure that drug companies make the public interest a priority, or should government agencies assume responsibility for developing critical drugs that may have little or no return on investment?",True,Acute and Chronic Diseases,,,,
a30f748c-4711-4025-8f5c-9aa63da8da62,https://open.oregonstate.education/microbiology/,10.5	Testing the Effectiveness of Antimicrobials,https://open.oregonstate.education/microbiology/chapter/14-5testing-the-effectiveness-of-antimicrobials/,The Kirby-Bauer Disk Diffusion Test,False,The Kirby-Bauer Disk Diffusion Test,,,,
5be9e5fc-b7a5-4d7e-bfd4-cf389937cf0f,https://open.oregonstate.education/microbiology/,10.5	Testing the Effectiveness of Antimicrobials,https://open.oregonstate.education/microbiology/chapter/14-5testing-the-effectiveness-of-antimicrobials/,"The Kirby-Bauer disk diffusion test has long been used as a starting point for determining the susceptibility of specific microbes to various antimicrobial drugs. The Kirby-Bauer assay starts with a Mueller-Hinton agar plate on which a confluent lawn is inoculated with a patient’s isolated bacterial pathogen. Filter paper disks impregnated with known amounts of antibacterial drugs to be tested are then placed on the agar plate. As the bacterial inoculum grows, antibiotic diffuses from the circular disk into the agar and interacts with the growing bacteria. Antibacterial activity is observed as a clear circular zone of inhibition around the drug-impregnated disk, similar to the disk-diffusion assay depicted in Figure 10.10. The diameter of the zone of inhibition, measured in millimeters and compared to a standardized chart, determines the susceptibility or resistance of the bacterial pathogen to the drug.",True,The Kirby-Bauer Disk Diffusion Test,Figure 10.10,10.5	Testing the Effectiveness of Antimicrobials,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-14.19.png,"Figure 10.10 In a dilution test, the lowest dilution that inhibits turbidity (cloudiness) is the MIC. In this example, the MIC is 8 μg/mL. Broth from samples without turbidity can be inoculated onto plates lacking the antimicrobial drug. The lowest dilution that kills ≥99.9% of the starting inoculum is observed on the plates is the MBC. (credit: modification of work by Suzanne Wakim)"
8df02335-df06-4043-b0f9-77ca4561d63e,https://open.oregonstate.education/microbiology/,10.5	Testing the Effectiveness of Antimicrobials,https://open.oregonstate.education/microbiology/chapter/14-5testing-the-effectiveness-of-antimicrobials/,"There are multiple factors that determine the size of a zone of inhibition in this assay, including drug solubility, rate of drug diffusion through agar, the thickness of the agar medium, and the drug concentration impregnated into the disk. Due to a lack of standardization of these factors, interpretation of the Kirby-Bauer disk diffusion assay provides only limited information on susceptibility and resistance to the drugs tested. The assay cannot distinguish between bacteriostatic and bactericidal activities, and differences in zone sizes cannot be used to compare drug potencies or efficacies. Comparison of zone sizes to a standardized chart will only provide information on the antibacterials to which a bacterial pathogen is susceptible or resistant.",True,The Kirby-Bauer Disk Diffusion Test,,,,
6f0eb607-568f-47ee-9e2d-6b6a03804898,https://open.oregonstate.education/microbiology/,10.5	Testing the Effectiveness of Antimicrobials,https://open.oregonstate.education/microbiology/chapter/14-5testing-the-effectiveness-of-antimicrobials/,Dilution Tests,False,Dilution Tests,,,,
f669f6ea-e4ce-4885-b90e-373b787ac49b,https://open.oregonstate.education/microbiology/,10.5	Testing the Effectiveness of Antimicrobials,https://open.oregonstate.education/microbiology/chapter/14-5testing-the-effectiveness-of-antimicrobials/,"As discussed, the limitations of the Kirby-Bauer disk diffusion test do not allow for a direct comparison of antibacterial potencies to guide selection of the best therapeutic choice. However, antibacterial dilution tests can be used to determine a particular drug’s minimal inhibitory concentration (MIC), the lowest concentration of drug that inhibits visible bacterial growth, and minimal bactericidal concentration (MBC), the lowest drug concentration that kills ≥99.9% of the starting inoculum. Determining these concentrations helps identify the correct drug for a particular pathogen. For the macrobroth dilution assay, a dilution series of the drug in broth is made in test tubes and the same number of cells of a test bacterial strain is added to each tube (Figure 10.10). The MIC is determined by examining the tubes to find the lowest drug concentration that inhibits visible growth; this is observed as turbidity (cloudiness) in the broth. Tubes with no visible growth are then inoculated onto agar media without antibiotic to determine the MBC. Generally, serum levels of an antibacterial should be at least three to five times above the MIC for treatment of an infection.",True,Dilution Tests,Figure 10.10,10.5	Testing the Effectiveness of Antimicrobials,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-14.19.png,"Figure 10.10 In a dilution test, the lowest dilution that inhibits turbidity (cloudiness) is the MIC. In this example, the MIC is 8 μg/mL. Broth from samples without turbidity can be inoculated onto plates lacking the antimicrobial drug. The lowest dilution that kills ≥99.9% of the starting inoculum is observed on the plates is the MBC. (credit: modification of work by Suzanne Wakim)"
5a105a7b-53e0-4161-9149-c7aed4ac5c07,https://open.oregonstate.education/microbiology/,10.5	Testing the Effectiveness of Antimicrobials,https://open.oregonstate.education/microbiology/chapter/14-5testing-the-effectiveness-of-antimicrobials/,"The MIC assay can also be performed using 96-well microdilution trays, which allow for the use of small volumes and automated dispensing devices, as well as the testing of multiple antimicrobials and/or microorganisms in one tray (Figure 10.11). MICs are interpreted as the lowest concentration that inhibits visible growth, the same as for the macrobroth dilution in test tubes. Growth may also be interpreted visually or by using a spectrophotometer or similar device to detect turbidity or a color change if an appropriate biochemical substrate that changes color in the presence of bacterial growth is also included in each well.",True,Dilution Tests,Figure 10.11,10.5	Testing the Effectiveness of Antimicrobials,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-14.20.png,"Figure 10.11 A microdilution tray can also be used to determine MICs of multiple antimicrobial drugs in a single assay. In this example, the drug concentrations increase from left to right and the rows with clindamycin, penicillin, and erythromycin have been indicated to the left of the plate. For penicillin and erythromycin, the lowest concentrations that inhibited visible growth are indicated by red circles and were 0.06 μg/mL for penicillin and 8 μg/ mL for erythromycin. For clindamycin, visible bacterial growth was observed at every concentration up to 32 μg/mL and the MIC is interpreted as >32 μg/mL. (credit: modification of work by Centers for Disease Control and Prevention)"
d509490f-99ae-4028-b0b5-c969a76f0f19,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,"Exposure of a pathogen to an antimicrobial compound can select for chromosomal mutations conferring resistance, which can be transferred vertically to subsequent microbial generations and eventually become predominant in a microbial population that is repeatedly exposed to the antimicrobial. Alternatively, many genes responsible for drug resistance are found on plasmids or in transposons that can be transferred easily between microbes through horizontal gene tranfer. Small pieces of DNA called transposons also have the ability to move resistance genes between plasmids and chromosomes to further promote the spread of resistance.",True,Dilution Tests,,,,
094b0710-c5df-4fe0-8205-f052d4902d7a,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,Mechanisms for Drug Resistance,False,Mechanisms for Drug Resistance,,,,
4ceae23a-b39d-42fa-bff2-d3bec84ca498,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,"There are several common mechanisms for drug resistance, which are summarized in Figure 10.9. These mechanisms include enzymatic modification of the drug, modification of the antimicrobial target, and prevention of drug penetration or accumulation.",True,Mechanisms for Drug Resistance,Figure 10.9,10.6	Current Strategies for Antimicrobial Discovery,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-14.22.jpg,"Figure 10.9 In recent decades, approvals of new antimicrobials by the FDA have steadily fallen. In the five- year period from 1983–1987, 16 new antimicrobial drugs were approved, compared to just two from 2008–2012."
4ceae23a-b39d-42fa-bff2-d3bec84ca498,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,"There are several common mechanisms for drug resistance, which are summarized in Figure 10.9. These mechanisms include enzymatic modification of the drug, modification of the antimicrobial target, and prevention of drug penetration or accumulation.",True,Mechanisms for Drug Resistance,Figure 10.9,10.4	Drug Resistance,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-10.18.png,"Figure 10.9 There are multiple strategies that microbes use to develop resistance to antimicrobial drugs. (Not shown: target overproduction, target mimicry, and enzymatic bypass). (credit: modification of work by Gerard D Wright)"
eab61dd4-36fd-4d75-bb4e-94a279cb3af1,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,Drug Inactivation,False,Drug Inactivation,,,,
06a077dc-e992-48da-9d71-9bf6f427c4de,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,"Resistance genes may code for enzymes that chemically modify an antimicrobial, thereby inactivating it, or destroy an antimicrobial through hydrolysis. Resistance to many types of antimicrobials occurs through this mechanism.",True,Drug Inactivation,,,,
72fd77c5-f0d7-4c62-8504-cbef2758f724,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,Prevention of Cellular Uptake or Efflux,False,Prevention of Cellular Uptake or Efflux,,,,
54a6c4e0-6a23-42f3-b766-01bf7fbb6219,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,"Microbes may develop resistance mechanisms that involve inhibiting the accumulation of an antimicrobial drug, which then prevents the drug from reaching its cellular target. This strategy is common among gram-negative pathogens and can involve changes in outer membrane lipid composition, porin channel selectivity, and/or porin channel concentrations. Additionally, many gram-positive and gram-negative pathogenic bacteria produce efflux pumps that actively transport an antimicrobial drug out of the cell and prevent the accumulation of drug to a level that would be antibacterial.",True,Prevention of Cellular Uptake or Efflux,,,,
6e9a644f-0d4c-4a85-a7a7-4af44d3a4878,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,Target Modification,False,Target Modification,,,,
cf5d57d3-8e53-43ec-86b1-9ed28cc97293,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,"Because antimicrobial drugs have very specific targets, structural changes to those targets can prevent drug binding, rendering the drug ineffective. Through spontaneous mutations in the genes encoding antibacterial drug targets, bacteria have an evolutionary advantage that allows them to develop resistance to drugs. This mechanism of resistance development is quite common. Examples of this resistance strategy include alterations in",True,Target Modification,,,,
c6a240fe-1e25-424c-aecc-2b9e6eb14264,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,Target Overproduction or Enzymatic Bypass,False,Target Overproduction or Enzymatic Bypass,,,,
4f330b13-6ac0-43c5-880e-1987d370706f,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,"When an antimicrobial drug functions as an antimetabolite, targeting a specific enzyme to inhibit its activity, there are additional ways that microbial resistance may occur. First, the microbe may overproduce the target enzyme such that there is a sufficient amount of antimicrobial-free enzyme to carry out the proper enzymatic reaction. Second, the bacterial cell may develop a bypass that circumvents the need for the functional target enzyme. Both of these strategies have been found as mechanisms of sulfonamide resistance.",True,Target Overproduction or Enzymatic Bypass,,,,
31ee6d82-851c-422d-9bc2-dc6de9cef620,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,Multidrug-Resistant Microbes and Cross Resistance,False,Multidrug-Resistant Microbes and Cross Resistance,,,,
97207a51-400b-4210-97f4-8c8fb87b7206,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,"From a clinical perspective, our greatest concerns are multidrug-resistant microbes (MDRs) and cross resistance. MDRs are colloquially known as “superbugs” and carry one or more resistance mechanism(s), making them resistant to multiple antimicrobials. In cross-resistance, a single resistance mechanism confers resistance to multiple antimicrobial drugs. For example, having an efflux pump that can export multiple antimicrobial drugs is a common way for microbes to be resistant to multiple drugs by using a single resistance mechanism.",True,Multidrug-Resistant Microbes and Cross Resistance,,,,
2a62bf9c-5425-440f-92cb-dca5b741f69b,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,Methicillin-Resistant Staphylococcus aureus (MRSA),False,Methicillin-Resistant Staphylococcus aureus (MRSA),,,,
50fd789c-adb0-4010-ac92-b8831602e90f,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,"Methicillin, a semisynthetic penicillin, was designed to resist inactivation by β-lactamases. Unfortunately, soon after the introduction of methicillin to clinical practice, methicillin-resistant strains of S. aureus appeared and started to spread. The mechanism of resistance, acquisition of a new low-affinity PBP, provided S. aureus with resistance to all available β-lactams. Strains of methicillin-resistant S. aureus (MRSA) are widespread opportunistic pathogens and a particular concern for skin and other wound infections, but may also cause pneumonia and septicemia. Although originally a problem in health-care settings (hospital-acquired MRSA [HA-MRSA]), MRSA infections are now also acquired through contact with contaminated members of the general public, called community-associated MRSA (CA-MRSA). Approximately one-third of the population carries S. aureus as a member of their normal nasal microbiota without illness, and about 6% of these strains are methicillin resistant.[1][2]",True,Methicillin-Resistant Staphylococcus aureus (MRSA),,,,
6de75102-b65c-4db6-8dd5-71e696064e44,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,Multidrug-Resistant Mycobacterium tuberculosis,False,Multidrug-Resistant Mycobacterium tuberculosis,,,,
521c5e4c-f10b-4994-a2a8-7e7ddc486d09,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,"The emergence of multidrug-resistant Mycobacterium tuberculosis (MDR-TB) and extensively drug-resistant Mycobacterium tuberculosis (XDR-TB) is also of significant global concern. MDR-TB strains are resistant to both rifampin and isoniazid, the drug combination typically prescribed for treatment of tuberculosis. XDR-TB strains are additionally resistant to any fluoroquinolone and at least one of three other drugs (amikacin, kanamycin, or capreomycin) used as a second line of treatment, leaving these patients very few treatment options. Both types of pathogens are particularly problematic in immunocompromised persons, including those suffering from HIV infection. The development of resistance in these strains often results from the incorrect use of antimicrobials for tuberculosis treatment, selecting for resistance.",True,Multidrug-Resistant Mycobacterium tuberculosis,,,,
f25530d1-28c3-4b7b-884e-d15281b05c48,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,"To learn more about the top 18 drug-resistant threats to the US, visit the CDC’s website (https://openstax.org/l/22CDC18drugres).",True,Multidrug-Resistant Mycobacterium tuberculosis,,,,
12f09942-8e4c-401d-b019-a6c0033f93f0,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,Multidrug-Resistant Microbes and Cross Resistance,False,Multidrug-Resistant Microbes and Cross Resistance,,,,
d60ce739-41bb-4ce7-ba16-abfe3dc90368,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,"From a clinical perspective, our greatest concerns are multidrug-resistant microbes (MDRs) and cross resistance. MDRs are colloquially known as “superbugs” and carry one or more resistance mechanism(s), making them resistant to multiple antimicrobials. In cross-resistance, a single resistance mechanism confers resistance to multiple antimicrobial drugs. For example, having an efflux pump that can export multiple antimicrobial drugs is a common way for microbes to be resistant to multiple drugs by using a single resistance mechanism.",True,Multidrug-Resistant Microbes and Cross Resistance,,,,
64d92be0-aa24-43ea-95e7-5323a3c828b6,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,Methicillin-Resistant Staphylococcus aureus (MRSA),False,Methicillin-Resistant Staphylococcus aureus (MRSA),,,,
eb148ed8-f1f9-4bfb-946f-432f8ab4c53d,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,"Methicillin, a semisynthetic penicillin, was designed to resist inactivation by β-lactamases. Unfortunately, soon after the introduction of methicillin to clinical practice, methicillin-resistant strains of S. aureus appeared and started to spread. The mechanism of resistance, acquisition of a new low-affinity PBP, provided S. aureus with resistance to all available β-lactams. Strains of methicillin-resistant S. aureus (MRSA) are widespread opportunistic pathogens and a particular concern for skin and other wound infections, but may also cause pneumonia and septicemia. Although originally a problem in health-care settings (hospital-acquired MRSA [HA-MRSA]), MRSA infections are now also acquired through contact with contaminated members of the general public, called community-associated MRSA (CA-MRSA). Approximately one-third of the population carries S. aureus as a member of their normal nasal microbiota without illness, and about 6% of these strains are methicillin resistant.[1][2]",True,Methicillin-Resistant Staphylococcus aureus (MRSA),,,,
91f1274f-2749-4ba1-b68a-3c27ff1b926e,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,Multidrug-Resistant Mycobacterium tuberculosis,False,Multidrug-Resistant Mycobacterium tuberculosis,,,,
47ee9ff7-72fd-43a7-8e1b-62a7eab00e73,https://open.oregonstate.education/microbiology/,10.4	Drug Resistance,https://open.oregonstate.education/microbiology/chapter/14-4drug-resistance/,"The emergence of multidrug-resistant Mycobacterium tuberculosis (MDR-TB) and extensively drug-resistant Mycobacterium tuberculosis (XDR-TB) is also of significant global concern. MDR-TB strains are resistant to both rifampin and isoniazid, the drug combination typically prescribed for treatment of tuberculosis. XDR-TB strains are additionally resistant to any fluoroquinolone and at least one of three other drugs (amikacin, kanamycin, or capreomycin) used as a second line of treatment, leaving these patients very few treatment options. Both types of pathogens are particularly problematic in immunocompromised persons, including those suffering from HIV infection. The development of resistance in these strains often results from the incorrect use of antimicrobials for tuberculosis treatment, selecting for resistance.",True,Multidrug-Resistant Mycobacterium tuberculosis,,,,
8931ca8e-848b-4bcd-a91e-97f64306b018,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,Antifungal Drugs,False,Antifungal Drugs,,,,
fde3a7bb-8606-4c4d-af2e-1f6a15abc276,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,"The most common mode of action for antifungal drugs is the disruption of the cell membrane. Antifungals take advantage of small differences between fungi and humans in the biochemical pathways that synthesize sterols. The sterols are important in maintaining proper membrane fluidity and, hence, proper function of the cell membrane. For most fungi, the predominant membrane sterol is ergosterol. Because human cell membranes use cholesterol, instead of ergosterol, antifungal drugs that target ergosterol synthesis are selectively toxic (Figure 10.7).",True,Antifungal Drugs,Figure 10.7,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-14.13.png,"Figure 10.7 The predominant sterol found in human cells is cholesterol, whereas the predominant sterol found in fungi is ergosterol, making ergosterol a good target for antifungal drug development."
ab89f688-c2f0-40db-b3a9-9bf3b62d4520,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,"Beyond targeting ergosterol in fungal cell membranes, there are a few antifungal drugs that target specific substances found in fungal cell walls, interfere with fungal cell division, or act as antimetbolites against fungal processes.",True,Antifungal Drugs,,,,
472f14f0-759a-4eae-9022-40f2b988d4fd,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,"Table 10.7 shows the various therapeutic classes of antifungal drugs, categorized by mode of action, with examples of each.",True,Antifungal Drugs,,,,
42ad8a55-e5e0-47f1-94d4-7be94ad27be0,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,Antiprotozoan Drugs,False,Antiprotozoan Drugs,,,,
77aab436-dab0-4822-8036-a2026536a7ce,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,"There are a few mechanisms by which antiprotozoan drugs target infectious protozoans (Table 10.8). Some are antimetabolites, others interfere with nucleic acid synthesis, and one class interferes with heme detoxification, which is necessary for the parasite’s effective breakdown of hemoglobin into amino acids inside red blood cells.",True,Antiprotozoan Drugs,,,,
22e2110d-4c42-4ebb-8fc1-cf6d3e76fc50,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,Antihelminthic Drugs,False,Antihelminthic Drugs,,,,
997ec406-8a21-4805-a312-075c0412fdb0,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,"Because helminths are multicellular eukaryotes like humans, developing drugs with selective toxicity against them is extremely challenging. Despite this, several effective classes have been developed (Table 10.9). Some bind to helminthic β-tubulin, preventing microtubule formation. Microtubules in the intestinal cells of the worms seem to be particularly affected, leading to a reduction in glucose uptake. Another type of drug binds to glutamate-gated chloride channels specific to invertebrates including helminths, blocking neuronal transmission and causing starvation, paralysis, and death of the worms. Many antihelminthic drugs have modes of action that are unclear, but appear to interfere with ATP formation, inhibit RNA synthesis, or result in calcium influx into the worm.",True,Antihelminthic Drugs,,,,
e66683a9-9c97-48a9-8677-8e812a5ed3a9,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,Antiviral Drugs,False,Antiviral Drugs,,,,
828cd059-31ec-4754-9dbc-da0bafbb1073,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,"Unlike the complex structure of fungi, protozoa, and helminths, viral structure is simple, consisting of nucleic acid, a protein coat, viral enzymes, and, sometimes, a lipid envelope. Furthermore, viruses are obligate intracellular pathogens that use the host’s cellular machinery to replicate. These characteristics make it difficult to develop drugs with selective toxicity against viruses.",True,Antiviral Drugs,,,,
9e054cea-a4f2-43c9-81b0-b6daa450a924,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,"Many antiviral drugs are nucleoside analogs and function by inhibiting nucleic acid biosynthesis. The mode of action of other antivirals is not entirely clear, but it appears that some prevent viral escape from the cell endosome, preventing viral replication, while others block uncoating of the viral particles inside the host cells. Neuraminidase inhibitors (i.e. Tamiflu) specifically target influenza viruses by blocking the activity of influenza virus neuraminidase, preventing the release of the virus from infected cells. These antivirals can decrease flu symptoms and shorten the duration of illness.",True,Antiviral Drugs,,,,
3a4b9772-c298-4f4b-a191-cdfcee0f4c00,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,"Viruses with complex life cycles, such as HIV, can be more difficult to treat. First, HIV targets CD4-positive white blood cells, which are necessary for a normal immune response to infection. Second, HIV is a retrovirus, meaning that it converts its RNA genome into a DNA copy that integrates into the host cell’s genome, thus hiding within host cell DNA. Third, the HIV reverse transcriptase lacks proofreading activity and introduces mutations that allow for rapid development of antiviral drug resistance. To help prevent the emergence of resistance, a combination of specific synthetic antiviral drugs is typically used to treat HIV with antiretroviral therapy (ART), including a reverse transcriptase inhibitor, a protease inhibitor, and an integrase inhibitor. (Figure 10.8).",True,Antiviral Drugs,Figure 10.8,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-14.17.png,Figure 10.8 Antiretroviral therapy (ART) is typically used for the treatment of HIV. The targets of drug classes currently in use are shown here. (credit: modification of work by Thomas Splettstoesser)
106f0ad2-dc02-49a5-a6a9-37f760b4c1b8,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,"Table 10.10 shows the various therapeutic classes of antiviral drugs, categorized by mode of action, with examples of each.",True,Antiviral Drugs,,,,
46409d8e-5e0f-42a9-b8cb-9a87b9a4f465,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,"To learn more about the various classes of antiretroviral drugs used in the ART of HIV infection, explore each of the drugs in the HIV drug classes provided by US Department of Health and Human Services at this website (https://openstax.org/l/22HIVUSDepthea).",True,Antiviral Drugs,,,,
ac2a0cde-0619-4491-87cb-b0d8afa83ae1,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,Antiprotozoan Drugs,False,Antiprotozoan Drugs,,,,
50d300a1-df36-400f-960c-9dfc4b95898d,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,"There are a few mechanisms by which antiprotozoan drugs target infectious protozoans (Table 10.8). Some are antimetabolites, others interfere with nucleic acid synthesis, and one class interferes with heme detoxification, which is necessary for the parasite’s effective breakdown of hemoglobin into amino acids inside red blood cells.",True,Antiprotozoan Drugs,,,,
4c29fdcc-f75f-4df1-a34c-f56802bb38c6,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,Antihelminthic Drugs,False,Antihelminthic Drugs,,,,
72c6c6f2-3906-4087-b8f9-a47909fdf515,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,"Because helminths are multicellular eukaryotes like humans, developing drugs with selective toxicity against them is extremely challenging. Despite this, several effective classes have been developed (Table 10.9). Some bind to helminthic β-tubulin, preventing microtubule formation. Microtubules in the intestinal cells of the worms seem to be particularly affected, leading to a reduction in glucose uptake. Another type of drug binds to glutamate-gated chloride channels specific to invertebrates including helminths, blocking neuronal transmission and causing starvation, paralysis, and death of the worms. Many antihelminthic drugs have modes of action that are unclear, but appear to interfere with ATP formation, inhibit RNA synthesis, or result in calcium influx into the worm.",True,Antihelminthic Drugs,,,,
bb2405a7-1c2d-4bc4-8acc-d477594efa8e,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,Antiviral Drugs,False,Antiviral Drugs,,,,
ea696a64-bcdb-4e26-ad16-9ea6c48c7706,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,"Unlike the complex structure of fungi, protozoa, and helminths, viral structure is simple, consisting of nucleic acid, a protein coat, viral enzymes, and, sometimes, a lipid envelope. Furthermore, viruses are obligate intracellular pathogens that use the host’s cellular machinery to replicate. These characteristics make it difficult to develop drugs with selective toxicity against viruses.",True,Antiviral Drugs,,,,
7cd0e7d6-2ccf-4092-a717-513dd1429f43,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,"Many antiviral drugs are nucleoside analogs and function by inhibiting nucleic acid biosynthesis. The mode of action of other antivirals is not entirely clear, but it appears that some prevent viral escape from the cell endosome, preventing viral replication, while others block uncoating of the viral particles inside the host cells. Neuraminidase inhibitors (i.e. Tamiflu) specifically target influenza viruses by blocking the activity of influenza virus neuraminidase, preventing the release of the virus from infected cells. These antivirals can decrease flu symptoms and shorten the duration of illness.",True,Antiviral Drugs,,,,
8cc066f1-d24c-46cc-bbd5-f4784dbe0674,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,"Viruses with complex life cycles, such as HIV, can be more difficult to treat. First, HIV targets CD4-positive white blood cells, which are necessary for a normal immune response to infection. Second, HIV is a retrovirus, meaning that it converts its RNA genome into a DNA copy that integrates into the host cell’s genome, thus hiding within host cell DNA. Third, the HIV reverse transcriptase lacks proofreading activity and introduces mutations that allow for rapid development of antiviral drug resistance. To help prevent the emergence of resistance, a combination of specific synthetic antiviral drugs is typically used to treat HIV with antiretroviral therapy (ART), including a reverse transcriptase inhibitor, a protease inhibitor, and an integrase inhibitor. (Figure 10.8).",True,Antiviral Drugs,Figure 10.8,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-14.17.png,Figure 10.8 Antiretroviral therapy (ART) is typically used for the treatment of HIV. The targets of drug classes currently in use are shown here. (credit: modification of work by Thomas Splettstoesser)
47983e1d-1ea0-421b-a9d7-c0f03d23beda,https://open.oregonstate.education/microbiology/,10.3	Mechanisms of Other Antimicrobial Drugs,https://open.oregonstate.education/microbiology/chapter/14-3mechanisms-of-other-antimicrobial-drugs/,"Table 10.10 shows the various therapeutic classes of antiviral drugs, categorized by mode of action, with examples of each.",True,Antiviral Drugs,,,,
859682fe-1c38-4a7a-809a-fa3e1b5d90a1,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Inhibitors of Cell Wall Biosynthesis,False,Inhibitors of Cell Wall Biosynthesis,,,,
ac4e949b-75c6-44ff-8ddf-07842f785de4,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"Several different classes of antibacterials block steps in the biosynthesis of peptidoglycan, making cells more susceptible to osmotic lysis (Table 10.2). Therefore, antibacterials that target cell wall biosynthesis are bactericidal in their action. Because human cells do not make peptidoglycan, this mode of action is an excellent example of selective toxicity. Antibiotics that inhibit the cell wall biosynthesis of bacteria include the penicillins (including ampicillin, amoxicillin, and methicillin), cephalosporins, vancomycin, and bacitracin. Although it may be administered orally or intramuscularly in some circumstances, bacitracin has been shown to be nephrotoxic (damaging to the kidneys). Therefore, it is more commonly combined with neomycin and polymyxin in topical ointments such as Neosporin.",True,Inhibitors of Cell Wall Biosynthesis,,,,
a40f6638-7178-41d7-afb2-20962893ba4e,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"Some of these antibiotics are natural antibiotics produced by fungi or bacteria, while others are semi-synthetic, where a natural antibiotic has been chemically modified in the lab.",True,Inhibitors of Cell Wall Biosynthesis,,,,
88d572db-f91f-4386-abfc-3d92dfd16327,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Spectrum of Activity,False,Spectrum of Activity,,,,
d2d6201f-51e6-4ebb-808b-3adaebaeda1f,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Inhibitors of Protein Biosynthesis,False,Inhibitors of Protein Biosynthesis,,,,
6e9ef415-99f0-476b-99ff-ceac7d61c98f,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"The cytoplasmic ribosomes found in animal cells (80S) are structurally distinct from those found in bacterial cells (70S), making protein biosynthesis a good selective target for antibacterial drugs. Several types of protein biosynthesis inhibitors are discussed in this section and are summarized in Figure 10.5 and Table 10.3.",True,Inhibitors of Protein Biosynthesis,Figure 10.5,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-14.11.png,Figure 10.5 The major classes of protein synthesis inhibitors target the 30S or 50S subunits of cytoplasmic ribosomes.
f81d0161-9bc4-46d1-8a38-f9272b3c716c,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Protein Synthesis Inhibitors That Bind the 30S Subunit,False,Protein Synthesis Inhibitors That Bind the 30S Subunit,,,,
cefe4b44-ab7f-4903-a03a-1f1a1420eb14,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"Another class of antibacterial compounds that bind to the 30S subunit is the tetracyclines. In contrast to aminoglycosides, these drugs are bacteriostatic and inhibit protein synthesis by blocking the association of tRNAs with the ribosome during translation. Although the tetracyclines are broad spectrum in their coverage of bacterial pathogens, side effects that can limit their use include phototoxicity, permanent discoloration of developing teeth, and liver toxicity with high doses or in patients with kidney impairment.",True,Protein Synthesis Inhibitors That Bind the 30S Subunit,,,,
88b485bf-226c-42f0-8242-98cb0401cd8d,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Protein Synthesis Inhibitors That Bind the 50S Subunit,False,Protein Synthesis Inhibitors That Bind the 50S Subunit,,,,
9e92f2ff-3523-4218-9aff-cfe7f09fcc32,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"There are several classes of antibacterial drugs that work through binding to the 50S subunit of bacterial ribosomes. Specific examples include erythromycin, azithromycin, and chloramphenicol. The first drug discovered in this category was erythromycin. It was isolated in 1952 from Streptomyces erythreus. Compared with erythromycin, azithromycin has a broader spectrum of activity, fewer side effects, and a significantly longer half-life (1.5 hours for erythromycin versus 68 hours for azithromycin) that allows for once-daily dosing and a short 3-day course of therapy (i.e., Zpac formulation) for most infections.",True,Protein Synthesis Inhibitors That Bind the 50S Subunit,,,,
cb6c0b4a-5d73-4158-9d0a-40a1863a89bf,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"The drug chloramphenicol represents yet another structurally distinct class of antibacterials that also bind to the 50S ribosome, inhibiting peptide bond formation. Chloramphenicol, produced by Streptomyces venezuelae, was discovered in 1947; in 1949, it became the first broad-spectrum antibiotic that was approved by the FDA. Although it is a natural antibiotic, it is also easily synthesized and was the first antibacterial drug synthetically mass produced. As a result of its mass production, broad-spectrum coverage, and ability to penetrate into tissues efficiently, chloramphenicol was historically used to treat a wide range of infections, from meningitis to typhoid fever to conjunctivitis. Unfortunately, serious side effects, such as lethal gray baby syndrome, and suppression of bone marrow production, have limited its clinical role. Because of toxicity concerns, chloramphenicol usage in humans is now rare in the United States and is limited to severe infections unable to be treated by less toxic antibiotics. Because its side effects are much less severe in animals, it is used in veterinary medicine.",True,Protein Synthesis Inhibitors That Bind the 50S Subunit,,,,
09ab7b3e-f3fb-4252-8756-a1ec8073b6d0,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,subunit,False,subunit,,,,
4e7a6de4-00f9-46e7-be96-f0f7dcbb6f3e,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,subunit,False,subunit,,,,
dde09699-3aec-4abd-8e0d-93aeedab92ef,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Inhibitors of Membrane Function,False,Inhibitors of Membrane Function,,,,
3d0aa1ae-6521-4f88-bb01-20bd2f88c035,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"A small group of antibacterials target the bacterial membrane as their mode of action (Table 10.4). The polymyxins are natural polypeptide antibiotics that were first discovered in 1947 as products of Bacillus polymyxa; only polymyxin B and polymyxin E (colistin) have been used clinically. They are lipophilic with detergent-like properties and interact with the lipopolysaccharide component of the outer membrane of gram-negative bacteria, ultimately disrupting both their outer and inner membranes and killing the bacterial cells. Unfortunately, the membrane-targeting mechanism is not a selective toxicity, and these drugs also target and damage the membrane of cells in the kidney and nervous system when administered systemically. Because of these serious side effects and their poor absorption from the digestive tract, polymyxin B is used in over-the-counter topical antibiotic ointments (e.g., Neosporin), and oral colistin was historically used only for bowel decontamination to prevent infections originating from bowel microbes in immunocompromised patients or for those undergoing certain abdominal surgeries. The antibacterial daptomycin is a cyclic lipopeptide produced by Streptomyces roseosporus that seems to work like the polymyxins, inserting in the bacterial cell membrane and disrupting it. However, in contrast to polymyxin B and colistin, which target only gram-negative bacteria, daptomycin specifically targets gram-positive bacteria. It is typically administered intravenously and seems to be well tolerated, showing reversible toxicity in skeletal muscles.",True,Inhibitors of Membrane Function,,,,
7828f019-3b64-4157-a71c-a3120c516ac6,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Inhibitors of Nucleic Acid Synthesis,False,Inhibitors of Nucleic Acid Synthesis,,,,
d10cfafc-a6ef-42ec-b037-8bad2246ec05,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"Some antibacterial drugs work by inhibiting nucleic acid synthesis (Table 10.5). The drug rifampin is a semisynthetic member of the rifamycin family and functions by blocking RNA polymerase activity in bacteria. The RNA polymerase enzymes in bacteria are structurally different from those in eukaryotes, providing for selective toxicity against bacterial cells. It is used for the treatment of a variety of infections, but its primary use, often in a cocktail with other antibacterial drugs, is against mycobacteria that cause tuberculosis. Despite the selectivity of its mechanism, rifampin can induce liver enzymes to increase metabolism of other drugs being administered (antagonism), leading to hepatotoxicity (liver toxicity) and negatively influencing the bioavailability and therapeutic effect of the companion drugs.",True,Inhibitors of Nucleic Acid Synthesis,,,,
728a81f1-2261-441c-8e30-b9027d50b5d8,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"Fluoroquinolones, such as ciprofloxacin, kills bacterial cells by blocking DNA replication.",True,Inhibitors of Nucleic Acid Synthesis,,,,
3ae1e78d-eff9-4105-887d-bd1ac5ea09b8,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Inhibitors of Metabolic Pathways,False,Inhibitors of Metabolic Pathways,,,,
49eaf9e1-bcbd-4bf1-bc01-51d34151adee,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"Some synthetic drugs control bacterial infections by functioning as antimetabolites, competitive inhibitors for bacterial metabolic enzymes (Table 10.6). The sulfonamides (sulfa drugs) are the oldest synthetic antibacterial agents and are structural analogues of para-aminobenzoic acid (PABA), an early intermediate in folic acid synthesis (Figure 10.6). By inhibiting the enzyme involved in the production of dihydrofolic acid, sulfonamides block bacterial biosynthesis of folic acid and, subsequently, pyrimidines and purines required for nucleic acid synthesis. This mechanism of action provides bacteriostatic inhibition of growth against a wide spectrum of gram-positive and gram-negative pathogens. Because humans obtain folic acid from food instead of synthesizing it intracellularly, sulfonamides are selectively toxic for bacteria. However, allergic reactions to sulfa drugs are common. Another example of an antimetabolite that inhibits the folic acid synthesis pathway is trimethoprim, a synthetic antimicrobial compound (Figure 10.6). Trimethoprim is used in combination with the sulfa drug sulfamethoxazole to treat urinary tract infections, ear infections, and bronchitis. When used alone, each antimetabolite only decreases production of folic acid to a level where bacteriostatic inhibition of growth occurs. However, when used in combination, inhibition of both steps in the metabolic pathway decreases folic acid synthesis to a level that is lethal to the bacterial cell. Because of the importance of folic acid during fetal development, sulfa drugs and trimethoprim use should be carefully considered during early pregnancy.",True,Inhibitors of Metabolic Pathways,Figure 10.6,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-14.12.png,"Figure 10.6 Sulfonamides and trimethoprim are examples of antimetabolites that interfere in the bacterial synthesis of folic acid by blocking purine and pyrimidine biosynthesis, thus inhibiting bacterial growth."
a23c2d8f-29f7-4357-b82c-d0e776e235e2,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Inhibitor of ATP Synthase,False,Inhibitor of ATP Synthase,,,,
952d212d-fca7-49c6-9692-c8b11d33410e,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"Bedaquiline, representing the synthetic antibacterial class of compounds called the diarylquinolines, uses a novel mode of action that specifically inhibits mycobacterial growth. Although the specific mechanism has yet to be elucidated, this compound appears to interfere with the function of ATP synthases, perhaps by interfering with the use of the hydrogen ion gradient for ATP synthesis by oxidative phosphorylation, leading to reduced ATP production. Due to its side effects, including hepatotoxicity and potentially lethal heart arrhythmia, its use is reserved for serious, otherwise untreatable cases of tuberculosis.",True,Inhibitor of ATP Synthase,,,,
bbba963c-bec7-401f-9498-acf36cf6b7d8,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Inhibitors of Cell Wall Biosynthesis,False,Inhibitors of Cell Wall Biosynthesis,,,,
8c03152b-b072-4e9b-a3f8-3e97c980e8d7,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"Some of these antibiotics are natural antibiotics produced by fungi or bacteria, while others are semi-synthetic, where a natural antibiotic has been chemically modified in the lab.",True,Inhibitors of Cell Wall Biosynthesis,,,,
b3f06482-815c-486e-b579-5b5bea5602fb,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Spectrum of Activity,False,Spectrum of Activity,,,,
5bcdd291-cc08-44cc-87d7-5fe68df2699c,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Inhibitors of Protein Biosynthesis,False,Inhibitors of Protein Biosynthesis,,,,
05e8543c-14b7-42fa-aa35-a2481087933c,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"The cytoplasmic ribosomes found in animal cells (80S) are structurally distinct from those found in bacterial cells (70S), making protein biosynthesis a good selective target for antibacterial drugs. Several types of protein biosynthesis inhibitors are discussed in this section and are summarized in Figure 10.5 and Table 10.3.",True,Inhibitors of Protein Biosynthesis,Figure 10.5,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-14.11.png,Figure 10.5 The major classes of protein synthesis inhibitors target the 30S or 50S subunits of cytoplasmic ribosomes.
08c2802b-aca5-4cee-aae5-fe49e243e76a,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Protein Synthesis Inhibitors That Bind the 30S Subunit,False,Protein Synthesis Inhibitors That Bind the 30S Subunit,,,,
bb0f18af-9d93-4c51-843d-70d56af00f81,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"Another class of antibacterial compounds that bind to the 30S subunit is the tetracyclines. In contrast to aminoglycosides, these drugs are bacteriostatic and inhibit protein synthesis by blocking the association of tRNAs with the ribosome during translation. Although the tetracyclines are broad spectrum in their coverage of bacterial pathogens, side effects that can limit their use include phototoxicity, permanent discoloration of developing teeth, and liver toxicity with high doses or in patients with kidney impairment.",True,Protein Synthesis Inhibitors That Bind the 30S Subunit,,,,
313307fa-c92b-4bf7-a3c7-140988a7f724,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Protein Synthesis Inhibitors That Bind the 50S Subunit,False,Protein Synthesis Inhibitors That Bind the 50S Subunit,,,,
17d6bf46-b29f-461a-8a80-107f86f47073,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"There are several classes of antibacterial drugs that work through binding to the 50S subunit of bacterial ribosomes. Specific examples include erythromycin, azithromycin, and chloramphenicol. The first drug discovered in this category was erythromycin. It was isolated in 1952 from Streptomyces erythreus. Compared with erythromycin, azithromycin has a broader spectrum of activity, fewer side effects, and a significantly longer half-life (1.5 hours for erythromycin versus 68 hours for azithromycin) that allows for once-daily dosing and a short 3-day course of therapy (i.e., Zpac formulation) for most infections.",True,Protein Synthesis Inhibitors That Bind the 50S Subunit,,,,
c0561208-3630-4ab6-a9d1-57fc053bced2,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"The drug chloramphenicol represents yet another structurally distinct class of antibacterials that also bind to the 50S ribosome, inhibiting peptide bond formation. Chloramphenicol, produced by Streptomyces venezuelae, was discovered in 1947; in 1949, it became the first broad-spectrum antibiotic that was approved by the FDA. Although it is a natural antibiotic, it is also easily synthesized and was the first antibacterial drug synthetically mass produced. As a result of its mass production, broad-spectrum coverage, and ability to penetrate into tissues efficiently, chloramphenicol was historically used to treat a wide range of infections, from meningitis to typhoid fever to conjunctivitis. Unfortunately, serious side effects, such as lethal gray baby syndrome, and suppression of bone marrow production, have limited its clinical role. Because of toxicity concerns, chloramphenicol usage in humans is now rare in the United States and is limited to severe infections unable to be treated by less toxic antibiotics. Because its side effects are much less severe in animals, it is used in veterinary medicine.",True,Protein Synthesis Inhibitors That Bind the 50S Subunit,,,,
ccb5a8e7-e528-4d65-b916-bb154024864f,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,subunit,False,subunit,,,,
ee126c0a-67ba-4b61-a98c-13c5e4a51718,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,subunit,False,subunit,,,,
b82abfe7-3544-4442-9bae-1f21685af1f7,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Inhibitors of Membrane Function,False,Inhibitors of Membrane Function,,,,
1fb2b0a3-18a8-4395-b2b1-1d07459f7dce,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"A small group of antibacterials target the bacterial membrane as their mode of action (Table 10.4). The polymyxins are natural polypeptide antibiotics that were first discovered in 1947 as products of Bacillus polymyxa; only polymyxin B and polymyxin E (colistin) have been used clinically. They are lipophilic with detergent-like properties and interact with the lipopolysaccharide component of the outer membrane of gram-negative bacteria, ultimately disrupting both their outer and inner membranes and killing the bacterial cells. Unfortunately, the membrane-targeting mechanism is not a selective toxicity, and these drugs also target and damage the membrane of cells in the kidney and nervous system when administered systemically. Because of these serious side effects and their poor absorption from the digestive tract, polymyxin B is used in over-the-counter topical antibiotic ointments (e.g., Neosporin), and oral colistin was historically used only for bowel decontamination to prevent infections originating from bowel microbes in immunocompromised patients or for those undergoing certain abdominal surgeries. The antibacterial daptomycin is a cyclic lipopeptide produced by Streptomyces roseosporus that seems to work like the polymyxins, inserting in the bacterial cell membrane and disrupting it. However, in contrast to polymyxin B and colistin, which target only gram-negative bacteria, daptomycin specifically targets gram-positive bacteria. It is typically administered intravenously and seems to be well tolerated, showing reversible toxicity in skeletal muscles.",True,Inhibitors of Membrane Function,,,,
7d06cf2d-3fee-4056-a8a0-3dea61f58910,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Inhibitors of Nucleic Acid Synthesis,False,Inhibitors of Nucleic Acid Synthesis,,,,
4556e8ad-118e-4838-af08-17be8c064dd0,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"Some antibacterial drugs work by inhibiting nucleic acid synthesis (Table 10.5). The drug rifampin is a semisynthetic member of the rifamycin family and functions by blocking RNA polymerase activity in bacteria. The RNA polymerase enzymes in bacteria are structurally different from those in eukaryotes, providing for selective toxicity against bacterial cells. It is used for the treatment of a variety of infections, but its primary use, often in a cocktail with other antibacterial drugs, is against mycobacteria that cause tuberculosis. Despite the selectivity of its mechanism, rifampin can induce liver enzymes to increase metabolism of other drugs being administered (antagonism), leading to hepatotoxicity (liver toxicity) and negatively influencing the bioavailability and therapeutic effect of the companion drugs.",True,Inhibitors of Nucleic Acid Synthesis,,,,
b57c396f-2a57-4611-a0ee-6f44d17e239e,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"Fluoroquinolones, such as ciprofloxacin, kills bacterial cells by blocking DNA replication.",True,Inhibitors of Nucleic Acid Synthesis,,,,
640ea42c-765b-4f93-80aa-1553b54ddd04,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Inhibitors of Metabolic Pathways,False,Inhibitors of Metabolic Pathways,,,,
741bb021-e9f1-42a8-96ef-9a0d685d1fe2,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"Some synthetic drugs control bacterial infections by functioning as antimetabolites, competitive inhibitors for bacterial metabolic enzymes (Table 10.6). The sulfonamides (sulfa drugs) are the oldest synthetic antibacterial agents and are structural analogues of para-aminobenzoic acid (PABA), an early intermediate in folic acid synthesis (Figure 10.6). By inhibiting the enzyme involved in the production of dihydrofolic acid, sulfonamides block bacterial biosynthesis of folic acid and, subsequently, pyrimidines and purines required for nucleic acid synthesis. This mechanism of action provides bacteriostatic inhibition of growth against a wide spectrum of gram-positive and gram-negative pathogens. Because humans obtain folic acid from food instead of synthesizing it intracellularly, sulfonamides are selectively toxic for bacteria. However, allergic reactions to sulfa drugs are common. Another example of an antimetabolite that inhibits the folic acid synthesis pathway is trimethoprim, a synthetic antimicrobial compound (Figure 10.6). Trimethoprim is used in combination with the sulfa drug sulfamethoxazole to treat urinary tract infections, ear infections, and bronchitis. When used alone, each antimetabolite only decreases production of folic acid to a level where bacteriostatic inhibition of growth occurs. However, when used in combination, inhibition of both steps in the metabolic pathway decreases folic acid synthesis to a level that is lethal to the bacterial cell. Because of the importance of folic acid during fetal development, sulfa drugs and trimethoprim use should be carefully considered during early pregnancy.",True,Inhibitors of Metabolic Pathways,Figure 10.6,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-14.12.png,"Figure 10.6 Sulfonamides and trimethoprim are examples of antimetabolites that interfere in the bacterial synthesis of folic acid by blocking purine and pyrimidine biosynthesis, thus inhibiting bacterial growth."
4e148407-c605-4896-ad65-18b291a52400,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,Inhibitor of ATP Synthase,False,Inhibitor of ATP Synthase,,,,
cc4f062d-622b-4c06-b9d5-70ae4c6e6c42,https://open.oregonstate.education/microbiology/,10.2 Mechanisms of Antibacterial Drugs,https://open.oregonstate.education/microbiology/chapter/14-2mechanisms-of-antibacterial-drugs/,"Bedaquiline, representing the synthetic antibacterial class of compounds called the diarylquinolines, uses a novel mode of action that specifically inhibits mycobacterial growth. Although the specific mechanism has yet to be elucidated, this compound appears to interfere with the function of ATP synthases, perhaps by interfering with the use of the hydrogen ion gradient for ATP synthesis by oxidative phosphorylation, leading to reduced ATP production. Due to its side effects, including hepatotoxicity and potentially lethal heart arrhythmia, its use is reserved for serious, otherwise untreatable cases of tuberculosis.",True,Inhibitor of ATP Synthase,,,,
9b4d7a53-6888-470e-8098-f9b497c7d4f2,https://open.oregonstate.education/microbiology/,10.1	Fundamentals of Antimicrobial Chemotherapy,https://open.oregonstate.education/microbiology/chapter/14-1fundamentals-of-antimicrobial-chemotherapy/,Bacteriostatic Versus Bactericidal,False,Bacteriostatic Versus Bactericidal,,,,
59d9ae9a-ce68-4ce8-8ab6-71806dbbb4f9,https://open.oregonstate.education/microbiology/,10.1	Fundamentals of Antimicrobial Chemotherapy,https://open.oregonstate.education/microbiology/chapter/14-1fundamentals-of-antimicrobial-chemotherapy/,"Antibacterial drugs can be either bacteriostatic or bactericidal in their interactions with target bacteria. Bacteriostatic drugs cause a reversible inhibition of growth, with bacterial growth restarting after elimination of the drug. By contrast, bactericidal drugs kill their target bacteria. The decision of whether to use a bacteriostatic or bactericidal drugs depends on the type of infection and the immune status of the patient. In a patient with strong immune defenses, bacteriostatic and bactericidal drugs can be effective in achieving clinical cure. However, when a patient is immunocompromised, a bactericidal drug is essential for the successful treatment of infections. Regardless of the immune status of the patient, life-threatening infections such as acute endocarditis require the use of a bactericidal drug.",True,Bacteriostatic Versus Bactericidal,,,,
9a331a40-ac34-410c-bc5e-b77c22de7c1d,https://open.oregonstate.education/microbiology/,10.1	Fundamentals of Antimicrobial Chemotherapy,https://open.oregonstate.education/microbiology/chapter/14-1fundamentals-of-antimicrobial-chemotherapy/,Spectrum of Activity,False,Spectrum of Activity,,,,
ef4e0c98-4926-4963-a324-ed144fb65c84,https://open.oregonstate.education/microbiology/,10.1	Fundamentals of Antimicrobial Chemotherapy,https://open.oregonstate.education/microbiology/chapter/14-1fundamentals-of-antimicrobial-chemotherapy/,"The spectrum of activity of an antibacterial drug relates to diversity of targeted bacteria. A narrow-spectrum antimicrobial targets only specific subsets of bacterial pathogens. For example, some narrow-spectrum drugs only target gram-positive bacteria, whereas others target only gram-negative bacteria. If the pathogen causing an infection has been identified, it is best to use a narrow-spectrum antimicrobial and minimize collateral damage to the normal microbiota. A broad-spectrum antimicrobial targets a wide variety of bacterial pathogens, including both gram- positive and gram-negative species, and is frequently used as empiric therapy to cover a wide range of potential pathogens while waiting on the laboratory identification of the infecting pathogen. Broad-spectrum antimicrobials are also used for polymicrobic infections (mixed infection with multiple bacterial species), or as prophylactic prevention of infections with surgery/invasive procedures. Finally, broad-spectrum antimicrobials may be selected to treat an infection when a narrow-spectrum drug fails because of development of drug resistance by the target pathogen.",True,Spectrum of Activity,,,,
90315252-4d6f-449a-9e40-706d01eae84a,https://open.oregonstate.education/microbiology/,10.1	Fundamentals of Antimicrobial Chemotherapy,https://open.oregonstate.education/microbiology/chapter/14-1fundamentals-of-antimicrobial-chemotherapy/,"The risk associated with using broad-spectrum antimicrobials is that they will also target a broad spectrum of the normal microbiota, increasing the risk of a superinfection, a secondary infection in a patient having a preexisting infection. A superinfection develops when the antibacterial intended for the preexisting infection kills the protective microbiota, allowing another pathogen resistant to the antibacterial to proliferate and cause a secondary infection (Figure 10.2)",True,Spectrum of Activity,Figure 10.2,10.1	Fundamentals of Antimicrobial Chemotherapy,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-14.6.png,Figure 10.2 Broad-spectrum antimicrobial use may lead to the development of a superinfection. (credit: modification of work by Centers for Disease Control and Prevention)
832062b7-0537-44fa-bb52-307818510fff,https://open.oregonstate.education/microbiology/,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/microbiology/chapter/13-2testing-the-effectiveness-of-antiseptics-and-disinfectants/,"However, several environmental conditions influence the potency of an antimicrobial agent and its effectiveness. For example, length of exposure is particularly important, with longer exposure increasing efficacy. Similarly, the concentration of the chemical agent is also important, with higher concentrations being more ef fective than lower ones. Temperature, pH, and other factors can also affect the potency of a disinfecting agent.",True,Spectrum of Activity,,,,
9e3662f6-a069-4e51-9c0a-e31410376c33,https://open.oregonstate.education/microbiology/,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/microbiology/chapter/13-2testing-the-effectiveness-of-antiseptics-and-disinfectants/,"One method to determine the effectiveness of a chemical agent includes swabbing surfaces before and after use to confirm whether a sterile field was maintained during use. Additional tests are described in the sections that follow. These tests allow for the maintenance of appropriate disinfection protocols in clinical settings, controlling microbial growth to protect patients, health-care workers, and the community.",True,Spectrum of Activity,,,,
a3a73166-874a-4b1b-8e50-1f76d7b94155,https://open.oregonstate.education/microbiology/,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/microbiology/chapter/13-2testing-the-effectiveness-of-antiseptics-and-disinfectants/,Phenol Coefficient,False,Phenol Coefficient,,,,
232dbff9-6320-43b2-b020-28bb490d0ae8,https://open.oregonstate.education/microbiology/,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/microbiology/chapter/13-2testing-the-effectiveness-of-antiseptics-and-disinfectants/,"The effectiveness of a disinfectant or antiseptic can be determined in a number of ways. Historically, a chemical agent’s effectiveness was often compared with that of phenol, the first chemical agent used by Joseph Lister. In 1903, British chemists Samuel Rideal (1863–1929) and J. T. Ainslie Walker (1868–1930) established a protocol to compare the effectiveness of a variety of chemicals with that of phenol, using as their test organisms Staphylococcus aureus (a gram-positive bacterium) and Salmonella enterica serovar Typhi (a gram-negative bacterium). They exposed the test bacteria to the antimicrobial chemical solutions diluted in water for 7.5 minutes. They then calculated a phenol coefficient for each chemical for each of the two bacteria tested. A phenol coefficient of 1.0 means that the chemical agent has about the same level of effectiveness as phenol. A chemical agent with a phenol coefficient of less than 1.0 is less effective than phenol. An example is formalin, with phenol coefficients of 0.3 (S. aureus) and 0.7 (S. enterica serovar Typhi). A chemical agent with a phenol coefficient greater than 1.0 is more effective than phenol, such as chloramine, with phenol coefficients of 133 and 100, respectively. Although the phenol coefficient was once a useful measure of effectiveness, it is no longer commonly used because the conditions and organisms used were arbitrarily chosen.",True,Phenol Coefficient,,,,
04969a3f-6041-48e6-8ad0-b09483866fec,https://open.oregonstate.education/microbiology/,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/microbiology/chapter/13-2testing-the-effectiveness-of-antiseptics-and-disinfectants/,Disk-Diffusion Method,False,Disk-Diffusion Method,,,,
e90d35e7-4e1a-45ec-93c4-4b48d2feb30b,https://open.oregonstate.education/microbiology/,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/microbiology/chapter/13-2testing-the-effectiveness-of-antiseptics-and-disinfectants/,"The disk-diffusion method involves applying different chemicals to separate, sterile filter paper disks (Figure 9.6). The disks are then placed on an agar plate that has been inoculated with the targeted bacterium and the chemicals diffuse out of the disks into the agar where the bacteria have been inoculated. As the “lawn” of bacteria grows, zones of inhibition of microbial growth are observed as clear areas around the disks. Although there are other factors that contribute to the sizes of zones of inhibition (e.g., whether the agent is water soluble and able to diffuse in the agar), larger zones typically correlate to increased inhibition effectiveness of the chemical agent. The diameter across each zone is measured in millimeters.",True,Disk-Diffusion Method,Figure 9.6,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-13.31.png,"Figure 9.6 A disk-diffusion assay is used to determine the effectiveness of chemical agents against a particular microbe. (a) A plate is inoculated with various antimicrobial discs. The zone of inhibition around each disc indicates how effective that antimicrobial is against the particular species being tested. (b) On these plates, four antimicrobial agents are tested for efficacy in killing Pseudomonas aeruginosa (left) and Staphylococcus aureus (right). These antimicrobials are much more effective at killing S. aureus, as indicated by the size of the zones of inhibition. (credit b: modification of work by American Society for Microbiology)"
667d6de4-8497-459c-863e-9797aa90818c,https://open.oregonstate.education/microbiology/,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/microbiology/chapter/13-2testing-the-effectiveness-of-antiseptics-and-disinfectants/,Use-Dilution Test,False,Use-Dilution Test,,,,
9cb8a1e5-ce8a-4ba1-a9b0-889abd8ebab8,https://open.oregonstate.education/microbiology/,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/microbiology/chapter/13-2testing-the-effectiveness-of-antiseptics-and-disinfectants/,"Other methods are also used for measuring the effectiveness of a chemical agent in clinical settings. The use-dilution test is commonly used to determine a chemical’s disinfection effectiveness on an inanimate surface. For this test, a cylinder of stainless steel is dipped in a culture of the targeted microorganism and then dried. The cylinder is then dipped in solutions of disinfectant at various concentrations for a specified amount of time. Finally, the cylinder is transferred to a new test tube containing fresh sterile medium that does not contain disinfectant, and this test tube is incubated. Bacterial survival is demonstrated by the presence of turbidity in the medium, whereas killing of the target organism on the cylinder by the disinfectant will produce no turbidity.",True,Use-Dilution Test,,,,
3ccf44c7-d2e0-41be-990e-33642cf670b1,https://open.oregonstate.education/microbiology/,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/microbiology/chapter/13-2testing-the-effectiveness-of-antiseptics-and-disinfectants/,"The Association of Official Agricultural Chemists International (AOAC), a nonprofit group that establishes many protocol standards, has determined that a minimum of 59 of 60 replicates must show no growth in such a test to achieve a passing result, and the results must be repeatable from different batches of disinfectant and when performed on different days. Disinfectant manufacturers perform use-dilution tests to validate the efficacy claims for their products, as designated by the EPA.",True,Use-Dilution Test,,,,
b63098c5-3e4c-4c4b-bbbf-1fe17db9fdd5,https://open.oregonstate.education/microbiology/,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/microbiology/chapter/13-2testing-the-effectiveness-of-antiseptics-and-disinfectants/,In-Use Test,False,In-Use Test,,,,
8ef97b08-e89d-4b02-9e1a-3b78f524c4c6,https://open.oregonstate.education/microbiology/,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/microbiology/chapter/13-2testing-the-effectiveness-of-antiseptics-and-disinfectants/,"An in-use test can determine whether an actively used solution of disinfectant in a clinical setting is microbially contaminated (Figure 9.7). A 1-mL sample of the used disinfectant is diluted into 9 mL of sterile broth medium that also contains a compound to inactivate the disinfectant. Ten drops, totaling approximately 0.2 mL of this mixture, are then inoculated onto each of two agar plates. One plate is incubated at 37 °C for 3 days and the other is incubated at room temperature for 7 days. The plates are monitored for growth of microbial colonies. Growth of five or more colonies on either plate suggests that viable microbial cells existed in the disinfectant solution and that it is contaminated. Such in-use tests monitor the effectiveness of disinfectants in the clinical setting.",True,In-Use Test,Figure 9.7,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-13.32.png,Figure 9.7 Used disinfectant solutions in a clinical setting can be checked with the in-use test for contamination with microbes.
14a87714-5f7d-4282-95ef-40a80aba7225,https://open.oregonstate.education/microbiology/,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/microbiology/chapter/13-2testing-the-effectiveness-of-antiseptics-and-disinfectants/,Use-Dilution Test,False,Use-Dilution Test,,,,
01e77c51-95ad-456d-ace8-81242a4c911d,https://open.oregonstate.education/microbiology/,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/microbiology/chapter/13-2testing-the-effectiveness-of-antiseptics-and-disinfectants/,"Other methods are also used for measuring the effectiveness of a chemical agent in clinical settings. The use-dilution test is commonly used to determine a chemical’s disinfection effectiveness on an inanimate surface. For this test, a cylinder of stainless steel is dipped in a culture of the targeted microorganism and then dried. The cylinder is then dipped in solutions of disinfectant at various concentrations for a specified amount of time. Finally, the cylinder is transferred to a new test tube containing fresh sterile medium that does not contain disinfectant, and this test tube is incubated. Bacterial survival is demonstrated by the presence of turbidity in the medium, whereas killing of the target organism on the cylinder by the disinfectant will produce no turbidity.",True,Use-Dilution Test,,,,
8c888c5d-5553-418b-adf8-e621127faf44,https://open.oregonstate.education/microbiology/,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/microbiology/chapter/13-2testing-the-effectiveness-of-antiseptics-and-disinfectants/,"The Association of Official Agricultural Chemists International (AOAC), a nonprofit group that establishes many protocol standards, has determined that a minimum of 59 of 60 replicates must show no growth in such a test to achieve a passing result, and the results must be repeatable from different batches of disinfectant and when performed on different days. Disinfectant manufacturers perform use-dilution tests to validate the efficacy claims for their products, as designated by the EPA.",True,Use-Dilution Test,,,,
6e786a92-2254-4354-b38f-6225d951e1f4,https://open.oregonstate.education/microbiology/,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/microbiology/chapter/13-2testing-the-effectiveness-of-antiseptics-and-disinfectants/,In-Use Test,False,In-Use Test,,,,
c9df2e73-c13d-4ef4-803f-45338bd78734,https://open.oregonstate.education/microbiology/,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/microbiology/chapter/13-2testing-the-effectiveness-of-antiseptics-and-disinfectants/,"An in-use test can determine whether an actively used solution of disinfectant in a clinical setting is microbially contaminated (Figure 9.7). A 1-mL sample of the used disinfectant is diluted into 9 mL of sterile broth medium that also contains a compound to inactivate the disinfectant. Ten drops, totaling approximately 0.2 mL of this mixture, are then inoculated onto each of two agar plates. One plate is incubated at 37 °C for 3 days and the other is incubated at room temperature for 7 days. The plates are monitored for growth of microbial colonies. Growth of five or more colonies on either plate suggests that viable microbial cells existed in the disinfectant solution and that it is contaminated. Such in-use tests monitor the effectiveness of disinfectants in the clinical setting.",True,In-Use Test,Figure 9.7,9.2 Testing the Effectiveness of Antiseptics and Disinfectants,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-13.32.png,Figure 9.7 Used disinfectant solutions in a clinical setting can be checked with the in-use test for contamination with microbes.
0cbc37f8-0484-41ca-b9b9-3690079d3c2c,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,Laboratory Biological Safety Levels,False,Laboratory Biological Safety Levels,,,,
9fce0428-59ec-4f71-a317-c1829babfb4c,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"For researchers or laboratory personnel working with pathogens, the risks associated with specific pathogens determine the levels of cleanliness and control required. The Centers for Disease Control and Prevention (CDC) and the National Institutes of Health (NIH) have established four classification levels, called “biological safety levels” (BSLs). Various organizations around the world, including the World Health Organization (WHO) and the European Union (EU), use a similar classification scheme. According to the CDC, the BSL is determined by the agent’s infectivity, ease of transmission, and potential disease severity, as well as the type of work being done with the agent.[1]",True,Laboratory Biological Safety Levels,,,,
65d5cd65-c44f-4715-be14-2aff42a0267a,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"Each BSL requires a different level of biocontainment to prevent contamination and spread of infectious agents to laboratory personnel and, ultimately, the community. For example, the lowest BSL, BSL-1, requires the fewest precautions because it applies to situations with the lowest risk for microbial infection.",True,Laboratory Biological Safety Levels,,,,
1a22006a-1ac5-43c2-8740-0c30a2257a36,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"BSL-1 agents are those that generally do not cause infection in healthy human adults. These include noninfectious bacteria, such as nonpathogenic strains of Escherichia coli and Bacillus subtilis, and viruses known to infect animals other than humans, such as baculoviruses (insect viruses). Because working with BSL-1 agents poses very little risk, few precautions are necessary. Laboratory workers use standard aseptic technique and may work with these agents at an open laboratory bench or table, wearing personal protective equipment (PPE) such as a laboratory coat, goggles, and gloves, as needed. Other than a sink for handwashing and doors to separate the laboratory from the rest of the building, no additional modifications are needed.",True,Laboratory Biological Safety Levels,,,,
dd4a35fe-f389-4499-833e-1062204506da,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"Agents classified as BSL-2 include those that pose moderate risk to laboratory workers and the community, and are typically “indigenous,” meaning that they are commonly found in that geographical area. These include bacteria such as Staphylococcus aureus and Salmonella spp., and viruses like hepatitis, mumps, and measles viruses. BSL-2 laboratories require additional precautions beyond those of BSL-1, including restricted access; required PPE, including a face shield in some circumstances; and the use of biological safety cabinets for procedures that may disperse agents through the air (called “aerosolization”). BSL-2 laboratories are equipped with self-closing doors, an eyewash station, and an autoclave, which is a specialized device for sterilizing materials with pressurized steam before use or disposal. BSL-1 laboratories may also have an autoclave.",True,Laboratory Biological Safety Levels,,,,
5d3cdaaf-4b8d-4ce6-94d1-89058ac0b516,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"BSL-4 agents are the most dangerous and often fatal. These microbes are typically exotic, are easily transmitted by inhalation, and cause infections for which there are no treatments or vaccinations. Examples include Ebola virus and Marburg virus, both of which cause hemorrhagic fevers, and smallpox virus. There are only a small number of laboratories in the United States and around the world appropriately equipped to work with these agents. In addition to BSL-3 precautions, laboratory workers in BSL-4 facilities must also change their clothing on entering the laboratory, shower on exiting, and decontaminate all material on exiting. While working in the laboratory, they must either wear a full-body protective suit with a designated air supply or conduct all work within a biological safety cabinet with a high-efficiency particulate air (HEPA)-filtered air supply and a doubly HEPA-filtered exhaust. If wearing a suit, the air pressure within the suit must be higher than that outside the suit, so that if a leak in the suit occurs, laboratory air that may be contaminated cannot be drawn into the suit (Figure 9.2). The laboratory itself must be located either in a separate building or in an isolated portion of a building and have its own air supply and exhaust system, as well as its own decontamination system. The BSLs are summarized in Figure 9.3.",True,Laboratory Biological Safety Levels,Figure 9.2,9.1 Controlling Microbial Growth,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-13.2.png,"Figure 9.2 A protective suit like this one is an additional precaution for those who work in BSL-4 laboratories. This suit has its own air supply and maintains a positive pressure relative to the outside, so that if a leak occurs, air will flow out of the suit, not into it from the laboratory. (credit: modification of work by Centers for Disease Control and Prevention)"
14ce8c82-0d27-49b1-beb1-f38d21bd64e2,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,Sterilization,False,Sterilization,,,,
cab746b3-75b3-4217-97b4-c45e0934938f,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"The most extreme protocols for microbial control aim to achieve sterilization: the complete removal or killing of all vegetative cells, endospores, and viruses from the targeted item or environment. Sterilization protocols are generally reserved for laboratory, medical, manufacturing, and food industry settings, where it may be imperative for certain items to be completely free of potentially infectious agents. Sterilization can be accomplished through either physical means, such as exposure to high heat, pressure, or filtration through an appropriate filter, or by chemical means. Chemicals that can be used to achieve sterilization are called sterilants. Sterilants effectively kill all microbes and viruses, and, with appropriate exposure time, can also kill endospores.",True,Sterilization,,,,
5b6342db-42fa-4591-8252-c690d4214dbe,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"For many clinical purposes, aseptic technique is necessary to prevent contamination of sterile surfaces. Aseptic technique involves a combination of protocols that collectively maintain sterility, or asepsis, thus preventing contamination of the patient with microbes and infectious agents. Failure to practice aseptic technique during many types of clinical procedures may introduce microbes to the patient’s body and put the patient at risk for sepsis, a systemic inflammatory response to an infection that results in high fever, increased heart and respiratory rates, shock, and, possibly, death. Medical procedures that carry risk of contamination must be performed in a sterile field, a designated area that is kept free of all vegetative microbes, endospores, and viruses. Sterile fields are created according to protocols requiring the use of sterilized materials, such as packaging and drapings, and strict procedures for washing and application of sterilants. Other protocols are followed to maintain the sterile field while the medical procedure is being performed.",True,Sterilization,,,,
d38c3425-28fd-4e5e-8f1d-ad4ce47e18b5,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"One food sterilization protocol, commercial sterilization, uses heat at a temperature low enough to preserve food quality but high enough to destroy common pathogens responsible for food poisoning, such as C. botulinum. Because botulinum and its endospores are commonly found in soil, they may easily contaminate crops during harvesting, and these endospores can later germinate within the anaerobic environment once foods are canned. Metal cans of food contaminated with C. botulinum will bulge due to the microbe’s production of gases; contaminated jars of food typically bulge at the metal lid. To eliminate the risk for C. botulinum contamination, commercial food-canning protocols are designed with a large margin of error. They assume an impossibly large population of endospores (1012 per can) and aim to reduce this population to 1 endospore per can to ensure the safety of canned foods. For example, low- and medium-acid foods are heated to 121 °C for a minimum of 2.52 minutes, which is the time it would take to reduce a population of 1012 endospores per can down to 1 endospore at this temperature. Even so, commercial sterilization does not eliminate the presence of all microbes; rather, it targets those pathogens that cause spoilage and foodborne diseases, while allowing many nonpathogenic organisms to survive. Therefore, “sterilization” is somewhat of a misnomer in this context, and commercial sterilization may be more accurately described as “quasi-sterilization.”",True,Sterilization,,,,
4554b99f-180c-481b-85f4-57eb612758f7,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,Other Methods of Control,False,Other Methods of Control,,,,
b96ff486-7b20-4746-9d89-ee028cdca797,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"The process of disinfection inactivates most microbes on the surface of a fomite by using antimicrobial chemicals or heat. Because some microbes remain, the disinfected item is not considered sterile. Ideally, disinfectants should be fast acting, stable, easy to prepare, inexpensive, and easy to use. An example of a natural disinfectant is vinegar; its acidity kills most microbes. Chemical disinfectants, such as chlorine bleach or products containing chlorine, are used to clean nonliving surfaces such as laboratory benches, clinical surfaces, and bathroom sinks. Typical disinfection does not lead to sterilization because endospores tend to survive even when all vegetative cells have been killed.",True,Other Methods of Control,,,,
bb0ed6e6-1dd0-415f-9754-93d390a070ff,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"Unlike disinfectants, antiseptics are antimicrobial chemicals safe for use on living skin or tissues. Examples of antiseptics include hydrogen peroxide and isopropyl alcohol. The process of applying an antiseptic is called antisepsis. In addition to the characteristics of a good disinfectant, antiseptics must also be selectively effective against microorganisms and able to penetrate tissue deeply without causing tissue damage.",True,Other Methods of Control,,,,
898288b2-ef7d-45ba-ab39-37d11f49f9ef,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"The type of protocol required to achieve the desired level of cleanliness depends on the particular item to be cleaned. For example, those used clinically are categorized as critical, semicritical, and noncritical. Critical items must be sterile because they will be used inside the body, often penetrating sterile tissues or the bloodstream; examples of critical items include surgical instruments, catheters, and intravenous fluids. Gastrointestinal endoscopes and various types of equipment for respiratory therapies are examples of semicritical items; they may contact mucous membranes or nonintact skin but do not penetrate tissues. Semicritical items do not typically need to be sterilized but do require a high level of disinfection. Items that may contact but not penetrate intact skin are noncritical items; examples are bed linens, furniture, crutches, stethoscopes, and blood pressure cuffs. These articles need to be clean but not highly disinfected.",True,Other Methods of Control,,,,
1cdeceec-51cc-4be5-8f9c-321e953af0be,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"The act of handwashing is an example of degerming, in which microbial numbers are significantly reduced by gently scrubbing living tissue, most commonly skin, with a mild chemical (e.g., soap) to avoid the transmission of pathogenic microbes. Wiping the skin with an alcohol swab at an injection site is another example of degerming. These degerming methods remove most (but not all) microbes from the skin’s surface.",True,Other Methods of Control,,,,
504971a6-ac71-4bc8-83c6-a07fb89291eb,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"The term sanitization refers to the cleansing of fomites to remove enough microbes to achieve levels deemed safe for public health. For example, commercial dishwashers used in the food service industry typically use very hot water and air for washing and drying; the high temperatures kill most microbes, sanitizing the dishes. Surfaces in hospital rooms are commonly sanitized using a chemical disinfectant to prevent disease transmission between patients. Figure 9.4 summarizes common protocols, definitions, applications, and agents used to control microbial growth.",True,Other Methods of Control,Figure 9.4,9.1 Controlling Microbial Growth,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-13.4.png,Figure 9.4 Details associated with the different protocols used for control of microbial growth.
aab835f3-b53d-4028-b921-9d240909302d,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,Measuring Microbial Control,False,Measuring Microbial Control,,,,
4f0c911e-032b-4c59-8aa3-d70550b3168a,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"Physical and chemical methods of microbial control that kill the targeted microorganism are identified by the suffix -cide (or -cidal). The prefix indicates the type of microbe or infectious agent killed by the treatment method: bactericides kill bacteria, while viricides kill or inactivate viruses. Other methods do not kill organisms but, instead, stop their growth, making their population static; such methods are identified by the suffix-stat (or -static). For example, bacteriostatic treatments inhibit the growth of bacteria. Factors that determine whether a particular treatment is -cidal or -static include the types of microorganisms targeted, the concentration of the chemical used, and the nature of the treatment applied.",True,Measuring Microbial Control,,,,
81646e98-5ee2-4d7b-b961-86e366515af6,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"Although -static treatments do not actually kill infectious agents, they are often less toxic to humans and other animals, and may also better preserve the integrity of the item treated. Such treatments are typically sufficient to keep the microbial population of an item in check. The reduced toxicity of some of these -static chemicals also allows them to be impregnated safely into plastics to prevent the growth of microbes on these surfaces. Such plastics are used in products such as toys for children and cutting boards for food preparation. When used to treat an infection, -static treatments are typically sufficient in an otherwise healthy individual, preventing the pathogen from multiplying, thus allowing the individual’s immune system to clear the infection.",True,Measuring Microbial Control,,,,
accfaf8f-5f07-4d6a-b401-81314c85755e,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"The degree of microbial control can be evaluated using a microbial death curve to describe the progress and effectiveness of a particular protocol. When exposed to a particular microbial control protocol, a fixed percentage of the microbes within the population will die. Because the rate of killing remains constant even when the population size varies, the percentage killed is more useful information than the absolute number of microbes killed. Death curves are often plotted as semilog plots just like microbial growth curves because the reduction in microorganisms is typically logarithmic (Figure 9.5). The amount of time it takes for a specific protocol to produce a one order- of-magnitude decrease in the number of organisms, or the death of 90% of the population, is called the decimal reduction time (DRT) or D-value.",True,Measuring Microbial Control,Figure 9.5,9.1 Controlling Microbial Growth,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-13.5.png,"Figure 9.5 Microbial death is logarithmic and easily observed using a semilog plot instead of an arithmetic one. The decimal reduction time (D-value) is the time it takes to kill 90% of the population (a 1-log decrease in the total population) when exposed to a specific microbial control protocol, as indicated by the purple bracket."
2d29b6a4-47fd-4180-82bf-a5bc6c1f1b74,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"Several factors contribute to the effectiveness of a disinfecting agent or microbial control protocol. First, as demonstrated in Figure 9.5, the length of time of exposure is important. Longer exposure times kill more microbes. Because microbial death of a population exposed to a specific protocol is logarithmic, it takes longer to kill a high-population load than a low-population load exposed to the same protocol. A shorter treatment time (measured in multiples of the D-value) is needed when starting with a smaller number of organisms. Effectiveness also depends on the susceptibility of the agent to that disinfecting agent or protocol. The concentration of disinfecting agent or intensity of exposure is also important. For example, higher temperatures and higher concentrations of disinfectants kill microbes more quickly and effectively. Conditions that limit contact between the agent and the targeted cells cells—for example, the presence of bodily fluids, tissue, organic debris (e.g., mud or feces), or biofilms on surfaces—increase the cleaning time or intensity of the microbial control protocol required to reach the desired level of cleanliness. All these factors must be considered when choosing the appropriate protocol to control microbial growth in a given situation.",True,Measuring Microbial Control,Figure 9.5,9.1 Controlling Microbial Growth,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-13.5.png,"Figure 9.5 Microbial death is logarithmic and easily observed using a semilog plot instead of an arithmetic one. The decimal reduction time (D-value) is the time it takes to kill 90% of the population (a 1-log decrease in the total population) when exposed to a specific microbial control protocol, as indicated by the purple bracket."
053eb919-c5c3-4664-a3b7-a1bf901db05f,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"BSL-4 agents are the most dangerous and often fatal. These microbes are typically exotic, are easily transmitted by inhalation, and cause infections for which there are no treatments or vaccinations. Examples include Ebola virus and Marburg virus, both of which cause hemorrhagic fevers, and smallpox virus. There are only a small number of laboratories in the United States and around the world appropriately equipped to work with these agents. In addition to BSL-3 precautions, laboratory workers in BSL-4 facilities must also change their clothing on entering the laboratory, shower on exiting, and decontaminate all material on exiting. While working in the laboratory, they must either wear a full-body protective suit with a designated air supply or conduct all work within a biological safety cabinet with a high-efficiency particulate air (HEPA)-filtered air supply and a doubly HEPA-filtered exhaust. If wearing a suit, the air pressure within the suit must be higher than that outside the suit, so that if a leak in the suit occurs, laboratory air that may be contaminated cannot be drawn into the suit (Figure 9.2). The laboratory itself must be located either in a separate building or in an isolated portion of a building and have its own air supply and exhaust system, as well as its own decontamination system. The BSLs are summarized in Figure 9.3.",True,Measuring Microbial Control,Figure 9.2,9.1 Controlling Microbial Growth,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-13.2.png,"Figure 9.2 A protective suit like this one is an additional precaution for those who work in BSL-4 laboratories. This suit has its own air supply and maintains a positive pressure relative to the outside, so that if a leak occurs, air will flow out of the suit, not into it from the laboratory. (credit: modification of work by Centers for Disease Control and Prevention)"
243a9a76-ce8a-4151-925c-701119ba50c0,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,Sterilization,False,Sterilization,,,,
0025869a-99b0-47ef-ae33-f178546ad09f,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"The most extreme protocols for microbial control aim to achieve sterilization: the complete removal or killing of all vegetative cells, endospores, and viruses from the targeted item or environment. Sterilization protocols are generally reserved for laboratory, medical, manufacturing, and food industry settings, where it may be imperative for certain items to be completely free of potentially infectious agents. Sterilization can be accomplished through either physical means, such as exposure to high heat, pressure, or filtration through an appropriate filter, or by chemical means. Chemicals that can be used to achieve sterilization are called sterilants. Sterilants effectively kill all microbes and viruses, and, with appropriate exposure time, can also kill endospores.",True,Sterilization,,,,
fa5a926e-330f-451a-a7a7-295c2e79f5ae,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"For many clinical purposes, aseptic technique is necessary to prevent contamination of sterile surfaces. Aseptic technique involves a combination of protocols that collectively maintain sterility, or asepsis, thus preventing contamination of the patient with microbes and infectious agents. Failure to practice aseptic technique during many types of clinical procedures may introduce microbes to the patient’s body and put the patient at risk for sepsis, a systemic inflammatory response to an infection that results in high fever, increased heart and respiratory rates, shock, and, possibly, death. Medical procedures that carry risk of contamination must be performed in a sterile field, a designated area that is kept free of all vegetative microbes, endospores, and viruses. Sterile fields are created according to protocols requiring the use of sterilized materials, such as packaging and drapings, and strict procedures for washing and application of sterilants. Other protocols are followed to maintain the sterile field while the medical procedure is being performed.",True,Sterilization,,,,
1d66008c-944b-4483-a616-978d64eb2bb6,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"One food sterilization protocol, commercial sterilization, uses heat at a temperature low enough to preserve food quality but high enough to destroy common pathogens responsible for food poisoning, such as C. botulinum. Because botulinum and its endospores are commonly found in soil, they may easily contaminate crops during harvesting, and these endospores can later germinate within the anaerobic environment once foods are canned. Metal cans of food contaminated with C. botulinum will bulge due to the microbe’s production of gases; contaminated jars of food typically bulge at the metal lid. To eliminate the risk for C. botulinum contamination, commercial food-canning protocols are designed with a large margin of error. They assume an impossibly large population of endospores (1012 per can) and aim to reduce this population to 1 endospore per can to ensure the safety of canned foods. For example, low- and medium-acid foods are heated to 121 °C for a minimum of 2.52 minutes, which is the time it would take to reduce a population of 1012 endospores per can down to 1 endospore at this temperature. Even so, commercial sterilization does not eliminate the presence of all microbes; rather, it targets those pathogens that cause spoilage and foodborne diseases, while allowing many nonpathogenic organisms to survive. Therefore, “sterilization” is somewhat of a misnomer in this context, and commercial sterilization may be more accurately described as “quasi-sterilization.”",True,Sterilization,,,,
edd0f6d7-b18f-404c-9343-04601e9b0347,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,Other Methods of Control,False,Other Methods of Control,,,,
aaa70f8d-fc0e-41c5-9e7a-a7bd8b286672,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"The process of disinfection inactivates most microbes on the surface of a fomite by using antimicrobial chemicals or heat. Because some microbes remain, the disinfected item is not considered sterile. Ideally, disinfectants should be fast acting, stable, easy to prepare, inexpensive, and easy to use. An example of a natural disinfectant is vinegar; its acidity kills most microbes. Chemical disinfectants, such as chlorine bleach or products containing chlorine, are used to clean nonliving surfaces such as laboratory benches, clinical surfaces, and bathroom sinks. Typical disinfection does not lead to sterilization because endospores tend to survive even when all vegetative cells have been killed.",True,Other Methods of Control,,,,
29a544f5-a93c-4f0a-9061-f5d5cf192149,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"Unlike disinfectants, antiseptics are antimicrobial chemicals safe for use on living skin or tissues. Examples of antiseptics include hydrogen peroxide and isopropyl alcohol. The process of applying an antiseptic is called antisepsis. In addition to the characteristics of a good disinfectant, antiseptics must also be selectively effective against microorganisms and able to penetrate tissue deeply without causing tissue damage.",True,Other Methods of Control,,,,
c9a4780e-97a6-4240-85ed-a607c4df62b4,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"The type of protocol required to achieve the desired level of cleanliness depends on the particular item to be cleaned. For example, those used clinically are categorized as critical, semicritical, and noncritical. Critical items must be sterile because they will be used inside the body, often penetrating sterile tissues or the bloodstream; examples of critical items include surgical instruments, catheters, and intravenous fluids. Gastrointestinal endoscopes and various types of equipment for respiratory therapies are examples of semicritical items; they may contact mucous membranes or nonintact skin but do not penetrate tissues. Semicritical items do not typically need to be sterilized but do require a high level of disinfection. Items that may contact but not penetrate intact skin are noncritical items; examples are bed linens, furniture, crutches, stethoscopes, and blood pressure cuffs. These articles need to be clean but not highly disinfected.",True,Other Methods of Control,,,,
7d3070ff-f74b-4dfb-9b52-a330cfc41fc8,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"The act of handwashing is an example of degerming, in which microbial numbers are significantly reduced by gently scrubbing living tissue, most commonly skin, with a mild chemical (e.g., soap) to avoid the transmission of pathogenic microbes. Wiping the skin with an alcohol swab at an injection site is another example of degerming. These degerming methods remove most (but not all) microbes from the skin’s surface.",True,Other Methods of Control,,,,
afc60161-ef7d-447e-ae9f-f0122e335704,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"The term sanitization refers to the cleansing of fomites to remove enough microbes to achieve levels deemed safe for public health. For example, commercial dishwashers used in the food service industry typically use very hot water and air for washing and drying; the high temperatures kill most microbes, sanitizing the dishes. Surfaces in hospital rooms are commonly sanitized using a chemical disinfectant to prevent disease transmission between patients. Figure 9.4 summarizes common protocols, definitions, applications, and agents used to control microbial growth.",True,Other Methods of Control,Figure 9.4,9.1 Controlling Microbial Growth,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-13.4.png,Figure 9.4 Details associated with the different protocols used for control of microbial growth.
63f7eec2-e987-4d0c-b8d1-ae050ec9723d,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,Measuring Microbial Control,False,Measuring Microbial Control,,,,
0b3b4ea3-c548-46d3-acc8-8b63aab549ed,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"Physical and chemical methods of microbial control that kill the targeted microorganism are identified by the suffix -cide (or -cidal). The prefix indicates the type of microbe or infectious agent killed by the treatment method: bactericides kill bacteria, while viricides kill or inactivate viruses. Other methods do not kill organisms but, instead, stop their growth, making their population static; such methods are identified by the suffix-stat (or -static). For example, bacteriostatic treatments inhibit the growth of bacteria. Factors that determine whether a particular treatment is -cidal or -static include the types of microorganisms targeted, the concentration of the chemical used, and the nature of the treatment applied.",True,Measuring Microbial Control,,,,
9b0ae1e8-1ce9-43b8-a62e-a9bd2279f86d,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"Although -static treatments do not actually kill infectious agents, they are often less toxic to humans and other animals, and may also better preserve the integrity of the item treated. Such treatments are typically sufficient to keep the microbial population of an item in check. The reduced toxicity of some of these -static chemicals also allows them to be impregnated safely into plastics to prevent the growth of microbes on these surfaces. Such plastics are used in products such as toys for children and cutting boards for food preparation. When used to treat an infection, -static treatments are typically sufficient in an otherwise healthy individual, preventing the pathogen from multiplying, thus allowing the individual’s immune system to clear the infection.",True,Measuring Microbial Control,,,,
233f79d1-67ed-4736-b80f-81974d02c5c6,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"The degree of microbial control can be evaluated using a microbial death curve to describe the progress and effectiveness of a particular protocol. When exposed to a particular microbial control protocol, a fixed percentage of the microbes within the population will die. Because the rate of killing remains constant even when the population size varies, the percentage killed is more useful information than the absolute number of microbes killed. Death curves are often plotted as semilog plots just like microbial growth curves because the reduction in microorganisms is typically logarithmic (Figure 9.5). The amount of time it takes for a specific protocol to produce a one order- of-magnitude decrease in the number of organisms, or the death of 90% of the population, is called the decimal reduction time (DRT) or D-value.",True,Measuring Microbial Control,Figure 9.5,9.1 Controlling Microbial Growth,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-13.5.png,"Figure 9.5 Microbial death is logarithmic and easily observed using a semilog plot instead of an arithmetic one. The decimal reduction time (D-value) is the time it takes to kill 90% of the population (a 1-log decrease in the total population) when exposed to a specific microbial control protocol, as indicated by the purple bracket."
d0cc94db-193a-44bb-812f-6c490d050f29,https://open.oregonstate.education/microbiology/,9.1 Controlling Microbial Growth,https://open.oregonstate.education/microbiology/chapter/13-1controlling-microbial-growth/,"Several factors contribute to the effectiveness of a disinfecting agent or microbial control protocol. First, as demonstrated in Figure 9.5, the length of time of exposure is important. Longer exposure times kill more microbes. Because microbial death of a population exposed to a specific protocol is logarithmic, it takes longer to kill a high-population load than a low-population load exposed to the same protocol. A shorter treatment time (measured in multiples of the D-value) is needed when starting with a smaller number of organisms. Effectiveness also depends on the susceptibility of the agent to that disinfecting agent or protocol. The concentration of disinfecting agent or intensity of exposure is also important. For example, higher temperatures and higher concentrations of disinfectants kill microbes more quickly and effectively. Conditions that limit contact between the agent and the targeted cells cells—for example, the presence of bodily fluids, tissue, organic debris (e.g., mud or feces), or biofilms on surfaces—increase the cleaning time or intensity of the microbial control protocol required to reach the desired level of cleanliness. All these factors must be considered when choosing the appropriate protocol to control microbial growth in a given situation.",True,Measuring Microbial Control,Figure 9.5,9.1 Controlling Microbial Growth,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-13.5.png,"Figure 9.5 Microbial death is logarithmic and easily observed using a semilog plot instead of an arithmetic one. The decimal reduction time (D-value) is the time it takes to kill 90% of the population (a 1-log decrease in the total population) when exposed to a specific microbial control protocol, as indicated by the purple bracket."
72263286-7fd1-46b3-912f-324a17c74a02,https://open.oregonstate.education/microbiology/,8.2 Gene Therapy,https://open.oregonstate.education/microbiology/chapter/12-2gene-therapy/,Mechanisms and Risks of Gene Therapy,False,Mechanisms and Risks of Gene Therapy,,,,
190b319c-b656-422b-9920-de7be6b38c49,https://open.oregonstate.education/microbiology/,8.2 Gene Therapy,https://open.oregonstate.education/microbiology/chapter/12-2gene-therapy/,"Human diseases that result from genetic mutations are often difficult to treat with drugs or other traditional forms of therapy because the signs and symptoms of disease result from abnormalities in a patient’s genome. For example, a patient may have a genetic mutation that prevents the expression of a specific protein required for the normal function of a particular cell type. This is the case in patients with Severe Combined Immunodeficiency (SCID), a genetic disease that impairs the function of certain white blood cells essential to the immune system.",True,Mechanisms and Risks of Gene Therapy,,,,
5153ed73-1d01-4bf9-ba27-0a755f66b75f,https://open.oregonstate.education/microbiology/,8.2 Gene Therapy,https://open.oregonstate.education/microbiology/chapter/12-2gene-therapy/,"Gene therapy attempts to correct genetic abnormalities by introducing a nonmutated, functional gene into the patient’s genome. The nonmutated gene encodes a functional protein that the patient would otherwise be unable to produce. Viral vectors are sometimes used to introduce the functional gene; part of the viral genome is removed and replaced with the desired gene (Figure 8.5). More advanced forms of gene therapy attempt to correct the mutation at the original site in the genome, such as is the case with treatment of SCID.",True,Mechanisms and Risks of Gene Therapy,Figure 8.5,8.2 Gene Therapy,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-12.29.png,Figure 8.5 Gene therapy using an adenovirus vector can be used to treat or cure certain genetic diseases in which a patient has a defective gene. (credit: modification of work by National Institutes of Health)
59a5f023-77c7-4e14-80db-9500a5d44ff4,https://open.oregonstate.education/microbiology/,8.2 Gene Therapy,https://open.oregonstate.education/microbiology/chapter/12-2gene-therapy/,"So far, gene therapies have proven relatively ineffective, with the possible exceptions of treatments for cystic fibrosis and adenosine deaminase deficiency, a type of SCID. Other trials have shown the clear hazards of attempting genetic manipulation in complex multicellular organisms like humans. In some patients, the use of an adenovirus vector can trigger an unanticipated inflammatory response from the immune system, which may lead to organ failure. Moreover, because viruses can often target multiple cell types, the virus vector may infect cells not targeted for the therapy, damaging these other cells and possibly leading to illnesses such as cancer. Another potential risk is that the modified virus could revert to being infectious and cause disease in the patient. Lastly, there is a risk that the inserted gene could unintentionally inactivate another important gene in the patient’s genome, disrupting normal cell cycling and possibly leading to tumor formation and cancer. Because gene therapy involves so many risks, candidates for gene therapy need to be fully informed of these risks before providing informed consent to undergo the therapy.",True,Mechanisms and Risks of Gene Therapy,,,,
31d24734-8e40-4a13-9eaa-7352c59f781f,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,"Genomics, Transcriptomics, and Proteomics",False,"Genomics, Transcriptomics, and Proteomics",,,,
f4a2ee70-98d0-4d5b-9c03-9625baaab102,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,"The study and comparison of entire genomes, including the complete set of genes and their nucleotide sequence  and organization, is called genomics. This field has great potential for future medical advances through the study of the human genome as well as the genomes of infectious organisms. Analysis of microbial genomes has contributed to the development of new antibiotics, diagnostic tools, vaccines, medical treatments, and environmental cleanup techniques.",True,"Genomics, Transcriptomics, and Proteomics",,,,
91268e44-6f1d-4061-9162-5ecce1990b9e,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,"The field of transcriptomics is the science of the entire collection of mRNA molecules produced by cells. Scientists compare gene expression patterns between infected and uninfected host cells, gaining important information about the cellular responses to infectious disease. Additionally, transcriptomics can be used to monitor the gene expression of virulence factors in microorganisms, aiding scientists in better understanding pathogenic processes from this viewpoint.",True,"Genomics, Transcriptomics, and Proteomics",,,,
3738e15e-e8d5-4d65-b341-34e098fe6c61,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,"When genomics and transcriptomics are applied to entire microbial communities, we use the terms metagenomics and metatranscriptomics, respectively. Metagenomics and metatranscriptomics allow researchers to study genes and gene expression from a collection of multiple species, many of which may not be easily cultured or cultured at all in the laboratory.",True,"Genomics, Transcriptomics, and Proteomics",,,,
600786f4-e599-455c-a6a2-63629a28c4d9,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,"Another up-and-coming clinical application of genomics and transcriptomics is pharmacogenomics, also called toxicogenomics, which involves evaluating the effectiveness and safety of drugs on the basis of information from an individual’s genomic sequence. Genomic responses to drugs can be studied using experimental animals (such as laboratory rats or mice) or live cells in the laboratory before embarking on studies with humans. Changes in gene expression in the presence of a drug can sometimes be an early indicator of the potential for toxic effects. Personal genome sequence information may someday be used to prescribe medications that will be most effective and least toxic on the basis of the individual patient’s genotype.",True,"Genomics, Transcriptomics, and Proteomics",,,,
233ab559-9770-4819-9843-346823baa05c,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,"The study of proteomics is an extension of genomics that allows scientists to study the entire complement of proteins in an organism, called the proteome. Even though all cells of a multicellular organism have the same set of genes, cells in various tissues produce different sets of proteins. Thus, the genome is constant, but the proteome varies and is dynamic within an organism. Proteomics may be used to study which proteins are expressed under various conditions within a single cell type or to compare protein expression patterns between different organisms.",True,"Genomics, Transcriptomics, and Proteomics",,,,
7bc06bef-a4fe-4875-8b76-e18e50534426,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,"A recent and developing proteomic analysis relies on identifying proteins called biomarkers, whose expression is affected by the disease process. Biomarkers are currently being used to detect various forms of cancer as well as infections caused by pathogens such as Yersinia pestis and Vaccinia virus.[1]",True,"Genomics, Transcriptomics, and Proteomics",,,,
a0ccb088-cdb0-4f1f-9aea-cd367930f6b5,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,"Additionally, researchers can use reverse genetics, a technique related to classic mutational analysis, to determine the function of specific genes. Classic methods of studying gene function involved searching for the genes responsible for a given phenotype. Reverse genetics uses the opposite approach, starting with a specific DNA sequence and attempting to determine what phenotype it produces. Alternatively, scientists can attach known genes (called reporter genes) that encode easily observable characteristics to genes of interest, and the location of expression of such genes of interest can be easily monitored. This gives the researcher important information about what the gene product might be doing or where it is located in the organism. A common reporter genes includes the gene encoding the jellyfish protein green fluorescent protein (GFP) whose activity can be visualized in colonies under ultraviolet light exposure (Figure 8.2).",True,"Genomics, Transcriptomics, and Proteomics",Figure 8.2,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-12.26.png,"Figure 8.2 (a) The gene encoding green fluorescence protein is a commonly used reporter gene for monitoring gene expression patterns in organisms. Under ultraviolet light, GFP fluoresces. Here, two mice are expressing GFP, while the middle mouse is not. (b) GFP can be used as a reporter gene in bacteria as well. Here, a plate containing bacterial colonies expressing GFP is shown. (c) Blue-white screening in bacteria is accomplished through the use of the lacZ reporter gene, followed by plating of bacteria onto medium containing X-gal. Cleavage of X-gal by the LacZ enzyme results in the formation of blue colonies. (credit a: modification of work by Ingrid Moen, Charlotte Jevne, Jian Wang, Karl-Henning Kalland, Martha Chekenya, Lars A Akslen, Linda Sleire, Per Ø Enger, Rolf K Reed, Anne M Øyan, Linda EB Stuhr; credit b: modification of work by “2.5JIGEN.com”/Flickr; credit c: modification of work by American Society for Microbiology)"
a3a461d5-9836-4e65-a61f-9cfa7a80859f,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,Recombinant DNA Technology and Pharmaceutical Production,False,Recombinant DNA Technology and Pharmaceutical Production,,,,
8ba4bb4c-27aa-49af-97ba-c410dc38247a,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,"Genetic engineering has provided a way to create new pharmaceutical products called recombinant DNA pharmaceuticals. Such products include antibiotic drugs, vaccines, and hormones used to treat various diseases. Table 8.1 lists examples of recombinant DNA products and their uses.",True,Recombinant DNA Technology and Pharmaceutical Production,,,,
639c8a17-7d4f-498f-86ff-02fbb027be0c,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,"For example, the naturally occurring antibiotic synthesis pathways of various Streptomyces spp., long known for their antibiotic production capabilities, can be modified to improve yields or to create new antibiotics through the introduction of genes encoding additional enzymes. More than 200 new antibiotics have been generated through the targeted inactivation of genes and the novel combination of antibiotic synthesis genes in antibiotic-producing Streptomyces hosts.[2]",True,Recombinant DNA Technology and Pharmaceutical Production,,,,
0a094b93-87e6-4e3f-8891-aae110f17118,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,"Genetic engineering is also used to manufacture subunit vaccines, which are safer than other vaccines because they contain only a single antigenic molecule and lack any part of the genome of the pathogen (see Vaccines). For example, a vaccine for hepatitis B is created by inserting a gene encoding a hepatitis B surface protein into a yeast; the yeast then produces this protein, which the human immune system recognizes as an antigen. The hepatitis B antigen is purified from yeast cultures and administered to patients as a vaccine. Even though the vaccine does not contain the hepatitis B virus, the presence of the antigenic protein stimulates the immune system to produce antibodies that will protect the patient against the virus in the event of exposure.[3][4]",True,Recombinant DNA Technology and Pharmaceutical Production,,,,
9abe4a90-ce13-476c-81fc-27b84bedc35c,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,"Genetic engineering has also been important in the production of other therapeutic proteins, such as insulin, interferons, and human growth hormone, to treat a variety of human medical conditions. For example, at one time, it was possible to treat diabetes only by giving patients pig insulin, which caused allergic reactions due to small differences between the proteins expressed in human and pig insulin. However, since 1978, recombinant DNA technology has been used to produce large-scale quantities of human insulin using E. coli in a relatively inexpensive process that yields a more consistently effective pharmaceutical product. Scientists have also genetically engineered coli capable of producing human growth hormone (HGH), which is used to treat growth disorders in children and certain other disorders in adults. The HGH gene was cloned from a cDNA library and inserted into E. coli cells by cloning it into a bacterial vector. Eventually, genetic engineering will be used to produce DNA vaccines and various gene therapies, as well as customized medicines for fighting cancer and other diseases.",True,Recombinant DNA Technology and Pharmaceutical Production,,,,
bdab1fef-752c-4a34-a401-c935122f2906,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,RNA Interference Technology,False,RNA Interference Technology,,,,
508aeac5-383c-4740-8c62-b0d24dcef68c,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,"Researchers are currently developing techniques to mimic the natural process of RNA interference as a way to treat viral infections in eukaryotic cells. RNA interference technology involves using small interfering RNAs (siRNAs) or microRNAs (miRNAs) (Figure 8.4). siRNAs are completely complementary to the mRNA transcript of a specific gene of interest while miRNAs are mostly complementary. These double-stranded RNAs are bound to DICER, an endonuclease that cleaves the RNA into short molecules (approximately 20 nucleotides long). The RNAs are then bound to RNA-induced silencing complex (RISC), a ribonucleoprotein. The siRNA-RISC complex binds to mRNA and cleaves it. For miRNA, only one of the two strands binds to RISC. The miRNA-RISC complex then binds to mRNA, inhibiting translation. If the miRNA is completely complementary to the target gene, then the mRNA can be cleaved. Taken together, these mechanisms are known as gene silencing.",True,RNA Interference Technology,Figure 8.4,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-12.28.png,Figure 8.4 This diagram illustrates the process of using siRNA or miRNA in a eukaryotic cell to silence genes involved in the pathogenesis of various diseases. (credit: modification of work by National Center for Biotechnology Information)
09b7003c-67d2-4459-807d-e22060e5b4e2,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,Recombinant DNA Technology and Pharmaceutical Production,False,Recombinant DNA Technology and Pharmaceutical Production,,,,
0f6b958e-74a9-4d11-95ee-04588767f662,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,"For example, the naturally occurring antibiotic synthesis pathways of various Streptomyces spp., long known for their antibiotic production capabilities, can be modified to improve yields or to create new antibiotics through the introduction of genes encoding additional enzymes. More than 200 new antibiotics have been generated through the targeted inactivation of genes and the novel combination of antibiotic synthesis genes in antibiotic-producing Streptomyces hosts.[2]",True,Recombinant DNA Technology and Pharmaceutical Production,,,,
31daf1d9-fef7-444c-bd4b-69ecd0a04f86,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,"Genetic engineering is also used to manufacture subunit vaccines, which are safer than other vaccines because they contain only a single antigenic molecule and lack any part of the genome of the pathogen (see Vaccines). For example, a vaccine for hepatitis B is created by inserting a gene encoding a hepatitis B surface protein into a yeast; the yeast then produces this protein, which the human immune system recognizes as an antigen. The hepatitis B antigen is purified from yeast cultures and administered to patients as a vaccine. Even though the vaccine does not contain the hepatitis B virus, the presence of the antigenic protein stimulates the immune system to produce antibodies that will protect the patient against the virus in the event of exposure.[3][4]",True,Recombinant DNA Technology and Pharmaceutical Production,,,,
93cf1fa1-2f50-4120-b1ed-13ce041a9c68,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,"Genetic engineering has also been important in the production of other therapeutic proteins, such as insulin, interferons, and human growth hormone, to treat a variety of human medical conditions. For example, at one time, it was possible to treat diabetes only by giving patients pig insulin, which caused allergic reactions due to small differences between the proteins expressed in human and pig insulin. However, since 1978, recombinant DNA technology has been used to produce large-scale quantities of human insulin using E. coli in a relatively inexpensive process that yields a more consistently effective pharmaceutical product. Scientists have also genetically engineered coli capable of producing human growth hormone (HGH), which is used to treat growth disorders in children and certain other disorders in adults. The HGH gene was cloned from a cDNA library and inserted into E. coli cells by cloning it into a bacterial vector. Eventually, genetic engineering will be used to produce DNA vaccines and various gene therapies, as well as customized medicines for fighting cancer and other diseases.",True,Recombinant DNA Technology and Pharmaceutical Production,,,,
6fd69821-11b9-4652-bb9f-53a8e4a1dfdd,https://open.oregonstate.education/microbiology/,8.1 Whole Genome Methods and Pharmaceutical Applications of Genetic Engineering,https://open.oregonstate.education/microbiology/chapter/12-1whole-genome-methods-and-pharmaceutical-applications-of-genetic-engineering/,RNA Interference Technology,False,RNA Interference Technology,,,,
4606fce3-6a2b-42c3-afdc-0657651774d9,https://open.oregonstate.education/microbiology/,7.4 Temperature and Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-4temperature-and-microbial-growth/,Temperature and Growth,False,Temperature and Growth,,,,
8e1c70b5-2edd-46af-bbe2-69b0fd863bb5,https://open.oregonstate.education/microbiology/,7.4 Temperature and Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-4temperature-and-microbial-growth/,Microbes can be roughly classified according to the range of temperature at which they can grow. The growth rates are the highest at the optimum growth temperature for the organism. The lowest temperature at which the organism can survive and replicate is its minimum growth temperature. The highest temperature at which growth can occur is its maximum growth temperature. The following ranges of permissive growth temperatures are approximate only and can vary according to other environmental factors.,True,Temperature and Growth,,,,
7b8f6899-5450-49bc-a4c6-80e9964f1a2f,https://open.oregonstate.education/microbiology/,7.4 Temperature and Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-4temperature-and-microbial-growth/,"Organisms categorized as mesophiles (“middle loving”) are adapted to moderate temperatures, with optimal growth temperatures ranging from room temperature (about 20 °C) to about 45 °C. As would be expected from the core temperature of the human body, 37 °C (98.6 °F), normal human microbiota and pathogens (e.g., E. coli and Lactobacillus spp.) are mesophiles.",True,Temperature and Growth,,,,
89842016-782d-4e6c-b72e-4390ec7f2424,https://open.oregonstate.education/microbiology/,7.4 Temperature and Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-4temperature-and-microbial-growth/,"Organisms called psychrotrophs, also known as psychrotolerant, prefer cooler environments, from a high temperature of 25 °C to refrigeration temperature about 4 °C. They are found in many natural environments in temperate climates. They are also responsible for the spoilage of refrigerated food.",True,Temperature and Growth,,,,
abd66a6e-6b69-41b0-b518-d6c3f2495a74,https://open.oregonstate.education/microbiology/,7.4 Temperature and Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-4temperature-and-microbial-growth/,"The organisms retrieved from arctic lakes such as Lake Whillans are considered extreme psychrophiles (cold loving). Psychrophiles are microorganisms that can grow at 0 °C and below, have an optimum growth temperature close to 15 °C, and usually do not survive at temperatures above 20 °C. They are found in permanently cold environments such as the deep waters of the oceans. Because they are active at low temperature, psychrophiles and psychrotrophs are important decomposers in cold climates.",True,Temperature and Growth,,,,
dd72a6c1-1be4-4cfa-a955-03b24a47ca68,https://open.oregonstate.education/microbiology/,7.4 Temperature and Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-4temperature-and-microbial-growth/,"Organisms that grow at optimum temperatures of 50 °C to a maximum of 80 °C are called thermophiles (“heat loving”). They do not multiply at room temperature. Thermophiles are widely distributed in hot springs, geothermal soils, and manmade environments such as garden compost piles where the microbes break down kitchen scraps and vegetal material. Higher up on the extreme temperature scale we find the hyperthermophiles, which are characterized by growth ranges from 80 °C to a maximum of 110 °C, with some extreme examples that survive temperatures above 121 °C, the average temperature of an autoclave. The hydrothermal vents at the bottom of the ocean are a prime example of extreme environments, with temperatures reaching an estimated 340 °C (Figure 7.14). Microbes isolated from the vents achieve optimal growth at temperatures higher than 100 °C. Some archaea grow at 105 °C and can survive autoclaving. Figure 7.15 shows the typical skewed curves of temperature-dependent growth for the categories of microorganisms we have discussed.",True,Temperature and Growth,Figure 7.14,7.4 Temperature and Microbial Growth,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-9.28.png,"Figure 7.14 A black smoker at the bottom of the ocean belches hot, chemical-rich water, and heats the surrounding waters. Sea vents provide an extreme environment that is nonetheless teeming with macroscopic life (the red tubeworms) supported by an abundant microbial ecosystem. (credit: NOAA)"
0e2ba2de-a5e5-45a3-b75d-2cedccf2b3da,https://open.oregonstate.education/microbiology/,7.4 Temperature and Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-4temperature-and-microbial-growth/,"Life in extreme environments raises fascinating questions about the adaptation of macromolecules and metabolic processes. Very low temperatures affect cells in many ways. Membranes lose their fluidity and are damaged by ice crystal formation. Chemical reactions and diffusion slow considerably. Proteins become too rigid to catalyze reactions and may undergo denaturation. At the opposite end of the temperature spectrum, heat denatures proteins and nucleic acids. Increased fluidity impairs metabolic processes in membranes. Some of the practical applications of the destructive effects of heat on microbes are sterilization by steam, pasteurization, and incineration of inoculating loops. Proteins in psychrophiles are, in general, rich in hydrophobic residues, display an increase in flexibility, and have a lower number of secondary stabilizing bonds when compared with homologous proteins from mesophiles. Antifreeze proteins and solutes that decrease the freezing temperature of the cytoplasm are common. The lipids in the membranes tend to be unsaturated to increase fluidity. Growth rates are much slower than those encountered at moderate temperatures. Under appropriate conditions, mesophiles and even thermophiles can survive freezing.",True,Temperature and Growth,,,,
ed5e4586-b6b5-4f8f-bc1c-9a000a5619e6,https://open.oregonstate.education/microbiology/,7.4 Temperature and Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-4temperature-and-microbial-growth/,"Macromolecules in thermophiles and hyperthermophiles show some notable structural differences from what is observed in the mesophiles. The ratio of saturated to polyunsaturated lipids increases to limit the fluidity of the cell membranes. Their DNA sequences show a higher proportion of guanine–cytosine nitrogenous bases, which are held together by three hydrogen bonds in contrast to adenine and thymine, which are connected in the double helix by two hydrogen bonds. Additional secondary ionic and covalent bonds, as well as the replacement of key amino acids to stabilize folding, contribute to the resistance of proteins to denaturation.",True,Temperature and Growth,,,,
4fabda83-c302-4872-b9be-c7fa3fb2134e,https://open.oregonstate.education/microbiology/,7.3 The Effects of pH on Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-3the-effects-of-ph-on-microbial-growth/,"The optimum growth pH is the most favorable pH for the growth of an organism. The lowest pH value that an organism can tolerate is called the minimum growth pH and the highest pH is the maximum growth pH. These values can cover a wide range, which is important for the preservation of food and to microorganisms’ survival in the stomach. For example, the optimum growth pH of Salmonella spp. is 7.0–7.5, but the minimum growth pH is closer to 4.2.",True,Temperature and Growth,,,,
44057f12-32fd-4f6d-abb1-1307b193a97d,https://open.oregonstate.education/microbiology/,7.3 The Effects of pH on Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-3the-effects-of-ph-on-microbial-growth/,"Most bacteria are neutrophiles, meaning they grow optimally at a pH within one or two pH units of the neutral pH of 7 (see Figure 7.12). Most familiar bacteria, like Escherichia coli, are neutrophiles and do not fare well in the acidic pH of the stomach. However, there are pathogenic strains of E. coli, and other species of intestinal pathogens that are much more resistant to stomach acid. In comparison, fungi thrive at slightly acidic pH values of 5.0–6.0.",True,Temperature and Growth,Figure 7.12,7.3 The Effects of pH on Microbial Growth,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-9.26.png,Figure 7.12 The curves show the approximate pH ranges for the growth of the different classes of pH-specific prokaryotes. Each curve has an optimal pH and extreme pH values at which growth is much reduced. Most bacteria are neutrophiles and grow best at near-neutral pH (center curve). Acidophiles have optimal growth at pH values near 3 and alkaliphiles have optimal growth at pH values above 9.
47cd7937-7b64-4d7c-a1e0-8d2b0ca72519,https://open.oregonstate.education/microbiology/,7.3 The Effects of pH on Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-3the-effects-of-ph-on-microbial-growth/,"Microorganisms that grow optimally at pH less than 5.55 are called acidophiles. For example, the sulfur-oxidizing Sulfolobus spp. isolated from sulfur mud fields and hot springs in Yellowstone National Park are extreme acidophiles. These archaea survive at pH values of 2.5–3.5. Species of the archaean genus Ferroplasma live in acid mine drainage at pH values of 0–2.9. Lactobacillus bacteria, which are an important part of the normal microbiota of the vagina, can tolerate acidic environments at pH values 3.5–6.8 and also contribute to the acidity of the vagina (pH of 4, except at the onset of menstruation) through their metabolic production of lactic acid. The vagina’s acidity plays an important role in inhibiting other microbes that are less tolerant of acidity. Acidophilic microorganisms display a number of adaptations to survive in strong acidic environments. For example, proteins show increased negative surface charge that stabilizes them at low pH. Pumps actively eject H+ ions out of the cells. The changes in the composition of membrane phospholipids probably reflect the need to maintain membrane fluidity at low pH.",True,Temperature and Growth,,,,
f9ab2eb5-2800-4de9-8d85-30ba3e586d8c,https://open.oregonstate.education/microbiology/,7.3 The Effects of pH on Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-3the-effects-of-ph-on-microbial-growth/,"Most bacteria are neutrophiles, meaning they grow optimally at a pH within one or two pH units of the neutral pH of 7 (see Figure 7.12). Most familiar bacteria, like Escherichia coli, are neutrophiles and do not fare well in the acidic pH of the stomach. However, there are pathogenic strains of E. coli, and other species of intestinal pathogens that are much more resistant to stomach acid. In comparison, fungi thrive at slightly acidic pH values of 5.0–6.0.",True,Temperature and Growth,Figure 7.12,7.3 The Effects of pH on Microbial Growth,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-9.26.png,Figure 7.12 The curves show the approximate pH ranges for the growth of the different classes of pH-specific prokaryotes. Each curve has an optimal pH and extreme pH values at which growth is much reduced. Most bacteria are neutrophiles and grow best at near-neutral pH (center curve). Acidophiles have optimal growth at pH values near 3 and alkaliphiles have optimal growth at pH values above 9.
65e9c77a-adaf-4f06-8f2e-a550ce8dd092,https://open.oregonstate.education/microbiology/,7.3 The Effects of pH on Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-3the-effects-of-ph-on-microbial-growth/,"Microorganisms that grow optimally at pH less than 5.55 are called acidophiles. For example, the sulfur-oxidizing Sulfolobus spp. isolated from sulfur mud fields and hot springs in Yellowstone National Park are extreme acidophiles. These archaea survive at pH values of 2.5–3.5. Species of the archaean genus Ferroplasma live in acid mine drainage at pH values of 0–2.9. Lactobacillus bacteria, which are an important part of the normal microbiota of the vagina, can tolerate acidic environments at pH values 3.5–6.8 and also contribute to the acidity of the vagina (pH of 4, except at the onset of menstruation) through their metabolic production of lactic acid. The vagina’s acidity plays an important role in inhibiting other microbes that are less tolerant of acidity. Acidophilic microorganisms display a number of adaptations to survive in strong acidic environments. For example, proteins show increased negative surface charge that stabilizes them at low pH. Pumps actively eject H+ ions out of the cells. The changes in the composition of membrane phospholipids probably reflect the need to maintain membrane fluidity at low pH.",True,Temperature and Growth,,,,
d1f7ee12-6405-4d67-a009-4e7beaf5c52f,https://open.oregonstate.education/microbiology/,7.2 Oxygen Requirements for Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-2oxygen-requirements-for-microbial-growth/,"The answer is that molecular oxygen (O2) is not always needed. The earliest signs of life are dated to a period when conditions on earth were highly reducing and free oxygen gas was essentially nonexistent. Only after cyanobacteria started releasing oxygen as a byproduct of photosynthesis and the capacity of iron in the oceans for taking up oxygen was exhausted did oxygen levels increase in the atmosphere. This event, often referred to as the Great Oxygenation Event or the Oxygen Revolution, caused a massive extinction. Most organisms could not survive the powerful oxidative properties of reactive oxygen species (ROS), highly unstable ions and molecules derived from partial reduction of oxygen that can damage virtually any macromolecule or structure with which they come in contact. Singlet oxygen (O2•), superoxide (O 2−), peroxides (H2O2), hydroxyl radical (OH•), and hypochlorite ion (OCl−), the active ingredient of household bleach, are all examples of ROS. The organisms that were able to detoxify reactive oxygen species harnessed the high electronegativity of oxygen to produce free energy for their metabolism and thrived in the new environment.",True,Temperature and Growth,,,,
6144d1a3-3749-479c-953f-adbf4b98247d,https://open.oregonstate.education/microbiology/,7.2 Oxygen Requirements for Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-2oxygen-requirements-for-microbial-growth/,Oxygen Requirements of Microorganisms,False,Oxygen Requirements of Microorganisms,,,,
0f182f0f-c3a5-47b6-ad55-043e9e913084,https://open.oregonstate.education/microbiology/,7.2 Oxygen Requirements for Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-2oxygen-requirements-for-microbial-growth/,"Many ecosystems are still free of molecular oxygen. Some are found in extreme locations, such as deep in the ocean or in earth’s crust; others are part of our everyday landscape, such as marshes, bogs, and sewers. Within the bodies of humans and other animals, regions with little or no oxygen provide an anaerobic environment for microorganisms. (Figure 7.9).",True,Oxygen Requirements of Microorganisms,Figure 7.9,7.2 Oxygen Requirements for Microbial Growth,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-9.19.png,"Figure 7.9 Anaerobic environments are still common on earth. They include environments like (a) a bog where undisturbed dense sediments are virtually devoid of oxygen, and (b) the rumen (the first compartment of a cow’s stomach), which provides an oxygen-free incubator for methanogens and other obligate anaerobic bacteria. (credit a: modification of work by National Park Service; credit b: modification of work by US Department of Agriculture)"
8878d5ad-3b3f-4901-9f6f-c27ab8942a4b,https://open.oregonstate.education/microbiology/,7.2 Oxygen Requirements for Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-2oxygen-requirements-for-microbial-growth/,"The growth of bacteria with varying oxygen requirements in thioglycolate tubes is illustrated in Figure 7.10. In tube A, all the growth is seen at the top of the tube. The bacteria are obligate (strict) aerobes that cannot grow without an abundant supply of oxygen. Tube B looks like the opposite of tube A. Bacteria grow at the bottom of tube B. Those are obligate anaerobes, which are killed by oxygen. Tube C shows heavy growth at the top of the tube and growth throughout the tube, a typical result with facultative anaerobes. Facultative anaerobes are organisms that thrive in the presence of oxygen but also grow in its absence by relying on fermentation or anaerobic respiration, if there is a suitable electron acceptor other than oxygen and the organism is able to perform anaerobic respiration. The aerotolerant anaerobes in tube D are indifferent to the presence of oxygen. They do not use oxygen because they usually have a fermentative metabolism, but they are not harmed by the presence of oxygen as obligate anaerobes are. Tube E on the right shows a “Goldilocks” culture. The oxygen level has to be just right for growth, not too much and not too little. These microaerophiles are bacteria that require a minimum level of oxygen for growth, about 1%–10%, well below the 21% found in the atmosphere.",True,Oxygen Requirements of Microorganisms,Figure 7.10,7.2 Oxygen Requirements for Microbial Growth,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-9.20.png,Figure 7.10 Diagram of bacterial cell distribution in thioglycolate tubes.
a906ef6a-3e61-4808-a397-ee46ef4b0794,https://open.oregonstate.education/microbiology/,7.2 Oxygen Requirements for Microbial Growth,https://open.oregonstate.education/microbiology/chapter/9-2oxygen-requirements-for-microbial-growth/,"The growth of bacteria with varying oxygen requirements in thioglycolate tubes is illustrated in Figure 7.10. In tube A, all the growth is seen at the top of the tube. The bacteria are obligate (strict) aerobes that cannot grow without an abundant supply of oxygen. Tube B looks like the opposite of tube A. Bacteria grow at the bottom of tube B. Those are obligate anaerobes, which are killed by oxygen. Tube C shows heavy growth at the top of the tube and growth throughout the tube, a typical result with facultative anaerobes. Facultative anaerobes are organisms that thrive in the presence of oxygen but also grow in its absence by relying on fermentation or anaerobic respiration, if there is a suitable electron acceptor other than oxygen and the organism is able to perform anaerobic respiration. The aerotolerant anaerobes in tube D are indifferent to the presence of oxygen. They do not use oxygen because they usually have a fermentative metabolism, but they are not harmed by the presence of oxygen as obligate anaerobes are. Tube E on the right shows a “Goldilocks” culture. The oxygen level has to be just right for growth, not too much and not too little. These microaerophiles are bacteria that require a minimum level of oxygen for growth, about 1%–10%, well below the 21% found in the atmosphere.",True,Oxygen Requirements of Microorganisms,Figure 7.10,7.2 Oxygen Requirements for Microbial Growth,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-9.20.png,Figure 7.10 Diagram of bacterial cell distribution in thioglycolate tubes.
7f93b772-dd4b-4dfc-8f9b-bd40af04f47c,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,Binary Fission,False,Binary Fission,,,,
3e067331-1976-4849-982d-c7bdb2b5ee71,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"The most common mechanism of cell replication in bacteria is a process called binary fission, which is depicted in Figure 7.2. Before dividing, the cell grows and increases its number of cellular components. Next, the replication of DNA starts at a location on the circular chromosome called the origin of replication, where the chromosome is attached to the inner cell membrane. Replication continues in opposite directions along the chromosome until the terminus is reached.",True,Binary Fission,Figure 7.2,7.1 How Microbes Grow,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-9.2.png,"Figure 7.2 (a) The electron micrograph depicts two cells of Salmonella typhimurium after a binary fission event. (b) Binary fission in bacteria starts with the replication of DNA as the cell elongates. A division septum forms in the center of the cell. Two daughter cells of similar size form and separate, each receiving a copy of the original chromosome. (credit a: modification of work by Centers for Disease Control and Prevention)"
8d5e8d7c-f500-40e3-a59b-50c4d4b338d2,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"The center of the enlarged cell constricts until two daughter cells are formed, each offspring receiving a complete copy of the parental genome and a division of the cytoplasm (cytokinesis). This process of cytokinesis and cell division is directed by a protein called FtsZ. FtsZ assembles into a Z ring on the cytoplasmic membrane (Figure 7.3). The Z ring is anchored by FtsZ-binding proteins and defines the division plane between the two daughter cells. Additional proteins required for cell division are added to the Z ring to form a structure called the divisome. The divisome activates to produce a peptidoglycan cell wall and build a septum that divides the two daughter cells. The daughter cells are separated by the division septum, where all of the cells’ outer layers (the cell wall and outer membranes, if present) must be remodeled to complete division.",True,Binary Fission,Figure 7.3,7.1 How Microbes Grow,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-9.3.png,Figure 7.3 FtsZ proteins assemble to form a Z ring that is anchored to the plasma membrane. The Z ring pinches the cell envelope to separate the cytoplasm of the new cells.
6b93cdfd-fe26-4646-a29f-880ad94c76c8,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,Generation Time,False,Generation Time,,,,
55f62a27-6ede-4269-b43b-ee9ffe1910ff,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"In eukaryotic organisms, the generation time is the time between the same points of the life cycle in two successive generations. For example, the typical generation time for the human population is 25 years. This definition is not practical for bacteria, which may reproduce rapidly or remain dormant for thousands of years. In prokaryotes (Bacteria and Archaea), the generation time is also called the doubling time and is defined as the time it takes for the population to double through one round of binary fission. Bacterial doubling times vary enormously. Whereas Escherichia coli can double in as little as 20 minutes under optimal growth conditions in the laboratory, bacteria of the same species may need several days to double in especially harsh environments. Most pathogens grow rapidly, like E.coli, but there are exceptions. For example, Mycobacterium tuberculosis, the causative agent of tuberculosis, has a generation time of between 15 and 20 hours. On the other hand, M. leprae, which causes Hansen’s disease (leprosy), grows much more slowly, with a doubling time of 14 days.",True,Generation Time,,,,
959f245b-ccc3-4af9-8b1e-88c24882ad53,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"The number of cells increases exponentially and can be expressed as 2n, where n is the number of generations. If cells divide every 30 minutes, after 24 hours, 48 divisions would have taken place. If we apply the formula 2n, where n is equal to 48, the single cell would give rise to 248 or 281,474,976,710,656 cells at 48 generations (24 hours). When dealing with such huge numbers, it is more practical to use scientific notation. Therefore, we express the number of cells as 2.8 × 1014 cells.",True,Generation Time,,,,
cedb7c51-450c-4d36-97bc-d3910348096e,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"In our example, we used one cell as the initial number of cells. For any number of starting cells, the formula is adapted as follows:",True,Generation Time,,,,
583a27f7-aa60-4b3f-aba1-d2f2ff811bdd,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,Nn = N02n,False,Nn = N02n,,,,
b339c224-8d95-4c45-889a-1c386b7e7702,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"Nn is the number of cells at any generation n, N0 is the initial number of cells, and n is the number of generations.",True,Nn = N02n,,,,
781042eb-ccd1-42f0-af5b-8469b41ebb45,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,The Growth Curve,False,The Growth Curve,,,,
32b367c0-f653-493e-99d5-b4aa709e4714,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"Microorganisms grown in closed culture (also known as a batch culture), in which no nutrients are added and most waste is not removed, follow a reproducible growth pattern referred to as the growth curve. An example of a batch culture in nature is a pond in which a small number of cells grow in a closed environment. The culture density is defined as the number of cells per unit volume. In a closed environment, the culture density is also a measure of the number of cells in the population. Infections of the body do not always follow the growth curve, but correlations can exist depending upon the site and type of infection. When the number of live cells is plotted against time, distinct phases can be observed in the curve (Figure 7.5).",True,The Growth Curve,Figure 7.5,7.1 How Microbes Grow,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-9.5.png,"Figure 7.5 The growth curve of a bacterial culture is represented by the logarithm of the number of live cells plotted as a function of time. The graph can be divided into four phases according to the slope, each of which matches events in the cell. The four phases are lag, log, stationary, and death."
b6c7a119-e202-4225-b929-3c8b3a887073,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"The beginning of the growth curve represents a small number of cells, referred to as an inoculum, that are added to a fresh culture medium, a nutritional broth that supports growth. The initial phase of the growth curve is called the lag phase, during which cells are gearing up for the next phase of growth. The number of cells does not change during the lag phase; however, cells grow larger and are metabolically active, synthesizing proteins needed to grow within the medium. If any cells were damaged or shocked during the transfer to the new medium, repair takes place during the lag phase. The duration of the lag phase is determined by many factors, including the species and genetic make-up of the cells, the composition of the medium, and the size of the original inoculum.",True,The Growth Curve,,,,
dbc5883b-b65d-4a61-ab61-7c229e13f146,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"In the logarithmic (log) phase, sometimes called exponential growth phase, the cells are actively dividing by binary fission and their number increases exponentially. During the log phase, the relationship between time and number of cells is not linear but exponential; however, the growth curve is often plotted on a semilogarithmic graph, as shown in Figure 7.6, which gives the appearance of a linear relationship.",True,The Growth Curve,Figure 7.6,7.1 How Microbes Grow,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-9.6.png,"Figure 7.6 Both graphs illustrate population growth during the log phase for a bacterial sample with an initial population of one cell and a doubling time of 1 hour. (a) When plotted on an arithmetic scale, the growth rate resembles a curve. (b) When plotted on a semilogarithmic scale (meaning the values on the y-axis are logarithmic), the growth rate appears linear."
a104ee7e-a07e-43a6-8255-1b27ec1cd995,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"As the number of cells increases through the log phase, several factors contribute to a slowing of the growth rate. Waste products accumulate and nutrients are gradually used up. In addition, gradual depletion of oxygen begins to limit aerobic cell growth. This combination of unfavorable conditions slows and finally stalls population growth. The total number of live cells reaches a plateau referred to as the stationary phase (Figure 7.5). In this phase, the number of new cells created by cell division is now equivalent to the number of cells dying; thus, the total population of living cells is relatively stagnant. The culture density in a stationary culture is constant. The culture’s carrying capacity, or maximum culture density, depends on the types of microorganisms in the culture and the specific conditions of the culture; however, carrying capacity is constant for a given organism grown under the same conditions.",True,The Growth Curve,Figure 7.5,7.1 How Microbes Grow,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-9.5.png,"Figure 7.5 The growth curve of a bacterial culture is represented by the logarithm of the number of live cells plotted as a function of time. The graph can be divided into four phases according to the slope, each of which matches events in the cell. The four phases are lag, log, stationary, and death."
9ba93f7e-12b5-48d8-a4c8-befe203883f2,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"During the stationary phase, cells switch to a survival mode of metabolism. As growth slows, so too does the synthesis of peptidoglycans, proteins, and nucleic-acids; thus, stationary cultures are less susceptible to antibiotics that disrupt these processes. In bacteria capable of producing endospores, many cells undergo sporulation during the stationary phase. Secondary metabolites, including antibiotics, are synthesized in the stationary phase. In certain pathogenic bacteria, the stationary phase is also associated with the expression of virulence factors, products that contribute to a microbe’s ability to survive, reproduce, and cause disease in a host organism. For example, quorum sensing in Staphylococcus aureus initiates the production of enzymes that can break down human tissue and cellular debris, clearing the way for bacteria to spread to new tissue where nutrients are more plentiful.",True,The Growth Curve,,,,
d6e2f7a1-5adb-476e-a7b8-c4350cc1f5d6,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,The Death Phase,False,The Death Phase,,,,
4903aa99-1303-47ac-8c5a-24a756fe9523,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"As a culture medium accumulates toxic waste and nutrients are exhausted, cells die in greater and greater numbers. Soon, the number of dying cells exceeds the number of dividing cells, leading to an exponential decrease in the number of cells (Figure 7.5). This is the aptly named death phase, sometimes called the decline phase. Many cells lyse and release nutrients into the medium, allowing surviving cells to maintain viability and form endospores. A few cells, the so-called persisters, are characterized by a slow metabolic rate. Persister cells are medically important because they are associated with certain chronic infections, such as tuberculosis, that do not respond to antibiotic treatment.",True,The Death Phase,Figure 7.5,7.1 How Microbes Grow,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-9.5.png,"Figure 7.5 The growth curve of a bacterial culture is represented by the logarithm of the number of live cells plotted as a function of time. The graph can be divided into four phases according to the slope, each of which matches events in the cell. The four phases are lag, log, stationary, and death."
35c2d477-4e76-4cd5-9a89-70977e52af8f,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"The growth pattern shown in Figure 7.5 takes place in a closed environment; nutrients are not added and waste and dead cells are not removed. In many cases, though, it is advantageous to maintain cells in the logarithmic phase of growth. One example is in industries that harvest microbial products. A chemostat (Figure 7.7) is used to maintain a continuous culture in which nutrients are supplied at a steady rate. A controlled amount of air is mixed in for aerobic processes. Bacterial suspension is removed at the same rate as nutrients flow in to maintain an optimal growth environment.",True,The Death Phase,Figure 7.5,7.1 How Microbes Grow,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-9.5.png,"Figure 7.5 The growth curve of a bacterial culture is represented by the logarithm of the number of live cells plotted as a function of time. The graph can be divided into four phases according to the slope, each of which matches events in the cell. The four phases are lag, log, stationary, and death."
0a2c6705-4262-440a-9861-086236c0e800,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,Biofilms,False,Biofilms,,,,
de65cb66-a49f-4210-855a-1e72c10aa073,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"In nature, microorganisms grow mainly in biofilms, complex and dynamic ecosystems that form on a variety of environmental surfaces, from industrial conduits and water treatment pipelines to rocks in river beds. Biofilms are not restricted to solid surface substrates, however. Almost any surface in a liquid environment containing some minimal nutrients will eventually develop a biofilm. Microbial mats that float on water, for example, are biofilms that contain large populations of photosynthetic microorganisms. Biofilms found in the human mouth may contain hundreds of bacterial species. Regardless of the environment where they occur, biofilms are not random collections of microorganisms; rather, they are highly structured communities that provide a selective advantage to their constituent microorganisms.",True,Biofilms,,,,
dcc6ab6d-3aa5-44aa-807e-9743bdcabebb,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"Observations using confocal microscopy have shown that environmental conditions influence the overall structure of biofilms. Filamentous biofilms called streamers form in rapidly flowing water, such as freshwater streams, eddies, and specially designed laboratory flow cells that replicate growth conditions in fast-moving fluids. The streamers are anchored to the substrate by a “head” and the “tail” floats downstream in the current. In still or slow-moving water, biofilms mainly assume a mushroom-like shape. The structure of biofilms may also change with other environmental conditions such as nutrient availability.",True,Biofilms,,,,
34e1c1e3-efd9-405c-85fc-1e5d524c711e,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"Detailed observations of biofilms under confocal laser and scanning electron microscopes reveal clusters of microorganisms embedded in a matrix interspersed with open water channels. The extracellular matrix consists of extracellular polymeric substances (EPS) secreted by the organisms in the biofilm. The extracellular matrix represents a large fraction of the biofilm, accounting for 50%–90% of the total dry mass. The properties of the EPS vary according to the resident organisms and environmental conditions but is composed primarily of polysaccharides and containing other macromolecules such as proteins, nucleic acids, and lipids. It plays a key role in maintaining the integrity and function of the biofilm. Channels in the EPS allow movement of nutrients, waste, and gases throughout the biofilm. This keeps the cells hydrated, preventing desiccation. EPS also shelters organisms in the biofilm from predation by other microbes or cells (e.g., protozoans, white blood cells in the human body).",True,Biofilms,,,,
98d66dc9-f003-4377-b7aa-195db11d93ad,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"Free-floating microbial cells that live in an aquatic environment are called planktonic cells. The formation of a biofilm essentially involves the attachment of planktonic cells to a substrate, where they become sessile (attached to a surface). This occurs in stages, as depicted in Figure 7.8. The first stage involves the attachment of planktonic cells to a surface coated with a conditioning film of organic material. At this point, attachment to the substrate is reversible, but as cells express new phenotypes that facilitate the formation of EPS, they transition from a planktonic to a sessile lifestyle. The biofilm develops characteristic structures, including an extensive matrix and water channels. Appendages such as fimbriae, pili, and flagella interact with the EPS, and microscopy and genetic analysis suggest that such structures are required for the establishment of a mature biofilm. In the last stage of the biofilm life cycle, cells on the periphery of the biofilm revert to a planktonic lifestyle, sloughing off the mature biofilm to colonize new sites. This stage is referred to as dispersal.",True,Biofilms,Figure 7.8,7.1 How Microbes Grow,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-9.17.png,Figure 7.8 Stages in the formation and life cycle of a biofilm. (credit: modification of work by Public Library of Science and American Society for Microbiology)
1197e456-c464-44a0-9800-e8ba6fba71ff,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"Within a biofilm, different species of microorganisms establish metabolic collaborations in which the waste product of one organism becomes the nutrient for another. For example, aerobic microorganisms consume oxygen, creating anaerobic regions that promote the growth of anaerobes. This occurs in many polymicrobial infections that involve both aerobic and anaerobic pathogens.",True,Biofilms,,,,
c62fac56-50d2-4a74-84f2-d832b284f6a7,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"The mechanism by which cells in a biofilm coordinate their activities in response to environmental stimuli is called quorum sensing. Quorum sensing—which can occur between cells of different species within a biofilm—enables microorganisms to detect their cell density through the release and binding of small, diffusible molecules called autoinducers. When the cell population reaches a critical threshold (a quorum), these autoinducers initiate a cascade of reactions that activate genes associated with cellular functions that are beneficial only when the population reaches a critical density. For example, in some pathogens, synthesis of virulence factors only begins when enough cells are present to overwhelm the immune defenses of the host. Although mostly studied in bacterial populations, quorum sensing takes place between bacteria and eukaryotes and between eukaryotic cells such as the fungus Candida albicans, a common member of the human microbiota that can cause infections in immunocompromised individuals.",True,Biofilms,,,,
5821b672-26a2-4454-b06a-6146f408c690,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"The human body harbors many types of biofilms, some beneficial and some harmful. For example, the layers of normal microbiota lining the intestinal and respiratory mucosa play a role in warding off infections by pathogens. However, other biofilms in the body can have a detrimental effect on health. For example, the plaque that forms on teeth is a biofilm that can contribute to dental and periodontal disease. Biofilms can also form in wounds, sometimes causing serious infections that can spread. The bacterium Pseudomonas aeruginosa often colonizes biofilms in the airways of patients with cystic fibrosis, causing chronic and sometimes fatal infections of the lungs. Biofilms can also form on medical devices used in or on the body, causing infections in patients with in-dwelling catheters, artificial joints, or contact lenses.",True,Biofilms,,,,
7518bbfb-dc7c-4d0e-a8db-a61967d9bb85,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"Pathogens embedded within biofilms exhibit a higher resistance to antibiotics than their free-floating counterparts. Several hypotheses have been proposed to explain why. Cells in the deep layers of a biofilm are metabolically inactive and may be less susceptible to the action of antibiotics that disrupt metabolic activities. The EPS may also slow the diffusion of antibiotics and antiseptics, preventing them from reaching cells in the deeper layers of the biofilm. Phenotypic changes may also contribute to the increased resistance exhibited by bacterial cells in biofilms. For example, the increased production of efflux pumps, membrane-embedded proteins that actively extrude antibiotics out of bacterial cells, have been shown to be an important mechanism of antibiotic resistance among biofilm-associated bacteria. Finally, biofilms provide an ideal environment for the exchange of extrachromosomal DNA, which often includes genes that confer antibiotic resistance.",True,Biofilms,,,,
d65b9cf7-8dc3-40d8-a0b9-a1fe02203969,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,Generation Time,False,Generation Time,,,,
baa235e8-15c9-4295-9bdc-9fcb5904768f,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"In eukaryotic organisms, the generation time is the time between the same points of the life cycle in two successive generations. For example, the typical generation time for the human population is 25 years. This definition is not practical for bacteria, which may reproduce rapidly or remain dormant for thousands of years. In prokaryotes (Bacteria and Archaea), the generation time is also called the doubling time and is defined as the time it takes for the population to double through one round of binary fission. Bacterial doubling times vary enormously. Whereas Escherichia coli can double in as little as 20 minutes under optimal growth conditions in the laboratory, bacteria of the same species may need several days to double in especially harsh environments. Most pathogens grow rapidly, like E.coli, but there are exceptions. For example, Mycobacterium tuberculosis, the causative agent of tuberculosis, has a generation time of between 15 and 20 hours. On the other hand, M. leprae, which causes Hansen’s disease (leprosy), grows much more slowly, with a doubling time of 14 days.",True,Generation Time,,,,
dd48f42a-5e7c-4be7-b74d-f5b9ad8a27ed,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"The number of cells increases exponentially and can be expressed as 2n, where n is the number of generations. If cells divide every 30 minutes, after 24 hours, 48 divisions would have taken place. If we apply the formula 2n, where n is equal to 48, the single cell would give rise to 248 or 281,474,976,710,656 cells at 48 generations (24 hours). When dealing with such huge numbers, it is more practical to use scientific notation. Therefore, we express the number of cells as 2.8 × 1014 cells.",True,Generation Time,,,,
43f7c543-02bb-4da2-a7b8-50e5a78adba0,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"In our example, we used one cell as the initial number of cells. For any number of starting cells, the formula is adapted as follows:",True,Generation Time,,,,
a8397d70-09c1-4c84-87bd-0e99b55933e3,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,Nn = N02n,False,Nn = N02n,,,,
3fba58c1-9563-469e-9eee-0aec0892fde1,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"Nn is the number of cells at any generation n, N0 is the initial number of cells, and n is the number of generations.",True,Nn = N02n,,,,
64fec694-279b-4bb3-b512-2d4550e950fd,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,The Growth Curve,False,The Growth Curve,,,,
08c37504-f177-4b75-b8f7-98c38fb6a3e2,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"In the logarithmic (log) phase, sometimes called exponential growth phase, the cells are actively dividing by binary fission and their number increases exponentially. During the log phase, the relationship between time and number of cells is not linear but exponential; however, the growth curve is often plotted on a semilogarithmic graph, as shown in Figure 7.6, which gives the appearance of a linear relationship.",True,The Growth Curve,Figure 7.6,7.1 How Microbes Grow,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-9.6.png,"Figure 7.6 Both graphs illustrate population growth during the log phase for a bacterial sample with an initial population of one cell and a doubling time of 1 hour. (a) When plotted on an arithmetic scale, the growth rate resembles a curve. (b) When plotted on a semilogarithmic scale (meaning the values on the y-axis are logarithmic), the growth rate appears linear."
ffd5e2f3-2239-4237-91e2-80478ae115c6,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"During the stationary phase, cells switch to a survival mode of metabolism. As growth slows, so too does the synthesis of peptidoglycans, proteins, and nucleic-acids; thus, stationary cultures are less susceptible to antibiotics that disrupt these processes. In bacteria capable of producing endospores, many cells undergo sporulation during the stationary phase. Secondary metabolites, including antibiotics, are synthesized in the stationary phase. In certain pathogenic bacteria, the stationary phase is also associated with the expression of virulence factors, products that contribute to a microbe’s ability to survive, reproduce, and cause disease in a host organism. For example, quorum sensing in Staphylococcus aureus initiates the production of enzymes that can break down human tissue and cellular debris, clearing the way for bacteria to spread to new tissue where nutrients are more plentiful.",True,The Growth Curve,,,,
e04d4df2-5bf4-4b01-bad3-2edd4524d02b,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"As a culture medium accumulates toxic waste and nutrients are exhausted, cells die in greater and greater numbers. Soon, the number of dying cells exceeds the number of dividing cells, leading to an exponential decrease in the number of cells (Figure 7.5). This is the aptly named death phase, sometimes called the decline phase. Many cells lyse and release nutrients into the medium, allowing surviving cells to maintain viability and form endospores. A few cells, the so-called persisters, are characterized by a slow metabolic rate. Persister cells are medically important because they are associated with certain chronic infections, such as tuberculosis, that do not respond to antibiotic treatment.",True,The Growth Curve,Figure 7.5,7.1 How Microbes Grow,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-9.5.png,"Figure 7.5 The growth curve of a bacterial culture is represented by the logarithm of the number of live cells plotted as a function of time. The graph can be divided into four phases according to the slope, each of which matches events in the cell. The four phases are lag, log, stationary, and death."
a8b8b419-0d04-4300-9095-c537f2c78bd9,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,Biofilms,False,Biofilms,,,,
31361e37-b3ad-43ab-bb3a-eccf55e061b9,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"In nature, microorganisms grow mainly in biofilms, complex and dynamic ecosystems that form on a variety of environmental surfaces, from industrial conduits and water treatment pipelines to rocks in river beds. Biofilms are not restricted to solid surface substrates, however. Almost any surface in a liquid environment containing some minimal nutrients will eventually develop a biofilm. Microbial mats that float on water, for example, are biofilms that contain large populations of photosynthetic microorganisms. Biofilms found in the human mouth may contain hundreds of bacterial species. Regardless of the environment where they occur, biofilms are not random collections of microorganisms; rather, they are highly structured communities that provide a selective advantage to their constituent microorganisms.",True,Biofilms,,,,
06d80679-7864-4364-aa8e-d5eeb6c1bd1d,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"Observations using confocal microscopy have shown that environmental conditions influence the overall structure of biofilms. Filamentous biofilms called streamers form in rapidly flowing water, such as freshwater streams, eddies, and specially designed laboratory flow cells that replicate growth conditions in fast-moving fluids. The streamers are anchored to the substrate by a “head” and the “tail” floats downstream in the current. In still or slow-moving water, biofilms mainly assume a mushroom-like shape. The structure of biofilms may also change with other environmental conditions such as nutrient availability.",True,Biofilms,,,,
7bdde067-2c28-47f7-9c96-a51d6c548728,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"Detailed observations of biofilms under confocal laser and scanning electron microscopes reveal clusters of microorganisms embedded in a matrix interspersed with open water channels. The extracellular matrix consists of extracellular polymeric substances (EPS) secreted by the organisms in the biofilm. The extracellular matrix represents a large fraction of the biofilm, accounting for 50%–90% of the total dry mass. The properties of the EPS vary according to the resident organisms and environmental conditions but is composed primarily of polysaccharides and containing other macromolecules such as proteins, nucleic acids, and lipids. It plays a key role in maintaining the integrity and function of the biofilm. Channels in the EPS allow movement of nutrients, waste, and gases throughout the biofilm. This keeps the cells hydrated, preventing desiccation. EPS also shelters organisms in the biofilm from predation by other microbes or cells (e.g., protozoans, white blood cells in the human body).",True,Biofilms,,,,
26c28e4a-0c75-4754-ab39-798b9d5165bf,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"Free-floating microbial cells that live in an aquatic environment are called planktonic cells. The formation of a biofilm essentially involves the attachment of planktonic cells to a substrate, where they become sessile (attached to a surface). This occurs in stages, as depicted in Figure 7.8. The first stage involves the attachment of planktonic cells to a surface coated with a conditioning film of organic material. At this point, attachment to the substrate is reversible, but as cells express new phenotypes that facilitate the formation of EPS, they transition from a planktonic to a sessile lifestyle. The biofilm develops characteristic structures, including an extensive matrix and water channels. Appendages such as fimbriae, pili, and flagella interact with the EPS, and microscopy and genetic analysis suggest that such structures are required for the establishment of a mature biofilm. In the last stage of the biofilm life cycle, cells on the periphery of the biofilm revert to a planktonic lifestyle, sloughing off the mature biofilm to colonize new sites. This stage is referred to as dispersal.",True,Biofilms,Figure 7.8,7.1 How Microbes Grow,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-9.17.png,Figure 7.8 Stages in the formation and life cycle of a biofilm. (credit: modification of work by Public Library of Science and American Society for Microbiology)
20ceab16-7766-4cf0-802c-6b785c056590,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"Within a biofilm, different species of microorganisms establish metabolic collaborations in which the waste product of one organism becomes the nutrient for another. For example, aerobic microorganisms consume oxygen, creating anaerobic regions that promote the growth of anaerobes. This occurs in many polymicrobial infections that involve both aerobic and anaerobic pathogens.",True,Biofilms,,,,
4258448b-2072-4f93-b9cc-533570726b95,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"The mechanism by which cells in a biofilm coordinate their activities in response to environmental stimuli is called quorum sensing. Quorum sensing—which can occur between cells of different species within a biofilm—enables microorganisms to detect their cell density through the release and binding of small, diffusible molecules called autoinducers. When the cell population reaches a critical threshold (a quorum), these autoinducers initiate a cascade of reactions that activate genes associated with cellular functions that are beneficial only when the population reaches a critical density. For example, in some pathogens, synthesis of virulence factors only begins when enough cells are present to overwhelm the immune defenses of the host. Although mostly studied in bacterial populations, quorum sensing takes place between bacteria and eukaryotes and between eukaryotic cells such as the fungus Candida albicans, a common member of the human microbiota that can cause infections in immunocompromised individuals.",True,Biofilms,,,,
e46387bb-b095-4143-a7e0-d6f27b304a73,https://open.oregonstate.education/microbiology/,7.1 How Microbes Grow,https://open.oregonstate.education/microbiology/chapter/9-1how-microbes-grow/,"Pathogens embedded within biofilms exhibit a higher resistance to antibiotics than their free-floating counterparts. Several hypotheses have been proposed to explain why. Cells in the deep layers of a biofilm are metabolically inactive and may be less susceptible to the action of antibiotics that disrupt metabolic activities. The EPS may also slow the diffusion of antibiotics and antiseptics, preventing them from reaching cells in the deeper layers of the biofilm. Phenotypic changes may also contribute to the increased resistance exhibited by bacterial cells in biofilms. For example, the increased production of efflux pumps, membrane-embedded proteins that actively extrude antibiotics out of bacterial cells, have been shown to be an important mechanism of antibiotic resistance among biofilm-associated bacteria. Finally, biofilms provide an ideal environment for the exchange of extrachromosomal DNA, which often includes genes that confer antibiotic resistance.",True,Biofilms,,,,
d0d75c86-1040-40ce-99ff-5c19ed17b94a,https://open.oregonstate.education/microbiology/,6.1 Microbial Biochemistry,https://open.oregonstate.education/microbiology/chapter/7-1using-biochemistry-to-identify-microorganisms/,"There are many ways to detect, characterize, and identify microorganisms. Some methods rely on phenotypic biochemical characteristics, while others use genotypic identification. The biochemical characteristics of a bacterium provide many traits that are useful for classification and identification. Analyzing the nutritional and metabolic capabilities of the bacterial isolate is a common approach for determining the genus and the species of the bacterium. In this section, we will discuss a few methods that use biochemical characteristics to identify microorganisms.",True,Biofilms,,,,
3e23e662-b3f3-404c-9f9b-ce4e93092f90,https://open.oregonstate.education/microbiology/,6.1 Microbial Biochemistry,https://open.oregonstate.education/microbiology/chapter/7-1using-biochemistry-to-identify-microorganisms/,"Some microorganisms store certain compounds as granules within their cytoplasm, and the contents of these granules can be used for identification purposes. Other systems rely on biochemical characteristics to identify microorganisms by their biochemical reactions, such as carbon utilization and other metabolic tests. In small laboratory settings or in teaching laboratories, those assays are carried out using a limited number of test tubes. However, more modern systems, such as the one developed by Biolog, Inc., are based on panels of biochemical reactions performed simultaneously and analyzed by software. Biolog’s system identifies cells based on their ability to metabolize certain biochemicals and on their physiological properties, including pH and chemical sensitivity. It uses all major classes of biochemicals in its analysis. Identifications can be performed manually or with the semi- or fully automated instruments.",True,Biofilms,,,,
0e53d1c9-8438-42eb-a3c7-6985c9784288,https://open.oregonstate.education/microbiology/,6.1 Microbial Biochemistry,https://open.oregonstate.education/microbiology/chapter/7-1using-biochemistry-to-identify-microorganisms/,"Another automated system identifies microorganisms by determining the specimen’s mass spectrum and then comparing it to a database that contains known mass spectra for thousands of microorganisms. This method is based on matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF) and uses disposable MALDI plates on which the microorganism is mixed with a specialized matrix reagent (Figure 6.2). The sample/ reagent mixture is irradiated with a high-intensity pulsed ultraviolet laser, resulting in the ejection of gaseous ions generated from the various chemical constituents of the microorganism. These gaseous ions are collected and accelerated through the mass spectrometer, with ions traveling at a velocity determined by their mass-to-charge ratio (m/z), thus, reaching the detector at different times. A plot of detector signal versus m/z yields a mass spectrum for the organism that is uniquely related to its biochemical composition. Comparison of the mass spectrum to a library of reference spectra obtained from identical analyses of known microorganisms permits identification of the unknown microbe.",True,Biofilms,Figure 6.2,6.1 Microbial Biochemistry,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-7.26.png,"Figure 6.2 MALDI-TOF methods are now routinely used for diagnostic procedures in clinical microbiology laboratories. This technology is able to rapidly identify some microorganisms that cannot be readily identified by more traditional methods. (credit “MALDI plate photo”: modification of work by Chen Q, Liu T, Chen G; credit “graphs”: modification of work by Bailes J, Vidal L, Ivanov DA, Soloviev M)"
65ab4c74-9ff1-4220-8024-c302b1ecb749,https://open.oregonstate.education/microbiology/,6.1 Microbial Biochemistry,https://open.oregonstate.education/microbiology/chapter/7-1using-biochemistry-to-identify-microorganisms/,"Microbes can also be identified by measuring their unique lipid profiles. As we have learned, fatty acids of lipids can vary in chain length, presence or absence of double bonds, and number of double bonds, hydroxyl groups, branches, and rings. To identify a microbe by its lipid composition, the fatty acids present in their membranes are analyzed. A common biochemical analysis used for this purpose is a technique used in clinical, public health, and food laboratories. It relies on detecting unique differences in fatty acids and is called fatty acid methyl ester (FAME) analysis. In a FAME analysis, fatty acids are extracted from the membranes of microorganisms, chemically altered to form volatile methyl esters, and analyzed by gas chromatography (GC). The resulting GC chromatogram is compared with reference chromatograms in a database containing data for thousands of bacterial isolates to identify the unknown microorganism (Figure 6.3).",True,Biofilms,Figure 6.3,6.1 Microbial Biochemistry,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-7.27.png,Figure 6.3 Fatty acid methyl ester (FAME) analysis in bacterial identification results in a chromatogram unique to each bacterium. Each peak in the gas chromatogram corresponds to a particular fatty acid methyl ester and its height is proportional to the amount present in the cell. (credit “culture”: modification of work by the Centers for Disease Control and Prevention; credit “graph”: modification of work by Zhang P. and Liu P.)
d9eb9c9b-dd34-49ad-a678-a3d75bf1e7fe,https://open.oregonstate.education/microbiology/,6.1 Microbial Biochemistry,https://open.oregonstate.education/microbiology/chapter/7-1using-biochemistry-to-identify-microorganisms/,"A related method for microorganism identification is called phospholipid-derived fatty acids (PLFA) analysis. Membranes are mostly composed of phospholipids, which can be saponified (hydrolyzed with alkali) to release the fatty acids. The resulting fatty acid mixture is then subjected to FAME analysis, and the measured lipid profiles can be compared with those of known microorganisms to identify the unknown microorganism.",True,Biofilms,,,,
0dd9cb62-a8c3-4902-bcc0-ac1112b89f6c,https://open.oregonstate.education/microbiology/,6.1 Microbial Biochemistry,https://open.oregonstate.education/microbiology/chapter/7-1using-biochemistry-to-identify-microorganisms/,"Bacterial identification can also be based on the proteins produced under specific growth conditions within the human body. These types of identification procedures are called proteomic analysis. To perform proteomic analysis, proteins from the pathogen are first separated by high-pressure liquid chromatography (HPLC), and the collected fractions are then digested to yield smaller peptide fragments. These peptides are identified by mass spectrometry and compared with those of known microorganisms to identify the unknown microorganism in the original specimen.",True,Biofilms,,,,
d86bb2ff-284e-47f5-91ea-ee0b2e35cabd,https://open.oregonstate.education/microbiology/,6.1 Microbial Biochemistry,https://open.oregonstate.education/microbiology/chapter/7-1using-biochemistry-to-identify-microorganisms/,"Microorganisms can also be identified by the carbohydrates attached to proteins (glycoproteins) in the plasma membrane or cell wall. Antibodies and other carbohydrate-binding proteins can attach to specific carbohydrates on cell surfaces, causing the cells to clump together. Serological tests (e.g., the Lancefield groups tests, which are used for identification of Streptococcus species) are performed to detect the unique carbohydrates located on the surface of the cell.",True,Biofilms,,,,
e632acd9-9312-4009-a7c7-0d346ddff5ed,https://open.oregonstate.education/microbiology/,5.3 Prions,https://open.oregonstate.education/microbiology/chapter/6-3prions/,Prions,False,Prions,,,,
8a414807-f65b-4675-837b-a2637df9cf46,https://open.oregonstate.education/microbiology/,5.3 Prions,https://open.oregonstate.education/microbiology/chapter/6-3prions/,"At one time, scientists believed that any infectious particle must contain DNA or RNA. Then, in 1982, Stanley Prusiner, a medical doctor studying scrapie (a fatal, degenerative disease in sheep) discovered that the disease was caused by proteinaceous infectious particles, or prions. Because proteins are acellular and do not contain DNA or RNA, Prusiner’s findings were originally met with resistance and skepticism; however, his research was eventually validated, and he received the Nobel Prize in Physiology or Medicine in 1997.",True,Prions,,,,
60a80bda-3ab8-4d05-9b8d-10637ab6eff5,https://open.oregonstate.education/microbiology/,5.3 Prions,https://open.oregonstate.education/microbiology/chapter/6-3prions/,"A prion is a misfolded rogue form of a normal protein (PrPc) found in the cell. This rogue prion protein (PrPsc), which may be caused by a genetic mutation or occur spontaneously, can be infectious, stimulating other endogenous normal proteins to become misfolded, forming plaques (see Figure 5.10). Today, prions are known to cause various forms of transmissible spongiform encephalopathy (TSE) in human and animals. TSE is a rare degenerative disorder that affects the brain and nervous system. The accumulation of rogue proteins causes the brain tissue to become sponge- like, killing brain cells and forming holes in the tissue, leading to brain damage, loss of motor coordination, and dementia. Infected individuals are mentally impaired and become unable to move or speak. There is no cure, and the disease progresses rapidly, eventually leading to death within a few months or years.",True,Prions,Figure 5.10,5.3 Prions,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-6.25.png,"Figure 5.10 Endogenous normal prion protein (PrPc) is converted into the disease-causing form (PrPsc) when it encounters this variant form of the protein. PrPsc may arise spontaneously in brain tissue, especially if a mutant form of the protein is present, or it may originate from misfolded prions consumed in food that eventually find their way into brain tissue. (credit b: modification of work by USDA)"
1ae0c830-07e6-442f-bcbf-d3fcdd813c9a,https://open.oregonstate.education/microbiology/,5.3 Prions,https://open.oregonstate.education/microbiology/chapter/6-3prions/,"TSEs in humans include kuru, fatal familial insomnia, and Creutzfeldt- Jakob disease (see Figure 5.11). TSEs in animals include mad cow disease, scrapie (in sheep and goats), and chronic wasting disease (in elk and deer). TSEs can be transmitted between animals and from animals to humans by eating contaminated meat or animal feed. Transmission between humans can occur through heredity (as is often the case with CJD) or by contact with contaminated tissue, as might occur during a blood transfusion or organ transplant. There is no evidence for transmission via casual contact with an infected person.",True,Prions,Figure 5.11,5.3 Prions,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-6.26.png,"Figure 5.11 Creutzfeldt-Jakob disease (CJD) is a fatal disease that causes degeneration of neural tissue. (a) These brain scans compare a normal brain to one with CJD. (b) Compared to a normal brain, the brain tissue of a CJD patient is full of sponge-like lesions, which result from abnormal formations of prion protein. (credit a (right): modification of work by Dr. Laughlin Dawes; credit b (top): modification of work by Suzanne Wakim; credit b (bottom): modification of work by Centers for Disease Control and Prevention)"
76e41402-f7b5-499d-a197-9b124661cdcb,https://open.oregonstate.education/microbiology/,5.3 Prions,https://open.oregonstate.education/microbiology/chapter/6-3prions/,"Prions are extremely difficult to destroy because they are resistant to heat, chemicals, and radiation. Even standard sterilization procedures do not ensure the destruction of these particles. Currently, there is no treatment or cure for TSE disease, and contaminated meats or infected animals must be handled according to federal guidelines to prevent transmission.",True,Prions,,,,
ad711fc2-b699-4c3f-afdd-110ebdc7cc9c,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,Life Cycle of Viruses with Animal Hosts,False,Life Cycle of Viruses with Animal Hosts,,,,
cba235b9-b9f7-4418-a8e9-a433f44228a7,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"Lytic animal viruses go through the following stages to replicate: attachment, penetration, uncoating, biosynthesis, maturation, and release (see Figure 5.7). After binding to host receptors, animal viruses enter through endocytosis (engulfment by the host cell) or through membrane fusion (viral envelope with the host cell membrane).",True,Life Cycle of Viruses with Animal Hosts,Figure 5.7,5.2 The Viral Life Cycle,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-6.10.png,"Figure 5.7 In influenza virus infection, viral glycoproteins attach the virus to a host epithelial cell. As a result, the virus is engulfed. Viral RNA and viral proteins are made and assembled into new virions that are released by budding."
22cbcb92-960d-44bf-bba5-44561af00394,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"Many viruses are host specific, meaning they only infect a certain type of host; and most viruses only infect certain types of cells within tissues. This specificity is called a tissue tropism.",True,Life Cycle of Viruses with Animal Hosts,,,,
edfc29c5-e32f-43f4-b3d0-09caa66ee94b,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"Animal viruses do not always express their genes using the normal flow of genetic information—from DNA to RNA to protein. Some viruses have a dsDNA genome like cellular organisms and can follow the normal flow. However, others may have ssDNA, dsRNA, or ssRNA genomes. The nature of the genome determines how the genome is replicated and expressed as viral proteins. If a genome is ssDNA, host enzymes will be used to synthesize a second strand that is complementary to the genome strand, thus producing dsDNA. The dsDNA can now be replicated, transcribed, and translated similar to host DNA.",True,Life Cycle of Viruses with Animal Hosts,,,,
7203fda4-2b1b-4c3e-8b01-469ceff599a5,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"If the viral genome is RNA, a different mechanism must be used. Single-stranded RNA viruses such as HIV carry a special enzyme called reverse transcriptase within the capsid that synthesizes a complementary ssDNA (cDNA) copy using the +ssRNA genome as a template. The ssDNA is then made into dsDNA, which can integrate into the host chromosome and become a permanent part of the host. The integrated viral genome is called a provirus. The virus now can remain in the host for a long time to establish a chronic infection.",True,Life Cycle of Viruses with Animal Hosts,,,,
b101e895-aa20-44dc-b977-dc827a3e7175,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,Persistent Infections,False,Persistent Infections,,,,
a3c7ba36-eecd-4b62-b993-cac2054bf0ed,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,Latent Infection,False,Latent Infection,,,,
7eb8787a-c732-4c52-95f2-b5cce1a824c6,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,Not all animal viruses undergo replication by the lytic cycle. There are viruses that are capable of remaining hidden or dormant inside the cell in a process called latency. These types of viruses are known as latent viruses and may cause latent infections. Viruses capable of latency may initially cause an acute infection before becoming dormant.,True,Latent Infection,,,,
f75356ec-1670-4bba-ba1e-b643a7543389,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"For example, the varicella-zoster virus infects many cells throughout the body and causes chickenpox, characterized by a rash of blisters covering the skin. About 10 to 12 days postinfection, the disease resolves and the virus goes dormant, living within nerve-cell ganglia for years. During this time, the virus does not kill the nerve cells or continue replicating. It is not clear why the virus stops replicating within the nerve cells and expresses few viral proteins but, in some cases, typically after many years of dormancy, the virus is reactivated and causes a new disease called shingles (Figure 5.8). Whereas chickenpox affects many areas throughout the body, shingles is a nerve cell-specific disease emerging from the ganglia in which the virus was dormant.",True,Latent Infection,Figure 5.8,5.2 The Viral Life Cycle,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-6.13.png,"Figure 5.8 (a) Varicella-zoster, the virus that causes chickenpox, has an enveloped icosahedral capsid visible in this transmission electron micrograph. Its double-stranded DNA genome becomes incorporated in the host DNA. (b) After a period of latency, the virus can reactivate in the form of shingles, usually manifesting as a painful, localized rash on one side of the body. (credit a: modification of work by Erskine Palmer and B.G. Partin—scale-bar data from Matt Russell; credit b: modification of work by Rosmarie Voegtli)"
1cb25962-e0d9-4daa-b026-3ed9ad5e1679,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"Latent viruses may remain dormant by existing as circular viral genome molecules outside of the host chromosome. Others become proviruses by integrating into the host genome. During dormancy, viruses do not cause any symptoms of disease and may be difficult to detect. A patient may be unaware that he or she is carrying the virus unless a viral diagnostic test has been performed.",True,Latent Infection,,,,
91cd0f3c-5de3-461d-ba4b-f1ca685b105e,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,Chronic Infection,False,Chronic Infection,,,,
f0dede48-078d-4b79-8414-757e175c1c69,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"A chronic infection is a disease with symptoms that are recurrent or persistent over a long time. Some viral infections can be chronic if the body is unable to eliminate the virus. HIV is an example of a virus that produces a chronic infection, often after a long period of latency. Once a person becomes infected with HIV, the virus can be detected in tissues continuously thereafter, but untreated patients often experience no symptoms for years. However, the virus maintains chronic persistence through several mechanisms that interfere with immune function, including preventing expression of viral antigens on the surface of infected cells, altering immune cells themselves, restricting expression of viral genes, and rapidly changing viral antigens through mutation. Eventually, the damage to the immune system results in progression of the disease leading to acquired immunodeficiency syndrome (AIDS). The various mechanisms that HIV uses to avoid being cleared by the immune system are also used by other chronically infecting viruses, including the hepatitis C virus.",True,Chronic Infection,,,,
ecf8b8a3-05bd-4eab-b2a1-4e9f6d256b60,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,Viral Growth Curve,False,Viral Growth Curve,,,,
bfa5bf2b-0db8-42ac-85b2-e8cc2b6036ad,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"Unlike the growth curve for a bacterial population, the growth curve for a virus population over its life cycle does not follow a sigmoidal curve. During the initial stage, an inoculum of virus causes infection. In the eclipse phase, viruses bind and penetrate the cells with no virions detected in the medium. The chief difference that next appears in the viral growth curve compared to a bacterial growth curve occurs when virions are released from the lysed host cell at the same time. Such an occurrence is called a burst, and the number of virions per bacterium released is described as the burst size. In a one-step multiplication curve for bacteriophage, the host cells lyse, releasing many viral particles to the medium, which leads to a very steep rise in viral titer (the number of virions per unit volume). If no viable host cells remain, the viral particles begin to degrade during the decline of the culture (see Figure 5.9).",True,Viral Growth Curve,Figure 5.9,5.2 The Viral Life Cycle,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-6.14.png,"Figure 5.9 The one-step multiplication curve for a bacteriophage population follows three steps: 1) inoculation, during which the virions attach to host cells; 2) eclipse, during which entry of the viral genome occurs; and 3) burst, when sufficient numbers of new virions are produced and emerge from the host cell. The burst size is the maximum number of virions produced per bacterium."
3c7ad1f4-a31d-4db5-83c4-08094355ff4e,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"Further investigations revealed that Duncan had just returned from Liberia, one of the countries in the midst of a severe Ebola epidemic. On September 15, nine days before he showed up at the hospital in Dallas, Duncan had helped transport an Ebola-stricken neighbor to a hospital in Liberia. The hospital continued to treat Duncan, but he died several days after being admitted.",True,Viral Growth Curve,,,,
922dc274-6b4c-4d6e-955e-33c40257bd85,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"The timeline of the Duncan case is indicative of the life cycle of the Ebola virus. The incubation time for Ebola ranges from 2 days to 21 days. Nine days passed between Duncan’s exposure to the virus infection and the appearance of his symptoms. This corresponds, in part, to the eclipse period in the growth of the virus population. During the eclipse phase, Duncan would have been unable to transmit the disease to others. However, once an infected individual begins exhibiting symptoms, the disease becomes very contagious. Ebola virus is transmitted through direct contact with droplets of bodily fluids such as saliva, blood, and vomit. Duncan could conceivably have transmitted the disease to others at any time after he began having symptoms, presumably some time before his arrival at the hospital in Dallas. Once a hospital realizes a patient like Duncan is infected with Ebola virus, the patient is immediately quarantined, and public health officials initiate a back trace to identify everyone with whom a patient like Duncan might have interacted during the period in which he was showing symptoms.",True,Viral Growth Curve,,,,
937c9227-e49c-412d-b53d-11ec6d00e9ff,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"Public health officials were able to track down 10 high-risk individuals (family members of Duncan) and 50 low-risk individuals to monitor them for signs of infection. None contracted the disease. However, one of the nurses charged with Duncan’s care did become infected. This, along with Duncan’s initial misdiagnosis, made it clear that US hospitals needed to provide additional training to medical personnel to prevent a possible Ebola outbreak in the US.",True,Viral Growth Curve,,,,
fc72755f-80b1-4257-a00d-4d93a09262a5,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"For additional information about Ebola, please visit the CDC website (https://www.openstax.org/l/22ebolacdc) .",True,Viral Growth Curve,,,,
77d59d5c-24c6-4f8b-9aa6-1e1ac8805c27,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,Persistent Infections,False,Persistent Infections,,,,
cab606be-2792-40ca-b726-25ad5b049772,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"For example, the varicella-zoster virus infects many cells throughout the body and causes chickenpox, characterized by a rash of blisters covering the skin. About 10 to 12 days postinfection, the disease resolves and the virus goes dormant, living within nerve-cell ganglia for years. During this time, the virus does not kill the nerve cells or continue replicating. It is not clear why the virus stops replicating within the nerve cells and expresses few viral proteins but, in some cases, typically after many years of dormancy, the virus is reactivated and causes a new disease called shingles (Figure 5.8). Whereas chickenpox affects many areas throughout the body, shingles is a nerve cell-specific disease emerging from the ganglia in which the virus was dormant.",True,Persistent Infections,Figure 5.8,5.2 The Viral Life Cycle,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-6.13.png,"Figure 5.8 (a) Varicella-zoster, the virus that causes chickenpox, has an enveloped icosahedral capsid visible in this transmission electron micrograph. Its double-stranded DNA genome becomes incorporated in the host DNA. (b) After a period of latency, the virus can reactivate in the form of shingles, usually manifesting as a painful, localized rash on one side of the body. (credit a: modification of work by Erskine Palmer and B.G. Partin—scale-bar data from Matt Russell; credit b: modification of work by Rosmarie Voegtli)"
f85538cd-f629-4405-9801-212fd1b93087,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"Latent viruses may remain dormant by existing as circular viral genome molecules outside of the host chromosome. Others become proviruses by integrating into the host genome. During dormancy, viruses do not cause any symptoms of disease and may be difficult to detect. A patient may be unaware that he or she is carrying the virus unless a viral diagnostic test has been performed.",True,Persistent Infections,,,,
ace49f44-3d07-4a7b-991c-adf89764c3cd,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"A chronic infection is a disease with symptoms that are recurrent or persistent over a long time. Some viral infections can be chronic if the body is unable to eliminate the virus. HIV is an example of a virus that produces a chronic infection, often after a long period of latency. Once a person becomes infected with HIV, the virus can be detected in tissues continuously thereafter, but untreated patients often experience no symptoms for years. However, the virus maintains chronic persistence through several mechanisms that interfere with immune function, including preventing expression of viral antigens on the surface of infected cells, altering immune cells themselves, restricting expression of viral genes, and rapidly changing viral antigens through mutation. Eventually, the damage to the immune system results in progression of the disease leading to acquired immunodeficiency syndrome (AIDS). The various mechanisms that HIV uses to avoid being cleared by the immune system are also used by other chronically infecting viruses, including the hepatitis C virus.",True,Persistent Infections,,,,
fa7fde71-6bdf-4bd3-9070-2d66c07236ec,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,Viral Growth Curve,False,Viral Growth Curve,,,,
b3921746-506a-47aa-ab93-aba7af4fde29,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"Unlike the growth curve for a bacterial population, the growth curve for a virus population over its life cycle does not follow a sigmoidal curve. During the initial stage, an inoculum of virus causes infection. In the eclipse phase, viruses bind and penetrate the cells with no virions detected in the medium. The chief difference that next appears in the viral growth curve compared to a bacterial growth curve occurs when virions are released from the lysed host cell at the same time. Such an occurrence is called a burst, and the number of virions per bacterium released is described as the burst size. In a one-step multiplication curve for bacteriophage, the host cells lyse, releasing many viral particles to the medium, which leads to a very steep rise in viral titer (the number of virions per unit volume). If no viable host cells remain, the viral particles begin to degrade during the decline of the culture (see Figure 5.9).",True,Viral Growth Curve,Figure 5.9,5.2 The Viral Life Cycle,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-6.14.png,"Figure 5.9 The one-step multiplication curve for a bacteriophage population follows three steps: 1) inoculation, during which the virions attach to host cells; 2) eclipse, during which entry of the viral genome occurs; and 3) burst, when sufficient numbers of new virions are produced and emerge from the host cell. The burst size is the maximum number of virions produced per bacterium."
53c7cbaa-a1e3-4202-8544-1a0982d7d746,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"Further investigations revealed that Duncan had just returned from Liberia, one of the countries in the midst of a severe Ebola epidemic. On September 15, nine days before he showed up at the hospital in Dallas, Duncan had helped transport an Ebola-stricken neighbor to a hospital in Liberia. The hospital continued to treat Duncan, but he died several days after being admitted.",True,Viral Growth Curve,,,,
6ffcad8b-49ec-4c44-b620-bd107c810054,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"The timeline of the Duncan case is indicative of the life cycle of the Ebola virus. The incubation time for Ebola ranges from 2 days to 21 days. Nine days passed between Duncan’s exposure to the virus infection and the appearance of his symptoms. This corresponds, in part, to the eclipse period in the growth of the virus population. During the eclipse phase, Duncan would have been unable to transmit the disease to others. However, once an infected individual begins exhibiting symptoms, the disease becomes very contagious. Ebola virus is transmitted through direct contact with droplets of bodily fluids such as saliva, blood, and vomit. Duncan could conceivably have transmitted the disease to others at any time after he began having symptoms, presumably some time before his arrival at the hospital in Dallas. Once a hospital realizes a patient like Duncan is infected with Ebola virus, the patient is immediately quarantined, and public health officials initiate a back trace to identify everyone with whom a patient like Duncan might have interacted during the period in which he was showing symptoms.",True,Viral Growth Curve,,,,
eb71950b-f54c-4857-a7c6-b2ef98279bf1,https://open.oregonstate.education/microbiology/,5.2 The Viral Life Cycle,https://open.oregonstate.education/microbiology/chapter/6-2the-viral-life-cycle/,"Public health officials were able to track down 10 high-risk individuals (family members of Duncan) and 50 low-risk individuals to monitor them for signs of infection. None contracted the disease. However, one of the nurses charged with Duncan’s care did become infected. This, along with Duncan’s initial misdiagnosis, made it clear that US hospitals needed to provide additional training to medical personnel to prevent a possible Ebola outbreak in the US.",True,Viral Growth Curve,,,,
4fb1cc37-d243-4f0b-828a-28aed1bdc973,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,"Today, we can see viruses using electron microscopes (Figure 5.2) and we know much more about them. Viruses are distinct biological entities; however, their evolutionary origin is still a matter of speculation. In terms of taxonomy, they are not included in the tree of life because they are acellular (not consisting of cells). In order to survive and reproduce, viruses must infect a cellular host, making them obligate intracellular parasites. The genome of a virus enters a host cell and directs the production of the viral components, proteins and nucleic acids, needed to form new virus particles called virions. New virions are made in the host cell by assembly of viral components. The new virions transport the viral genome to another host cell to carry out another round of infection. Table 5.1 summarizes the properties of viruses.",True,Viral Growth Curve,Figure 5.2,5.1 Viruses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-6.2.png,"Figure 5.2 (a) Tobacco mosaic virus (TMV) viewed with transmission electron microscope. (b) Plants infected with tobacco mosaic disease (TMD), caused by TMV. (credit a: modification of work by USDA Agricultural Research Service—scale-bar data from Matt Russell; credit b: modification of work by USDA Forest Service, Department of Plant Pathology Archive North Carolina State University)"
2fc210a8-ae38-4f84-8cc2-856be2a7850d,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,Hosts and Viral Transmission,False,Hosts and Viral Transmission,,,,
031ffcd6-f67a-47db-ac23-93071ff474e3,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,"Viruses can infect every type of host cell, including those of plants, animals, fungi, protists, bacteria, and archaea. Most viruses will only be able to infect the cells of one or a few species of organism. This is called the host range. However, having a wide host range is not common and viruses will typically only infect specific hosts and only specific cell types within those hosts. The viruses that infect bacteria are called bacteriophages, or simply phages. The word phage comes from the Greek word for devour. Other viruses are just identified by their host group, such as animal or plant viruses. Once a cell is infected, the effects of the virus can vary depending on the type of virus.",True,Hosts and Viral Transmission,,,,
b50c1060-c568-4a7c-a8e7-1fb1140e4fc5,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,"Viruses may cause abnormal growth of the cell or cell death, alter the cell’s genome, or cause little noticeable effect in the cell.",True,Hosts and Viral Transmission,,,,
5bea5989-d32f-4e4c-98cc-d8a3415a4f78,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,"Viruses can be transmitted through direct contact, indirect contact with fomites, or through a vector: an animal that transmits a pathogen from one host to another. Arthropods such as mosquitoes, ticks, and flies, are typical vectors for viral diseases, and they may act as mechanical vectors or biological vectors. Mechanical transmission occurs when the arthropod carries a viral pathogen on the outside of its body and transmits it to a new host by physical contact. Biological transmission occurs when the arthropod carries the viral pathogen inside its body and transmits it to the new host through biting.",True,Hosts and Viral Transmission,,,,
3f483338-6123-4ec9-8f11-0b569455b7bd,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,"In humans, a wide variety of viruses are capable of causing various infections and diseases. Some of the deadliest emerging pathogens in humans are viruses, yet we have few treatments or drugs to deal with viral infections, making them difficult to eradicate.",True,Hosts and Viral Transmission,,,,
1873d75d-e88c-4263-96fc-b9d76879c71d,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,"Viruses that can be transmitted from an animal host to a human host can cause zoonoses. For example, the avian influenza virus originates in birds, but can cause disease in humans. Reverse zoonoses are caused by infection of an animal by a virus that originated in a human.",True,Hosts and Viral Transmission,,,,
ce788767-9fe7-4120-964f-013aa96b5301,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,"One potential solution is the use of phage therapy, a procedure that uses bacteria-killing viruses (bacteriophages) to treat bacterial infections. Phage therapy is not a new idea. The discovery of bacteriophages dates back to the early 20th century, and phage therapy was first used in Europe in 1915 by the English bacteriologist Frederick Twort.[3] However, the subsequent discovery of penicillin and other antibiotics led to the near abandonment of this form of therapy, except in the former Soviet Union and a few countries in Eastern Europe. Interest in phage therapy outside of the countries of the former Soviet Union is only recently re-emerging because of the rise in antibiotic-resistant bacteria.[4]",True,Hosts and Viral Transmission,,,,
1fac0ae8-4083-42bf-b4e5-c951f9635c5c,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,"Phage therapy has some advantages over antibiotics in that phages kill only one specific bacterium, whereas antibiotics kill not only the pathogen but also beneficial bacteria of the normal microbiota. Development of new antibiotics is also expensive for drug companies and for patients, especially for those who live in countries with high poverty rates.",True,Hosts and Viral Transmission,,,,
5ad971f1-20e8-47a1-8859-9bee48101410,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,"Phages have also been used to prevent food spoilage. In 2006, the US Food and Drug Administration approved the use of a solution containing six bacteriophages that can be sprayed on lunch meats such as bologna, ham, and turkey to kill Listeria monocytogenes, a bacterium responsible for listeriosis, a form of food poisoning. Some consumers have concerns about the use of phages on foods, however, especially given the rising popularity of organic products. Foods that have been treated with phages must declare “bacteriophage preparation” in the list of ingredients or include a label declaring that the meat has been “treated with antimicrobial solution to reduce microorganisms.”[5]",True,Hosts and Viral Transmission,,,,
c38a2dfb-a487-4a73-b10c-aa450aaac560,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,Viral Structures,False,Viral Structures,,,,
0f544937-666d-4f32-8a2d-72e6c869bc87,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,"The size of a virion can range from 20 nm for small viruses up to 900 nm for typical, large viruses (see Figure 5.4). Recent discoveries, however, have identified new giant viral species, with sizes approaching that of a bacterial cell.[6]In 1935, after the development of the electron microscope, Wendell Stanley was the first scientist to crystallize the structure of the tobacco mosaic virus and discovered that it is composed of RNA and protein. In 1943, he isolated Influenza B virus, which contributed to the development of an influenza (flu) vaccine. Stanley’s discoveries unlocked the mystery of the nature of viruses that had been puzzling scientists for over 40 years and his contributions to the field of virology led to him being awarded the Nobel Prize in 1946.",True,Viral Structures,Figure 5.4,5.1 Viruses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-6.4.png,Figure 5.4 The size of a virus is small relative to the size of most bacterial and eukaryotic cells and their organelles.
4b9889d5-734d-4b38-baef-99b01c242e44,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,There are two categories of viruses based on general composition. Viruses formed from only a nucleic acid and capsid are called naked viruses or nonenveloped viruses. Viruses formed with a nucleic-acid packed capsid surrounded by a lipid layer are called enveloped viruses (see Figure 5.5). The viral envelope is a small portion of phospholipid membrane obtained as the virion buds from a host cell.,True,Viral Structures,Figure 5.5,5.1 Viruses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-6.5.png,Figure 5.5 (a) The naked atadenovirus uses spikes made of glycoproteins from its capsid to bind to host cells. (b) The enveloped human immunodeficiency virus uses spikes made of glycoproteins embedded in its envelope to bind to host cells (credit a “micrograph”: modification of work by NIAID; credit b “micrograph”: modification of work by Centers for Disease Control and Prevention)
33ff78d7-f91b-48d2-929c-87528f945186,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,"Extending outward and away from the capsid on some naked viruses and enveloped viruses are protein structures called spikes. At the tips of these spikes are structures that allow the virus to attach and enter a cell, like the influenza virus hemagglutinin spikes (H) or enzymes like the neuraminidase (N) influenza virus spikes that allow the virus to detach from the cell surface during release of new virions.",True,Viral Structures,,,,
b65c1689-0afb-4a0d-8ec3-1cfb5d351f24,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,"Viruses vary in the shape of their capsids, which can be either helical, polyhedral, or complex. A helical capsid forms the shape of tobacco mosaic virus (TMV), a naked helical virus, and Ebola virus, an enveloped helical virus. The capsid is cylindrical or rod shaped, with the genome fitting just inside the length of the capsid. Polyhedral capsids form the shapes of poliovirus and rhinovirus, and consist of a nucleic acid surrounded by a polyhedral (many- sided) capsid in the form of an icosahedron. An icosahedral capsid is a three-dimensional, 20-sided structure with 12 vertices. These capsids somewhat resemble a soccer ball. Both helical and polyhedral viruses can have envelopes. Some viruses may have features of both polyhedral and helical viruses so they are described as a complex viral shape (see Figure 5.6).",True,Viral Structures,Figure 5.6,5.1 Viruses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-6.6.png,"Figure 5.6 Viral capsids can be (a) helical, (b) polyhedral, or (c) have a complex shape. (credit a “micrograph”: modification of work by USDA ARS; credit b “micrograph”: modification of work by U.S. Department of Energy)"
0ab0d56a-2505-43e6-aa11-952c38ab5d8e,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,Viral Structures,False,Viral Structures,,,,
576a1caf-0534-40d4-9ae3-2afc48d105c1,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,"The size of a virion can range from 20 nm for small viruses up to 900 nm for typical, large viruses (see Figure 5.4). Recent discoveries, however, have identified new giant viral species, with sizes approaching that of a bacterial cell.[6]In 1935, after the development of the electron microscope, Wendell Stanley was the first scientist to crystallize the structure of the tobacco mosaic virus and discovered that it is composed of RNA and protein. In 1943, he isolated Influenza B virus, which contributed to the development of an influenza (flu) vaccine. Stanley’s discoveries unlocked the mystery of the nature of viruses that had been puzzling scientists for over 40 years and his contributions to the field of virology led to him being awarded the Nobel Prize in 1946.",True,Viral Structures,Figure 5.4,5.1 Viruses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-6.4.png,Figure 5.4 The size of a virus is small relative to the size of most bacterial and eukaryotic cells and their organelles.
f1671303-a0d5-461b-829e-08b1e666ffc8,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,There are two categories of viruses based on general composition. Viruses formed from only a nucleic acid and capsid are called naked viruses or nonenveloped viruses. Viruses formed with a nucleic-acid packed capsid surrounded by a lipid layer are called enveloped viruses (see Figure 5.5). The viral envelope is a small portion of phospholipid membrane obtained as the virion buds from a host cell.,True,Viral Structures,Figure 5.5,5.1 Viruses,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-6.5.png,Figure 5.5 (a) The naked atadenovirus uses spikes made of glycoproteins from its capsid to bind to host cells. (b) The enveloped human immunodeficiency virus uses spikes made of glycoproteins embedded in its envelope to bind to host cells (credit a “micrograph”: modification of work by NIAID; credit b “micrograph”: modification of work by Centers for Disease Control and Prevention)
4307f023-9e11-4ef2-8752-30727ffd32c7,https://open.oregonstate.education/microbiology/,5.1 Viruses,https://open.oregonstate.education/microbiology/chapter/6-1viruses/,"Extending outward and away from the capsid on some naked viruses and enveloped viruses are protein structures called spikes. At the tips of these spikes are structures that allow the virus to attach and enter a cell, like the influenza virus hemagglutinin spikes (H) or enzymes like the neuraminidase (N) influenza virus spikes that allow the virus to detach from the cell surface during release of new virions.",True,Viral Structures,,,,
18e0ec4a-b274-4c90-8c17-1d08585c2187,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"Fungi are important to humans in a variety of ways. Both microscopic and macroscopic fungi have medical relevance, with some pathogenic species that can cause mycoses (illnesses caused by fungi). Some pathogenic fungi are opportunistic, meaning that they mainly cause infections when the host’s immune defenses are compromised and do not normally cause illness in healthy individuals. Fungi are important in other ways. They act as decomposers in the environment, and they are critical for the production of certain foods such as cheeses. Fungi are also major sources of antibiotics, such as penicillin from the fungus Penicillium.",True,Viral Structures,,,,
21ee6d99-70fd-4d48-8474-9656efc7cfa0,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,Characteristics of Fungi,False,Characteristics of Fungi,,,,
b8ae9711-a862-48b4-9e63-9229e89a0cc7,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"Fungi have well-defined characteristics that set them apart from other organisms. Most multicellular fungal bodies, commonly called molds, are made up of filaments called hyphae. Hyphae can form a tangled network called a mycelium and form the thallus (body) of fleshy fungi. Hyphae that have walls between the cells are called septate hyphae; hyphae that lack walls and cell membranes between the cells are called nonseptate or coenocytic hyphae. (Figure 4.14).",True,Characteristics of Fungi,Figure 4.14,4.3 Fungi,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-5.25.png,"Figure 4.14 Multicellular fungi (molds) form hyphae, which may be septate or nonseptate. Unicellular fungi (yeasts) cells form pseudohyphae from individual yeast cells."
9023dcc2-1eb1-4284-b342-19e57c6c7571,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"In contrast to molds, yeasts are unicellular fungi. The budding yeasts reproduce asexually by budding off a smaller daughter cell; the resulting cells may sometimes stick together as a short chain or pseudohypha (Figure 4.14).",True,Characteristics of Fungi,Figure 4.14,4.3 Fungi,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-5.25.png,"Figure 4.14 Multicellular fungi (molds) form hyphae, which may be septate or nonseptate. Unicellular fungi (yeasts) cells form pseudohyphae from individual yeast cells."
a30b05e7-3c17-4fd5-9c8c-33d3e8f2fe98,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"Some fungi are dimorphic, having more than one appearance during their life cycle. These dimorphic fungi may be able to appear as yeasts or molds, which can be important for infectivity. They are capable of changing their appearance in response to environmental changes such as nutrient availability or fluctuations in temperature, growing as a mold, for example, at 25 °C (77 °F), and as yeast cells at 37 °C (98.6 °F). This ability helps dimorphic fungi to survive in diverse environments.",True,Characteristics of Fungi,,,,
efed8dd2-8d10-4e32-85da-95cf8a73543b,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"There are notable unique features in fungal cell walls and membranes. Fungal cell walls contain chitin, as opposed to the cellulose found in the cell walls of plants and many protists. Additionally, whereas animals have cholesterol in their cell membranes, fungal cell membranes have different sterols called ergosterols. Ergosterols are often exploited as targets for antifungal drugs.",True,Characteristics of Fungi,,,,
9abfaa29-e901-4bc7-8e98-3f322c12d3bb,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,Fungal life cycles are unique and complex. Fungi reproduce sexually either through cross- or self-fertilization.,True,Characteristics of Fungi,,,,
cdc9da09-40bc-4c87-9bef-87e97cbe8e03,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"Fungi may also exhibit asexual reproduction budding, fragmentation of hyphae, and formation of asexual spores. These spores are specialized cells that, depending on the organism, may have unique characteristics for survival, reproduction, and dispersal. Fungi exhibit several types of asexual spores and these can be important in classification (Figure 4.15).",True,Characteristics of Fungi,Figure 4.15,4.3 Fungi,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-5.28.png,"Figure 4.15 These images show asexually produced spores. (a) This brightfield micrograph shows the release of spores from a sporangium at the end of a hypha called a sporangiophore. The organism is a Mucor sp. fungus, a mold often found indoors. (b) Sporangia grow at the ends of stalks, which appear as the white fuzz seen on this bread mold, Rhizopus stolonifer. The tips of bread mold are the dark, spore-containing sporangia. (credit a: modification of work by Centers for Disease Control and Prevention; credit b right: modification of work by “Andrew”/Flickr)"
e5cda0a3-7761-4785-b9e2-e3a4ec060318,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,Fungal Diversity,False,Fungal Diversity,,,,
e574c8ba-c756-4c6b-88e8-d35d0ca5a0dc,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"The fungi are very diverse, comprising seven major groups. Not all of the seven groups contain pathogens. Some of these groups are generally associated with plants and include plant pathogens. Because of their medical importance, we will focus on Zygomycota, Ascomycota, Basidiomycota, and Microsporidia. Figure 4.17 summarizes the characteristics of these medically important groups of fungi.",True,Fungal Diversity,Figure 4.17,4.3 Fungi,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-5.33.png,"Figure 4.17 Table showing the groups of fungi of particular importance for human health. (Credit “Ascomycota”: modification of work by Dr. Lucille Georg, Centers for Disease Control and Prevention; credit “Microsporidia”: modification of work by Centers for Disease Control and Prevention)"
d6efbb91-5fc6-479a-94b7-8ec1ccf03a4d,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"The Zygomycota (zygomycetes) are mainly saprophytes with coenocytic hyphae and haploid nuclei. They use sporangiospores for asexual reproduction. The group name comes from the zygospores that they use for sexual reproduction, which have hard walls formed from the fusion of reproductive cells from two individuals. Zygomycetes are important for food science and as crop pathogens.",True,Fungal Diversity,,,,
459decaa-80c6-4a20-b40f-83fa996db9a9,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"The Ascomycota include fungi that are used as food (edible mushrooms, morels, and truffles), others that are common causes of food spoilage (bread molds and plant pathogens), and still others that are human pathogens. Some genera of Ascomycota use sexually produced ascospores (Figure 4.16) as well as asexual spores called conidia, but sexual phases have not been discovered or described for others. Some produce an ascus containing ascospores within an ascocarp.",True,Fungal Diversity,Figure 4.16,4.3 Fungi,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-5.29.png,"Figure 4.16 (a) This brightfield micrograph shows ascospores being released from asci in the fungus Talaromyces flavus var. flavus. (b) This electron micrograph shows the conidia (spores) borne on the conidiophore of Aspergillus, a type of toxic fungus found mostly in soil and plants. (c) This brightfield micrograph shows the yeast Candida albicans, the causative agent of candidiasis and thrush. (credit a, b, c: modification of work by Centers for Disease Control and Prevention)"
2a3309d2-038a-482d-a7f3-d6e2a9735605,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"Examples of the Ascomycota include several bread molds and minor pathogens, as well as species capable of causing more serious mycoses. The fungus Aspergillus flavus, a contaminant of nuts and stored grains, produces an aflatoxin that is both a toxin and the most potent known natural carcinogen. Penicillium produces the antibiotic penicillin. Many species of ascomycetes are medically important, causing a range of conditions such as skin infections, respiratory infections, and vaginal yeast infections.",True,Fungal Diversity,,,,
e5d99579-3f14-4343-9f2e-47c1f4a97848,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"The Basidiomycota (basidiomycetes) are fungi that produce basidiospores (spores produced through budding) within fruiting bodies called basidiocarps. They are important as decomposers and as food. This group includes rusts, stinkhorns, puffballs, and mushrooms. Several species are of clinical importance, causing lung infections or other health issues.",True,Fungal Diversity,,,,
0bc315c9-55de-4bf7-9c90-bacec057d7ae,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"Finally, the Microsporidia are unicellular fungi that are obligate intracellular parasites. They lack mitochondria, peroxisomes, and centrioles, but their spores release a unique polar tubule that pierces the host cell membrane to allow the fungus to gain entry into the cell. A number of microsporidia are human pathogens, and infections with microsporidia are called microsporidiosis.",True,Fungal Diversity,,,,
381c18c0-6cd4-46c2-bcb5-eda19d80d345,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"Some fungi are dimorphic, having more than one appearance during their life cycle. These dimorphic fungi may be able to appear as yeasts or molds, which can be important for infectivity. They are capable of changing their appearance in response to environmental changes such as nutrient availability or fluctuations in temperature, growing as a mold, for example, at 25 °C (77 °F), and as yeast cells at 37 °C (98.6 °F). This ability helps dimorphic fungi to survive in diverse environments.",True,Fungal Diversity,,,,
075a9c66-bba0-44b7-a4a2-8abe9d0a839a,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"There are notable unique features in fungal cell walls and membranes. Fungal cell walls contain chitin, as opposed to the cellulose found in the cell walls of plants and many protists. Additionally, whereas animals have cholesterol in their cell membranes, fungal cell membranes have different sterols called ergosterols. Ergosterols are often exploited as targets for antifungal drugs.",True,Fungal Diversity,,,,
bba2e990-e31f-4efe-95b7-8e9ef732d7d2,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,Fungal life cycles are unique and complex. Fungi reproduce sexually either through cross- or self-fertilization.,True,Fungal Diversity,,,,
6ff0836d-58fd-4e5b-9f14-a13a7bfba9d0,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"Fungi may also exhibit asexual reproduction budding, fragmentation of hyphae, and formation of asexual spores. These spores are specialized cells that, depending on the organism, may have unique characteristics for survival, reproduction, and dispersal. Fungi exhibit several types of asexual spores and these can be important in classification (Figure 4.15).",True,Fungal Diversity,Figure 4.15,4.3 Fungi,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-5.28.png,"Figure 4.15 These images show asexually produced spores. (a) This brightfield micrograph shows the release of spores from a sporangium at the end of a hypha called a sporangiophore. The organism is a Mucor sp. fungus, a mold often found indoors. (b) Sporangia grow at the ends of stalks, which appear as the white fuzz seen on this bread mold, Rhizopus stolonifer. The tips of bread mold are the dark, spore-containing sporangia. (credit a: modification of work by Centers for Disease Control and Prevention; credit b right: modification of work by “Andrew”/Flickr)"
1de2f538-2164-4f80-b0b4-68cdccf7b772,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,Fungal Diversity,False,Fungal Diversity,,,,
a1cfe298-5bad-4354-85a7-cd1f82a1f147,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"The fungi are very diverse, comprising seven major groups. Not all of the seven groups contain pathogens. Some of these groups are generally associated with plants and include plant pathogens. Because of their medical importance, we will focus on Zygomycota, Ascomycota, Basidiomycota, and Microsporidia. Figure 4.17 summarizes the characteristics of these medically important groups of fungi.",True,Fungal Diversity,Figure 4.17,4.3 Fungi,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-5.33.png,"Figure 4.17 Table showing the groups of fungi of particular importance for human health. (Credit “Ascomycota”: modification of work by Dr. Lucille Georg, Centers for Disease Control and Prevention; credit “Microsporidia”: modification of work by Centers for Disease Control and Prevention)"
a975ecb8-ff30-4333-a5bd-0306effaa2cb,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"The Zygomycota (zygomycetes) are mainly saprophytes with coenocytic hyphae and haploid nuclei. They use sporangiospores for asexual reproduction. The group name comes from the zygospores that they use for sexual reproduction, which have hard walls formed from the fusion of reproductive cells from two individuals. Zygomycetes are important for food science and as crop pathogens.",True,Fungal Diversity,,,,
63fb2e0a-aa4f-4501-bfe0-ae68c74a6c16,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"The Ascomycota include fungi that are used as food (edible mushrooms, morels, and truffles), others that are common causes of food spoilage (bread molds and plant pathogens), and still others that are human pathogens. Some genera of Ascomycota use sexually produced ascospores (Figure 4.16) as well as asexual spores called conidia, but sexual phases have not been discovered or described for others. Some produce an ascus containing ascospores within an ascocarp.",True,Fungal Diversity,Figure 4.16,4.3 Fungi,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-5.29.png,"Figure 4.16 (a) This brightfield micrograph shows ascospores being released from asci in the fungus Talaromyces flavus var. flavus. (b) This electron micrograph shows the conidia (spores) borne on the conidiophore of Aspergillus, a type of toxic fungus found mostly in soil and plants. (c) This brightfield micrograph shows the yeast Candida albicans, the causative agent of candidiasis and thrush. (credit a, b, c: modification of work by Centers for Disease Control and Prevention)"
002abd14-ace4-4edd-b615-5456a4535bb2,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"Examples of the Ascomycota include several bread molds and minor pathogens, as well as species capable of causing more serious mycoses. The fungus Aspergillus flavus, a contaminant of nuts and stored grains, produces an aflatoxin that is both a toxin and the most potent known natural carcinogen. Penicillium produces the antibiotic penicillin. Many species of ascomycetes are medically important, causing a range of conditions such as skin infections, respiratory infections, and vaginal yeast infections.",True,Fungal Diversity,,,,
3cc6fe15-db58-4bb5-838c-1ce0ebe2729a,https://open.oregonstate.education/microbiology/,4.3 Fungi,https://open.oregonstate.education/microbiology/chapter/5-3fungi/,"Finally, the Microsporidia are unicellular fungi that are obligate intracellular parasites. They lack mitochondria, peroxisomes, and centrioles, but their spores release a unique polar tubule that pierces the host cell membrane to allow the fungus to gain entry into the cell. A number of microsporidia are human pathogens, and infections with microsporidia are called microsporidiosis.",True,Fungal Diversity,,,,
afd94c27-d60a-48d3-80e6-b6daa23365ea,https://open.oregonstate.education/microbiology/,4.2 Parasitic Helminths,https://open.oregonstate.education/microbiology/chapter/5-2parasitic-helminths/,Learning Objectives,False,Learning Objectives,,,,
70f04ff0-cccb-405d-860b-3155c7f3469d,https://open.oregonstate.education/microbiology/,4.2 Parasitic Helminths,https://open.oregonstate.education/microbiology/chapter/5-2parasitic-helminths/,Nematoda (Roundworms),False,Nematoda (Roundworms),,,,
922a2e5b-c259-4a47-a6d6-55cace69fef4,https://open.oregonstate.education/microbiology/,4.2 Parasitic Helminths,https://open.oregonstate.education/microbiology/chapter/5-2parasitic-helminths/,"Phylum Nematoda (the roundworms) is a diverse group containing more than 15,000 species, of which several are important human parasites (Figure 4.11). These unsegmented worms have a full digestive system even when parasitic. Some are common intestinal parasites, and their eggs can sometimes be identified in feces or around the anus of infected individuals. Ascaris lumbricoides is the largest nematode intestinal parasite found in humans; females may reach lengths greater than 1 meter. A. lumbricoides is also very widespread, even in developed nations, although it is now a relatively uncommon problem in the United States. It may cause symptoms ranging from relatively mild (such as a cough and mild abdominal pain) to severe (such as intestinal blockage and impaired growth).",True,Nematoda (Roundworms),Figure 4.11,4.2 Parasitic Helminths,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-5.19.png,"Figure 4.11 A micrograph of the nematode Enterobius vermicularis, also known as the pinworm. (credit: modification of work by Centers for Disease Control and Prevention)"
e28507f4-c6fd-4c7c-b27a-c034552cba93,https://open.oregonstate.education/microbiology/,4.2 Parasitic Helminths,https://open.oregonstate.education/microbiology/chapter/5-2parasitic-helminths/,"Trichinellosis, also called trichinosis, caused by Trichinella spiralis, is contracted by consuming undercooked meat, which releases the larvae and allows them to encyst in muscles. Infection can cause fever, muscle pains, and digestive system problems; severe infections can lead to lack of coordination, breathing and heart problems, and even death. Finally, heartworm in dogs and other animals is caused by a nematode.",True,Nematoda (Roundworms),,,,
155fab10-4b3a-42f1-b824-938cf44f6bb1,https://open.oregonstate.education/microbiology/,4.2 Parasitic Helminths,https://open.oregonstate.education/microbiology/chapter/5-2parasitic-helminths/,Platyhelminths (Flatworms),False,Platyhelminths (Flatworms),,,,
3279f615-a9ed-4433-a9ba-ff6490937eca,https://open.oregonstate.education/microbiology/,4.2 Parasitic Helminths,https://open.oregonstate.education/microbiology/chapter/5-2parasitic-helminths/,"Phylum Platyhelminthes (the platyhelminths) are flatworms. This group includes the flukes and tapeworms, as medically important parasites.",True,Platyhelminths (Flatworms),,,,
98116788-c17d-4b99-8e68-39f7a5060e67,https://open.oregonstate.education/microbiology/,4.2 Parasitic Helminths,https://open.oregonstate.education/microbiology/chapter/5-2parasitic-helminths/,"The flukes (trematodes) are nonsegmented flatworms that have an oral sucker (Figure 4.12) (and sometimes a second ventral sucker) and attach to the inner walls of intestines, lungs, large blood vessels, or the liver. Trematodes have complex life cycles, often with multiple hosts. Several important examples are the liver flukes, the intestinal fluke, and the oriental lung fluke. Schistosomiasis is a serious parasitic disease, considered second in the scale of its impact on human populations only to malaria. Immature forms burrow through the skin into the blood. They migrate to the lungs, then to the liver and, later, other organs. Symptoms include anemia, malnutrition, fever, abdominal pain, fluid buildup, and sometimes death.",True,Platyhelminths (Flatworms),Figure 4.12,4.2 Parasitic Helminths,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-5.21.png,"Figure 4.12 (a) The oral sucker is visible on the anterior end of this liver fluke, Opisthorchis viverrini. (b) This micrograph shows the scolex of the cestode Taenia solium, also known as the pork tapeworm. The visible suckers and hooks allow the worm to attach itself to the inner wall of the intestine. (credit a: modification of work by Sripa B, Kaewkes S, Sithithaworn P, Mairiang E, Laha T, and Smout M; credit b: modification of work by Centers for Disease Control and Prevention)"
37f31917-d4f3-4296-a66f-7d70610071e8,https://open.oregonstate.education/microbiology/,4.2 Parasitic Helminths,https://open.oregonstate.education/microbiology/chapter/5-2parasitic-helminths/,Learning Objectives,False,Learning Objectives,,,,
603cc86c-ba5e-4866-b3fb-dd9155e4ee33,https://open.oregonstate.education/microbiology/,4.2 Parasitic Helminths,https://open.oregonstate.education/microbiology/chapter/5-2parasitic-helminths/,Nematoda (Roundworms),False,Nematoda (Roundworms),,,,
8936b998-bbe8-4815-82ed-7aad3c636e39,https://open.oregonstate.education/microbiology/,4.2 Parasitic Helminths,https://open.oregonstate.education/microbiology/chapter/5-2parasitic-helminths/,"Phylum Nematoda (the roundworms) is a diverse group containing more than 15,000 species, of which several are important human parasites (Figure 4.11). These unsegmented worms have a full digestive system even when parasitic. Some are common intestinal parasites, and their eggs can sometimes be identified in feces or around the anus of infected individuals. Ascaris lumbricoides is the largest nematode intestinal parasite found in humans; females may reach lengths greater than 1 meter. A. lumbricoides is also very widespread, even in developed nations, although it is now a relatively uncommon problem in the United States. It may cause symptoms ranging from relatively mild (such as a cough and mild abdominal pain) to severe (such as intestinal blockage and impaired growth).",True,Nematoda (Roundworms),Figure 4.11,4.2 Parasitic Helminths,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-5.19.png,"Figure 4.11 A micrograph of the nematode Enterobius vermicularis, also known as the pinworm. (credit: modification of work by Centers for Disease Control and Prevention)"
c5b2a585-da52-4577-a11e-9a6b06bc5410,https://open.oregonstate.education/microbiology/,4.2 Parasitic Helminths,https://open.oregonstate.education/microbiology/chapter/5-2parasitic-helminths/,"Phylum Platyhelminthes (the platyhelminths) are flatworms. This group includes the flukes and tapeworms, as medically important parasites.",True,Nematoda (Roundworms),,,,
44b7ed5b-10f4-473f-a11c-d76049975ab0,https://open.oregonstate.education/microbiology/,4.2 Parasitic Helminths,https://open.oregonstate.education/microbiology/chapter/5-2parasitic-helminths/,"The flukes (trematodes) are nonsegmented flatworms that have an oral sucker (Figure 4.12) (and sometimes a second ventral sucker) and attach to the inner walls of intestines, lungs, large blood vessels, or the liver. Trematodes have complex life cycles, often with multiple hosts. Several important examples are the liver flukes, the intestinal fluke, and the oriental lung fluke. Schistosomiasis is a serious parasitic disease, considered second in the scale of its impact on human populations only to malaria. Immature forms burrow through the skin into the blood. They migrate to the lungs, then to the liver and, later, other organs. Symptoms include anemia, malnutrition, fever, abdominal pain, fluid buildup, and sometimes death.",True,Nematoda (Roundworms),Figure 4.12,4.2 Parasitic Helminths,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-5.21.png,"Figure 4.12 (a) The oral sucker is visible on the anterior end of this liver fluke, Opisthorchis viverrini. (b) This micrograph shows the scolex of the cestode Taenia solium, also known as the pork tapeworm. The visible suckers and hooks allow the worm to attach itself to the inner wall of the intestine. (credit a: modification of work by Sripa B, Kaewkes S, Sithithaworn P, Mairiang E, Laha T, and Smout M; credit b: modification of work by Centers for Disease Control and Prevention)"
5ed86a4d-f3e8-4363-8f64-7fb582d4e7eb,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,Characteristics of Protists,False,Characteristics of Protists,,,,
43d18f1e-bbf6-4366-9847-4b2d609b6c26,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"The word protist is a historical term that is now used informally to refer to a diverse group of microscopic eukaryotic organisms. It is not considered a formal taxonomic term because the organisms it describes do not have a shared evolutionary origin. Historically, the protists were informally grouped into the “animal-like” protozoans, the “plant- like” algae, and the “fungus-like” protists such as water molds. These three groups of protists differ greatly in terms of their basic characteristics. For example, algae are photosynthetic organisms that can be unicellular or multicellular. Protozoa, on the other hand, are nonphotosynthetic, motile organisms that are always unicellular. Other informal terms may also be used to describe various groups of protists. For example, microorganisms that drift or float in water, moved by currents, are referred to as plankton. Types of plankton include zooplankton, which are motile and nonphotosynthetic, and phytoplankton, which are photosynthetic.",True,Characteristics of Protists,,,,
0f5f2f94-2f48-4efe-892a-546422afb046,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"Protozoans inhabit a wide variety of habitats, both aquatic and terrestrial. Many are free-living, while others are parasitic, carrying out a life cycle within a host or hosts and potentially causing illness. There are also beneficial symbionts that provide metabolic services to their hosts. During the feeding and growth part of their life cycle, they are called trophozoites; these feed on small particulate food sources such as bacteria. While some types of protozoa exist exclusively in the trophozoite form, others can develop from trophozoite to an encapsulated cyst stage when environmental conditions are too harsh for the trophozoite. A cyst is a cell with a protective wall.",True,Characteristics of Protists,,,,
8fcd6df5-5bb2-4181-87ea-230428bd822a,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"Protozoans have a variety of reproductive mechanisms. Some protozoans reproduce asexually and others reproduce sexually; still others are capable of both sexual and asexual reproduction. In protozoans, asexual reproduction occurs by binary fission, budding, or schizogony. In schizogony, the nucleus of a cell divides multiple times before the cell divides into many smaller cells. Protozoans may also reproduce sexually, which increases genetic diversity and can lead to complex life cycles.",True,Characteristics of Protists,,,,
0a49efea-9c1f-44d1-92dd-ef235f8f82d3,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"All protozoans have a plasma membrane, or plasmalemma. Many protists have whip-like flagella or hair-like cilia made of microtubules that can be used for locomotion (Figure 4.3). Other protists use cytoplasmic extensions known as pseudopodia (“false feet”) to attach the cell to a surface; they then allow cytoplasm to flow into the extension, thus moving themselves forward.",True,Characteristics of Protists,Figure 4.3,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-5.5.png,Figure 4.3 (a) Paramecium spp. have hair-like appendages called cilia for locomotion. (b) Amoeba spp. use lobe- like pseudopodia to anchor the cell to a solid surface and pull forward. (c) Euglena spp. use a whip-like structure called a flagellum to propel the cell.
26cd1870-6e84-4b32-bcab-91ef5afe811e,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"Protozoans have a variety of unique organelles and sometimes lack organelles found in other cells. Some have contractile vacuoles, organelles that can be used to move water out of the cell for osmotic regulation (salt and water balance) (Figure 4.3). Mitochondria may be absent in parasites or altered to kinetoplastids (modified mitochondria) or hydrogenosomes.",True,Characteristics of Protists,Figure 4.3,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-5.5.png,Figure 4.3 (a) Paramecium spp. have hair-like appendages called cilia for locomotion. (b) Amoeba spp. use lobe- like pseudopodia to anchor the cell to a solid surface and pull forward. (c) Euglena spp. use a whip-like structure called a flagellum to propel the cell.
df3bbdce-4faa-4753-814f-3a6d503d1510,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,Taxonomy of Protists,False,Taxonomy of Protists,,,,
81ec45a4-31fb-4925-9487-cffc86002139,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"The protists are a polyphyletic group, meaning they lack a shared evolutionary origin. Since the current taxonomy is based on evolutionary history (as determined by biochemistry, morphology, and genetics), protists are scattered across many different taxonomic groups within the domain Eukarya. Eukarya is currently divided into six supergroups that are further divided into subgroups, as illustrated in (Figure 4.4). In this section, we will primarily be concerned with the subgroups Formicata, Parabasalids, Eugoenozoans, Apicomplexan, Ciliates, and Entamoebas, ; since these subgroups include many protozoans of clinical significance. Figure 4.5 and Figure 4.6 summarize the characteristics of each supergroup and subgroup and list representatives of each.",True,Taxonomy of Protists,Figure 4.4,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-4.4-1.png,"Figure 4.4 This tree shows a proposed classification of the domain Eukarya based on evolutionary relationships. Currently, the domain Eukarya is divided into six supergroups. Within each supergroup are multiple kingdoms. Dotted lines indicate suggested evolutionary relationships that remain under debate. The subgroups with members of clinical relevance have a start next to them."
f65bf71f-2222-4fdd-9271-1af897e04a7d,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,Subgroup Entamoeba,False,Subgroup Entamoeba,,,,
fe1dfd00-95c8-488a-ad7c-1d3a4eb2b6e9,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,Subgroups Apicomplexan and Ciliates,False,Subgroups Apicomplexan and Ciliates,,,,
1e78e88e-618f-430b-bdc0-e1e2b100375e,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"The subgroups Apicomplexan and Ciliates are united by similar origins of its members’ plastids. The apicomplexans are intra- or extracellular parasites that have an apical complex at one end of the cell. The apical complex is a concentration of organelles, vacuoles, and microtubules that allows the parasite to enter host cells (Figure 4.7). Many are capable of infecting a variety of animal cells, from insects to livestock to humans, and their life cycles often depend on transmission between multiple hosts.",True,Subgroups Apicomplexan and Ciliates,Figure 4.7,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-5.12.png,Figure 4.7 (a) Apicomplexans are parasitic protists. They have a characteristic apical complex that enables them to infect host cells. (b) A colorized electron microscope image of a Plasmodium sporozoite. (credit b: modification of work by Ute Frevert)
51a5ea73-1f94-4fec-b33e-954a2fac9c32,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"The ciliates (Ciliaphora) are a large, very diverse group characterized by the presence of cilia on their cell surface. Although the cilia may be used for locomotion, they are often used for feeding, as well, and some forms are nonmotile. Balantidium coli (Figure 4.8) is the only parasitic ciliate that affects humans by causing intestinal illness, although it rarely causes serious medical issues except in the immunocompromised (those having a weakened immune system). Perhaps the most familiar ciliate is Paramecium, a motile organism with a clearly visible cytostome and cytoproct that is often studied in biology laboratories (Figure 4.9).",True,Subgroups Apicomplexan and Ciliates,Figure 4.8,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-5.13.png,"Figure 4.8 This specimen of the ciliate Balantidium coli is a trophozoite form isolated from the gut of a primate. B. coli is the only ciliate capable of parasitizing humans. (credit: modification of work by Kouassi RYW, McGraw SW, Yao PK, Abou-Bacar A, Brunet J, Pesson B, Bonfoh B, N’goran EK & Candolfi E)"
403d90d3-42c2-48ce-9374-61d45d28f5db,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"Ciliates are able to reproduce through conjugation, in which two cells attach to each other and exchange DNA, forming cells that are genetically different from each other and from their previous versions.",True,Subgroups Apicomplexan and Ciliates,,,,
7a358b2d-8c4c-49f1-8b25-8b51a56231f9,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"Subgroups Fornicata, Parabasalia, Euglenozoa",False,"Subgroups Fornicata, Parabasalia, Euglenozoa",,,,
4e82791b-6caa-43e9-b504-99118c32a97a,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"The subgroups Fornicata, Parabasalia, and Euglenozoa includes primitive eukaryotes and many parasites with limited metabolic abilities. These organisms have complex cell shapes and structures, often including a depression on the surface of the cell. The Fornicata lack mitochondria but have flagella. Parabasalia are frequent animal endosymbionts; they live in the guts of animals like termites and cockroaches. They have basal bodies and modified mitochondria (kinetoplastids). They also have a large, complex cell structure with an undulating membrane and often have many flagella. The trichomonads (a subgroup of the Parabasalia) include pathogens such as Trichomonas vaginalis, which causes the human sexually transmitted disease trichomoniasis.",True,"Subgroups Fornicata, Parabasalia, Euglenozoa",,,,
0188dea7-fc65-48cf-b230-45dc0bb7a46f,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"The Euglenozoa are common in the environment and include photosynthetic and nonphotosynthetic species. Their cells have two flagella, a pellicle, a stigma (eyespot) to sense light, and chloroplasts for photosynthesis (Figure 4.10). Members of the genus Euglena are typically not pathogenic, but include the trypanosomes, which are parasitic pathogens that cause African sleeping sickness and American trypanosomiasis (Chagas disease). These tropical diseases are spread by insect bites. The early symptoms include confusion, difficulty sleeping, and lack of coordination. Left untreated, it is fatal.",True,"Subgroups Fornicata, Parabasalia, Euglenozoa",Figure 4.10,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-5.17.png,"Figure 4.10 (a) This illustration of a Euglena shows the characteristic structures, such as the stigma and flagellum. (b) The pellicle, under the cell membrane, gives the cell its distinctive shape and is visible in this image as delicate parallel striations over the surface of the entire cell (especially visible over the grey contractile vacuole). (credit a: modification of work by Claudio Miklos; credit b: modification of work by David Shykind)"
1bc74f5d-01ab-42d1-9234-4688af0f87b4,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,Characteristics of Protists,False,Characteristics of Protists,,,,
1de864eb-bd21-46f5-9e81-05a4cc2fb23b,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"Protozoans inhabit a wide variety of habitats, both aquatic and terrestrial. Many are free-living, while others are parasitic, carrying out a life cycle within a host or hosts and potentially causing illness. There are also beneficial symbionts that provide metabolic services to their hosts. During the feeding and growth part of their life cycle, they are called trophozoites; these feed on small particulate food sources such as bacteria. While some types of protozoa exist exclusively in the trophozoite form, others can develop from trophozoite to an encapsulated cyst stage when environmental conditions are too harsh for the trophozoite. A cyst is a cell with a protective wall.",True,Characteristics of Protists,,,,
a871a05d-e995-4693-b73b-c94ba9bb1c57,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"Protozoans have a variety of reproductive mechanisms. Some protozoans reproduce asexually and others reproduce sexually; still others are capable of both sexual and asexual reproduction. In protozoans, asexual reproduction occurs by binary fission, budding, or schizogony. In schizogony, the nucleus of a cell divides multiple times before the cell divides into many smaller cells. Protozoans may also reproduce sexually, which increases genetic diversity and can lead to complex life cycles.",True,Characteristics of Protists,,,,
9682a147-4ab3-41a5-98d4-de744255975d,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"All protozoans have a plasma membrane, or plasmalemma. Many protists have whip-like flagella or hair-like cilia made of microtubules that can be used for locomotion (Figure 4.3). Other protists use cytoplasmic extensions known as pseudopodia (“false feet”) to attach the cell to a surface; they then allow cytoplasm to flow into the extension, thus moving themselves forward.",True,Characteristics of Protists,Figure 4.3,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-5.5.png,Figure 4.3 (a) Paramecium spp. have hair-like appendages called cilia for locomotion. (b) Amoeba spp. use lobe- like pseudopodia to anchor the cell to a solid surface and pull forward. (c) Euglena spp. use a whip-like structure called a flagellum to propel the cell.
502ec6dd-62ba-4921-91df-336992e397a4,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"Protozoans have a variety of unique organelles and sometimes lack organelles found in other cells. Some have contractile vacuoles, organelles that can be used to move water out of the cell for osmotic regulation (salt and water balance) (Figure 4.3). Mitochondria may be absent in parasites or altered to kinetoplastids (modified mitochondria) or hydrogenosomes.",True,Characteristics of Protists,Figure 4.3,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-5.5.png,Figure 4.3 (a) Paramecium spp. have hair-like appendages called cilia for locomotion. (b) Amoeba spp. use lobe- like pseudopodia to anchor the cell to a solid surface and pull forward. (c) Euglena spp. use a whip-like structure called a flagellum to propel the cell.
0bd37b66-4e10-4aca-ba4f-e6c1f03e2967,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,Taxonomy of Protists,False,Taxonomy of Protists,,,,
f1e954b8-df27-4e09-bbf9-7ce78e2b7abe,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"The protists are a polyphyletic group, meaning they lack a shared evolutionary origin. Since the current taxonomy is based on evolutionary history (as determined by biochemistry, morphology, and genetics), protists are scattered across many different taxonomic groups within the domain Eukarya. Eukarya is currently divided into six supergroups that are further divided into subgroups, as illustrated in (Figure 4.4). In this section, we will primarily be concerned with the subgroups Formicata, Parabasalids, Eugoenozoans, Apicomplexan, Ciliates, and Entamoebas, ; since these subgroups include many protozoans of clinical significance. Figure 4.5 and Figure 4.6 summarize the characteristics of each supergroup and subgroup and list representatives of each.",True,Taxonomy of Protists,Figure 4.4,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-4.4-1.png,"Figure 4.4 This tree shows a proposed classification of the domain Eukarya based on evolutionary relationships. Currently, the domain Eukarya is divided into six supergroups. Within each supergroup are multiple kingdoms. Dotted lines indicate suggested evolutionary relationships that remain under debate. The subgroups with members of clinical relevance have a start next to them."
47707092-bba6-4e34-a41d-dbebcdca34bd,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"The subgroups Apicomplexan and Ciliates are united by similar origins of its members’ plastids. The apicomplexans are intra- or extracellular parasites that have an apical complex at one end of the cell. The apical complex is a concentration of organelles, vacuoles, and microtubules that allows the parasite to enter host cells (Figure 4.7). Many are capable of infecting a variety of animal cells, from insects to livestock to humans, and their life cycles often depend on transmission between multiple hosts.",True,Taxonomy of Protists,Figure 4.7,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-5.12.png,Figure 4.7 (a) Apicomplexans are parasitic protists. They have a characteristic apical complex that enables them to infect host cells. (b) A colorized electron microscope image of a Plasmodium sporozoite. (credit b: modification of work by Ute Frevert)
157279cd-33cd-4417-a9a0-99f769675b5d,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"The ciliates (Ciliaphora) are a large, very diverse group characterized by the presence of cilia on their cell surface. Although the cilia may be used for locomotion, they are often used for feeding, as well, and some forms are nonmotile. Balantidium coli (Figure 4.8) is the only parasitic ciliate that affects humans by causing intestinal illness, although it rarely causes serious medical issues except in the immunocompromised (those having a weakened immune system). Perhaps the most familiar ciliate is Paramecium, a motile organism with a clearly visible cytostome and cytoproct that is often studied in biology laboratories (Figure 4.9).",True,Taxonomy of Protists,Figure 4.8,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-5.13.png,"Figure 4.8 This specimen of the ciliate Balantidium coli is a trophozoite form isolated from the gut of a primate. B. coli is the only ciliate capable of parasitizing humans. (credit: modification of work by Kouassi RYW, McGraw SW, Yao PK, Abou-Bacar A, Brunet J, Pesson B, Bonfoh B, N’goran EK & Candolfi E)"
405a4f7a-02ce-41bd-bf90-0a23ab546c4f,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"Ciliates are able to reproduce through conjugation, in which two cells attach to each other and exchange DNA, forming cells that are genetically different from each other and from their previous versions.",True,Taxonomy of Protists,,,,
bb80e040-4e1a-4437-b780-92fc5052111d,https://open.oregonstate.education/microbiology/,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/microbiology/chapter/5-1unicellular-eukaryotic-parasites/,"The Euglenozoa are common in the environment and include photosynthetic and nonphotosynthetic species. Their cells have two flagella, a pellicle, a stigma (eyespot) to sense light, and chloroplasts for photosynthesis (Figure 4.10). Members of the genus Euglena are typically not pathogenic, but include the trypanosomes, which are parasitic pathogens that cause African sleeping sickness and American trypanosomiasis (Chagas disease). These tropical diseases are spread by insect bites. The early symptoms include confusion, difficulty sleeping, and lack of coordination. Left untreated, it is fatal.",True,Taxonomy of Protists,Figure 4.10,4.1 Unicellular Eukaryotic Parasites,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-5.17.png,"Figure 4.10 (a) This illustration of a Euglena shows the characteristic structures, such as the stigma and flagellum. (b) The pellicle, under the cell membrane, gives the cell its distinctive shape and is visible in this image as delicate parallel striations over the surface of the entire cell (especially visible over the grey contractile vacuole). (credit a: modification of work by Claudio Miklos; credit b: modification of work by David Shykind)"
fc5d907a-c2a6-4de7-9bea-eba38b10dbbc,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,Learning Objectives,False,Learning Objectives,,,,
56bf01f8-d5a7-436d-a3e8-405e4ce7b081,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Microorganisms differ from each other not only in size, but also in structure, habitat, metabolism, and many other characteristics. While we typically think of microorganisms as being unicellular, there are also many multicellular organisms that are too small to be seen without a microscope. Some microbes, such as viruses, are even acellular (not composed of cells).",True,Learning Objectives,,,,
0aaea719-0b2c-4e8b-b57f-bfb74e02592e,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Microorganisms are found in each of the three domains of life: Archaea, Bacteria, and Eukarya. Microbes within the domains Bacteria and Archaea are all prokaryotes (their cells lack a nucleus), whereas microbes in the domain Eukarya are eukaryotes (their cells have a nucleus). Some microorganisms, such as viruses, do not fall within any of the three domains of life. In this section, we will briefly introduce each of the broad groups of microbes. Later chapters will go into greater depth about the diverse species within each group.",True,Learning Objectives,,,,
8d90c924-cf86-4b47-a242-0c08c56cf76e,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,Prokaryotic Microorganisms,False,Prokaryotic Microorganisms,,,,
7e51e093-6ef6-40f8-b434-3ac5d903add3,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Bacteria are found in nearly every habitat on earth, including within and on humans. Most bacteria are harmless or helpful, but some are pathogens, causing disease in humans and other animals. Bacteria are prokaryotic because their genetic material (DNA) is not housed within a true nucleus. Most bacteria have cell walls that contain peptidoglycan.",True,Prokaryotic Microorganisms,,,,
aa2eaefb-1ffb-49be-81e3-35a42b5f79d1,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Bacteria are often described in terms of their general shape. Common shapes include spherical (coccus), rod-shaped (bacillus), or curved (spirillum, spirochete, or vibrio). Figure 1.11 shows examples of these shapes.",True,Prokaryotic Microorganisms,Figure 1.11,1.3 Types of Microorganisms,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-1.13.png,"Figure 1.11 Common bacterial shapes. Note how coccobacillus is a combination of spherical (coccus) and rod- shaped (bacillus). (credit “Coccus”: modification of work by Janice Haney Carr, Centers for Disease Control and Prevention; credit “Coccobacillus”: modification of work by Janice Carr, Centers for Disease Control and Prevention; credit “Spirochete”: Centers for Disease Control and Prevention)"
106f2e9b-45e8-4794-93de-52ac9aec2191,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"They have a wide range of metabolic capabilities and can grow in a variety of environments, using different combinations of nutrients. Some bacteria are photosynthetic, such as oxygenic cyanobacteria and anoxygenic green sulfur and green nonsulfur bacteria; these bacteria use energy derived from sunlight, and fix carbon dioxide for growth. Other types of bacteria are nonphotosynthetic, obtaining their energy from organic or inorganic compounds in their environment.",True,Prokaryotic Microorganisms,,,,
ce67389e-2138-4adc-adcd-bf3c89f6655a,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Archaea are also unicellular prokaryotic organisms. Archaea and bacteria have different evolutionary histories, as well as significant differences in genetics, metabolic pathways, and the composition of their cell walls and membranes. Unlike most bacteria, archaeal cell walls do not contain peptidoglycan, but their cell walls are often composed of a similar substance called pseudopeptidoglycan. Like bacteria, archaea are found in nearly every habitat on earth, even extreme environments that are very cold, very hot, very basic, or very acidic (Figure 1.12). Some archaea live in the human body, but none have been shown to be human pathogens.",True,Prokaryotic Microorganisms,Figure 1.12,1.3 Types of Microorganisms,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-1.14.png,"Figure 1.12 Some archaea live in extreme environments, such as the Morning Glory pool, a hot spring in Yellowstone National Park. The color differences in the pool result from the different communities of microbes that are able to thrive at various water temperatures."
fbdf9f88-fdd8-4d93-bff0-6500d4564e57,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,Eukaryotic Microorganisms,False,Eukaryotic Microorganisms,,,,
52d6853c-f6cf-45de-8406-deb3adc65b39,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"The domain Eukarya contains all eukaryotes, including uni- or multicellular eukaryotes such as protists, fungi, plants, and animals. The major defining characteristic of eukaryotes is that their cells contain a nucleus.",True,Eukaryotic Microorganisms,,,,
9e43558b-7c4d-41d8-a6b8-9e1e577bd9e3,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Protists are an informal grouping of eukaryotes that are not plants, animals, or fungi. Algae and protozoa are examples of protists.",True,Eukaryotic Microorganisms,,,,
fbdc3204-8d9e-46f6-a14b-38ea6caf321c,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Algae (singular: alga) are protists that can be either unicellular or multicellular and vary widely in size, appearance, and habitat (Figure 1.13). Their cells are surrounded by cell walls made of cellulose, a type of carbohydrate. Algae are photosynthetic organisms that extract energy from the sun and release oxygen and carbohydrates into their environment. Because other organisms can use their waste products for energy, algae are important parts of many ecosystems. Many consumer products contain ingredients derived from algae, such as carrageenan or alginic acid, which are found in some brands of ice cream, salad dressing, beverages, lipstick, and toothpaste. A derivative of algae also plays a prominent role in the microbiology laboratory. Agar, a gel derived from algae, can be mixed with various nutrients and used to grow microorganisms in a Petri dish. Algae are also being developed as a possible source for biofuels.",True,Eukaryotic Microorganisms,Figure 1.13,1.3 Types of Microorganisms,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-1.15.png,"Figure 1.13 Assorted diatoms, a kind of algae, live in annual sea ice in McMurdo Sound, Antarctica. Diatoms range in size from 2 μm to 200 μm and are visualized here using light microscopy. (credit: modification of work by National Oceanic and Atmospheric Administration)"
96b2cf06-043e-4f76-907f-7ceaf1fd856b,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Fungi (singular: fungus) are also eukaryotes. Some multicellular fungi, such as mushrooms, resemble plants, but they are actually quite different. Fungi are not photosynthetic, and their cell walls are usually made out of chitin rather than cellulose.",True,Eukaryotic Microorganisms,,,,
699422dc-552b-4317-8e88-5b2f1f2e2d0d,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Unicellular fungi—yeasts—are included within the study of microbiology. There are more than 1000 known species. Yeasts are found in many different environments, from the deep sea to the human navel. Some yeasts have beneficial uses, such as causing bread to rise and beverages to ferment; but yeasts can also cause food to spoil. Some even cause diseases, such as vaginal yeast infections and oral thrush (Figure 1.15).",True,Eukaryotic Microorganisms,Figure 1.15,1.3 Types of Microorganisms,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-1.17.png,"Figure 1.15 Candida albicans is a unicellular fungus, or yeast. It is the causative agent of vaginal yeast infections as well as oral thrush, a yeast infection of the mouth that commonly afflicts infants. C. albicans has a morphology similar to that of coccus bacteria; however, yeast is a eukaryotic organism (note the nuclei) and is much larger. (credit: modification of work by Centers for Disease Control and Prevention)"
459950f0-c3cb-4450-ab6a-90ae15589af9,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Other fungi of interest to microbiologists are multicellular organisms called molds. Molds are made up of long filaments that form visible colonies (Figure 1.16). Molds are found in many different environments, from soil to rotting food to dank bathroom corners. Molds play a critical role in the decomposition of dead plants and animals. Some molds can cause allergies, and others produce disease-causing metabolites called mycotoxins. Molds have been used to make pharmaceuticals, including penicillin, which is one of the most commonly prescribed antibiotics, and cyclosporine, used to prevent organ rejection following a transplant.",True,Eukaryotic Microorganisms,Figure 1.16,1.3 Types of Microorganisms,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-1.18.png,"Figure 1.16 Large colonies of microscopic fungi can often be observed with the naked eye, as seen on the surface of these moldy oranges."
fa8e58e0-0079-4fdc-afb5-762f0a85d203,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,Helminths,False,Helminths,,,,
9015dced-9161-4207-a0cf-a0bd92339749,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Multicellular parasitic worms called helminths are not technically microorganisms, as most are large enough to see without a microscope. However, these worms fall within the field of microbiology because diseases caused by helminths involve microscopic eggs and larvae. One example of a helminth is the guinea worm, or Dracunculus medinensis, which causes dizziness, vomiting, diarrhea, and painful ulcers on the legs and feet when the worm works its way out of the skin (Figure 1.17). Infection typically occurs after a person drinks water containing water fleas infected by guinea-worm larvae. In the mid-1980s, there were an estimated 3.5 million cases of guinea-worm disease, but the disease has been largely eradicated. In 2014, there were only 126 cases reported, thanks to the coordinated efforts of the World Health Organization (WHO) and other groups committed to improvements in drinking water sanitation.[1][2]",True,Helminths,Figure 1.17,1.3 Types of Microorganisms,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-1.19.png,"Figure 1.17 (a) The beef tapeworm, Taenia saginata, infects both cattle and humans. T. saginata eggs are microscopic (around 50 µm), but adult worms like the one shown here can reach 4–10 m, taking up residence in the digestive system. (b) An adult guinea worm, Dracunculus medinensis, is removed through a lesion in the patient’s skin by winding it around a matchstick. (credit a, b: modification of work by Centers for Disease Control and Prevention)"
75ffab7e-aa60-4e18-8b4d-00960c111532,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,Viruses,False,Viruses,,,,
6b3ab769-0f45-434b-a8fb-2dbefd86c497,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Viruses are acellular microorganisms, which means they are not composed of cells. Essentially, a virus consists of proteins and genetic material—either DNA or RNA, but never both—that are inert outside of a host organism. However, by incorporating themselves into a host cell, viruses are able to co-opt the host’s cellular mechanisms to multiply and infect other hosts.",True,Viruses,,,,
9cdd693b-16d4-4cd0-8a87-9c6b5ba99ed7,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Viruses can infect all types of cells, from human cells to the cells of other microorganisms. In humans, viruses are responsible for numerous diseases, from the common cold to deadly Ebola (Figure 1.18). However, many viruses do not cause disease.",True,Viruses,Figure 1.18,1.3 Types of Microorganisms,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-1.20.jpg,"Figure 1.18 (a) Members of the Coronavirus family can cause respiratory infections like the common cold, severe acute respiratory syndrome (SARS), and Middle East respiratory syndrome (MERS). Here they are viewed under a transmission electron microscope (TEM). (b) Ebolavirus, a member of the Filovirus family, as visualized using a TEM. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by Thomas W. Geisbert)"
5cb7e392-12d3-493e-9dd9-0fe3e526ed1e,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,Microbiology as a Field of Study,False,Microbiology as a Field of Study,,,,
7e3648d9-4d04-448a-a94d-7686d3235eeb,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Microbiology is a broad term that encompasses the study of all different types of microorganisms. But in practice, microbiologists tend to specialize in one of several subfields. For example, bacteriology is the study of bacteria; mycology is the study of fungi; protozoology is the study of protozoa; parasitology is the study of helminths and other parasites; and virology is the study of viruses (Figure 1.18). Immunology, the study of the immune system, is often included in the study of microbiology because host–pathogen interactions are central to our understanding of infectious disease processes. Microbiologists can also specialize in certain areas of microbiology, such as clinical microbiology, environmental microbiology, applied microbiology, or food microbiology.",True,Microbiology as a Field of Study,Figure 1.18,1.3 Types of Microorganisms,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-1.20.jpg,"Figure 1.18 (a) Members of the Coronavirus family can cause respiratory infections like the common cold, severe acute respiratory syndrome (SARS), and Middle East respiratory syndrome (MERS). Here they are viewed under a transmission electron microscope (TEM). (b) Ebolavirus, a member of the Filovirus family, as visualized using a TEM. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by Thomas W. Geisbert)"
c6eb23cc-bb5d-483a-a47f-d9ef32eb7f6b,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"In this textbook, we are primarily concerned with clinical applications of microbiology, but since the various subfields of microbiology are highly interrelated, we will often discuss applications that are not strictly clinical.",True,Microbiology as a Field of Study,,,,
c28e073c-6d37-41c7-a06e-13381f5e56be,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,Learning Objectives,False,Learning Objectives,,,,
49c49281-2c27-47d6-a440-9e4fbac8d6bc,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Microorganisms differ from each other not only in size, but also in structure, habitat, metabolism, and many other characteristics. While we typically think of microorganisms as being unicellular, there are also many multicellular organisms that are too small to be seen without a microscope. Some microbes, such as viruses, are even acellular (not composed of cells).",True,Learning Objectives,,,,
681c0c19-0d22-427b-8293-ac48494a0c96,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Microorganisms are found in each of the three domains of life: Archaea, Bacteria, and Eukarya. Microbes within the domains Bacteria and Archaea are all prokaryotes (their cells lack a nucleus), whereas microbes in the domain Eukarya are eukaryotes (their cells have a nucleus). Some microorganisms, such as viruses, do not fall within any of the three domains of life. In this section, we will briefly introduce each of the broad groups of microbes. Later chapters will go into greater depth about the diverse species within each group.",True,Learning Objectives,,,,
d49ea0ce-4123-457b-9272-028abd19c5a0,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,Prokaryotic Microorganisms,False,Prokaryotic Microorganisms,,,,
b54b8a90-3e16-408d-bb37-e58acd3ef760,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Bacteria are found in nearly every habitat on earth, including within and on humans. Most bacteria are harmless or helpful, but some are pathogens, causing disease in humans and other animals. Bacteria are prokaryotic because their genetic material (DNA) is not housed within a true nucleus. Most bacteria have cell walls that contain peptidoglycan.",True,Prokaryotic Microorganisms,,,,
6a6ab6d0-ce65-44b1-a7d9-1ae80d4adc0d,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Bacteria are often described in terms of their general shape. Common shapes include spherical (coccus), rod-shaped (bacillus), or curved (spirillum, spirochete, or vibrio). Figure 1.11 shows examples of these shapes.",True,Prokaryotic Microorganisms,Figure 1.11,1.3 Types of Microorganisms,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-1.13.png,"Figure 1.11 Common bacterial shapes. Note how coccobacillus is a combination of spherical (coccus) and rod- shaped (bacillus). (credit “Coccus”: modification of work by Janice Haney Carr, Centers for Disease Control and Prevention; credit “Coccobacillus”: modification of work by Janice Carr, Centers for Disease Control and Prevention; credit “Spirochete”: Centers for Disease Control and Prevention)"
22530cd9-0334-4ddd-a470-fbad2cb5cd60,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"They have a wide range of metabolic capabilities and can grow in a variety of environments, using different combinations of nutrients. Some bacteria are photosynthetic, such as oxygenic cyanobacteria and anoxygenic green sulfur and green nonsulfur bacteria; these bacteria use energy derived from sunlight, and fix carbon dioxide for growth. Other types of bacteria are nonphotosynthetic, obtaining their energy from organic or inorganic compounds in their environment.",True,Prokaryotic Microorganisms,,,,
97446238-0a71-4d0e-b9ce-721d60e5ddfa,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Archaea are also unicellular prokaryotic organisms. Archaea and bacteria have different evolutionary histories, as well as significant differences in genetics, metabolic pathways, and the composition of their cell walls and membranes. Unlike most bacteria, archaeal cell walls do not contain peptidoglycan, but their cell walls are often composed of a similar substance called pseudopeptidoglycan. Like bacteria, archaea are found in nearly every habitat on earth, even extreme environments that are very cold, very hot, very basic, or very acidic (Figure 1.12). Some archaea live in the human body, but none have been shown to be human pathogens.",True,Prokaryotic Microorganisms,Figure 1.12,1.3 Types of Microorganisms,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-1.14.png,"Figure 1.12 Some archaea live in extreme environments, such as the Morning Glory pool, a hot spring in Yellowstone National Park. The color differences in the pool result from the different communities of microbes that are able to thrive at various water temperatures."
64d34bb6-8e9b-422a-a45a-7abdc58fe287,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,Eukaryotic Microorganisms,False,Eukaryotic Microorganisms,,,,
1b1c67d9-431a-4023-b056-488266407d7f,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"The domain Eukarya contains all eukaryotes, including uni- or multicellular eukaryotes such as protists, fungi, plants, and animals. The major defining characteristic of eukaryotes is that their cells contain a nucleus.",True,Eukaryotic Microorganisms,,,,
6181b438-0885-436c-9653-9d5f05671c4e,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Protists are an informal grouping of eukaryotes that are not plants, animals, or fungi. Algae and protozoa are examples of protists.",True,Eukaryotic Microorganisms,,,,
916475d8-ca6b-47bd-acb1-02035aa1c4f2,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Algae (singular: alga) are protists that can be either unicellular or multicellular and vary widely in size, appearance, and habitat (Figure 1.13). Their cells are surrounded by cell walls made of cellulose, a type of carbohydrate. Algae are photosynthetic organisms that extract energy from the sun and release oxygen and carbohydrates into their environment. Because other organisms can use their waste products for energy, algae are important parts of many ecosystems. Many consumer products contain ingredients derived from algae, such as carrageenan or alginic acid, which are found in some brands of ice cream, salad dressing, beverages, lipstick, and toothpaste. A derivative of algae also plays a prominent role in the microbiology laboratory. Agar, a gel derived from algae, can be mixed with various nutrients and used to grow microorganisms in a Petri dish. Algae are also being developed as a possible source for biofuels.",True,Eukaryotic Microorganisms,Figure 1.13,1.3 Types of Microorganisms,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-1.15.png,"Figure 1.13 Assorted diatoms, a kind of algae, live in annual sea ice in McMurdo Sound, Antarctica. Diatoms range in size from 2 μm to 200 μm and are visualized here using light microscopy. (credit: modification of work by National Oceanic and Atmospheric Administration)"
b874ddb9-fb5f-441e-a18b-341988b5dc32,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Fungi (singular: fungus) are also eukaryotes. Some multicellular fungi, such as mushrooms, resemble plants, but they are actually quite different. Fungi are not photosynthetic, and their cell walls are usually made out of chitin rather than cellulose.",True,Eukaryotic Microorganisms,,,,
7d40865b-0a82-4696-8625-3975d66a8211,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Unicellular fungi—yeasts—are included within the study of microbiology. There are more than 1000 known species. Yeasts are found in many different environments, from the deep sea to the human navel. Some yeasts have beneficial uses, such as causing bread to rise and beverages to ferment; but yeasts can also cause food to spoil. Some even cause diseases, such as vaginal yeast infections and oral thrush (Figure 1.15).",True,Eukaryotic Microorganisms,Figure 1.15,1.3 Types of Microorganisms,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-1.17.png,"Figure 1.15 Candida albicans is a unicellular fungus, or yeast. It is the causative agent of vaginal yeast infections as well as oral thrush, a yeast infection of the mouth that commonly afflicts infants. C. albicans has a morphology similar to that of coccus bacteria; however, yeast is a eukaryotic organism (note the nuclei) and is much larger. (credit: modification of work by Centers for Disease Control and Prevention)"
b1c58e69-daac-4753-b347-5e29e1c32163,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,Helminths,False,Helminths,,,,
79319621-f768-4335-9133-b96d667119f2,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Multicellular parasitic worms called helminths are not technically microorganisms, as most are large enough to see without a microscope. However, these worms fall within the field of microbiology because diseases caused by helminths involve microscopic eggs and larvae. One example of a helminth is the guinea worm, or Dracunculus medinensis, which causes dizziness, vomiting, diarrhea, and painful ulcers on the legs and feet when the worm works its way out of the skin (Figure 1.17). Infection typically occurs after a person drinks water containing water fleas infected by guinea-worm larvae. In the mid-1980s, there were an estimated 3.5 million cases of guinea-worm disease, but the disease has been largely eradicated. In 2014, there were only 126 cases reported, thanks to the coordinated efforts of the World Health Organization (WHO) and other groups committed to improvements in drinking water sanitation.[1][2]",True,Helminths,Figure 1.17,1.3 Types of Microorganisms,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-1.19.png,"Figure 1.17 (a) The beef tapeworm, Taenia saginata, infects both cattle and humans. T. saginata eggs are microscopic (around 50 µm), but adult worms like the one shown here can reach 4–10 m, taking up residence in the digestive system. (b) An adult guinea worm, Dracunculus medinensis, is removed through a lesion in the patient’s skin by winding it around a matchstick. (credit a, b: modification of work by Centers for Disease Control and Prevention)"
264f5548-6c45-459b-bc60-6486767a8413,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,Viruses,False,Viruses,,,,
bf37dfd0-0903-411f-9534-37d2c0ad450e,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Viruses are acellular microorganisms, which means they are not composed of cells. Essentially, a virus consists of proteins and genetic material—either DNA or RNA, but never both—that are inert outside of a host organism. However, by incorporating themselves into a host cell, viruses are able to co-opt the host’s cellular mechanisms to multiply and infect other hosts.",True,Viruses,,,,
a6f6a189-1b33-49fe-b66c-e5dc41fdfb8b,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Viruses can infect all types of cells, from human cells to the cells of other microorganisms. In humans, viruses are responsible for numerous diseases, from the common cold to deadly Ebola (Figure 1.18). However, many viruses do not cause disease.",True,Viruses,Figure 1.18,1.3 Types of Microorganisms,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-1.20.jpg,"Figure 1.18 (a) Members of the Coronavirus family can cause respiratory infections like the common cold, severe acute respiratory syndrome (SARS), and Middle East respiratory syndrome (MERS). Here they are viewed under a transmission electron microscope (TEM). (b) Ebolavirus, a member of the Filovirus family, as visualized using a TEM. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by Thomas W. Geisbert)"
383177be-1703-4c84-b88e-68504b0ea049,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,Microbiology as a Field of Study,False,Microbiology as a Field of Study,,,,
e07bfb30-9763-471d-a3a1-6822463d75ec,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"Microbiology is a broad term that encompasses the study of all different types of microorganisms. But in practice, microbiologists tend to specialize in one of several subfields. For example, bacteriology is the study of bacteria; mycology is the study of fungi; protozoology is the study of protozoa; parasitology is the study of helminths and other parasites; and virology is the study of viruses (Figure 1.18). Immunology, the study of the immune system, is often included in the study of microbiology because host–pathogen interactions are central to our understanding of infectious disease processes. Microbiologists can also specialize in certain areas of microbiology, such as clinical microbiology, environmental microbiology, applied microbiology, or food microbiology.",True,Microbiology as a Field of Study,Figure 1.18,1.3 Types of Microorganisms,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig.-1.20.jpg,"Figure 1.18 (a) Members of the Coronavirus family can cause respiratory infections like the common cold, severe acute respiratory syndrome (SARS), and Middle East respiratory syndrome (MERS). Here they are viewed under a transmission electron microscope (TEM). (b) Ebolavirus, a member of the Filovirus family, as visualized using a TEM. (credit a: modification of work by Centers for Disease Control and Prevention; credit b: modification of work by Thomas W. Geisbert)"
dfd7f3b1-b52d-4c8d-895f-b40d3bd132d2,https://open.oregonstate.education/microbiology/,1.3 Types of Microorganisms,https://open.oregonstate.education/microbiology/chapter/1-3types-of-microorganisms/,"In this textbook, we are primarily concerned with clinical applications of microbiology, but since the various subfields of microbiology are highly interrelated, we will often discuss applications that are not strictly clinical.",True,Microbiology as a Field of Study,,,,
925b7c08-463d-4c6d-bdad-abe55ab0d6ef,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,The Science of Taxonomy,False,The Science of Taxonomy,,,,
eee72024-34f9-4726-be61-56d72dbd3b74,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"Taxonomy is the classification, description, identification, and naming of living organisms. Classification is the practice of organizing organisms into different groups based on their shared characteristics. The most famous early taxonomist was a Swedish botanist, zoologist, and physician named Carolus Linnaeus (1701–1778). In 1735, Linnaeus published Systema Naturae, an 11-page booklet in which he proposed the Linnaean taxonomy, a system of categorizing and naming organisms using a standard format so scientists could discuss organisms using consistent terminology. He continued to revise and add to the book, which grew into multiple volumes (Figure 1.6).",True,The Science of Taxonomy,Figure 1.6,1.2 A Systematic Approach,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-1.8-1.png,"Figure 1.6 Swedish botanist, zoologist, and physician Carolus Linnaeus developed a new system for categorizing plants and animals. In this 1853 portrait by Hendrik Hollander, Linnaeus is holding a twinflower, named Linnaea borealis in his honor."
fffe4d3e-b250-492d-a783-bca803e707f9,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"In his taxonomy, Linnaeus divided the natural world into three kingdoms: animal, plant, and mineral (the mineral kingdom was later abandoned). Within the animal and plant kingdoms, he grouped organisms using a hierarchy of increasingly specific levels and sublevels based on their similarities. The names of the levels in Linnaeus’s original taxonomy were kingdom, class, order, family, genus (plural: genera), and species. Species was, and continues to be, the most specific and basic taxonomic unit.",True,The Science of Taxonomy,,,,
d7a20314-be5e-4765-ad80-303eccb2f41d,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,Evolving Trees of Life (Phylogenies),False,Evolving Trees of Life (Phylogenies),,,,
320b4104-f8ba-4923-babd-7a7bee3cbf0e,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"With advances in technology, other scientists gradually made refinements to the Linnaean system and eventually created new systems for classifying organisms. In the 1800s, there was a growing interest in developing taxonomies that took into account the evolutionary relationships, or phylogenies, of all different species of organisms on earth. One way to depict these relationships is via a diagram called a phylogenetic tree (or tree of life). In these diagrams, groups of organisms are arranged by how closely related they are thought to be. In early phylogenetic trees, the relatedness of organisms was inferred by their visible similarities, such as the presence or absence of hair or the number of limbs. Now, the analysis is more complicated. Today, phylogenic analyses include genetic, biochemical, and embryological comparisons, as will be discussed later in this chapter.",True,Evolving Trees of Life (Phylogenies),,,,
9b389008-3b8e-41df-a82d-3a715726a076,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"Linnaeus’s tree of life contained just two main branches for all living things: the animal and plant kingdoms. In 1866, Ernst Haeckel, a German biologist, philosopher, and physician, proposed another kingdom, Protista, for unicellular organisms (Figure 1.7). He later proposed a fourth kingdom, Monera, for unicellular organisms whose cells lack nuclei, like bacteria.",True,Evolving Trees of Life (Phylogenies),Figure 1.7,1.2 A Systematic Approach,https://open.oregonstate.education/app/uploads/sites/8/2019/06/b0de7b2434ccb8cece67d06d598ea539c716f852.jpeg,"Figure 1.7 Ernst Haeckel’s rendering of the tree of life, from his 1866 book General Morphology of Organisms, contained three kingdoms: Plantae, Protista, and Animalia. He later added a fourth kingdom, Monera, for unicellular organisms lacking a nucleus."
dcc0257d-cdc0-4318-93d4-ca8ad3309b3f,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,Figure 1.8 shows how the tree of life has changed over time. Note that viruses are not found in any of these trees. That is because they are not made up of cells and thus it is difficult to determine where they would fit into a tree of life.,True,Evolving Trees of Life (Phylogenies),Figure 1.8,1.2 A Systematic Approach,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-1.10.png,"Figure 1.8 This timeline shows how the shape of the tree of life has changed over the centuries. Even today, the taxonomy of living organisms is continually being reevaluated and refined with advances in technology."
9b5d980f-44db-4dd5-83f4-b9df7e348182,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,The Role of Genetics in Modern Taxonomy,False,The Role of Genetics in Modern Taxonomy,,,,
93a7221b-1b5d-4c05-9bcf-1a941559c9d3,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"Haeckel’s and Whittaker’s trees presented hypotheses about the phylogeny of different organisms based on readily observable characteristics. But the advent of molecular genetics in the late 20th century revealed other ways to organize phylogenetic trees. Genetic methods allow for a standardized way to compare all living organisms without relying on observable characteristics that can often be subjective. Modern taxonomy relies heavily on comparing the nucleic acids (deoxyribonucleic acid [DNA] or ribonucleic acid [RNA]) or proteins from different organisms. The more similar the nucleic acids and proteins are between two organisms, the more closely related they are considered to be.",True,The Role of Genetics in Modern Taxonomy,,,,
5918c445-573d-44db-bc7c-6492f1b9144a,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"In the 1970s, American microbiologist Carl Woese discovered what appeared to be a “living record” of the evolution of organisms. He and his collaborator George Fox created a genetics-based tree of life based on similarities and differences they observed in the gene sequences coding for small subunit ribosomal RNA (rRNA) of different organisms. In the process, they discovered that a certain type of bacteria, called archaebacteria (now known simply as archaea), were significantly different from other bacteria and eukaryotes in terms of their small subunit rRNA gene sequences. To accommodate this difference, they created a tree with three Domains above the level of Kingdom: Archaea, Bacteria, and Eukarya (Figure 1.9). Analysis of small subunit rRNA gene sequences suggests archaea, bacteria, and eukaryotes all evolved from a common ancestral cell type. The tree is skewed to show a closer evolutionary relationship between Archaea and Eukarya than they have to Bacteria.",True,The Role of Genetics in Modern Taxonomy,Figure 1.9,1.2 A Systematic Approach,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-1.11.png,"Figure 1.9 Woese and Fox’s phylogenetic tree contains three domains: Bacteria, Archaea, and Eukarya. Domains Archaea and Bacteria contain all prokaryotic organisms, and Eukarya contains all eukaryotic organisms. (credit: modification of work by Eric Gaba)"
149cb310-ca7f-4727-a556-d4b43446ef7a,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"Scientists continue to use analysis of RNA, DNA, and proteins to determine how organisms are related. One interesting, and complicating, discovery is that of horizontal gene transfer—when a gene of one species is absorbed into another organism’s genome. Horizontal gene transfer is especially common in microorganisms and can make it difficult to determine how organisms are evolutionarily related. Consequently, some scientists now think in terms of “webs of life” rather than “trees of life.”",True,The Role of Genetics in Modern Taxonomy,,,,
4fb9305f-bcda-49c1-a922-cb3d504de561,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,Naming Microbes,False,Naming Microbes,,,,
9c8993db-2a3b-4a0a-a05a-8f938a0d519a,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"In developing his taxonomy, Linnaeus used a system of binomial nomenclature, a two-word naming system for identifying organisms by genus and specific epithet. For example, modern humans are in the genus Homo and have the specific epithet name sapiens, so their scientific name in binomial nomenclature is Homo sapiens. In binomial nomenclature, the genus part of the name is always capitalized; it is followed by the specific epithet name, which is not capitalized. Both names are italicized. When referring to the species of humans, the binomial nomenclature would be Homo sapiens.",True,Naming Microbes,,,,
d6094399-424f-49b4-938a-81ad88d2af49,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"Taxonomic names in the 18th through 20th centuries were typically derived from Latin, since that was the common language used by scientists when taxonomic systems were first created. Today, newly discovered organisms can be given names derived from Latin, Greek, or English. Sometimes these names reflect some distinctive trait of the organism; in other cases, microorganisms are named after the scientists who discovered them. The archaeon Haloquadratum walsbyi is an example of both of these naming schemes. The genus, Haloquadratum, describes the microorganism’s saltwater habitat (halo is derived from the Greek word for “salt”) as well as the arrangement of its square cells, which are arranged in square clusters of four cells (quadratum is Latin for “foursquare”). The species, walsbyi, is named after Anthony Edward Walsby, the microbiologist who discovered Haloquadratum walsbyi in in 1980. While it might seem easier to give an organism a common descriptive name—like a red- headed woodpecker—we can imagine how that could become problematic. What happens when another species of woodpecker with red head coloring is discovered? The systematic nomenclature scientists use eliminates this potential problem by assigning each organism a single, unique two-word name that is recognized by scientists all over the world.",True,Naming Microbes,,,,
45004bdb-7515-4698-858c-c32988b8be10,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"In this text, we will typically abbreviate an organism’s genus and species after its first mention. The abbreviated form is simply the first initial of the genus, followed by a period and the full name of the species. For example, the bacterium Escherichia coli is shortened to E. coli in its abbreviated form. You will encounter this same convention in other scientific texts as well.",True,Naming Microbes,,,,
4ee4acd0-f42d-451f-a2ef-36480ef91c1f,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"One pathogenic (disease-causing) E. coli strain that you may have heard of is E. coli O157:H7. In humans, infection from E. coli O157:H7 can cause abdominal cramps and diarrhea. Infection usually originates from contaminated water or food, particularly raw vegetables and undercooked meat. In the 1990s, there were several large outbreaks of E. coli O157:H7 thought to have originated in undercooked hamburgers.",True,Naming Microbes,,,,
acb37b3e-0e7b-4aa7-a100-895e9c62b4ae,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"While E. coli O157:H7 and some other strains have given E. coli a bad name, most E. coli strains do not cause disease. In fact, some can be helpful. Different strains of E. coli found naturally in our gut help us digest our food, provide us with some needed chemicals, and fight against pathogenic microbes.",True,Naming Microbes,,,,
93e8d188-1b6d-4908-85b8-acd5f7a23f5d,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,Evolving Trees of Life (Phylogenies),False,Evolving Trees of Life (Phylogenies),,,,
2c9f6baa-d381-4e38-b06c-71d454160428,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"Linnaeus’s tree of life contained just two main branches for all living things: the animal and plant kingdoms. In 1866, Ernst Haeckel, a German biologist, philosopher, and physician, proposed another kingdom, Protista, for unicellular organisms (Figure 1.7). He later proposed a fourth kingdom, Monera, for unicellular organisms whose cells lack nuclei, like bacteria.",True,Evolving Trees of Life (Phylogenies),Figure 1.7,1.2 A Systematic Approach,https://open.oregonstate.education/app/uploads/sites/8/2019/06/b0de7b2434ccb8cece67d06d598ea539c716f852.jpeg,"Figure 1.7 Ernst Haeckel’s rendering of the tree of life, from his 1866 book General Morphology of Organisms, contained three kingdoms: Plantae, Protista, and Animalia. He later added a fourth kingdom, Monera, for unicellular organisms lacking a nucleus."
171fe3a4-4398-465d-b402-509b4e3ae668,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,Figure 1.8 shows how the tree of life has changed over time. Note that viruses are not found in any of these trees. That is because they are not made up of cells and thus it is difficult to determine where they would fit into a tree of life.,True,Evolving Trees of Life (Phylogenies),Figure 1.8,1.2 A Systematic Approach,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-1.10.png,"Figure 1.8 This timeline shows how the shape of the tree of life has changed over the centuries. Even today, the taxonomy of living organisms is continually being reevaluated and refined with advances in technology."
a921ebdc-dadb-4c41-9f8a-e44766227588,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,The Role of Genetics in Modern Taxonomy,False,The Role of Genetics in Modern Taxonomy,,,,
1e51bff8-a9e6-4962-88e9-c1cdbfe505a0,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"In the 1970s, American microbiologist Carl Woese discovered what appeared to be a “living record” of the evolution of organisms. He and his collaborator George Fox created a genetics-based tree of life based on similarities and differences they observed in the gene sequences coding for small subunit ribosomal RNA (rRNA) of different organisms. In the process, they discovered that a certain type of bacteria, called archaebacteria (now known simply as archaea), were significantly different from other bacteria and eukaryotes in terms of their small subunit rRNA gene sequences. To accommodate this difference, they created a tree with three Domains above the level of Kingdom: Archaea, Bacteria, and Eukarya (Figure 1.9). Analysis of small subunit rRNA gene sequences suggests archaea, bacteria, and eukaryotes all evolved from a common ancestral cell type. The tree is skewed to show a closer evolutionary relationship between Archaea and Eukarya than they have to Bacteria.",True,The Role of Genetics in Modern Taxonomy,Figure 1.9,1.2 A Systematic Approach,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-1.11.png,"Figure 1.9 Woese and Fox’s phylogenetic tree contains three domains: Bacteria, Archaea, and Eukarya. Domains Archaea and Bacteria contain all prokaryotic organisms, and Eukarya contains all eukaryotic organisms. (credit: modification of work by Eric Gaba)"
16632252-47e0-450b-aa6f-b44d5f00380b,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"Scientists continue to use analysis of RNA, DNA, and proteins to determine how organisms are related. One interesting, and complicating, discovery is that of horizontal gene transfer—when a gene of one species is absorbed into another organism’s genome. Horizontal gene transfer is especially common in microorganisms and can make it difficult to determine how organisms are evolutionarily related. Consequently, some scientists now think in terms of “webs of life” rather than “trees of life.”",True,The Role of Genetics in Modern Taxonomy,,,,
c08ac34d-074c-42e0-bd02-a23d8fc5e6e1,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,Naming Microbes,False,Naming Microbes,,,,
88119e0c-8921-4bc2-b986-5a4d4ea2b4ad,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"Taxonomic names in the 18th through 20th centuries were typically derived from Latin, since that was the common language used by scientists when taxonomic systems were first created. Today, newly discovered organisms can be given names derived from Latin, Greek, or English. Sometimes these names reflect some distinctive trait of the organism; in other cases, microorganisms are named after the scientists who discovered them. The archaeon Haloquadratum walsbyi is an example of both of these naming schemes. The genus, Haloquadratum, describes the microorganism’s saltwater habitat (halo is derived from the Greek word for “salt”) as well as the arrangement of its square cells, which are arranged in square clusters of four cells (quadratum is Latin for “foursquare”). The species, walsbyi, is named after Anthony Edward Walsby, the microbiologist who discovered Haloquadratum walsbyi in in 1980. While it might seem easier to give an organism a common descriptive name—like a red- headed woodpecker—we can imagine how that could become problematic. What happens when another species of woodpecker with red head coloring is discovered? The systematic nomenclature scientists use eliminates this potential problem by assigning each organism a single, unique two-word name that is recognized by scientists all over the world.",True,Naming Microbes,,,,
74be6cb4-95ef-4af2-80ef-dbbb69660394,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"In this text, we will typically abbreviate an organism’s genus and species after its first mention. The abbreviated form is simply the first initial of the genus, followed by a period and the full name of the species. For example, the bacterium Escherichia coli is shortened to E. coli in its abbreviated form. You will encounter this same convention in other scientific texts as well.",True,Naming Microbes,,,,
5bdb87b9-eebe-4a0c-ac00-20fc55f6db5e,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"One pathogenic (disease-causing) E. coli strain that you may have heard of is E. coli O157:H7. In humans, infection from E. coli O157:H7 can cause abdominal cramps and diarrhea. Infection usually originates from contaminated water or food, particularly raw vegetables and undercooked meat. In the 1990s, there were several large outbreaks of E. coli O157:H7 thought to have originated in undercooked hamburgers.",True,Naming Microbes,,,,
4fbfccc8-7b6c-4d3c-8f71-2acf8d3b4c8d,https://open.oregonstate.education/microbiology/,1.2 A Systematic Approach,https://open.oregonstate.education/microbiology/chapter/1-2-a-systematic-approach/,"While E. coli O157:H7 and some other strains have given E. coli a bad name, most E. coli strains do not cause disease. In fact, some can be helpful. Different strains of E. coli found naturally in our gut help us digest our food, provide us with some needed chemicals, and fight against pathogenic microbes.",True,Naming Microbes,,,,
9fda17ee-c96e-4269-8661-dbd987481d4b,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,Learning Objectives,False,Learning Objectives,,,,
5ff85c30-6c2e-4c7d-9dd2-06e5bf6527d3,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"Humans have been living with—and using—microorganisms for much longer than they have been able to see them. Historical evidence suggests that humans have had some notion of microbial life since prehistoric times and have used that knowledge to develop foods as well as prevent and treat disease. In this section, we will explore some of the historical applications of microbiology as well as the early beginnings of microbiology as a science.",True,Learning Objectives,,,,
248f2fca-3d8c-4fd6-b8cb-8d60957bd531,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,Fermented Foods and Beverages,False,Fermented Foods and Beverages,,,,
80ba72a1-5b68-4dd9-8733-7542945fd584,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"People across the world have enjoyed fermented foods and beverages like beer, wine, bread, yogurt, cheese, and pickled vegetables for all of recorded history. Discoveries from several archeological sites suggest that even prehistoric people took advantage of fermentation to preserve and enhance the taste of food. Archaeologists studying pottery jars from a Neolithic village in China found that people were making a fermented beverage from rice, honey, and fruit as early as 7000 BC.[1]",True,Fermented Foods and Beverages,,,,
4e7e27ed-78d9-47cd-b8ba-03b1ac455adb,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"Production of these foods and beverages requires microbial fermentation, a process that uses bacteria, mold, or yeast to convert sugars (carbohydrates) to alcohol, gases, and organic acids (Figure 1.2). While it is likely that people first learned about fermentation by accident—perhaps by drinking old milk that had curdled or old grape juice that had fermented—they later learned to harness the power of fermentation to make products like bread, cheese, and wine.",True,Fermented Foods and Beverages,Figure 1.2,1.1 What Our Ancestors Knew,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-1.3.png,"Figure 1.2 A microscopic view of Saccharomyces cerevisiae, the yeast responsible for making bread rise (left). Yeast is a microorganism. Its cells metabolize the carbohydrates in flour (middle) and produce carbon dioxide, which causes the bread to rise (right). (credit middle: modification of work by Janus Sandsgaard; credit right: modification of work by “MDreibelbis”/Flickr)"
dc8cbdaa-c9db-4daa-95ae-5f02ff720fd3,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"Several ancient civilizations appear to have had some understanding that disease could be transmitted by things they could not see. This is especially evident in historical attempts to contain the spread of disease. For example, the Bible refers to the practice of quarantining people with leprosy and other diseases, suggesting that people understood that diseases could be communicable. Ironically, while leprosy is communicable, it is also a disease that progresses slowly. This means that people were likely quarantined after they had already spread the disease to others.",True,Fermented Foods and Beverages,,,,
37a36a21-55e4-4a18-8df8-df65c9b4040c,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"The ancient Greeks attributed disease to bad air, mal’aria, which they called “miasmatic odors.” They developed hygiene practices that built on this idea. The Romans also believed in the miasma hypothesis and created a complex sanitation infrastructure to deal with sewage. In Rome, they built aqueducts, which brought fresh water into the city, and a giant sewer, the Cloaca Maxima, which carried waste away and into the river Tiber (Figure 1.3). Some researchers believe that this infrastructure helped protect the Romans from epidemics of waterborne illnesses.",True,Fermented Foods and Beverages,Figure 1.3,1.1 What Our Ancestors Knew,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-1.4.png,"Figure 1.3 (a) The Cloaca Maxima, or “Greatest Sewer” (shown in red), ran through ancient Rome. It was an engineering marvel that carried waste away from the city and into the river Tiber. (b) These ancient latrines emptied into the Cloaca Maxima."
870de38e-b645-46b0-8481-c5606b0001ee,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"Even before the invention of the microscope, some doctors, philosophers, and scientists made great strides in understanding the invisible forces—what we now know as microbes—that can cause infection, disease, and death.",True,Fermented Foods and Beverages,,,,
4c67fab1-4747-4a48-9eda-9375077c78a9,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"The Greek physician Hippocrates (460–370 BC) is considered the “father of Western medicine” (Figure 1.4). Unlike many of his ancestors and contemporaries, he dismissed the idea that disease was caused by supernatural forces. Instead, he posited that diseases had natural causes from within patients or their environments. Hippocrates and his heirs are believed to have written the Hippocratic Corpus, a collection of texts that make up some of the oldest surviving medical books.[2] Hippocrates is also often credited as the author of the Hippocratic Oath, taken by new physicians to pledge their dedication to diagnosing and treating patients without causing harm.",True,Fermented Foods and Beverages,Figure 1.4,1.1 What Our Ancestors Knew,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-1.5.png,"Figure 1.4 (a) Hippocrates, the “father of Western medicine,” believed that diseases had natural, not supernatural, causes. (b) The historian Thucydides observed that survivors of the Athenian plague were subsequently immune to the infection. (c) Marcus Terentius Varro proposed that disease could be caused by “certain minute creatures . . . which cannot be seen by the eye.” (credit c: modification of work by Alessandro Antonelli)"
9a993d4d-c968-415e-8266-13a22efdb337,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"While Hippocrates is considered the father of Western medicine, the Greek philosopher and historian Thucydides (460–395 BC) is considered the father of scientific history because he advocated for evidence-based analysis of cause-and-effect reasoning (Figure 1.4). Among his most important contributions are his observations regarding the Athenian plague that killed one-third of the population of Athens between 430 and 410 BC. Having survived the epidemic himself, Thucydides made the important observation that survivors did not get re-infected with the disease, even when taking care of actively sick people.[3] This observation shows an early understanding of the concept of immunity.",True,Fermented Foods and Beverages,Figure 1.4,1.1 What Our Ancestors Knew,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-1.5.png,"Figure 1.4 (a) Hippocrates, the “father of Western medicine,” believed that diseases had natural, not supernatural, causes. (b) The historian Thucydides observed that survivors of the Athenian plague were subsequently immune to the infection. (c) Marcus Terentius Varro proposed that disease could be caused by “certain minute creatures . . . which cannot be seen by the eye.” (credit c: modification of work by Alessandro Antonelli)"
e0e2fae4-238f-4b7b-b7b9-b170959da1c8,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"Marcus Terentius Varro (116–27 BC) was a prolific Roman writer who was one of the first people to propose the concept that things we cannot see (what we now call microorganisms) can cause disease (Figure 1.4). In Res Rusticae (On Farming), published in 36 BC, he said that “precautions must also be taken in neighborhood swamps . . . because certain minute creatures [animalia minuta] grow there which cannot be seen by the eye, which float in the air and enter the body through the mouth and nose and there cause serious diseases.”[4]",True,Fermented Foods and Beverages,Figure 1.4,1.1 What Our Ancestors Knew,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-1.5.png,"Figure 1.4 (a) Hippocrates, the “father of Western medicine,” believed that diseases had natural, not supernatural, causes. (b) The historian Thucydides observed that survivors of the Athenian plague were subsequently immune to the infection. (c) Marcus Terentius Varro proposed that disease could be caused by “certain minute creatures . . . which cannot be seen by the eye.” (credit c: modification of work by Alessandro Antonelli)"
efac2b2f-b7d4-4d0e-a0fb-960c117a0b2b,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,The Birth of Microbiology,False,The Birth of Microbiology,,,,
3b74bcb5-3bfe-4199-8d9f-7542886b4a31,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"While the ancients may have suspected the existence of invisible “minute creatures,” it wasn’t until the invention of the microscope that their existence was definitively confirmed. While it is unclear who exactly invented the microscope, a Dutch cloth merchant named Antonie van Leeuwenhoek (1632–1723) was the first to develop a lens powerful enough to view microbes. In 1675, using a simple but powerful microscope, Leeuwenhoek was able to observe single-celled organisms, which he described as “animalcules” or “wee little beasties,” swimming in a drop of rain water. From his drawings of these little organisms, we now know he was looking at bacteria and protists.",True,The Birth of Microbiology,,,,
9494c3f2-7603-411a-b958-822cedc11852,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"Nearly 200 years after van Leeuwenhoek got his first glimpse of microbes, the “Golden Age of Microbiology” spawned a host of new discoveries between 1857 and 1914. Two famous microbiologists, Louis Pasteur and Robert Koch, were especially active in advancing our understanding of the unseen world of microbes (Figure 1.5). Pasteur, a French chemist, showed that individual microbial strains had unique properties and demonstrated that fermentation is caused by microorganisms. He also invented pasteurization, a process used to kill microorganisms responsible for spoilage, and developed vaccines for the treatment of diseases, including rabies, in animals and humans. Koch, a German physician, was the first to demonstrate the connection between a single, isolated microbe and a known human disease. For example, he discovered the bacteria that cause anthrax (Bacillus anthracis), cholera (Vibrio cholera), and tuberculosis (Mycobacterium tuberculosis).[5] We will discuss these famous microbiologists, and others, in later chapters.",True,The Birth of Microbiology,Figure 1.5,1.1 What Our Ancestors Knew,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-1.6.png,"Figure 1.5 (a) Louis Pasteur (1822–1895) is credited with numerous innovations that advanced the fields of microbiology and immunology. (b) Robert Koch (1843–1910) identified the specific microbes that cause anthrax, cholera, and tuberculosis."
55d806e3-9c34-40ba-b89b-accd23e6549f,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"As microbiology has developed, it has allowed the broader discipline of biology to grow and flourish in previously unimagined ways. Much of what we know about human cells comes from our understanding of microbes, and many of the tools we use today to study cells and their genetics derive from work with microbes.",True,The Birth of Microbiology,,,,
a03c2795-95b6-40a1-b50d-c167e4a94a29,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,Learning Objectives,False,Learning Objectives,,,,
7d751b1a-3f4f-493d-a3bb-ecdb0686b7ef,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"Humans have been living with—and using—microorganisms for much longer than they have been able to see them. Historical evidence suggests that humans have had some notion of microbial life since prehistoric times and have used that knowledge to develop foods as well as prevent and treat disease. In this section, we will explore some of the historical applications of microbiology as well as the early beginnings of microbiology as a science.",True,Learning Objectives,,,,
9255af42-f6c4-4b8e-82d7-83e81c11f8f1,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,Fermented Foods and Beverages,False,Fermented Foods and Beverages,,,,
a8b6d074-99d9-49a2-a03c-9400df56ce0f,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"People across the world have enjoyed fermented foods and beverages like beer, wine, bread, yogurt, cheese, and pickled vegetables for all of recorded history. Discoveries from several archeological sites suggest that even prehistoric people took advantage of fermentation to preserve and enhance the taste of food. Archaeologists studying pottery jars from a Neolithic village in China found that people were making a fermented beverage from rice, honey, and fruit as early as 7000 BC.[1]",True,Fermented Foods and Beverages,,,,
53b56531-e22d-441d-ac5f-58ae8c3f85be,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"Production of these foods and beverages requires microbial fermentation, a process that uses bacteria, mold, or yeast to convert sugars (carbohydrates) to alcohol, gases, and organic acids (Figure 1.2). While it is likely that people first learned about fermentation by accident—perhaps by drinking old milk that had curdled or old grape juice that had fermented—they later learned to harness the power of fermentation to make products like bread, cheese, and wine.",True,Fermented Foods and Beverages,Figure 1.2,1.1 What Our Ancestors Knew,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-1.3.png,"Figure 1.2 A microscopic view of Saccharomyces cerevisiae, the yeast responsible for making bread rise (left). Yeast is a microorganism. Its cells metabolize the carbohydrates in flour (middle) and produce carbon dioxide, which causes the bread to rise (right). (credit middle: modification of work by Janus Sandsgaard; credit right: modification of work by “MDreibelbis”/Flickr)"
4bb92dfc-181f-4ed6-a40f-4824583b1cec,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"Several ancient civilizations appear to have had some understanding that disease could be transmitted by things they could not see. This is especially evident in historical attempts to contain the spread of disease. For example, the Bible refers to the practice of quarantining people with leprosy and other diseases, suggesting that people understood that diseases could be communicable. Ironically, while leprosy is communicable, it is also a disease that progresses slowly. This means that people were likely quarantined after they had already spread the disease to others.",True,Fermented Foods and Beverages,,,,
15a1a191-fb12-47e3-ad2f-6ff9f5fa199f,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"The ancient Greeks attributed disease to bad air, mal’aria, which they called “miasmatic odors.” They developed hygiene practices that built on this idea. The Romans also believed in the miasma hypothesis and created a complex sanitation infrastructure to deal with sewage. In Rome, they built aqueducts, which brought fresh water into the city, and a giant sewer, the Cloaca Maxima, which carried waste away and into the river Tiber (Figure 1.3). Some researchers believe that this infrastructure helped protect the Romans from epidemics of waterborne illnesses.",True,Fermented Foods and Beverages,Figure 1.3,1.1 What Our Ancestors Knew,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-1.4.png,"Figure 1.3 (a) The Cloaca Maxima, or “Greatest Sewer” (shown in red), ran through ancient Rome. It was an engineering marvel that carried waste away from the city and into the river Tiber. (b) These ancient latrines emptied into the Cloaca Maxima."
28712c08-4541-4006-9f3f-4f6352166cd8,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"Even before the invention of the microscope, some doctors, philosophers, and scientists made great strides in understanding the invisible forces—what we now know as microbes—that can cause infection, disease, and death.",True,Fermented Foods and Beverages,,,,
4baee253-69c5-4d70-9313-0c857260a94c,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"The Greek physician Hippocrates (460–370 BC) is considered the “father of Western medicine” (Figure 1.4). Unlike many of his ancestors and contemporaries, he dismissed the idea that disease was caused by supernatural forces. Instead, he posited that diseases had natural causes from within patients or their environments. Hippocrates and his heirs are believed to have written the Hippocratic Corpus, a collection of texts that make up some of the oldest surviving medical books.[2] Hippocrates is also often credited as the author of the Hippocratic Oath, taken by new physicians to pledge their dedication to diagnosing and treating patients without causing harm.",True,Fermented Foods and Beverages,Figure 1.4,1.1 What Our Ancestors Knew,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-1.5.png,"Figure 1.4 (a) Hippocrates, the “father of Western medicine,” believed that diseases had natural, not supernatural, causes. (b) The historian Thucydides observed that survivors of the Athenian plague were subsequently immune to the infection. (c) Marcus Terentius Varro proposed that disease could be caused by “certain minute creatures . . . which cannot be seen by the eye.” (credit c: modification of work by Alessandro Antonelli)"
18253bc1-baf1-48de-9ade-ee32ebafb29b,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"While Hippocrates is considered the father of Western medicine, the Greek philosopher and historian Thucydides (460–395 BC) is considered the father of scientific history because he advocated for evidence-based analysis of cause-and-effect reasoning (Figure 1.4). Among his most important contributions are his observations regarding the Athenian plague that killed one-third of the population of Athens between 430 and 410 BC. Having survived the epidemic himself, Thucydides made the important observation that survivors did not get re-infected with the disease, even when taking care of actively sick people.[3] This observation shows an early understanding of the concept of immunity.",True,Fermented Foods and Beverages,Figure 1.4,1.1 What Our Ancestors Knew,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-1.5.png,"Figure 1.4 (a) Hippocrates, the “father of Western medicine,” believed that diseases had natural, not supernatural, causes. (b) The historian Thucydides observed that survivors of the Athenian plague were subsequently immune to the infection. (c) Marcus Terentius Varro proposed that disease could be caused by “certain minute creatures . . . which cannot be seen by the eye.” (credit c: modification of work by Alessandro Antonelli)"
96b1fee9-c415-4a63-919c-425fad6da9f9,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"Marcus Terentius Varro (116–27 BC) was a prolific Roman writer who was one of the first people to propose the concept that things we cannot see (what we now call microorganisms) can cause disease (Figure 1.4). In Res Rusticae (On Farming), published in 36 BC, he said that “precautions must also be taken in neighborhood swamps . . . because certain minute creatures [animalia minuta] grow there which cannot be seen by the eye, which float in the air and enter the body through the mouth and nose and there cause serious diseases.”[4]",True,Fermented Foods and Beverages,Figure 1.4,1.1 What Our Ancestors Knew,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-1.5.png,"Figure 1.4 (a) Hippocrates, the “father of Western medicine,” believed that diseases had natural, not supernatural, causes. (b) The historian Thucydides observed that survivors of the Athenian plague were subsequently immune to the infection. (c) Marcus Terentius Varro proposed that disease could be caused by “certain minute creatures . . . which cannot be seen by the eye.” (credit c: modification of work by Alessandro Antonelli)"
714ad608-380e-4d21-accb-d763d7e9a2e2,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,The Birth of Microbiology,False,The Birth of Microbiology,,,,
cb9def0f-e548-43b0-b707-b75e28905457,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"While the ancients may have suspected the existence of invisible “minute creatures,” it wasn’t until the invention of the microscope that their existence was definitively confirmed. While it is unclear who exactly invented the microscope, a Dutch cloth merchant named Antonie van Leeuwenhoek (1632–1723) was the first to develop a lens powerful enough to view microbes. In 1675, using a simple but powerful microscope, Leeuwenhoek was able to observe single-celled organisms, which he described as “animalcules” or “wee little beasties,” swimming in a drop of rain water. From his drawings of these little organisms, we now know he was looking at bacteria and protists.",True,The Birth of Microbiology,,,,
6fc44031-13ce-4589-9304-cbbccef420cd,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"Nearly 200 years after van Leeuwenhoek got his first glimpse of microbes, the “Golden Age of Microbiology” spawned a host of new discoveries between 1857 and 1914. Two famous microbiologists, Louis Pasteur and Robert Koch, were especially active in advancing our understanding of the unseen world of microbes (Figure 1.5). Pasteur, a French chemist, showed that individual microbial strains had unique properties and demonstrated that fermentation is caused by microorganisms. He also invented pasteurization, a process used to kill microorganisms responsible for spoilage, and developed vaccines for the treatment of diseases, including rabies, in animals and humans. Koch, a German physician, was the first to demonstrate the connection between a single, isolated microbe and a known human disease. For example, he discovered the bacteria that cause anthrax (Bacillus anthracis), cholera (Vibrio cholera), and tuberculosis (Mycobacterium tuberculosis).[5] We will discuss these famous microbiologists, and others, in later chapters.",True,The Birth of Microbiology,Figure 1.5,1.1 What Our Ancestors Knew,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-1.6.png,"Figure 1.5 (a) Louis Pasteur (1822–1895) is credited with numerous innovations that advanced the fields of microbiology and immunology. (b) Robert Koch (1843–1910) identified the specific microbes that cause anthrax, cholera, and tuberculosis."
0ac6f73d-c223-4503-a143-1f98652a5266,https://open.oregonstate.education/microbiology/,1.1 What Our Ancestors Knew,https://open.oregonstate.education/microbiology/chapter/1-1-what-our-ancestors-knew/,"As microbiology has developed, it has allowed the broader discipline of biology to grow and flourish in previously unimagined ways. Much of what we know about human cells comes from our understanding of microbes, and many of the tools we use today to study cells and their genetics derive from work with microbes.",True,The Birth of Microbiology,,,,
2efed08d-534e-4bee-8c9d-cb35bdc2cd88,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Beyond these basic components, cells can vary greatly between organisms, and even within the same multicellular organism. The two largest categories of cells—prokaryotic cells and eukaryotic cells—are defined by major differences in several cell structures. Prokaryotic cells lack a nucleus surrounded by a complex nuclear membrane and generally have a single, circular chromosome located in a nucleoid. Eukaryotic cells have a nucleus surrounded by a complex nuclear membrane that contains multiple, rod-shaped chromosomes.[1]",True,The Birth of Microbiology,,,,
ca176db8-05d9-48c4-863b-cc28a694a16a,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"All plant cells and animal cells are eukaryotic. Some microorganisms are composed of prokaryotic cells, whereas others are composed of eukaryotic cells. Prokaryotic microorganisms are classified within the domains Archaea and Bacteria, whereas eukaryotic organisms are classified within the domain Eukarya.",True,The Birth of Microbiology,,,,
15ca5410-ae32-4028-bfe7-c4d20a427673,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"The structures inside a cell are analogous to the organs inside a human body, with unique structures suited to specific functions. Some of the structures found in prokaryotic cells are similar to those found in some eukaryotic cells; others are unique to prokaryotes. Although there are some exceptions, eukaryotic cells tend to be larger than prokaryotic cells. The comparatively larger size of eukaryotic cells dictates the need to compartmentalize various chemical processes within different areas of the cell, using complex membrane-bound organelles. In contrast, prokaryotic cells generally lack membrane-bound organelles; however, they often contain inclusions that compartmentalize their cytoplasm. Figure 2.10 illustrates structures typically associated with prokaryotic cells. These structures are described in more detail in the next section.",True,The Birth of Microbiology,Figure 2.10,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.12.png,"Figure 2.10 A typical prokaryotic cell contains a cell membrane, chromosomal DNA that is concentrated in a nucleoid, ribosomes, and a cell wall. Some prokaryotic cells may also possess flagella, pili, fimbriae, and capsules."
8ba0da9c-f755-4efb-80d5-99e00c3ae6f6,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,Common Cell Morphologies and Arrangements,False,Common Cell Morphologies and Arrangements,,,,
f94ccced-3db6-498e-b83d-31d84bf64517,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Individual cells of a particular prokaryotic organism are typically similar in shape, or cell morphology. Although thousands of prokaryotic organisms have been identified, only a handful of cell morphologies are commonly seen microscopically. Figure 2.11 names and illustrates cell morphologies commonly found in prokaryotic cell.",True,Common Cell Morphologies and Arrangements,Figure 2.11,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.13.png,"Figure 2.11 (credit “Coccus” micrograph: modification of work by Janice Haney Carr, Centers for Disease Control and Prevention; credit “Coccobacillus” micrograph: modification of work by Janice Carr, Centers for Disease Control and Prevention; credit “Spirochete” micrograph: modification of work by Centers for Disease Control and Prevention."
c45125bc-03a4-48fe-a20e-d853c4a428ab,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,The Nucleoid,False,The Nucleoid,,,,
b026f864-91ad-4352-8ba1-51539d26af5c,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"All cellular life has a DNA genome organized into one or more chromosomes. Prokaryotic chromosomes are typically circular, haploid (unpaired), and not bound by a complex nuclear membrane. Prokaryotic DNA and DNA-associated proteins are concentrated within the nucleoid region of the cell (Figure 2.12). In general, prokaryotic DNA interacts with nucleoid-associated proteins (NAPs) that assist in the organization and packaging of the chromosome. In bacteria, NAPs function similar to histones, which are the DNA-organizing proteins found in eukaryotic cells. In archaea, the nucleoid is organized by either NAPs or histone-like DNA organizing proteins.",True,The Nucleoid,Figure 2.12,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.17.png,"Figure 2.12 The nucleoid region (the area enclosed by the green dashed line) is a condensed area of DNA found within prokaryotic cells. Because of the density of the area, it does not readily stain and appears lighter in color when viewed with a transmission electron microscope."
43750804-d744-4a43-af74-7f1afb432864,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,Plasmids,False,Plasmids,,,,
cdb89b9d-1533-45ad-a254-15f16dfd483c,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Prokaryotic cells may also contain extrachromosomal DNA, or DNA that is not part of the chromosome. This extrachromosomal DNA is found in plasmids, which are small, circular, double-stranded DNA molecules. Cells that have plasmids often have hundreds of them within a single cell. Plasmids are more commonly found in bacteria; however, plasmids have been found in archaea and eukaryotic organisms. Plasmids often carry genes that confer advantageous traits such as antibiotic resistance; thus, they are important to the survival of the organism.",True,Plasmids,,,,
bd695e1b-7ae9-4acf-8912-79d90fc26546,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,Ribosomes,False,Ribosomes,,,,
56dd55c8-fb4f-4ebb-8ca1-9f587cc3dad2,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"All cellular life synthesizes proteins, and organisms in all three domains of life possess ribosomes, structures responsible for protein synthesis. However, ribosomes in each of the three domains are structurally different. Ribosomes, themselves, are constructed from proteins, along with ribosomal RNA (rRNA). Prokaryotic ribosomes are found in the cytoplasm. They are called 70S ribosomes because they have a size of 70S (Figure 2.13), whereas eukaryotic cytoplasmic ribosomes have a size of 80S. (The S stands for Svedberg unit, a measure of sedimentation in an ultracentrifuge, which is based on size, shape, and surface qualities of the structure being analyzed). Although they are the same size, bacterial and archaeal ribosomes have different proteins and rRNA molecules, and the archaeal versions are more similar to their eukaryotic counterparts than to those found in bacteria.",True,Ribosomes,Figure 2.13,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.18.png,"Figure 2.13 Prokaryotic ribosomes (70S) are composed of two subunits: the 30S (small subunit) and the 50S (large subunit), each of which are composed of protein and rRNA components."
148bec1c-5b14-486d-beb5-8526f6dd07f2,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,Endospores,False,Endospores,,,,
665a310f-a3ec-4055-bc17-d45cce1ae5f3,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Bacterial cells are generally observed as vegetative cells, but some genera of bacteria have the ability to form endospores, structures that essentially protect the bacterial genome in a dormant state when environmental conditions are unfavorable. Endospores (not to be confused with the reproductive spores formed by fungi) allow some bacterial cells to survive long periods without food or water, as well as exposure to chemicals, extreme temperatures, and even radiation. Table 2.1 compares the characteristics of vegetative cells and endospores.",True,Endospores,,,,
5bb286b6-320c-40be-b971-edca558a27e3,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"The process by which vegetative cells transform into endospores is called sporulation, and it generally begins when nutrients become depleted or environmental conditions become otherwise unfavorable (Figure 2.14). The process begins with the formation of a septum in the vegetative bacterial cell. The septum divides the cell asymmetrically, separating a DNA forespore from the mother cell. The forespore, which will form the core of the endospore, is essentially a copy of the cell’s chromosomes, and is separated from the mother cell by a second membrane. A cortex gradually forms around the forespore by laying down layers of calcium and dipicolinic acid between membranes. A protein spore coat then forms around the cortex while the DNA of the mother cell disintegrates. Further maturation of the endospore occurs with the formation of an outermost exosporium. The endospore is released upon disintegration of the mother cell, completing sporulation.",True,Endospores,Figure 2.14,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.20.png,"Figure 2.14 (a) Sporulation begins following asymmetric cell division. The forespore becomes surrounded by a double layer of membrane, a cortex, and a protein spore coat, before being released as a mature endospore upon disintegration of the mother cell. (b) An electron micrograph of a Carboxydothermus hydrogenoformans endospore. These Bacillus spp. cells are undergoing sporulation. The endospores have been visualized using Malachite Green spore stain. (credit b: modification of work by Jonathan Eisen)"
1ab1a5ee-0f65-454e-aad9-e5f106488707,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Endospores of certain species have been shown to persist in a dormant state for extended periods of time, up to thousands of years.[2] However, when living conditions improve, endospores undergo germination, reentering a vegetative state. After germination, the cell becomes metabolically active again and is able to carry out all of its normal functions, including growth and cell division.",True,Endospores,,,,
5130c141-af8d-40cc-881e-1f6fea82ad56,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Not all bacteria have the ability to form endospores; however, there are a number of clinically significant endospore- forming gram-positive bacteria of the genera Bacillus and Clostridium. Pathogens such as these are particularly difficult to combat because their endospores are so hard to kill.",True,Endospores,,,,
baa92ae9-f00e-4041-9c14-791aabcff8f6,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Structures that enclose the cytoplasm and internal structures of the cell are known collectively as the cell envelope. In prokaryotic cells, the structures of the cell envelope vary depending on the type of cell and organism. Most (but not all) prokaryotic cells have a cell wall, but the makeup of this cell wall varies. All cells (prokaryotic and eukaryotic) have a plasma membrane (also called cytoplasmic membrane or cell membrane) that exhibits selective permeability, allowing some molecules to enter or leave the cell while restricting the passage of others.",True,Endospores,,,,
295c04de-851d-413e-8737-cf37549bfcc2,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"The structure of the plasma membrane is often described in terms of the fluid mosaic model, which refers to the ability of membrane components to move fluidly within the plane of the membrane, as well as the mosaic-like composition of the components, which include a diverse array of lipid and protein components (Figure 2.15). The plasma membrane structure of most bacterial and eukaryotic cell types is a bilayer composed mainly of phospholipids formed with ester linkages and proteins. These phospholipids and proteins have the ability to move laterally within the plane of the membranes as well as between the two phospholipid layers.",True,Endospores,Figure 2.15,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.21.png,"Figure 2.15 The bacterial plasma membrane is a phospholipid bilayer with a variety of embedded proteins that perform various functions for the cell. Note the presence of glycoproteins and glycolipids, whose carbohydrate components extend out from the surface of the cell. The abundance and arrangement of these proteins and lipids can vary greatly between species."
c0f19001-e79a-46d4-a04d-9043e6f09d75,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Archaeal membranes are fundamentally different from bacterial and eukaryotic membranes in a few significant ways. First, archaeal membrane phospholipids are formed with ether linkages, in contrast to the ester linkages found in bacterial or eukaryotic cell membranes. Second, archaeal phospholipids have branched chains, whereas those of bacterial and eukaryotic cells are straight chained. Finally, although some archaeal membranes can be formed of bilayers like those found in bacteria and eukaryotes, other archaeal plasma membranes are lipid monolayers.",True,Endospores,,,,
60896d1f-74bf-4569-9b58-dd27196dcd81,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Proteins on the cell’s surface are important for a variety of functions, including cell-to-cell communication, and sensing environmental conditions and pathogenic virulence factors. Membrane proteins and phospholipids may have carbohydrates (sugars) associated with them and are called glycoproteins or glycolipids, respectively. These glycoprotein and glycolipid complexes extend out from the surface of the cell, allowing the cell to interact with the external environment (Figure 2.15). Glycoproteins and glycolipids in the plasma membrane can vary considerably in chemical composition among archaea, bacteria, and eukaryotes, allowing scientists to use them to characterize unique species.",True,Endospores,Figure 2.15,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.21.png,"Figure 2.15 The bacterial plasma membrane is a phospholipid bilayer with a variety of embedded proteins that perform various functions for the cell. Note the presence of glycoproteins and glycolipids, whose carbohydrate components extend out from the surface of the cell. The abundance and arrangement of these proteins and lipids can vary greatly between species."
64718d94-990f-4daf-976f-b68172836fd4,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Plasma membranes from different cells types also contain unique phospholipids, which contain fatty acids. Phospholipid-derived fatty acid analysis (PLFA) profiles can be used to identify unique types of cells based on differences in fatty acids. Archaea, bacteria, and eukaryotes each have a unique PFLA profile.",True,Endospores,,,,
516794c5-2c9b-47b5-8e1f-b75c44a34f8d,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,Photosynthetic Membrane Structures,False,Photosynthetic Membrane Structures,,,,
ff5694a5-e268-4af2-9908-a1a2287a07ad,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,Cell Wall,False,Cell Wall,,,,
537dcb3f-17ab-4f6b-8827-db13dfd0317d,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"The primary function of the cell wall is to protect the cell from harsh conditions in the outside environment. When present, there are notable similarities and differences among the cell walls of archaea, bacteria, and eukaryotes.",True,Cell Wall,,,,
12229c7f-51b9-4af4-abd6-706e02a7303b,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"The major component of bacterial cell walls is called peptidoglycan (or murein); it is only found in bacteria. Structurally, peptidoglycan resembles a layer of meshwork or fabric (Figure 2.16). Each layer is composed of long chains of alternating molecules of N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM). The structure of the long chains has significant two-dimensional tensile strength due to the formation of peptide bridges that connect NAG and NAM within each peptidoglycan layer. In gram-negative bacteria, tetrapeptide chains extending from each NAM unit are directly cross-linked, whereas in gram-positive bacteria, these tetrapeptide chains are linked by pentaglycine cross-bridges. Peptidoglycan subunits are made inside of the bacterial cell and then exported and assembled in layers, giving the cell its shape.",True,Cell Wall,Figure 2.16,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.25.png,"Figure 2.16 Peptidoglycan is composed of polymers of alternating NAM and NAG subunits, which are cross-linked by peptide bridges linking NAM subunits from various glycan chains. This provides the cell wall with tensile strength in two dimensions."
aed1443d-dafa-4254-b547-00e2a4c2b67e,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"The Gram staining protocol is used to differentiate two common types of cell wall structures (Figure 2.17). Gram-positive cells have a cell wall consisting of many layers of peptidoglycan totaling 30–100 nm in thickness. These peptidoglycan layers are commonly embedded with teichoic acids (TAs), carbohydrate chains that extend through and beyond the peptidoglycan layer.[3] TA is thought to stabilize peptidoglycan by increasing its rigidity. TA also plays a role in the ability of pathogenic gram-positive bacteria such as Streptococcus to bind to certain proteins on the surface of host cells, enhancing their ability to cause infection.",True,Cell Wall,Figure 2.17,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.26.png,"Figure 2.17 Bacteria contain two common cell wall structural types. Gram-positive cell walls are structurally simple, containing a thick layer of peptidoglycan with embedded teichoic acid external to the plasma membrane.[footnote]B. Zuber et al. “Granular Layer in the Periplasmic Space of Gram-Positive Bacteria and Fine Structures of Enterococcus gallinarum and Streptococcus gordonii Septa Revealed by Cryo-Electron Microscopy of Vitreous Sections.” Journal of Bacteriology 188 no. 18 (2006):6652–6660[/footnote] Gram- negative cell walls are structurally more complex, containing three layers: the inner membrane, a thin layer of peptidoglycan, and an outer membrane containing lipopolysaccharide. (credit: modification of work by “Franciscosp2”/Wikimedia Commons)"
d780febd-85c5-41a0-8b3e-5d6b6a57ddd1,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Gram-negative cells have a much thinner layer of peptidoglycan (no more than about 4 nm thick[4]) than gram- positive cells, and the overall structure of their cell envelope is more complex. In gram-negative cells, a gel-like matrix occupies the periplasmic space between the cell wall and the plasma membrane, and there is a second lipid bilayer called the outer membrane, which is external to the peptidoglycan layer (Figure 2.17). This outer membrane is attached to the peptidoglycan by murein lipoprotein. The outer leaflet of the outer membrane contains the molecule lipopolysaccharide (LPS), which functions as an endotoxin in infections involving gram-negative bacteria, contributing to symptoms such as fever, hemorrhaging, and septic shock. Each LPS molecule is composed of Lipid A, a core polysaccharide, and an O side chain that is composed of sugar-like molecules that comprise the external face of the LPS (Figure 2.18). The composition of the O side chain varies between different species and strains of bacteria. Parts of the O side chain called antigens can be detected using serological or immunological tests to identify specific pathogenic strains like Escherichia coli O157:H7, a deadly strain of bacteria that causes bloody diarrhea and kidney failure.",True,Cell Wall,Figure 2.17,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.26.png,"Figure 2.17 Bacteria contain two common cell wall structural types. Gram-positive cell walls are structurally simple, containing a thick layer of peptidoglycan with embedded teichoic acid external to the plasma membrane.[footnote]B. Zuber et al. “Granular Layer in the Periplasmic Space of Gram-Positive Bacteria and Fine Structures of Enterococcus gallinarum and Streptococcus gordonii Septa Revealed by Cryo-Electron Microscopy of Vitreous Sections.” Journal of Bacteriology 188 no. 18 (2006):6652–6660[/footnote] Gram- negative cell walls are structurally more complex, containing three layers: the inner membrane, a thin layer of peptidoglycan, and an outer membrane containing lipopolysaccharide. (credit: modification of work by “Franciscosp2”/Wikimedia Commons)"
f5beb033-23fe-4c5a-954b-0983180a9786,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Archaeal cell wall structure differs from that of bacteria in several significant ways. First, archaeal cell walls do not contain peptidoglycan; instead, they contain a similar polymer called pseudopeptidoglycan (pseudomurein) in which NAM is replaced with a different subunit. Other archaea may have a layer of glycoproteins or polysaccharides that serves as the cell wall instead of pseudopeptidoglycan. Last, as is the case with some bacterial species, there are a few archaea that appear to lack cell walls entirely.",True,Cell Wall,,,,
d945e03f-ff19-49fd-8250-cd4b5ebcd191,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,Glycocalyces and S-Layers,False,Glycocalyces and S-Layers,,,,
4ba4cd4f-643c-4aab-acba-d9345cc7814f,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Although most prokaryotic cells have cell walls, some may have additional cell envelope structures exterior to the cell wall, such as glycocalyces and S-layers. A glycocalyx is a sugar coat, of which there are two important types: capsules and slime layers. A capsule is an organized layer located outside of the cell wall and usually composed of polysaccharides or proteins (Figure 2.19). A slime layer is a less tightly organized layer that is only loosely attached to the cell wall and can be more easily washed off. Slime layers may be composed of polysaccharides, glycoproteins, or glycolipids.",True,Glycocalyces and S-Layers,Figure 2.19,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.29.png,"Figure 2.19 (a) Capsules are a type of glycocalyx composed of an organized layer of polysaccharides. (b) A capsule stain of Pseudomonas aeruginosa, a bacterial pathogen capable of causing many different types of infections in humans. (credit b: modification of work by American Society for Microbiology)"
09abbfbb-457b-445a-8822-091ece08e41a,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Glycocalyces allows cells to adhere to surfaces, aiding in the formation of biofilms (colonies of microbes that form in layers on surfaces). In nature, most microbes live in mixed communities within biofilms, partly because the biofilm affords them some level of protection. Biofilms generally hold water like a sponge, preventing desiccation. They also protect cells from predation and hinder the action of antibiotics and disinfectants. All of these properties are advantageous to the microbes living in a biofilm, but they present challenges in a clinical setting, where the goal is often to eliminate microbes.",True,Glycocalyces and S-Layers,,,,
50d0781e-681a-442a-b917-0972fa84ed59,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"The ability to produce a capsule can contribute to a microbe’s pathogenicity (ability to cause disease) because the capsule can make it more difficult for phagocytic cells (such as white blood cells) to engulf and kill the microorganism. Streptococcus pneumoniae, for example, produces a capsule that is well known to aid in this bacterium’s pathogenicity.",True,Glycocalyces and S-Layers,,,,
72e7dd58-b061-4ec0-bb88-04e35293f89a,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"An S-layer is another type of cell envelope structure; it is composed of a mixture of structural proteins and glycoproteins. In bacteria, S-layers are found outside the cell wall, but in some archaea, the S-layer serves as the cell wall. The exact function of S-layers is not entirely understood, and they are difficult to study; but available evidence suggests that they may play a variety of functions in different prokaryotic cells, such as helping the cell withstand osmotic pressure and, for certain pathogens, interacting with the host immune system.",True,Glycocalyces and S-Layers,,,,
dcdc4608-f0f1-4632-85c6-274f4a2bf747,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,Filamentous Appendages,False,Filamentous Appendages,,,,
81377376-2845-44c4-8dcb-72fda14dc0ec,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Many bacterial cells have protein appendages embedded within their cell envelopes that extend outward, allowing interaction with the environment. These appendages can attach to other surfaces, transfer DNA, or provide movement. Filamentous appendages include fimbriae, pili, and flagella.",True,Filamentous Appendages,,,,
48124798-8806-4b96-a40e-8e50bd3c26e3,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Fimbriae and pili are structurally similar and, because differentiation between the two is problematic, these terms are often used interchangeably.[5][6] The term fimbriae commonly refers to short bristle-like proteins projecting from the cell surface by the hundreds. Fimbriae enable a cell to attach to surfaces and to other cells. For pathogenic bacteria, adherence to host cells is important for colonization, infectivity, and virulence. Adherence to surfaces is also important in biofilm formation.",True,Filamentous Appendages,,,,
669eb60d-442d-47c6-af93-6e23e96feeda,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"The term pili (singular: pilus) commonly refers to longer, less numerous protein appendages that aid in attachment to surfaces (Figure 2.20). A specific type of pilus, called the F pilus or sex pilus, is important in the transfer of DNA between bacterial cells, which occurs between members of the same generation when two cells physically transfer or exchange parts of their respective genomes.",True,Filamentous Appendages,Figure 2.20,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.30.png,"Figure 2.20 Bacteria may produce two different types of protein appendages that aid in surface attachment. Fimbriae typically are more numerous and shorter, whereas pili (shown here) are longer and less numerous per cell. (credit: modification of work by American Society for Microbiology)"
dcfaac68-9c2d-4e70-8c8c-302fcb745660,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,Flagella are structures used by cells to move in aqueous environments. Bacterial flagella act like propellers. They are stiff spiral filaments composed of flagellin protein subunits that extend outward from the cell and spin in solution. The basal body is the motor for the flagellum and is embedded in the plasma membrane (Figure 2.21). A hook region connects the basal body to the filament. Gram-positive and gram-negative bacteria have different basal body configurations due to differences in cell wall structure.,True,Filamentous Appendages,Figure 2.21,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.31.png,"Figure 2.21 The basic structure of a bacterial flagellum consists of a basal body, hook, and filament. The basal body composition and arrangement differ between gram-positive and gram-negative bacteria. (credit: modification of work by “LadyofHats”/Mariana Ruiz Villareal)"
19f93d1f-d553-46ae-8012-95855d55a5b6,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,The Nucleoid,False,The Nucleoid,,,,
41269202-032a-44d1-8c51-b7374c5cca57,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"All cellular life has a DNA genome organized into one or more chromosomes. Prokaryotic chromosomes are typically circular, haploid (unpaired), and not bound by a complex nuclear membrane. Prokaryotic DNA and DNA-associated proteins are concentrated within the nucleoid region of the cell (Figure 2.12). In general, prokaryotic DNA interacts with nucleoid-associated proteins (NAPs) that assist in the organization and packaging of the chromosome. In bacteria, NAPs function similar to histones, which are the DNA-organizing proteins found in eukaryotic cells. In archaea, the nucleoid is organized by either NAPs or histone-like DNA organizing proteins.",True,The Nucleoid,Figure 2.12,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.17.png,"Figure 2.12 The nucleoid region (the area enclosed by the green dashed line) is a condensed area of DNA found within prokaryotic cells. Because of the density of the area, it does not readily stain and appears lighter in color when viewed with a transmission electron microscope."
5e81c344-24ae-4655-919f-ede5bd8118b5,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,Plasmids,False,Plasmids,,,,
78583161-cb83-425a-b800-8c80cb1b05b0,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Prokaryotic cells may also contain extrachromosomal DNA, or DNA that is not part of the chromosome. This extrachromosomal DNA is found in plasmids, which are small, circular, double-stranded DNA molecules. Cells that have plasmids often have hundreds of them within a single cell. Plasmids are more commonly found in bacteria; however, plasmids have been found in archaea and eukaryotic organisms. Plasmids often carry genes that confer advantageous traits such as antibiotic resistance; thus, they are important to the survival of the organism.",True,Plasmids,,,,
e447cdf4-3bdc-4d37-9d26-016f27aa5eff,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,Ribosomes,False,Ribosomes,,,,
0523c73f-ca4a-487a-9b7b-3100b51520b9,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"All cellular life synthesizes proteins, and organisms in all three domains of life possess ribosomes, structures responsible for protein synthesis. However, ribosomes in each of the three domains are structurally different. Ribosomes, themselves, are constructed from proteins, along with ribosomal RNA (rRNA). Prokaryotic ribosomes are found in the cytoplasm. They are called 70S ribosomes because they have a size of 70S (Figure 2.13), whereas eukaryotic cytoplasmic ribosomes have a size of 80S. (The S stands for Svedberg unit, a measure of sedimentation in an ultracentrifuge, which is based on size, shape, and surface qualities of the structure being analyzed). Although they are the same size, bacterial and archaeal ribosomes have different proteins and rRNA molecules, and the archaeal versions are more similar to their eukaryotic counterparts than to those found in bacteria.",True,Ribosomes,Figure 2.13,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.18.png,"Figure 2.13 Prokaryotic ribosomes (70S) are composed of two subunits: the 30S (small subunit) and the 50S (large subunit), each of which are composed of protein and rRNA components."
c521a4ce-c78f-4475-a9f0-f8836caa0ac7,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,Endospores,False,Endospores,,,,
e0e8825b-6239-4033-82df-c71978c0cb0e,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Bacterial cells are generally observed as vegetative cells, but some genera of bacteria have the ability to form endospores, structures that essentially protect the bacterial genome in a dormant state when environmental conditions are unfavorable. Endospores (not to be confused with the reproductive spores formed by fungi) allow some bacterial cells to survive long periods without food or water, as well as exposure to chemicals, extreme temperatures, and even radiation. Table 2.1 compares the characteristics of vegetative cells and endospores.",True,Endospores,,,,
4a131e44-0bf6-4616-ac80-87dd80fc9922,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"The process by which vegetative cells transform into endospores is called sporulation, and it generally begins when nutrients become depleted or environmental conditions become otherwise unfavorable (Figure 2.14). The process begins with the formation of a septum in the vegetative bacterial cell. The septum divides the cell asymmetrically, separating a DNA forespore from the mother cell. The forespore, which will form the core of the endospore, is essentially a copy of the cell’s chromosomes, and is separated from the mother cell by a second membrane. A cortex gradually forms around the forespore by laying down layers of calcium and dipicolinic acid between membranes. A protein spore coat then forms around the cortex while the DNA of the mother cell disintegrates. Further maturation of the endospore occurs with the formation of an outermost exosporium. The endospore is released upon disintegration of the mother cell, completing sporulation.",True,Endospores,Figure 2.14,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.20.png,"Figure 2.14 (a) Sporulation begins following asymmetric cell division. The forespore becomes surrounded by a double layer of membrane, a cortex, and a protein spore coat, before being released as a mature endospore upon disintegration of the mother cell. (b) An electron micrograph of a Carboxydothermus hydrogenoformans endospore. These Bacillus spp. cells are undergoing sporulation. The endospores have been visualized using Malachite Green spore stain. (credit b: modification of work by Jonathan Eisen)"
26fc23ca-0529-4710-b69e-73db0f7bbf89,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Endospores of certain species have been shown to persist in a dormant state for extended periods of time, up to thousands of years.[2] However, when living conditions improve, endospores undergo germination, reentering a vegetative state. After germination, the cell becomes metabolically active again and is able to carry out all of its normal functions, including growth and cell division.",True,Endospores,,,,
ef0e5303-eae6-424e-9010-e443cfabae06,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Not all bacteria have the ability to form endospores; however, there are a number of clinically significant endospore- forming gram-positive bacteria of the genera Bacillus and Clostridium. Pathogens such as these are particularly difficult to combat because their endospores are so hard to kill.",True,Endospores,,,,
8d39760b-0660-4eba-806b-7a34f75ae0f2,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"The structure of the plasma membrane is often described in terms of the fluid mosaic model, which refers to the ability of membrane components to move fluidly within the plane of the membrane, as well as the mosaic-like composition of the components, which include a diverse array of lipid and protein components (Figure 2.15). The plasma membrane structure of most bacterial and eukaryotic cell types is a bilayer composed mainly of phospholipids formed with ester linkages and proteins. These phospholipids and proteins have the ability to move laterally within the plane of the membranes as well as between the two phospholipid layers.",True,Endospores,Figure 2.15,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.21.png,"Figure 2.15 The bacterial plasma membrane is a phospholipid bilayer with a variety of embedded proteins that perform various functions for the cell. Note the presence of glycoproteins and glycolipids, whose carbohydrate components extend out from the surface of the cell. The abundance and arrangement of these proteins and lipids can vary greatly between species."
33a135fc-4fd8-478e-ad6b-30cfc1b1c390,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Archaeal membranes are fundamentally different from bacterial and eukaryotic membranes in a few significant ways. First, archaeal membrane phospholipids are formed with ether linkages, in contrast to the ester linkages found in bacterial or eukaryotic cell membranes. Second, archaeal phospholipids have branched chains, whereas those of bacterial and eukaryotic cells are straight chained. Finally, although some archaeal membranes can be formed of bilayers like those found in bacteria and eukaryotes, other archaeal plasma membranes are lipid monolayers.",True,Endospores,,,,
7bee579c-28bb-4f25-8cae-270208efe586,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Proteins on the cell’s surface are important for a variety of functions, including cell-to-cell communication, and sensing environmental conditions and pathogenic virulence factors. Membrane proteins and phospholipids may have carbohydrates (sugars) associated with them and are called glycoproteins or glycolipids, respectively. These glycoprotein and glycolipid complexes extend out from the surface of the cell, allowing the cell to interact with the external environment (Figure 2.15). Glycoproteins and glycolipids in the plasma membrane can vary considerably in chemical composition among archaea, bacteria, and eukaryotes, allowing scientists to use them to characterize unique species.",True,Endospores,Figure 2.15,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.21.png,"Figure 2.15 The bacterial plasma membrane is a phospholipid bilayer with a variety of embedded proteins that perform various functions for the cell. Note the presence of glycoproteins and glycolipids, whose carbohydrate components extend out from the surface of the cell. The abundance and arrangement of these proteins and lipids can vary greatly between species."
6205ba4d-cbb2-421e-9299-93ee40f7966e,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Plasma membranes from different cells types also contain unique phospholipids, which contain fatty acids. Phospholipid-derived fatty acid analysis (PLFA) profiles can be used to identify unique types of cells based on differences in fatty acids. Archaea, bacteria, and eukaryotes each have a unique PFLA profile.",True,Endospores,,,,
0799a74d-b909-4bac-8d52-83b363963318,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,Photosynthetic Membrane Structures,False,Photosynthetic Membrane Structures,,,,
b467a934-ca6c-4b32-9599-8d8400eebe81,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,Cell Wall,False,Cell Wall,,,,
b9110cdb-d282-4c68-a515-b5f83ef7092c,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"The primary function of the cell wall is to protect the cell from harsh conditions in the outside environment. When present, there are notable similarities and differences among the cell walls of archaea, bacteria, and eukaryotes.",True,Cell Wall,,,,
6429db61-ce91-4baf-86d0-9e7dc0351ad7,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"The major component of bacterial cell walls is called peptidoglycan (or murein); it is only found in bacteria. Structurally, peptidoglycan resembles a layer of meshwork or fabric (Figure 2.16). Each layer is composed of long chains of alternating molecules of N-acetylglucosamine (NAG) and N-acetylmuramic acid (NAM). The structure of the long chains has significant two-dimensional tensile strength due to the formation of peptide bridges that connect NAG and NAM within each peptidoglycan layer. In gram-negative bacteria, tetrapeptide chains extending from each NAM unit are directly cross-linked, whereas in gram-positive bacteria, these tetrapeptide chains are linked by pentaglycine cross-bridges. Peptidoglycan subunits are made inside of the bacterial cell and then exported and assembled in layers, giving the cell its shape.",True,Cell Wall,Figure 2.16,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.25.png,"Figure 2.16 Peptidoglycan is composed of polymers of alternating NAM and NAG subunits, which are cross-linked by peptide bridges linking NAM subunits from various glycan chains. This provides the cell wall with tensile strength in two dimensions."
ed38ac24-cb5a-428a-b8a5-bc75d1a583e7,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"The Gram staining protocol is used to differentiate two common types of cell wall structures (Figure 2.17). Gram-positive cells have a cell wall consisting of many layers of peptidoglycan totaling 30–100 nm in thickness. These peptidoglycan layers are commonly embedded with teichoic acids (TAs), carbohydrate chains that extend through and beyond the peptidoglycan layer.[3] TA is thought to stabilize peptidoglycan by increasing its rigidity. TA also plays a role in the ability of pathogenic gram-positive bacteria such as Streptococcus to bind to certain proteins on the surface of host cells, enhancing their ability to cause infection.",True,Cell Wall,Figure 2.17,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.26.png,"Figure 2.17 Bacteria contain two common cell wall structural types. Gram-positive cell walls are structurally simple, containing a thick layer of peptidoglycan with embedded teichoic acid external to the plasma membrane.[footnote]B. Zuber et al. “Granular Layer in the Periplasmic Space of Gram-Positive Bacteria and Fine Structures of Enterococcus gallinarum and Streptococcus gordonii Septa Revealed by Cryo-Electron Microscopy of Vitreous Sections.” Journal of Bacteriology 188 no. 18 (2006):6652–6660[/footnote] Gram- negative cell walls are structurally more complex, containing three layers: the inner membrane, a thin layer of peptidoglycan, and an outer membrane containing lipopolysaccharide. (credit: modification of work by “Franciscosp2”/Wikimedia Commons)"
513148a3-239d-4fda-99b8-cbd1591c45ce,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Gram-negative cells have a much thinner layer of peptidoglycan (no more than about 4 nm thick[4]) than gram- positive cells, and the overall structure of their cell envelope is more complex. In gram-negative cells, a gel-like matrix occupies the periplasmic space between the cell wall and the plasma membrane, and there is a second lipid bilayer called the outer membrane, which is external to the peptidoglycan layer (Figure 2.17). This outer membrane is attached to the peptidoglycan by murein lipoprotein. The outer leaflet of the outer membrane contains the molecule lipopolysaccharide (LPS), which functions as an endotoxin in infections involving gram-negative bacteria, contributing to symptoms such as fever, hemorrhaging, and septic shock. Each LPS molecule is composed of Lipid A, a core polysaccharide, and an O side chain that is composed of sugar-like molecules that comprise the external face of the LPS (Figure 2.18). The composition of the O side chain varies between different species and strains of bacteria. Parts of the O side chain called antigens can be detected using serological or immunological tests to identify specific pathogenic strains like Escherichia coli O157:H7, a deadly strain of bacteria that causes bloody diarrhea and kidney failure.",True,Cell Wall,Figure 2.17,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.26.png,"Figure 2.17 Bacteria contain two common cell wall structural types. Gram-positive cell walls are structurally simple, containing a thick layer of peptidoglycan with embedded teichoic acid external to the plasma membrane.[footnote]B. Zuber et al. “Granular Layer in the Periplasmic Space of Gram-Positive Bacteria and Fine Structures of Enterococcus gallinarum and Streptococcus gordonii Septa Revealed by Cryo-Electron Microscopy of Vitreous Sections.” Journal of Bacteriology 188 no. 18 (2006):6652–6660[/footnote] Gram- negative cell walls are structurally more complex, containing three layers: the inner membrane, a thin layer of peptidoglycan, and an outer membrane containing lipopolysaccharide. (credit: modification of work by “Franciscosp2”/Wikimedia Commons)"
d60d583c-d92b-42c7-a449-7f689bbe59b7,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Archaeal cell wall structure differs from that of bacteria in several significant ways. First, archaeal cell walls do not contain peptidoglycan; instead, they contain a similar polymer called pseudopeptidoglycan (pseudomurein) in which NAM is replaced with a different subunit. Other archaea may have a layer of glycoproteins or polysaccharides that serves as the cell wall instead of pseudopeptidoglycan. Last, as is the case with some bacterial species, there are a few archaea that appear to lack cell walls entirely.",True,Cell Wall,,,,
f6e9d335-bd3f-4bc5-af20-6e08ebc5bc4f,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,Glycocalyces and S-Layers,False,Glycocalyces and S-Layers,,,,
3b3ad9fe-72e5-46b5-8e18-4818f0d9ac2b,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Although most prokaryotic cells have cell walls, some may have additional cell envelope structures exterior to the cell wall, such as glycocalyces and S-layers. A glycocalyx is a sugar coat, of which there are two important types: capsules and slime layers. A capsule is an organized layer located outside of the cell wall and usually composed of polysaccharides or proteins (Figure 2.19). A slime layer is a less tightly organized layer that is only loosely attached to the cell wall and can be more easily washed off. Slime layers may be composed of polysaccharides, glycoproteins, or glycolipids.",True,Glycocalyces and S-Layers,Figure 2.19,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.29.png,"Figure 2.19 (a) Capsules are a type of glycocalyx composed of an organized layer of polysaccharides. (b) A capsule stain of Pseudomonas aeruginosa, a bacterial pathogen capable of causing many different types of infections in humans. (credit b: modification of work by American Society for Microbiology)"
29ea81e8-48fe-4a79-969d-f31d0075ea73,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Glycocalyces allows cells to adhere to surfaces, aiding in the formation of biofilms (colonies of microbes that form in layers on surfaces). In nature, most microbes live in mixed communities within biofilms, partly because the biofilm affords them some level of protection. Biofilms generally hold water like a sponge, preventing desiccation. They also protect cells from predation and hinder the action of antibiotics and disinfectants. All of these properties are advantageous to the microbes living in a biofilm, but they present challenges in a clinical setting, where the goal is often to eliminate microbes.",True,Glycocalyces and S-Layers,,,,
1ae7ad23-95a1-489e-b921-63d050c59514,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"The ability to produce a capsule can contribute to a microbe’s pathogenicity (ability to cause disease) because the capsule can make it more difficult for phagocytic cells (such as white blood cells) to engulf and kill the microorganism. Streptococcus pneumoniae, for example, produces a capsule that is well known to aid in this bacterium’s pathogenicity.",True,Glycocalyces and S-Layers,,,,
9996b964-7c09-4e21-a927-7a7d2365ee59,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"An S-layer is another type of cell envelope structure; it is composed of a mixture of structural proteins and glycoproteins. In bacteria, S-layers are found outside the cell wall, but in some archaea, the S-layer serves as the cell wall. The exact function of S-layers is not entirely understood, and they are difficult to study; but available evidence suggests that they may play a variety of functions in different prokaryotic cells, such as helping the cell withstand osmotic pressure and, for certain pathogens, interacting with the host immune system.",True,Glycocalyces and S-Layers,,,,
7d92c43f-02cc-4bd5-9d99-f6efb167a394,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,Filamentous Appendages,False,Filamentous Appendages,,,,
a2c980f2-46e3-4ae9-be5e-1d98d8ef4daa,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"Fimbriae and pili are structurally similar and, because differentiation between the two is problematic, these terms are often used interchangeably.[5][6] The term fimbriae commonly refers to short bristle-like proteins projecting from the cell surface by the hundreds. Fimbriae enable a cell to attach to surfaces and to other cells. For pathogenic bacteria, adherence to host cells is important for colonization, infectivity, and virulence. Adherence to surfaces is also important in biofilm formation.",True,Filamentous Appendages,,,,
f0e93ecc-18b7-470d-a090-ffc1522eb609,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,"The term pili (singular: pilus) commonly refers to longer, less numerous protein appendages that aid in attachment to surfaces (Figure 2.20). A specific type of pilus, called the F pilus or sex pilus, is important in the transfer of DNA between bacterial cells, which occurs between members of the same generation when two cells physically transfer or exchange parts of their respective genomes.",True,Filamentous Appendages,Figure 2.20,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.30.png,"Figure 2.20 Bacteria may produce two different types of protein appendages that aid in surface attachment. Fimbriae typically are more numerous and shorter, whereas pili (shown here) are longer and less numerous per cell. (credit: modification of work by American Society for Microbiology)"
58e4b4ae-0d83-4bc7-8115-2081bfdfd88a,https://open.oregonstate.education/microbiology/,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/microbiology/chapter/3-3unique-characteristics-of-prokaryotic-cells/,Flagella are structures used by cells to move in aqueous environments. Bacterial flagella act like propellers. They are stiff spiral filaments composed of flagellin protein subunits that extend outward from the cell and spin in solution. The basal body is the motor for the flagellum and is embedded in the plasma membrane (Figure 2.21). A hook region connects the basal body to the filament. Gram-positive and gram-negative bacteria have different basal body configurations due to differences in cell wall structure.,True,Filamentous Appendages,Figure 2.21,2.3 Unique Characteristics of Prokaryotic Cells,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.31.png,"Figure 2.21 The basic structure of a bacterial flagellum consists of a basal body, hook, and filament. The basal body composition and arrangement differ between gram-positive and gram-negative bacteria. (credit: modification of work by “LadyofHats”/Mariana Ruiz Villareal)"
945dfabf-78e6-4785-a0e0-31658d31c6a9,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Today, these tenets are fundamental to our understanding of life on earth. However, modern cell theory grew out of the collective work of many scientists.",True,Filamentous Appendages,,,,
1cf904ec-9105-4039-994b-cf5a53c93a1d,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,The Origins of Cell Theory,False,The Origins of Cell Theory,,,,
d325288c-026d-46e3-9189-be010623e72e,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"The English scientist Robert Hooke first used the term “cells” in 1665 to describe the small chambers within cork that he observed under a microscope of his own design. To Hooke, thin sections of cork resembled “Honey-comb,” or “small Boxes or Bladders of Air.” He noted that each “Cavern, Bubble, or Cell” was distinct from the others (Figure 2.5). At the time, Hooke was not aware that the cork cells were long dead and, therefore, lacked the internal structures found within living cells.",True,The Origins of Cell Theory,Figure 2.5,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.5.png,Figure 2.5 Robert Hooke (1635–1703) was the first to describe cells based upon his microscopic observations of cork. This illustration was published in his work Micrographia.
a0b20f0c-1409-412f-840d-80a9b31fc715,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Despite Hooke’s early description of cells, their significance as the fundamental unit of life was not yet recognized. Nearly 200 years later, in 1838, Matthias Schleiden (1804–1881), a German botanist who made extensive microscopic observations of plant tissues, described them as being composed of cells. Visualizing plant cells was relatively easy because plant cells are clearly separated by their thick cell walls. Schleiden believed that cells formed through crystallization, rather than cell division.",True,The Origins of Cell Theory,,,,
aac4c7d8-40ee-4439-b612-49a31f407215,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Theodor Schwann (1810–1882), a noted German physiologist, made similar microscopic observations of animal tissue. In 1839, after a conversation with Schleiden, Schwann realized that similarities existed between plant and animal tissues. This laid the foundation for the idea that cells are the fundamental components of plants and animals.",True,The Origins of Cell Theory,,,,
eaadd3f3-63c6-4f4c-b4d6-8dfce16e425d,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"In the 1850s, two Polish scientists living in Germany pushed this idea further, culminating in what we recognize today as the modern cell theory. In 1852, Robert Remak (1815–1865), a prominent neurologist and embryologist, published convincing evidence that cells are derived from other cells as a result of cell division. However, this idea was questioned by many in the scientific community. Three years later, Rudolf Virchow (1821–1902), a well- respected pathologist, published an editorial essay entitled “Cellular Pathology,” which popularized the concept of cell theory using the Latin phrase omnis cellula a cellula (“all cells arise from cells”), which is essentially the second tenet of modern cell theory.[1] Given the similarity of Virchow’s work to Remak’s, there is some controversy as to which scientist should receive credit for articulating cell theory.",True,The Origins of Cell Theory,,,,
daef08cb-2592-4e59-9f0e-4ce4e07fde99,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,Endosymbiotic Theory,False,Endosymbiotic Theory,,,,
f01d430b-5323-4d2d-92cb-36d7defad491,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"As scientists were making progress toward understanding the role of cells in plant and animal tissues, others were examining the structures within the cells themselves. In 1831, Scottish botanist Robert Brown (1773–1858) was the first to describe observations of nuclei, which he observed in plant cells. Then, in the early 1880s, German botanist Andreas Schimper (1856–1901) was the first to describe the chloroplasts of plant cells, identifying their role in starch formation during photosynthesis and noting that they divided independent of the nucleus.",True,Endosymbiotic Theory,,,,
b087c094-166a-477d-8417-f9bf5d4e16f6,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Based upon the chloroplasts’ ability to reproduce independently, Russian botanist Konstantin Mereschkowski (1855–1921) suggested in 1905 that chloroplasts may have originated from ancestral photosynthetic bacteria living symbiotically inside a eukaryotic cell. He proposed a similar origin for the nucleus of plant cells. This was the first articulation of the endosymbiotic hypothesis, and would explain how eukaryotic cells evolved from ancestral bacteria.",True,Endosymbiotic Theory,,,,
cb2921f8-df2d-4e84-acfb-dbf612beabae,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Mereschkowski’s endosymbiotic hypothesis was furthered by American anatomist Ivan Wallin (1883–1969), who began to experimentally examine the similarities between mitochondria, chloroplasts, and bacteria—in other words, to put the endosymbiotic hypothesis to the test using objective investigation. Wallin published a series of papers in the 1920s supporting the endosymbiotic hypothesis, including a 1926 publication co-authored with Mereschkowski. Wallin claimed he could culture mitochondria outside of their eukaryotic host cells. Many scientists dismissed his cultures of mitochondria as resulting from bacterial contamination. Modern genome sequencing work supports the dissenting scientists by showing that much of the genome of mitochondria had been transferred to the host cell’s nucleus, preventing the mitochondria from being able to live on their own.[2][3]",True,Endosymbiotic Theory,,,,
674d4390-f68b-44f6-97bc-54fb76224006,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Wallin’s ideas regarding the endosymbiotic hypothesis were largely ignored for the next 50 years because scientists were unaware that these organelles contained their own DNA. However, with the discovery of mitochondrial and chloroplast DNA in the 1960s, the endosymbiotic hypothesis was resurrected. Lynn Margulis (1938–2011), an American geneticist, published her ideas regarding the endosymbiotic hypothesis of the origins of mitochondria and chloroplasts in 1967.[4] In the decade leading up to her publication, advances in microscopy had allowed scientists to differentiate prokaryotic cells from eukaryotic cells. In her publication, Margulis reviewed the literature and argued that the eukaryotic organelles such as mitochondria and chloroplasts are of prokaryotic origin. She presented a growing body of microscopic, genetic, molecular biology, fossil, and geological data to support her claims.",True,Endosymbiotic Theory,,,,
8a148e1a-7a57-4415-87f8-828fa7356c9e,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Again, this hypothesis was not initially popular, but mounting genetic evidence due to the advent of DNA sequencing supported the endosymbiotic theory, which is now defined as the theory that mitochondria and chloroplasts arose as a result of prokaryotic cells establishing a symbiotic relationship within a eukaryotic host (Figure 2.6). With Margulis’ initial endosymbiotic theory gaining wide acceptance, she expanded on the theory in her 1981 book Symbiosis in Cell Evolution. In it, she explains how endosymbiosis is a major driving factor in the evolution of organisms. More recent genetic sequencing and phylogenetic analysis show that mitochondrial DNA and chloroplast DNA are highly related to their bacterial counterparts, both in DNA sequence and chromosome structure. However, mitochondrial DNA and chloroplast DNA are reduced compared with nuclear DNA because many of the genes have moved from the organelles into the host cell’s nucleus. Additionally, mitochondrial and chloroplast ribosomes are structurally similar to bacterial ribosomes, rather than to the eukaryotic ribosomes of their hosts. Last, the binary fission of these organelles strongly resembles the binary fission of bacteria, as compared with mitosis performed by eukaryotic cells. Since Margulis’ original proposal, scientists have observed several examples of bacterial endosymbionts in modern-day eukaryotic cells. Examples include the endosymbiotic bacteria found within the guts of certain insects, such as cockroaches,[5] and photosynthetic bacteria-like organelles found in protists.[6]",True,Endosymbiotic Theory,Figure 2.6,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.7.png,"Figure 2.6 According to the endosymbiotic theory, mitochondria and chloroplasts are each derived from the uptake of bacteria. These bacteria established a symbiotic relationship with their host cell that eventually led to the bacteria evolving into mitochondria and chloroplasts."
f0d38660-31a7-48ab-aafd-1a2422f2c038,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,The Germ Theory of Disease,False,The Germ Theory of Disease,,,,
b7cf4a82-87ab-479a-b2a4-5b013f03ee85,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Prior to the discovery of microbes during the 17th century, other theories circulated about the origins of disease. For example, the ancient Greeks proposed the miasma theory, which held that disease originated from particles emanating from decomposing matter, such as that in sewage or cesspits. Such particles infected humans in close proximity to the rotting material. Diseases including the Black Death, which ravaged Europe’s population during the Middle Ages, were thought to have originated in this way.",True,The Germ Theory of Disease,,,,
8c854f81-c1ab-4864-a863-4badf8ff1a79,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"In 1546, Italian physician Girolamo Fracastoro proposed, in his essay De Contagione et Contagiosis Morbis, that seed-like spores may be transferred between individuals through direct contact, exposure to contaminated clothing, or through the air. We now recognize Fracastoro as an early proponent of the germ theory of disease, which states that diseases may result from microbial infection. However, in the 16th century, Fracastoro’s ideas were not widely accepted and would be largely forgotten until the 19th century.",True,The Germ Theory of Disease,,,,
5a45d1a3-0d38-41a2-9132-0839e7ae472a,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"In 1847, Hungarian obstetrician Ignaz Semmelweis (Figure 2.7) observed that mothers who gave birth in hospital wards staffed by physicians and medical students were more likely to suffer and die from puerperal fever after childbirth (10%–20% mortality rate) than were mothers in wards staffed by midwives (1% mortality rate). Semmelweis observed medical students performing autopsies and then subsequently carrying out vaginal examinations on living patients without washing their hands in between. He suspected that the students carried diseasefrom the autopsies to the patients they examined. His suspicions were supported by the untimely death of a friend, a physician who contracted a fatal wound infection after a postmortem examination of a woman who had died of a puerperal infection. The dead physician’s wound had been caused by a scalpel used during the examination, and his subsequent illness and death closely paralleled that of the dead patient.",True,The Germ Theory of Disease,Figure 2.7,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.8.png,Figure 2.7 Ignaz Semmelweis (1818–1865) was a proponent of the importance of handwashing to prevent transfer of disease between patients by physicians.
dfa6087d-7fa6-488c-a77d-5b1d8259a8aa,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Although Semmelweis did not know the true cause of puerperal fever, he proposed that physicians were somehow transferring the causative agent to their patients. He suggested that the number of puerperal fever cases could be reduced if physicians and medical students simply washed their hands with chlorinated lime water before and after examining every patient. When this practice was implemented, the maternal mortality rate in mothers cared for by physicians dropped to the same 1% mortality rate observed among mothers cared for by midwives. This demonstrated that handwashing was a very effective method for preventing disease transmission. Despite this great success, many discounted Semmelweis’s work at the time, and physicians were slow to adopt the simple procedure of handwashing to prevent infections in their patients because it contradicted established norms for that time period.",True,The Germ Theory of Disease,,,,
77f0c8f6-1145-42e6-8286-83f596134fb5,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Around the same time Semmelweis was promoting handwashing, in 1848, British physician John Snow conducted studies to track the source of cholera outbreaks in London. By tracing the outbreaks to two specific water sources, both of which were contaminated by sewage, Snow ultimately demonstrated that cholera bacteria were transmitted via drinking water. Snow’s work is influential in that it represents the first known epidemiological study, and it resulted in the first known public health response to an epidemic. The work of both Semmelweis and Snow clearly refuted the prevailing miasma theory of the day, showing that disease is not only transmitted through the air but also through contaminated items.",True,The Germ Theory of Disease,,,,
11ad93d3-948c-4ad6-90dc-c9c8744f51b8,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Although the work of Semmelweis and Snow successfully showed the role of sanitation in preventing infectious disease, the cause of disease was not fully understood. The subsequent work of Louis Pasteur, Robert Koch, and Joseph Lister would further substantiate the germ theory of disease.",True,The Germ Theory of Disease,,,,
0cde3efa-2264-4b51-8bc9-ef9101667d15,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"While studying the causes of beer and wine spoilage in 1856, Pasteur discovered properties of fermentation by microorganisms. He had demonstrated with his swan-neck flask experiments (Figure 2.4) that airborne microbes, not spontaneous generation, were the cause of food spoilage, and he suggested that if microbes were responsible for food spoilage and fermentation, they could also be responsible for causing infection. This was the foundation for the germ theory of disease.",True,The Germ Theory of Disease,Figure 2.4,2.1 Spontaneous Generation,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.4.png,"Figure 2.4 (a) French scientist Louis Pasteur, who definitively refuted the long-disputed theory of spontaneous generation. (b) The unique swan-neck feature of the flasks used in Pasteur ’s experiment allowed air to enter the flask but prevented the entry of bacterial and fungal spores. (c) Pasteur’s experiment consisted of two parts. In the first part, the broth in the flask was boiled to sterilize it. When this broth was cooled, it remained free of contamination. In the second part of the experiment, the flask was boiled and then the neck was broken off. The broth in this flask became contaminated. (credit b: modification of work by “Wellcome Images”/Wikimedia Commons)"
1aeed67b-87f1-4ee8-8b34-43c489bd38ff,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Meanwhile, British surgeon Joseph Lister (Figure 2.8) was trying to determine the causes of postsurgical infections. Many physicians did not give credence to the idea that microbes on their hands, on their clothes, or in the air could infect patients’ surgical wounds, despite the fact that 50% of surgical patients, on average, were dying of postsurgical infections.[7] Lister, however, was familiar with the work of Semmelweis and Pasteur; therefore, he insisted onhandwashing and extreme cleanliness during surgery. In 1867, to further decrease the incidence of postsurgical wound infections, Lister began using carbolic acid (phenol) spray disinfectant/antiseptic during surgery. His extremely successful efforts to reduce postsurgical infection caused his techniques to become a standard medical practice.",True,The Germ Theory of Disease,Figure 2.8,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.9.png,Figure 2.8 (a) Joseph Lister developed procedures for the proper care of surgical wounds and the sterilization of surgical equipment. (b) Robert Koch established a protocol to determine the cause of infectious disease. Both scientists contributed significantly to the acceptance of the germ theory of disease.
ff3e912f-52d3-4a99-b784-a79fb15f1759,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"A few years later, Robert Koch (Figure 2.8) proposed a series of postulates (Koch’s postulates) based on the idea that the cause of a specific disease could be attributed to a specific microbe. Using these postulates, Koch and his colleagues were able to definitively identify the causative pathogens of specific diseases, including anthrax, tuberculosis, and cholera. Koch’s “one microbe, one disease” concept was the culmination of the 19th century’s paradigm shift away from miasma theory and toward the germ theory of disease.",True,The Germ Theory of Disease,Figure 2.8,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.9.png,Figure 2.8 (a) Joseph Lister developed procedures for the proper care of surgical wounds and the sterilization of surgical equipment. (b) Robert Koch established a protocol to determine the cause of infectious disease. Both scientists contributed significantly to the acceptance of the germ theory of disease.
7149c793-9387-40ac-851d-84991699f418,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,Endosymbiotic Theory,False,Endosymbiotic Theory,,,,
04a86e43-0a3e-4809-b38d-d5a620d41128,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"As scientists were making progress toward understanding the role of cells in plant and animal tissues, others were examining the structures within the cells themselves. In 1831, Scottish botanist Robert Brown (1773–1858) was the first to describe observations of nuclei, which he observed in plant cells. Then, in the early 1880s, German botanist Andreas Schimper (1856–1901) was the first to describe the chloroplasts of plant cells, identifying their role in starch formation during photosynthesis and noting that they divided independent of the nucleus.",True,Endosymbiotic Theory,,,,
1c09174d-3687-4346-a4f1-0e7513f90e7c,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Based upon the chloroplasts’ ability to reproduce independently, Russian botanist Konstantin Mereschkowski (1855–1921) suggested in 1905 that chloroplasts may have originated from ancestral photosynthetic bacteria living symbiotically inside a eukaryotic cell. He proposed a similar origin for the nucleus of plant cells. This was the first articulation of the endosymbiotic hypothesis, and would explain how eukaryotic cells evolved from ancestral bacteria.",True,Endosymbiotic Theory,,,,
042abc9b-08c6-41a6-b9e5-9a9325d571e8,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Mereschkowski’s endosymbiotic hypothesis was furthered by American anatomist Ivan Wallin (1883–1969), who began to experimentally examine the similarities between mitochondria, chloroplasts, and bacteria—in other words, to put the endosymbiotic hypothesis to the test using objective investigation. Wallin published a series of papers in the 1920s supporting the endosymbiotic hypothesis, including a 1926 publication co-authored with Mereschkowski. Wallin claimed he could culture mitochondria outside of their eukaryotic host cells. Many scientists dismissed his cultures of mitochondria as resulting from bacterial contamination. Modern genome sequencing work supports the dissenting scientists by showing that much of the genome of mitochondria had been transferred to the host cell’s nucleus, preventing the mitochondria from being able to live on their own.[2][3]",True,Endosymbiotic Theory,,,,
8238d6ea-e59e-4158-9912-160e7485b57e,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Wallin’s ideas regarding the endosymbiotic hypothesis were largely ignored for the next 50 years because scientists were unaware that these organelles contained their own DNA. However, with the discovery of mitochondrial and chloroplast DNA in the 1960s, the endosymbiotic hypothesis was resurrected. Lynn Margulis (1938–2011), an American geneticist, published her ideas regarding the endosymbiotic hypothesis of the origins of mitochondria and chloroplasts in 1967.[4] In the decade leading up to her publication, advances in microscopy had allowed scientists to differentiate prokaryotic cells from eukaryotic cells. In her publication, Margulis reviewed the literature and argued that the eukaryotic organelles such as mitochondria and chloroplasts are of prokaryotic origin. She presented a growing body of microscopic, genetic, molecular biology, fossil, and geological data to support her claims.",True,Endosymbiotic Theory,,,,
067a9069-aff2-49b6-8de1-ad2fea963112,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Again, this hypothesis was not initially popular, but mounting genetic evidence due to the advent of DNA sequencing supported the endosymbiotic theory, which is now defined as the theory that mitochondria and chloroplasts arose as a result of prokaryotic cells establishing a symbiotic relationship within a eukaryotic host (Figure 2.6). With Margulis’ initial endosymbiotic theory gaining wide acceptance, she expanded on the theory in her 1981 book Symbiosis in Cell Evolution. In it, she explains how endosymbiosis is a major driving factor in the evolution of organisms. More recent genetic sequencing and phylogenetic analysis show that mitochondrial DNA and chloroplast DNA are highly related to their bacterial counterparts, both in DNA sequence and chromosome structure. However, mitochondrial DNA and chloroplast DNA are reduced compared with nuclear DNA because many of the genes have moved from the organelles into the host cell’s nucleus. Additionally, mitochondrial and chloroplast ribosomes are structurally similar to bacterial ribosomes, rather than to the eukaryotic ribosomes of their hosts. Last, the binary fission of these organelles strongly resembles the binary fission of bacteria, as compared with mitosis performed by eukaryotic cells. Since Margulis’ original proposal, scientists have observed several examples of bacterial endosymbionts in modern-day eukaryotic cells. Examples include the endosymbiotic bacteria found within the guts of certain insects, such as cockroaches,[5] and photosynthetic bacteria-like organelles found in protists.[6]",True,Endosymbiotic Theory,Figure 2.6,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.7.png,"Figure 2.6 According to the endosymbiotic theory, mitochondria and chloroplasts are each derived from the uptake of bacteria. These bacteria established a symbiotic relationship with their host cell that eventually led to the bacteria evolving into mitochondria and chloroplasts."
08fac3aa-2c49-4c23-9e23-82ea492c7df8,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,The Germ Theory of Disease,False,The Germ Theory of Disease,,,,
cb839cfb-6a7f-45c5-8ae9-8b136fa15728,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Prior to the discovery of microbes during the 17th century, other theories circulated about the origins of disease. For example, the ancient Greeks proposed the miasma theory, which held that disease originated from particles emanating from decomposing matter, such as that in sewage or cesspits. Such particles infected humans in close proximity to the rotting material. Diseases including the Black Death, which ravaged Europe’s population during the Middle Ages, were thought to have originated in this way.",True,The Germ Theory of Disease,,,,
c0f91496-4340-4658-87ff-370fdb5166e6,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"In 1546, Italian physician Girolamo Fracastoro proposed, in his essay De Contagione et Contagiosis Morbis, that seed-like spores may be transferred between individuals through direct contact, exposure to contaminated clothing, or through the air. We now recognize Fracastoro as an early proponent of the germ theory of disease, which states that diseases may result from microbial infection. However, in the 16th century, Fracastoro’s ideas were not widely accepted and would be largely forgotten until the 19th century.",True,The Germ Theory of Disease,,,,
ebf81796-5465-4535-8ead-5ec8c3cb2d16,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"In 1847, Hungarian obstetrician Ignaz Semmelweis (Figure 2.7) observed that mothers who gave birth in hospital wards staffed by physicians and medical students were more likely to suffer and die from puerperal fever after childbirth (10%–20% mortality rate) than were mothers in wards staffed by midwives (1% mortality rate). Semmelweis observed medical students performing autopsies and then subsequently carrying out vaginal examinations on living patients without washing their hands in between. He suspected that the students carried diseasefrom the autopsies to the patients they examined. His suspicions were supported by the untimely death of a friend, a physician who contracted a fatal wound infection after a postmortem examination of a woman who had died of a puerperal infection. The dead physician’s wound had been caused by a scalpel used during the examination, and his subsequent illness and death closely paralleled that of the dead patient.",True,The Germ Theory of Disease,Figure 2.7,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.8.png,Figure 2.7 Ignaz Semmelweis (1818–1865) was a proponent of the importance of handwashing to prevent transfer of disease between patients by physicians.
aa7e3f99-6a16-43cf-b66a-5d2aaa492310,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Although Semmelweis did not know the true cause of puerperal fever, he proposed that physicians were somehow transferring the causative agent to their patients. He suggested that the number of puerperal fever cases could be reduced if physicians and medical students simply washed their hands with chlorinated lime water before and after examining every patient. When this practice was implemented, the maternal mortality rate in mothers cared for by physicians dropped to the same 1% mortality rate observed among mothers cared for by midwives. This demonstrated that handwashing was a very effective method for preventing disease transmission. Despite this great success, many discounted Semmelweis’s work at the time, and physicians were slow to adopt the simple procedure of handwashing to prevent infections in their patients because it contradicted established norms for that time period.",True,The Germ Theory of Disease,,,,
172f495e-9a52-4c21-af82-a3eebe064acb,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Around the same time Semmelweis was promoting handwashing, in 1848, British physician John Snow conducted studies to track the source of cholera outbreaks in London. By tracing the outbreaks to two specific water sources, both of which were contaminated by sewage, Snow ultimately demonstrated that cholera bacteria were transmitted via drinking water. Snow’s work is influential in that it represents the first known epidemiological study, and it resulted in the first known public health response to an epidemic. The work of both Semmelweis and Snow clearly refuted the prevailing miasma theory of the day, showing that disease is not only transmitted through the air but also through contaminated items.",True,The Germ Theory of Disease,,,,
5febb54a-27d3-439d-9e55-9a3e60adbf47,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Although the work of Semmelweis and Snow successfully showed the role of sanitation in preventing infectious disease, the cause of disease was not fully understood. The subsequent work of Louis Pasteur, Robert Koch, and Joseph Lister would further substantiate the germ theory of disease.",True,The Germ Theory of Disease,,,,
4c9c97e0-e7a0-430c-9fa7-6bf500c97965,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"While studying the causes of beer and wine spoilage in 1856, Pasteur discovered properties of fermentation by microorganisms. He had demonstrated with his swan-neck flask experiments (Figure 2.4) that airborne microbes, not spontaneous generation, were the cause of food spoilage, and he suggested that if microbes were responsible for food spoilage and fermentation, they could also be responsible for causing infection. This was the foundation for the germ theory of disease.",True,The Germ Theory of Disease,Figure 2.4,2.1 Spontaneous Generation,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.4.png,"Figure 2.4 (a) French scientist Louis Pasteur, who definitively refuted the long-disputed theory of spontaneous generation. (b) The unique swan-neck feature of the flasks used in Pasteur ’s experiment allowed air to enter the flask but prevented the entry of bacterial and fungal spores. (c) Pasteur’s experiment consisted of two parts. In the first part, the broth in the flask was boiled to sterilize it. When this broth was cooled, it remained free of contamination. In the second part of the experiment, the flask was boiled and then the neck was broken off. The broth in this flask became contaminated. (credit b: modification of work by “Wellcome Images”/Wikimedia Commons)"
afba1ad1-0c0e-45e5-b061-ebd0d345ad73,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"Meanwhile, British surgeon Joseph Lister (Figure 2.8) was trying to determine the causes of postsurgical infections. Many physicians did not give credence to the idea that microbes on their hands, on their clothes, or in the air could infect patients’ surgical wounds, despite the fact that 50% of surgical patients, on average, were dying of postsurgical infections.[7] Lister, however, was familiar with the work of Semmelweis and Pasteur; therefore, he insisted onhandwashing and extreme cleanliness during surgery. In 1867, to further decrease the incidence of postsurgical wound infections, Lister began using carbolic acid (phenol) spray disinfectant/antiseptic during surgery. His extremely successful efforts to reduce postsurgical infection caused his techniques to become a standard medical practice.",True,The Germ Theory of Disease,Figure 2.8,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.9.png,Figure 2.8 (a) Joseph Lister developed procedures for the proper care of surgical wounds and the sterilization of surgical equipment. (b) Robert Koch established a protocol to determine the cause of infectious disease. Both scientists contributed significantly to the acceptance of the germ theory of disease.
af53649e-8826-4dca-9bb2-693b41e673bf,https://open.oregonstate.education/microbiology/,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/microbiology/chapter/3-2foundations-of-modern-cell-theory/,"A few years later, Robert Koch (Figure 2.8) proposed a series of postulates (Koch’s postulates) based on the idea that the cause of a specific disease could be attributed to a specific microbe. Using these postulates, Koch and his colleagues were able to definitively identify the causative pathogens of specific diseases, including anthrax, tuberculosis, and cholera. Koch’s “one microbe, one disease” concept was the culmination of the 19th century’s paradigm shift away from miasma theory and toward the germ theory of disease.",True,The Germ Theory of Disease,Figure 2.8,2.2 Foundations of Modern Cell Theory,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.9.png,Figure 2.8 (a) Joseph Lister developed procedures for the proper care of surgical wounds and the sterilization of surgical equipment. (b) Robert Koch established a protocol to determine the cause of infectious disease. Both scientists contributed significantly to the acceptance of the germ theory of disease.
116ee5ff-da47-4050-950f-dd974b9a0069,https://open.oregonstate.education/microbiology/,2.1 Spontaneous Generation,https://open.oregonstate.education/microbiology/chapter/3-1spontaneous-generation/,The Theory of Spontaneous Generation,False,The Theory of Spontaneous Generation,,,,
4eca15b4-707d-4c53-8655-780b998528bb,https://open.oregonstate.education/microbiology/,2.1 Spontaneous Generation,https://open.oregonstate.education/microbiology/chapter/3-1spontaneous-generation/,"The Greek philosopher Aristotle (384–322 BC) was one of the earliest recorded scholars to articulate the theory of spontaneous generation, the notion that life can arise from nonliving matter. Aristotle proposed that life arose from nonliving material if the material contained pneuma (“vital heat”). As evidence, he noted several instances of the appearance of animals from environments previously devoid of such animals, such as the seemingly sudden appearance of fish in a new puddle of water.[1]",True,The Theory of Spontaneous Generation,,,,
db87dad9-2f23-4c4b-b010-feb784c62372,https://open.oregonstate.education/microbiology/,2.1 Spontaneous Generation,https://open.oregonstate.education/microbiology/chapter/3-1spontaneous-generation/,"This theory persisted into the 17th century, when scientists undertook additional experimentation to support or disprove it. By this time, the proponents of the theory cited how frogs simply seem to appear along the muddy banks of the Nile River in Egypt during the annual flooding. Others observed that mice simply appeared among grain stored in barns with thatched roofs. When the roof leaked and the grain molded, mice appeared. Jan Baptista van Helmont, a 17th century Flemish scientist, proposed that mice could arise from rags and wheat kernels left in an open container for 3 weeks. In reality, such habitats provided ideal food sources and shelter for mouse populations to flourish.",True,The Theory of Spontaneous Generation,,,,
4851e132-42c3-49ee-9173-b557b8a48041,https://open.oregonstate.education/microbiology/,2.1 Spontaneous Generation,https://open.oregonstate.education/microbiology/chapter/3-1spontaneous-generation/,"However, one of van Helmont’s contemporaries, Italian physician Francesco Redi (1626–1697), performed an experiment in 1668 that was one of the first to refute the idea that maggots (the larvae of flies) spontaneously generate on meat left out in the open air. He predicted that preventing flies from having direct contact with the meat would also prevent the appearance of maggots. Redi left meat in each of six containers (Figure 2.2). Two were open to the air, two were covered with gauze, and two were tightly sealed. His hypothesis was supported when maggots developed in the uncovered jars, but no maggots appeared in either the gauze-covered or the tightly sealed jars. He concluded that maggots could only form when flies were allowed to lay eggs in the meat, and that the maggots were the offspring of flies, not the product of spontaneous generation.",True,The Theory of Spontaneous Generation,Figure 2.2,2.1 Spontaneous Generation,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.2.png,"Figure 2.2 Francesco Redi’s experimental setup consisted of an open container, a container sealed with a cork top, and a container covered in mesh that let in air but not flies. Maggots only appeared on the meat in the open container. However, maggots were also found on the gauze of the gauze-covered container."
d850bc5d-a8fd-4562-84f6-4419837d680a,https://open.oregonstate.education/microbiology/,2.1 Spontaneous Generation,https://open.oregonstate.education/microbiology/chapter/3-1spontaneous-generation/,"Lazzaro Spallanzani (1729–1799) did not agree with Needham’s conclusions, however, and performed hundreds of carefully executed experiments using heated broth.[3] As in Needham’s experiment, broth in sealed jars and unsealed jars was infused with plant and animal matter. Spallanzani’s results contradicted the findings of Needham: Heated but sealed flasks remained clear, without any signs of spontaneous growth, unless the flasks were subsequently opened to the air. This suggested that microbes were introduced into these flasks from the air. In response to Spallanzani’s findings, Needham argued that life originates from a “life force” that was destroyed during Spallanzani’s extended boiling. Any subsequent sealing of the flasks then prevented new life force from entering and causing spontaneous generation (Figure 2.3).",True,The Theory of Spontaneous Generation,Figure 2.3,2.1 Spontaneous Generation,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.3.png,"Figure 2.3 (a) Francesco Redi, who demonstrated that maggots were the offspring of flies, not products of spontaneous generation. (b) John Needham, who argued that microbes arose spontaneously in broth from a “life force.” (c) Lazzaro Spallanzani, whose experiments with broth aimed to disprove those of Needham."
6d9f5714-7036-413a-aa35-72b90bf293d6,https://open.oregonstate.education/microbiology/,2.1 Spontaneous Generation,https://open.oregonstate.education/microbiology/chapter/3-1spontaneous-generation/,Disproving Spontaneous Generation,False,Disproving Spontaneous Generation,,,,
dbe52788-309a-43a3-849e-38b989db4883,https://open.oregonstate.education/microbiology/,2.1 Spontaneous Generation,https://open.oregonstate.education/microbiology/chapter/3-1spontaneous-generation/,"The debate over spontaneous generation continued well into the 19th century, with scientists serving as proponents of both sides. To settle the debate, the Paris Academy of Sciences offered a prize for resolution of the problem. Louis Pasteur, a prominent French chemist who had been studying microbial fermentation and the causes of wine spoilage, accepted the challenge. In 1858, Pasteur filtered air through a gun-cotton filter and, upon microscopic examination of the cotton, found it full of microorganisms, suggesting that the exposure of a broth to air was not introducing a “life force” to the broth but rather airborne microorganisms.",True,Disproving Spontaneous Generation,,,,
b8a2af6d-210c-4321-a218-66578bc1c21c,https://open.oregonstate.education/microbiology/,2.1 Spontaneous Generation,https://open.oregonstate.education/microbiology/chapter/3-1spontaneous-generation/,"Later, Pasteur made a series of flasks with long, twisted necks (“swan-neck” flasks), in which he boiled broth to sterilize it (Figure 2.4). His design allowed air inside the flasks to be exchanged with air from the outside, but prevented the introduction of any airborne microorganisms, which would get caught in the twists and bends of the flasks’ necks. If a life force besides the airborne microorganisms were responsible for microbial growth within the sterilized flasks, it would have access to the broth, whereas the microorganisms would not. He correctly predicted that sterilized broth in his swan-neck flasks would remain sterile as long as the swan necks remained intact. However, should the necks be broken, microorganisms would be introduced, contaminating the flasks and allowing microbial growth within the broth.",True,Disproving Spontaneous Generation,Figure 2.4,2.1 Spontaneous Generation,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.4.png,"Figure 2.4 (a) French scientist Louis Pasteur, who definitively refuted the long-disputed theory of spontaneous generation. (b) The unique swan-neck feature of the flasks used in Pasteur ’s experiment allowed air to enter the flask but prevented the entry of bacterial and fungal spores. (c) Pasteur’s experiment consisted of two parts. In the first part, the broth in the flask was boiled to sterilize it. When this broth was cooled, it remained free of contamination. In the second part of the experiment, the flask was boiled and then the neck was broken off. The broth in this flask became contaminated. (credit b: modification of work by “Wellcome Images”/Wikimedia Commons)"
0edf2c86-1667-4fd7-90ce-5f7ad9c2a1a3,https://open.oregonstate.education/microbiology/,2.1 Spontaneous Generation,https://open.oregonstate.education/microbiology/chapter/3-1spontaneous-generation/,"Pasteur’s set of experiments irrefutably disproved the theory of spontaneous generation and earned him the prestigious Alhumbert Prize from the Paris Academy of Sciences in 1862. In a subsequent lecture in 1864, Pasteur articulated “Omne vivum ex vivo” (“Life only comes from life”). In this lecture, Pasteur recounted his famous swan- neck flask experiment, stating that “…life is a germ and a germ is life. Never will the doctrine of spontaneous generation recover from the mortal blow of this simple experiment.”[4] To Pasteur’s credit, it never has.",True,Disproving Spontaneous Generation,,,,
a6937f7b-45b6-4c6f-901f-308b3980e690,https://open.oregonstate.education/microbiology/,2.1 Spontaneous Generation,https://open.oregonstate.education/microbiology/chapter/3-1spontaneous-generation/,"Lazzaro Spallanzani (1729–1799) did not agree with Needham’s conclusions, however, and performed hundreds of carefully executed experiments using heated broth.[3] As in Needham’s experiment, broth in sealed jars and unsealed jars was infused with plant and animal matter. Spallanzani’s results contradicted the findings of Needham: Heated but sealed flasks remained clear, without any signs of spontaneous growth, unless the flasks were subsequently opened to the air. This suggested that microbes were introduced into these flasks from the air. In response to Spallanzani’s findings, Needham argued that life originates from a “life force” that was destroyed during Spallanzani’s extended boiling. Any subsequent sealing of the flasks then prevented new life force from entering and causing spontaneous generation (Figure 2.3).",True,Disproving Spontaneous Generation,Figure 2.3,2.1 Spontaneous Generation,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.3.png,"Figure 2.3 (a) Francesco Redi, who demonstrated that maggots were the offspring of flies, not products of spontaneous generation. (b) John Needham, who argued that microbes arose spontaneously in broth from a “life force.” (c) Lazzaro Spallanzani, whose experiments with broth aimed to disprove those of Needham."
9c6c6138-515a-4059-8714-dc0fb4e261f7,https://open.oregonstate.education/microbiology/,2.1 Spontaneous Generation,https://open.oregonstate.education/microbiology/chapter/3-1spontaneous-generation/,Disproving Spontaneous Generation,False,Disproving Spontaneous Generation,,,,
c8be371d-adce-47b2-9576-3307a834cd50,https://open.oregonstate.education/microbiology/,2.1 Spontaneous Generation,https://open.oregonstate.education/microbiology/chapter/3-1spontaneous-generation/,"The debate over spontaneous generation continued well into the 19th century, with scientists serving as proponents of both sides. To settle the debate, the Paris Academy of Sciences offered a prize for resolution of the problem. Louis Pasteur, a prominent French chemist who had been studying microbial fermentation and the causes of wine spoilage, accepted the challenge. In 1858, Pasteur filtered air through a gun-cotton filter and, upon microscopic examination of the cotton, found it full of microorganisms, suggesting that the exposure of a broth to air was not introducing a “life force” to the broth but rather airborne microorganisms.",True,Disproving Spontaneous Generation,,,,
d8067e9f-30fe-40f4-b3a5-83172392d306,https://open.oregonstate.education/microbiology/,2.1 Spontaneous Generation,https://open.oregonstate.education/microbiology/chapter/3-1spontaneous-generation/,"Later, Pasteur made a series of flasks with long, twisted necks (“swan-neck” flasks), in which he boiled broth to sterilize it (Figure 2.4). His design allowed air inside the flasks to be exchanged with air from the outside, but prevented the introduction of any airborne microorganisms, which would get caught in the twists and bends of the flasks’ necks. If a life force besides the airborne microorganisms were responsible for microbial growth within the sterilized flasks, it would have access to the broth, whereas the microorganisms would not. He correctly predicted that sterilized broth in his swan-neck flasks would remain sterile as long as the swan necks remained intact. However, should the necks be broken, microorganisms would be introduced, contaminating the flasks and allowing microbial growth within the broth.",True,Disproving Spontaneous Generation,Figure 2.4,2.1 Spontaneous Generation,https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-2.4.png,"Figure 2.4 (a) French scientist Louis Pasteur, who definitively refuted the long-disputed theory of spontaneous generation. (b) The unique swan-neck feature of the flasks used in Pasteur ’s experiment allowed air to enter the flask but prevented the entry of bacterial and fungal spores. (c) Pasteur’s experiment consisted of two parts. In the first part, the broth in the flask was boiled to sterilize it. When this broth was cooled, it remained free of contamination. In the second part of the experiment, the flask was boiled and then the neck was broken off. The broth in this flask became contaminated. (credit b: modification of work by “Wellcome Images”/Wikimedia Commons)"
ebb877e8-5320-4f7b-9aa9-4d54002408a5,https://open.oregonstate.education/microbiology/,2.1 Spontaneous Generation,https://open.oregonstate.education/microbiology/chapter/3-1spontaneous-generation/,"Pasteur’s set of experiments irrefutably disproved the theory of spontaneous generation and earned him the prestigious Alhumbert Prize from the Paris Academy of Sciences in 1862. In a subsequent lecture in 1864, Pasteur articulated “Omne vivum ex vivo” (“Life only comes from life”). In this lecture, Pasteur recounted his famous swan- neck flask experiment, stating that “…life is a germ and a germ is life. Never will the doctrine of spontaneous generation recover from the mortal blow of this simple experiment.”[4] To Pasteur’s credit, it never has.",True,Disproving Spontaneous Generation,,,,
ab40a96a-5bd7-442d-bc32-5385849f2864,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,Learning Objectives,False,Learning Objectives,,,,
4d63f118-7572-4796-be06-f11660c8397c,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,Prokaryote Habitats and Functions,False,Prokaryote Habitats and Functions,,,,
be79aa1a-dd1e-46a3-99d1-5418addbb16f,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Prokaryotes are ubiquitous. They can be found everywhere on our planet, even in hot springs, in the Antarctic ice shield, and under extreme pressure two miles under water. One bacterium, Paracoccus denitrificans, has even been shown to survive when scientists removed it from its native environment (soil) and used a centrifuge to subject it to forces of gravity as strong as those found on the surface of Jupiter.",True,Prokaryote Habitats and Functions,,,,
d2893580-89e2-4cb4-a714-ced02ad08aa0,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Prokaryotes also are abundant on and within the human body. According to a report by National Institutes of Health, prokaryotes, especially bacteria, outnumber human cells 10:1.[1] More recent studies suggest the ratio could be closer to 1:1, but even that ratio means that there are a great number of bacteria within the human body.[2] Bacteria thrive in the human mouth, nasal cavity, throat, ears, gastrointestinal tract, and vagina. Large colonies of bacteria can be found on healthy human skin, especially in moist areas (armpits, navel, and areas behind ears). However, even drier areas of the skin are not free from bacteria.",True,Prokaryote Habitats and Functions,,,,
155c3871-d6c3-4c6d-a800-bae4a009e365,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"The existence of prokaryotes is very important for the stability and thriving of ecosystems. For example, they are a necessary part of soil formation and stabilization processes through the breakdown of organic matter and development of biofilms. One gram of soil contains up to 10 billion microorganisms (most of them prokaryotic) belonging to about 1,000 species. Many species of bacteria use substances released from plant roots, such as acids and carbohydrates, as nutrients. The bacteria metabolize these plant substances and release the products of bacterial metabolism back to the soil, forming humus and thus increasing the soil’s fertility. In salty lakes such as the Dead Sea (Figure 3.2), salt-loving halobacteria decompose dead brine shrimp and nourish young brine shrimp and flies with the products of bacterial metabolism.",True,Prokaryote Habitats and Functions,Figure 3.2,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-3.2.png,"Figure 3.2 (a) Some prokaryotes, called halophiles, can thrive in extremely salty environments such as the Dead Sea, pictured here. (b) The archaeon Halobacterium salinarum, shown here in an electron micrograph, is a halophile that lives in the Dead Sea. (credit a: modification of work by Jullen Menichini; credit b: modification of work by NASA)"
23baefb9-6081-4401-bc24-f208c41be9cb,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"In addition to living in the ground and the water, prokaryotic microorganisms are abundant in the air, even high in the atmosphere. There may be up to 2,000 different kinds of bacteria in the air, similar to their diversity in the soil.",True,Prokaryote Habitats and Functions,,,,
ff0cf27a-b684-4e91-8b1d-7bbb230c7618,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Prokaryotes can be found everywhere on earth because they are extremely resilient and adaptable. They are often metabolically flexible, which means that they might easily switch from one energy source to another, depending on the availability of the sources, or from one metabolic pathway to another. For example, certain prokaryotic cyanobacteria can switch from a conventional type of lipid metabolism, which includes production of fatty aldehydes, to a different type of lipid metabolism that generates biofuel, such as fatty acids and wax esters. Groundwater bacteria store complex high-energy carbohydrates when grown in pure groundwater, but they metabolize these molecules when the groundwater is enriched with phosphates.",True,Prokaryote Habitats and Functions,,,,
2c230b8e-c902-4cc5-a933-284122c8c005,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Prokaryotes perform functions vital to life on earth by capturing (or “fixing”) and recycling elements like carbon and nitrogen. Organisms such as animals require organic carbon to grow, but, unlike prokaryotes, they are unable to use inorganic carbon sources like carbon dioxide. Thus, animals rely on prokaryotes to convert carbon dioxide into organic carbon products that they can use. This process of converting carbon dioxide to organic carbon products is called carbon fixation.",True,Prokaryote Habitats and Functions,,,,
ee8b2ac3-02a6-4c81-afe4-861cc7844194,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Plants and animals also rely heavily on prokaryotes for nitrogen fixation, the conversion of atmospheric nitrogen into ammonia, a compound that some plants can use to form many different biomolecules necessary to their survival. Bacteria in the genus Rhizobium, for example, are nitrogen-fixing bacteria; they live in the roots of legume plants such as clover, alfalfa, and peas (Figure 3.3). Ammonia produced by Rhizobium helps these plants to survive by enabling them to make building blocks of nucleic acids. In turn, these plants may be eaten by animals—sustaining their growth and survival—or they may die, in which case the products of nitrogen fixation will enrich the soil and be used by other plants.",True,Prokaryote Habitats and Functions,Figure 3.3,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-3.3.png,Figure 3.3 (a) Nitrogen-fixing bacteria such as Rhizobium live in the root nodules of legumes such as clover. (b) This micrograph of the root nodule shows bacteroids (bacterium-like cells or modified bacterial cells) within the plant cells. The bacteroids are visible as darker ovals within the larger plant cell. (credit a: modification of work by USDA)
4a95cb80-e050-44bf-884c-5dd94b81e68f,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Another positive function of prokaryotes is in cleaning up the environment. Recently, some researchers focused on the diversity and functions of prokaryotes in manmade environments. They found that some bacteria play a unique role in degrading toxic chemicals that pollute water and soil.[3]",True,Prokaryote Habitats and Functions,,,,
7c326811-29c5-4a6f-aad4-42fab68d6e73,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Despite all of the positive and helpful roles prokaryotes play, some are human pathogens that may cause illness or infection when they enter the body. In addition, some bacteria can contaminate food, causing spoilage or foodborne illness, which makes them subjects of concern in food preparation and safety. Less than 1% of prokaryotes (all of them bacteria) are thought to be human pathogens, but collectively these species are responsible for a large number of the diseases that afflict humans.",True,Prokaryote Habitats and Functions,,,,
25daff2b-c8ce-46fc-ab2d-6c8d54291c24,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Besides pathogens, which have a direct impact on human health, prokaryotes also affect humans in many indirect ways. For example, prokaryotes are now thought to be key players in the processes of climate change. In recent years, as temperatures in the earth’s polar regions have risen, soil that was formerly frozen year-round (permafrost) has begun to thaw. Carbon trapped in the permafrost is gradually released and metabolized by prokaryotes. This produces massive amounts of carbon dioxide and methane, greenhouse gases that escape into the atmosphere and contribute to the greenhouse effect.",True,Prokaryote Habitats and Functions,,,,
8ce5b897-a6a9-4b72-b1ea-2ae05d4834ae,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,Symbiotic Relationships,False,Symbiotic Relationships,,,,
4579f22a-f55c-4291-872d-cc9247688706,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"As we have learned, prokaryotic microorganisms can associate with plants and animals. Often, this association results in unique relationships between organisms. For example, bacteria living on the roots or leaves of a plant get nutrients from the plant and, in return, produce substances that protect the plant from pathogens. On the other hand, some bacteria are plant pathogens that use mechanisms of infection similar to bacterial pathogens of animals and humans.",True,Symbiotic Relationships,,,,
79596e40-40d4-4e75-a043-051778e32ada,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Prokaryotes live in a community, or a group of interacting populations of organisms. A population is a group of individual organisms belonging to the same biological species and limited to a certain geographic area. Populations can have cooperative interactions, which benefit the populations, or competitive interactions, in which one population competes with another for resources. The study of these interactions between microbial populations and their environment is called microbial ecology.",True,Symbiotic Relationships,,,,
b0135091-021e-49ca-ab41-d9e4172face4,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Any interaction between different species that are associated with each other within a community is called symbiosis. Such interactions fall along a continuum between opposition and cooperation. Interactions in a symbiotic relationship may be beneficial or harmful, or have no effect on one or both of the species involved. Table 3.1 summarizes the main types of symbiotic interactions among prokaryotes.",True,Symbiotic Relationships,,,,
976ec713-c360-4415-b181-6a72a6c4a7f7,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"When two species benefit from each other, the symbiosis is called mutualism (or syntropy, or crossfeeding). For example, humans have a mutualistic relationship with the bacterium Bacteroides thetaiotaomicron, which lives in the intestinal tract. Bacteroides thetaiotaomicron digests complex polysaccharide plant materials that human digestive enzymes cannot break down, converting them into monosaccharides that can be absorbed by human cells. Humans also have a mutualistic relationship with certain strains of Escherichia coli, another bacterium found in the gut. E. coli relies on intestinal contents for nutrients, and humans derive certain vitamins from E. coli, particularly vitamin K, which is required for the formation of blood clotting factors. (This is only true for some strains of E. coli, however. Other strains are pathogenic and do not have a mutualistic relationship with humans.)",True,Symbiotic Relationships,,,,
11dc7462-ba8a-476c-9086-f0f5200107a3,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"A type of symbiosis in which one population harms another but remains unaffected itself is called amensalism. In the case of bacteria, some amensalist species produce bactericidal substances that kill other species of bacteria. The microbiota of the skin is composed of a variety of bacterial species, including Staphylococcus epidermidis and Propionibacterium acnes. Although both species have the potential to cause infectious diseases when protective barriers are breached, they both produce a variety of antibacterial bacteriocins and bacteriocin-like compounds. S. epidermidis and P. acnes are unaffected by the bacteriocins and bacteriocin-like compounds they produce, but these compounds can target and kill other potential pathogens.",True,Symbiotic Relationships,,,,
4da4e8b3-88e4-415f-929e-e4210eb00ec8,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"In another type of symbiosis, called commensalism, one organism benefits while the other is unaffected. This occurs when the bacterium Staphylococcus epidermidis uses the dead cells of the human skin as nutrients. Billions of these bacteria live on our skin, but in most cases (especially when our immune system is healthy), we do not react to them in any way. S. epidermidis provides an excellent example of how the classifications of symbiotic relationships are not always distinct. One could also consider the symbiotic relationship of S. epidermidis with humans as mutualism. Humans provide a food source of dead skin cells to the bacterium, and in turn the production of bacteriocin can provide an defense against potential pathogens.",True,Symbiotic Relationships,,,,
af12f679-12b0-40da-b671-0d4bd3034135,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"If neither of the symbiotic organisms is affected in any way, we call this type of symbiosis neutralism. An example of neutralism is the coexistence of metabolically active (vegetating) bacteria and endospores (dormant, metabolically passive bacteria). For example, the bacterium Bacillus anthracis typically forms endospores in soil when conditions are unfavorable. If the soil is warmed and enriched with nutrients, some B. anthracis endospores germinate and remain in symbiosis with other species of endospores that have not germinated.",True,Symbiotic Relationships,,,,
c3edddf3-58c5-420b-a518-d98fb5cf7b42,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"A type of symbiosis in which one organism benefits while harming the other is called parasitism. The relationship between humans and many pathogenic prokaryotes can be characterized as parasitic because these organisms invade the body, producing toxic substances or infectious diseases that cause harm. Diseases such as tetanus, diphtheria, pertussis, tuberculosis, and leprosy all arise from interactions between bacteria and humans.",True,Symbiotic Relationships,,,,
102c2e1f-5168-450e-84f3-faf19f80c25a,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Scientists have coined the term microbiome to refer to all prokaryotic and eukaryotic microorganisms that are associated with a certain organism or environment. Within the human microbiome, there are resident microbiota and transient microbiota. The resident microbiota consists of microorganisms that constantly live in or on our bodies. The term transient microbiota refers to microorganisms that are only temporarily found in the human body, and these may include pathogenic microorganisms. Hygiene and diet can alter both the resident and transient microbiota.",True,Symbiotic Relationships,,,,
c423f9d8-8467-42af-b788-a551387a3565,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"The resident microbiota is amazingly diverse, not only in terms of the variety of species but also in terms of the preference of different microorganisms for different areas of the human body. For example, in the human mouth, there are thousands of commensal or mutualistic species of bacteria. Some of these bacteria prefer to inhabit the surface of the tongue, whereas others prefer the internal surface of the cheeks, and yet others prefer the front or back teeth or gums. The inner surface of the cheek has the least diverse microbiota because of its exposure to oxygen. [4]",True,Symbiotic Relationships,,,,
95a639df-0e12-45a3-bce3-2ffb835d42be,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,There are also significant differences between the microbiota of different sites of the same human body.,True,Symbiotic Relationships,,,,
c055a891-9479-4710-b545-b0a83a5521d4,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Not only can the microbiota vary from one body site to another, the microbiome can also change over time within the same individual. Humans acquire their first inoculations of normal flora during natural birth and shortly after birth. Before birth, there is a rapid increase in the population of Lactobacillus spp. in the vagina, and this population serves as the first colonization of microbiota during natural birth. After birth, additional microbes are acquired from health- care providers, parents, other relatives, and individuals who come in contact with the baby. This process establishes a microbiome that will continue to evolve over the course of the individual’s life as new microbes colonize and are eliminated from the body. For example, it is estimated that within a 9-hour period, the microbiota of the small intestine can change so that half of the microbial inhabitants will be different.[5] The importance of the initial Lactobacillus colonization during vaginal child birth is highlighted by studies demonstrating a higher incidence of diseases in individuals born by cesarean section, compared to those born vaginally. Studies have shown that babies born vaginally are predominantly colonized by vaginal lactobacillus, whereas babies born by cesarean section are more frequently colonized by microbes of the normal skin microbiota, including common hospital-acquired pathogens.",True,Symbiotic Relationships,,,,
a1070a76-35cf-4ca0-96cf-f9883c1a3527,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"One of the challenges in understanding the human microbiome has been the difficulty of culturing many of the microbes that inhabit the human body. It has been estimated that we are only able to culture 1% of the bacteria in nature and that we are unable to grow the remaining 99%. To address this challenge, researchers have used metagenomic analysis, which studies genetic material harvested directly from microbial communities, as opposed to that of individual species grown in a culture. This allows researchers to study the genetic material of all microbes in the microbiome, rather than just those that can be cultured.[6]",True,Symbiotic Relationships,,,,
06f9d533-20c5-4697-818d-47fe3e008f9c,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"One important achievement of the Human Microbiome Project is establishing the first reference database on microorganisms living in and on the human body. Many of the microbes in the microbiome are beneficial, but some are not. It was found, somewhat unexpectedly, that all of us have some serious microbial pathogens in our microbiota. For example, the conjunctiva of the human eye contains 24 genera of bacteria and numerous pathogenic species.[7] A healthy human mouth contains a number of species of the genus Streptococcus, including pathogenic species S. pyogenes and S. pneumoniae.[8] This raises the question of why certain prokaryotic organisms exist commensally in certain individuals but act as deadly pathogens in others. Also unexpected was the number of organisms that had never been cultured. For example, in one metagenomic study of the human gut microbiota, 174 new species of bacteria were identified.[9]",True,Symbiotic Relationships,,,,
1569edc6-ba08-4c9d-8012-067523733aeb,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,Another goal for the near future is to characterize the human microbiota in patients with different diseases and to find out whether there are any relationships between the contents of an individual’s microbiota and risk for or susceptibility to specific diseases. Analyzing the microbiome in a person with a specific disease may reveal new ways to fight diseases.,True,Symbiotic Relationships,,,,
a180ed23-4fa4-4197-b664-ca0c9644d0b5,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,Learning Objectives,False,Learning Objectives,,,,
09a38bf4-869f-410b-b56d-c34406324013,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,Prokaryote Habitats and Functions,False,Prokaryote Habitats and Functions,,,,
4fe471e2-7f85-4e66-9e5c-7470a892b0ba,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Prokaryotes are ubiquitous. They can be found everywhere on our planet, even in hot springs, in the Antarctic ice shield, and under extreme pressure two miles under water. One bacterium, Paracoccus denitrificans, has even been shown to survive when scientists removed it from its native environment (soil) and used a centrifuge to subject it to forces of gravity as strong as those found on the surface of Jupiter.",True,Prokaryote Habitats and Functions,,,,
7cb6b3c1-07c4-4f30-9734-57f951a0df95,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Prokaryotes also are abundant on and within the human body. According to a report by National Institutes of Health, prokaryotes, especially bacteria, outnumber human cells 10:1.[1] More recent studies suggest the ratio could be closer to 1:1, but even that ratio means that there are a great number of bacteria within the human body.[2] Bacteria thrive in the human mouth, nasal cavity, throat, ears, gastrointestinal tract, and vagina. Large colonies of bacteria can be found on healthy human skin, especially in moist areas (armpits, navel, and areas behind ears). However, even drier areas of the skin are not free from bacteria.",True,Prokaryote Habitats and Functions,,,,
6811af1a-9f50-449d-ab1a-25176b31f4b0,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"The existence of prokaryotes is very important for the stability and thriving of ecosystems. For example, they are a necessary part of soil formation and stabilization processes through the breakdown of organic matter and development of biofilms. One gram of soil contains up to 10 billion microorganisms (most of them prokaryotic) belonging to about 1,000 species. Many species of bacteria use substances released from plant roots, such as acids and carbohydrates, as nutrients. The bacteria metabolize these plant substances and release the products of bacterial metabolism back to the soil, forming humus and thus increasing the soil’s fertility. In salty lakes such as the Dead Sea (Figure 3.2), salt-loving halobacteria decompose dead brine shrimp and nourish young brine shrimp and flies with the products of bacterial metabolism.",True,Prokaryote Habitats and Functions,Figure 3.2,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-3.2.png,"Figure 3.2 (a) Some prokaryotes, called halophiles, can thrive in extremely salty environments such as the Dead Sea, pictured here. (b) The archaeon Halobacterium salinarum, shown here in an electron micrograph, is a halophile that lives in the Dead Sea. (credit a: modification of work by Jullen Menichini; credit b: modification of work by NASA)"
f98388eb-babe-4579-92a0-34acdeafe8ae,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"In addition to living in the ground and the water, prokaryotic microorganisms are abundant in the air, even high in the atmosphere. There may be up to 2,000 different kinds of bacteria in the air, similar to their diversity in the soil.",True,Prokaryote Habitats and Functions,,,,
e1286e48-2fda-406b-a081-79060026ca47,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Prokaryotes can be found everywhere on earth because they are extremely resilient and adaptable. They are often metabolically flexible, which means that they might easily switch from one energy source to another, depending on the availability of the sources, or from one metabolic pathway to another. For example, certain prokaryotic cyanobacteria can switch from a conventional type of lipid metabolism, which includes production of fatty aldehydes, to a different type of lipid metabolism that generates biofuel, such as fatty acids and wax esters. Groundwater bacteria store complex high-energy carbohydrates when grown in pure groundwater, but they metabolize these molecules when the groundwater is enriched with phosphates.",True,Prokaryote Habitats and Functions,,,,
539ebce5-4dea-4783-8d31-67cf96d0d0f4,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Prokaryotes perform functions vital to life on earth by capturing (or “fixing”) and recycling elements like carbon and nitrogen. Organisms such as animals require organic carbon to grow, but, unlike prokaryotes, they are unable to use inorganic carbon sources like carbon dioxide. Thus, animals rely on prokaryotes to convert carbon dioxide into organic carbon products that they can use. This process of converting carbon dioxide to organic carbon products is called carbon fixation.",True,Prokaryote Habitats and Functions,,,,
bb53ff1c-3689-423c-b59a-48d4e5da027c,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Plants and animals also rely heavily on prokaryotes for nitrogen fixation, the conversion of atmospheric nitrogen into ammonia, a compound that some plants can use to form many different biomolecules necessary to their survival. Bacteria in the genus Rhizobium, for example, are nitrogen-fixing bacteria; they live in the roots of legume plants such as clover, alfalfa, and peas (Figure 3.3). Ammonia produced by Rhizobium helps these plants to survive by enabling them to make building blocks of nucleic acids. In turn, these plants may be eaten by animals—sustaining their growth and survival—or they may die, in which case the products of nitrogen fixation will enrich the soil and be used by other plants.",True,Prokaryote Habitats and Functions,Figure 3.3,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/app/uploads/sites/8/2019/06/Fig-3.3.png,Figure 3.3 (a) Nitrogen-fixing bacteria such as Rhizobium live in the root nodules of legumes such as clover. (b) This micrograph of the root nodule shows bacteroids (bacterium-like cells or modified bacterial cells) within the plant cells. The bacteroids are visible as darker ovals within the larger plant cell. (credit a: modification of work by USDA)
e06135d0-22d8-467a-a7a9-b65424e3c717,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Another positive function of prokaryotes is in cleaning up the environment. Recently, some researchers focused on the diversity and functions of prokaryotes in manmade environments. They found that some bacteria play a unique role in degrading toxic chemicals that pollute water and soil.[3]",True,Prokaryote Habitats and Functions,,,,
f07cbcb8-fc16-47f8-b733-b62c491d476d,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Despite all of the positive and helpful roles prokaryotes play, some are human pathogens that may cause illness or infection when they enter the body. In addition, some bacteria can contaminate food, causing spoilage or foodborne illness, which makes them subjects of concern in food preparation and safety. Less than 1% of prokaryotes (all of them bacteria) are thought to be human pathogens, but collectively these species are responsible for a large number of the diseases that afflict humans.",True,Prokaryote Habitats and Functions,,,,
57994767-53ec-4c2a-8cda-440216b467ce,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Besides pathogens, which have a direct impact on human health, prokaryotes also affect humans in many indirect ways. For example, prokaryotes are now thought to be key players in the processes of climate change. In recent years, as temperatures in the earth’s polar regions have risen, soil that was formerly frozen year-round (permafrost) has begun to thaw. Carbon trapped in the permafrost is gradually released and metabolized by prokaryotes. This produces massive amounts of carbon dioxide and methane, greenhouse gases that escape into the atmosphere and contribute to the greenhouse effect.",True,Prokaryote Habitats and Functions,,,,
708381ac-7f7e-47ba-a861-e1c672719959,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,Symbiotic Relationships,False,Symbiotic Relationships,,,,
844ce4ba-c6e9-47ef-819a-85ed2b0ae467,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"As we have learned, prokaryotic microorganisms can associate with plants and animals. Often, this association results in unique relationships between organisms. For example, bacteria living on the roots or leaves of a plant get nutrients from the plant and, in return, produce substances that protect the plant from pathogens. On the other hand, some bacteria are plant pathogens that use mechanisms of infection similar to bacterial pathogens of animals and humans.",True,Symbiotic Relationships,,,,
5d848ff3-c68e-4faf-9e88-ce9184a7ceaf,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Prokaryotes live in a community, or a group of interacting populations of organisms. A population is a group of individual organisms belonging to the same biological species and limited to a certain geographic area. Populations can have cooperative interactions, which benefit the populations, or competitive interactions, in which one population competes with another for resources. The study of these interactions between microbial populations and their environment is called microbial ecology.",True,Symbiotic Relationships,,,,
64a84c9b-a7f6-43a7-97c9-e7284198416e,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Any interaction between different species that are associated with each other within a community is called symbiosis. Such interactions fall along a continuum between opposition and cooperation. Interactions in a symbiotic relationship may be beneficial or harmful, or have no effect on one or both of the species involved. Table 3.1 summarizes the main types of symbiotic interactions among prokaryotes.",True,Symbiotic Relationships,,,,
37d52b3a-76c5-43ba-93da-4b29b611c27d,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"When two species benefit from each other, the symbiosis is called mutualism (or syntropy, or crossfeeding). For example, humans have a mutualistic relationship with the bacterium Bacteroides thetaiotaomicron, which lives in the intestinal tract. Bacteroides thetaiotaomicron digests complex polysaccharide plant materials that human digestive enzymes cannot break down, converting them into monosaccharides that can be absorbed by human cells. Humans also have a mutualistic relationship with certain strains of Escherichia coli, another bacterium found in the gut. E. coli relies on intestinal contents for nutrients, and humans derive certain vitamins from E. coli, particularly vitamin K, which is required for the formation of blood clotting factors. (This is only true for some strains of E. coli, however. Other strains are pathogenic and do not have a mutualistic relationship with humans.)",True,Symbiotic Relationships,,,,
62fd1f5e-30b1-424b-9eb0-6da81cef3a65,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"A type of symbiosis in which one population harms another but remains unaffected itself is called amensalism. In the case of bacteria, some amensalist species produce bactericidal substances that kill other species of bacteria. The microbiota of the skin is composed of a variety of bacterial species, including Staphylococcus epidermidis and Propionibacterium acnes. Although both species have the potential to cause infectious diseases when protective barriers are breached, they both produce a variety of antibacterial bacteriocins and bacteriocin-like compounds. S. epidermidis and P. acnes are unaffected by the bacteriocins and bacteriocin-like compounds they produce, but these compounds can target and kill other potential pathogens.",True,Symbiotic Relationships,,,,
3b88b048-7bb5-481a-9319-f00b127c6710,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"In another type of symbiosis, called commensalism, one organism benefits while the other is unaffected. This occurs when the bacterium Staphylococcus epidermidis uses the dead cells of the human skin as nutrients. Billions of these bacteria live on our skin, but in most cases (especially when our immune system is healthy), we do not react to them in any way. S. epidermidis provides an excellent example of how the classifications of symbiotic relationships are not always distinct. One could also consider the symbiotic relationship of S. epidermidis with humans as mutualism. Humans provide a food source of dead skin cells to the bacterium, and in turn the production of bacteriocin can provide an defense against potential pathogens.",True,Symbiotic Relationships,,,,
419b6e72-aa23-4f62-beb3-dce54c6db2d6,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"If neither of the symbiotic organisms is affected in any way, we call this type of symbiosis neutralism. An example of neutralism is the coexistence of metabolically active (vegetating) bacteria and endospores (dormant, metabolically passive bacteria). For example, the bacterium Bacillus anthracis typically forms endospores in soil when conditions are unfavorable. If the soil is warmed and enriched with nutrients, some B. anthracis endospores germinate and remain in symbiosis with other species of endospores that have not germinated.",True,Symbiotic Relationships,,,,
a53e3033-1d7c-465c-821e-85e9480f34de,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"A type of symbiosis in which one organism benefits while harming the other is called parasitism. The relationship between humans and many pathogenic prokaryotes can be characterized as parasitic because these organisms invade the body, producing toxic substances or infectious diseases that cause harm. Diseases such as tetanus, diphtheria, pertussis, tuberculosis, and leprosy all arise from interactions between bacteria and humans.",True,Symbiotic Relationships,,,,
d11dadb6-22a0-4ac6-9553-240297c9858f,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Scientists have coined the term microbiome to refer to all prokaryotic and eukaryotic microorganisms that are associated with a certain organism or environment. Within the human microbiome, there are resident microbiota and transient microbiota. The resident microbiota consists of microorganisms that constantly live in or on our bodies. The term transient microbiota refers to microorganisms that are only temporarily found in the human body, and these may include pathogenic microorganisms. Hygiene and diet can alter both the resident and transient microbiota.",True,Symbiotic Relationships,,,,
b1fa7d05-9bfa-47b5-88a7-51449f78510f,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"The resident microbiota is amazingly diverse, not only in terms of the variety of species but also in terms of the preference of different microorganisms for different areas of the human body. For example, in the human mouth, there are thousands of commensal or mutualistic species of bacteria. Some of these bacteria prefer to inhabit the surface of the tongue, whereas others prefer the internal surface of the cheeks, and yet others prefer the front or back teeth or gums. The inner surface of the cheek has the least diverse microbiota because of its exposure to oxygen. [4]",True,Symbiotic Relationships,,,,
4aa4587a-08dd-41ce-8ba6-884276b34ff3,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,There are also significant differences between the microbiota of different sites of the same human body.,True,Symbiotic Relationships,,,,
ee99c83e-4c2b-4b7b-8b45-164ee5601b99,https://open.oregonstate.education/microbiology/,"3.1 Prokaryote Habitats, Relationships, and Microbiomes",https://open.oregonstate.education/microbiology/chapter/4-1prokaryote-habitats-relationships-and-microbiomes/,"Not only can the microbiota vary from one body site to another, the microbiome can also change over time within the same individual. Humans acquire their first inoculations of normal flora during natural birth and shortly after birth. Before birth, there is a rapid increase in the population of Lactobacillus spp. in the vagina, and this population serves as the first colonization of microbiota during natural birth. After birth, additional microbes are acquired from health- care providers, parents, other relatives, and individuals who come in contact with the baby. This process establishes a microbiome that will continue to evolve over the course of the individual’s life as new microbes colonize and are eliminated from the body. For example, it is estimated that within a 9-hour period, the microbiota of the small intestine can change so that half of the microbial inhabitants will be different.[5] The importance of the initial Lactobacillus colonization during vaginal child birth is highlighted by studies demonstrating a higher incidence of diseases in individuals born by cesarean section, compared to those born vaginally. Studies have shown that babies born vaginally are predominantly colonized by vaginal lactobacillus, whereas babies born by cesarean section are more frequently colonized by microbes of the normal skin microbiota, including common hospital-acquired pathogens.",True,Symbiotic Relationships,,,,