Article about Bunyaviridae.
- Viral taxonomy and vectors
- Genus Orthobunyavirus
- Genus Hantavirus
- Genus Nairovirus
- Genus Phlebovirus
- Unassigned viruses and viruses causing only minor disease in humans
- Further reading
Viruses of the family Bunyaviridae contain a 3-segmented, single-stranded, negative-sense RNA genome. They are divided into five genera, of which four are known to include human pathogens—Orthobunyavirus, Phlebovirus, Hantavirus, and Nairovirus. These viruses are found throughout the world and are transmitted between vertebrate hosts and to humans through the bite of infected arthropod vectors (mosquitoes, ticks, others), or from infectious excreta of rodents and other small mammals, and rarely person to person. Many of viruses are transmitted from infected arthropod vector females to the next generation by transovarial transmission, thereby surviving adverse environmental conditions and leading to marked seasonal distribution of disease. There are few vaccines available to protect against infection. Prevention is by avoidance of exposure to potentially infected arthropod and small-mammal vectors.
Bunyaviridae cause a wide range of clinical illnesses, ranging from self-limited febrile disease to severe, life-threatening haemorrhagic fever, acute respiratory distress, or encephalitis. The most important human diseases include those caused by:
La Crosse virus—the commonest cause of ‘California encephalitis’, most cases of which are relatively mild and with good prognosis; treatment is supportive.
Oropouche fever—causes epidemics of febrile illness, sometimes with meningitis, throughout the Amazon basin; prognosis is good; treatment is supportive.
Haemorrhagic fever with renal syndrome—caused by four distinct viruses (Hantaan, Dobrava, Puumala, Seoul); Hantaan and Dobrava cause the most severe disease, characterized sequentially by (1) febrile phase with features including headache, myalgias, petechiae and conjunctival haemorrhage, (2) hypotensive phase with shock, (3) oliguric phase, when one-third of cases have severe haemorrhage, (4) diuretic phase, (5) convalescent phase, which may be prolonged; ribavirin is effective if started early in disease. Inactivated vaccines against Hantaviruses are available for use in Asia.
Hantavirus pulmonary syndrome – most commonly reported from the western United States, Canada, Central and South America; symptoms are primarily those of acute unexplained adult respiratory distress syndrome; treatment is supportive; mortality is 20-40%.
Other diseases caused by Bunyaviridae—these include sandfly fever, Rift Valley fever and Crimean-Congo haemorrhagic fever. Some viruses of the family, e.g. Rift Valley fever virus and Nairobi sheep disease virus, are important pathogens of domestic animals.
Viral taxonomy and vectors
The family Bunyaviridae currently contains around 300 viruses, and is divided into five genera (Table 1). The family name, and that of the genus Orthobunyavirus, is derived from the type species Bunyamwera virus, which was isolated in Uganda from Aedes mosquitoes. The other genera are Hantavirus named after Hantaan virus (the cause of Korean haemorrhagic fever), Nairovirus after Nairobi sheep disease virus, Phlebovirus after phlebotomus or sandfly fever virus, and Tospovirus after tomato spotted wilt virus. All members of the family share structural, biochemical, and genetic properties, such as a spherical enveloped virion 80 to 120 nm in diameter and a genome of single-stranded negative-sense RNA divided into three segments (L, M, S). Members of different genera vary substantially in their biological and biochemical properties and in their mechanisms of replication. Orthobunyaviruses, nairoviruses, and phleboviruses, which together make up most of the family, are all arthropod-borne animal viruses (arboviruses). These circulate in a wide variety of different vertebrate hosts and are transmitted between vertebrates, including humans, by the bites of blood-sucking arthropods, principally mosquitoes for orthobunyaviruses, sandflies for phleboviruses, and ticks for nairoviruses. Hantaviruses are zoonotic agents infecting rodents and other small mammals. They may spread to humans who are in close contact with infected excreta. Tospoviruses are arthropod-transmitted plant viruses of no known medical importance.
Viruses within the larger genera are further subdivided into serogroups; orthobunyaviruses have at least 18 serogroups and nairoviruses have 7 (Table 1). Of over 60 Bunyaviridae that are known to infect humans, the type species and those causing major human diseases are shown in bold type in Table 1 and are described in more detail. Table 2 lists the distribution of the remaining viruses that cause minor human infections with their principal arthropod vectors. The habitats of the different viruses and their vectors range from arctic to tropical. The enzootic cycles of arboviruses are poorly understood. Most viruses undergo alternate cycles of replication in vertebrate and invertebrate hosts, but transovarial and trans-stadial transmission within some mosquitoes, ticks, and phlebotomine flies, and venereal transmission from vertically infected male mosquitoes to uninfected females is also known to occur. Most arboviruses have a narrow host range, occur within a limited area, and are transmitted by specific vectors to a limited number of vertebrate hosts, but some viruses infect a wider host range, are transmitted by more than one type of vector, and may occur in more than a single continent. Tick transmission predominates in Asia, but is unknown in South or Central America, and although some Bunyaviridae have been isolated in Australia, none is known to infect humans in that continent. Viruses of this family are among the most common apparently emerging diseases. Following viral entry, whether through the skin after the bite of an infected arthropod or by another route, there is replication in draining lymph nodes, which may be enlarged, and then viraemia. Symptoms develop when virus is deposited and replicates in other sites. The viruses are killed by bleach, phenolic disinfectants and detergents, autoclaving, boiling, and γ-irradiation. Enzymes such as nucleases also inactivate these viruses. Biosafety level 3 is recommended for handling most human pathogens with the ability to spread by aerosol (e.g. hantaviruses and Oropouche virus), but level 4 is required for Crimean–Congo haemorrhagic fever virus. Added precautions are necessary when handling hantavirus-infected animals and virus concentrates.
Studies with Bunyamwera and similar viruses show reassortment within the three-segmented genome when two closely related viruses infect the same cell, either in nature or in the laboratory. Such studies have been used to analyse the molecular basis of virulence for vertebrate and invertebrate hosts. Two orthobunyaviruses, Akabane and Aino viruses in the Simbu serogroup, produce congenital deformities in sheep, goats, and cattle in Japan, Australia, Africa, and the Middle East. However, there is no evidence that any member of the genus or family produces teratogenic effects in humans, but there is concern that Oropouche virus, a Simbu serogroup pathogen of Central and South America, may be a threat to pregnant women.
A mild febrile illness, usually with headache, joint and back pains, sometimes with a rash, and occasionally with mild involvement of the central nervous system. Serological surveys indicate widespread human infection in sub-Saharan Africa but it is rarely recognized. Laboratory infections have been recorded. Garissa virus, isolated from haemorrhagic fever patients during outbreak investigations in Kenya and Somalia, has genome segments virtually identical to both Bunyamwera and Cache Valley viruses, but neither of these is known to cause haemorrhagic disease in humans.
Treatment and prognosis
No treatment is necessary and the prognosis is excellent.
California encephalitis, Inkoo, Jamestown Canyon, La Crosse, Tahyna, and snowshoe hare viruses
The viruses named above, and perhaps others currently unrecognized, are responsible for the clinical condition known as California encephalitis. The viruses are widely distributed throughout many parts of North America, Europe, and Eurasia. In the United States of America most reported human infections are due to La Crosse virus in Ohio, Wisconsin, West Virginia, and Minnesota. From 1995 to 2005, 70 to 167 cases were reported annually. Most occurred in children, usually in boys, although Jamestown Canyon virus is found more often in adults. There is nearly always a history of outdoor exposure during warmer months in areas where woodland mosquitoes are prevalent. The incubation period is 5 to 10 days. Most cases of La Crosse encephalitis are relatively mild with headache, fever, and vomiting, progressing to lethargy, behavioural changes, and occasional brief seizures, followed by improvement. Severe cases (10–20%) develop sudden fever and headache, disorientation, and seizures during the first 24 h of illness, sometimes progressing to coma and requiring intensive supportive care. Overall, about 50% of symptomatic children have seizures with status epilepticus in 10 to 15%. The case fatality rate approaches 1%. Residual seizures occur in 6 to 13%, persistent hemiparesis in about 1%, and cognitive dysfunction in a few. In appropriate epidemiological settings, the disease should be considered in children presenting with aseptic meningitis or encephalitis.
|Table 1 The family Bunyaviridae: its genera, serogroups, vectors, and viruses infecting humans|
|Genus||Serogroup||Vector||Viruses infecting humans|
|Orthobunyavirus (over 150)||Anopheles A (12)||Mosquito||Tacaiuma|
|Anopheles B (2)||Mosquito|
|Bunyamwera (33)||Mosquito||Bunyamwera, Calovo, Garissa, Germiston, Ilesha, Maguari, Shokwe, Tensaw, Wyeomyia|
|Bwamba (2)||Mosquito||Bwamba, Pongola|
|C group (14)||Mosquito||Apeu, Caraparu, Itaqui, Madrid, Marituba, Murutucu, Nepuyo, Oriboca, Ossa, Restan|
|California (14)||Mosquito||California encephalitis, Guaroa, Inkoo, Jamestown Canyon, Keystone La Crosse, snowshoe hare, Tahyna, trivittatus|
|Guama (12)||Mosquito||Catu, Guama|
|Simbu (24)||Mosquito||Oropouche, Shuni|
|Hantavirus (8)||Hantaan (26)||None||Andes, Bayou, Black Creek Canal, Dobrava, Hantaan, Juquitiba, Laguna Negra, Lechiguanas, Monongahela, Oran, Prospect Hill, Puumala, Seoul, Sin Nombre|
|Nairovirus (32)||Crimean–Congo (3)||Tick||Crimean–Congo haemorrhagic fever, Hazara|
|Dera Ghazi Khan (6)||Tick|
|Nairobi sheep disease (3)||Tick||Dugbe, Ganjam, Nairobi sheep disease|
|Phlebovirus (57)||Phlebotomus (44)||Sandflya||Alenquer, Candiru, Chagres, Corfou, Punta Toro, Rift Valley fever a , Naples, sandfly fever, Sicilian, Toscana|
|Uukuniemi (13)||Tick||Uukuniemi, Zaliv-Terpeniya|
|Unassigned (53)||Mosquito||Bangui, Kasokero, Tataguine|
|Tick||Bhanja, Issyk-kul Keterah, Tamdy, Wanowrie|
Numbers in parentheses indicate the approximate number of viruses in the genus or serogroup.
Bold type indicates the type species and viruses causing major disease in humans.
a Mosquito vector for Rift Valley fever virus.
In Europe, Tahyna virus is widely distributed in Austria, former Czechoslovakia, France, Germany, Italy, Norway, Romania, former Yugoslavia, and the former Soviet Union. Seroprevalence exceeds 95% in parts of former Czechoslovakia, and is about 50% in the Rhone valley in France and the Danube basin near Vienna, but overt disease is seldom recognized. Inkoo virus is prevalent in Finland and also in neighbouring regions of Russia. Most adult Lapps have antibodies. Small children may have signs of central nervous system involvement during acute infection. Antibodies reactive with California serogroup viruses have also been found in human sera collected in Sri Lanka, China, and in the far northern latitudes of Eurasia where several California serogroup viruses have been isolated from mosquitoes, some related to Inkoo and Tahyna viruses, but others to snowshoe hare virus. In another Russian study of c.50 people, mainly 14 to 30 years old, with infections caused by California serogroup viruses, about two-thirds had influenza-like illnesses without central nervous system involvement, while the remaining one-third had aseptic meningitis.
Control, treatment, and prognosis
Measures to limit mosquito breeding, particularly of Aedes triseriatus, are useful in endemic regions. No vaccines are available, and there is no specific treatment. Fluid and electrolyte balance must be maintained, and anticonvulsive drugs may be required to control seizures. Intravenous ribavirin has been used to treat severe La Crosse encephalitis.
Before 1961, Oropouche virus was known to have caused only a mild fever in a single forest worker in Trinidad, but that year it was responsible for a substantial epidemic in the Belém area of northern Brazil, where c.7000 people were affected. Over the ensuing 50 years, massive epidemics of febrile illness have been recorded throughout the Amazon Basin and beyond, with many thousands infected. Symptoms include headache, generalized pain including back pain, prostration, and fever (40°C). Rash, meningitis, or meningism occasionally accompany infection. Illness lasts from 2 to 5 days, occasionally with protracted convalescence. No fatalities have been reported.
Control, treatment, and prognosis
No vaccine is available. Transmission is probably by the biting midge Culicoides paraensis and outbreaks appear to be a consequence of agricultural development of the Amazon Basin. Accumulated organic waste from cacao and banana production provides ideal breeding sites for Culicoides, leading to massive populations and subsequent epidemic Oropouche disease. Measures to reduce Culicoides breeding may be beneficial. Treatment is supportive and the prognosis is good, although convalescence may be protracted.
Haemorrhagic fever with renal syndrome Hantaan virus of the genus Hantavirus is the cause of Korean haemorrhagic fever in Korea. The Hantaan River is near the demilitarized zone between North and South Korea where the virus was first recovered in 1976 from its rodent host Apodemus agrarius. The clinical diseases caused by Hantaan and related viruses in the Eurasian continent have long been known by different synonyms: epidemic haemorrhagic fever, Korean haemorrhagic fever, or nephropathia epidemica, but haemorrhagic fever with renal syndrome (HFRS) is preferred. Four distinct viruses are responsible for most recognized cases of HFRS: Hantaan virus, found primarily in Asia; Dobrava virus in an enclave of disease in the Balkan region and sparsely elsewhere in Europe; Puumala virus in Scandinavia, western Russia, and much of Europe; and Seoul virus is probably global wherever uncontrolled populations of Rattus norvegicus exist. Hantaan and Dobrava viruses cause severe life-threatening disease with mortality of about 5%, reaching up to 30% in select populations. Puumala virus infections are less severe, although patients still require admission to hospital, but fewer than 1% of admitted patients die. Seoul virus is thought to be the least severe of the pathogenic strains of Old World hantaviruses, although it has been associated with human deaths.
|Table 2 Bunyaviridae causing only mild or trivial infections in humans, arranged on a geographical basis|
|Africa||North America||Central America||South America||Europe||Asia|
|Bangui (M)||Avalon (T)||Fort Sherman||Alenquer (P)||Bhanja (T)||Batai (M)|
|Bhanja (T)||Keystone (M)||Madrid (M)||Apeu (M)||Calovo (M)||Bhanja (T)|
|Dugbe (T)||Prospect Hill||Nepuyo||Candiru (P)||Corfou (P)||Issyk-Kul (T)|
|Germiston (M)||Tensaw (M)||Ossa (M)||Caraparu (M)||Tamdy (T)||Ganjam (T)|
|Ilesha (M)||Trivittatus (M)||Restan (M)||Catu (M)||Uukuniemi (T)||Hazara (T)|
|Kasokero (M)||Soldado||Guama (M, P)||Keterah (T)|
|Nairobi sheep disease||Trivittatus (M)||Guaroa (M)||Wanowrie (T)|
|Nyando (M)||Itaqui||Zaliv-Terpeniya (M, T)|
|Pongola (M)||Maguari (M)|
|Shokwe (M)||Marituba (M)|
|Shuni (M)||Murutucu (M)|
|Wanowrie (T)||Tacaiuma (M)|
M, virus transmitted by mosquitoes; P, virus transmitted by phlebotomine flies; T, virus transmitted by ticks.
Each hantavirus is associated with a particular rodent host: Hantaan virus with the striped field mouse Apodemus agrarius; Dobrava virus with the yellow-necked mouse Apodemus flavicollis; Puumala virus with the bank vole Myodes; and Seoul virus with the Norway rat Rattus norvegicus. Humans are infected by aerosols of rodent excreta, or rarely by rodent bites. It is seen among adult men in rural environments and may be an occupational disease. Those at greatest risk include farmers, woodcutters, shepherds, and, especially, soldiers in the field. Most hantavirus disease is seasonal, with a peak incidence in late autumn and early winter, although the Balkan form is found most often during summer months in Greece and adjacent countries.
Symptoms The incubation period for hantaviruses is variable; it is usually 12 to 16 days but it can be up to 2 months. Severe disease, typically associated with Hantaan or Dobrava virus infections in Asia or the Balkans, is characterized by five phases:
- Febrile: 3- to 7-day duration
- Hypotensive: lasting from a few hours to 3 days
- Oliguric: from 3 to 7 days
- Diuretic: from a few days to weeks
- Convalescent: prolonged
Signs and symptoms of the febrile phase include fever, malaise, headache, myalgia, back pain, abdominal pain, nausea and vomiting, facial flushing, petechiae, and conjunctival haemorrhage. In the hypotensive phase, patients have nausea, vomiting, tachycardia, hypotension, blurred vision, haemorrhagic signs, and shock. About one-third of fatalities occur during this phase. In the oliguric phase, nausea and vomiting may persist and blood pressure may rise. Renal failure develops with anuria, and about one-third of cases have severe haemorrhage (epistaxis, gastrointestinal, cutaneous, or bleeding at other sites). Nearly one-half of the deaths occur during the oliguric phase. In the diuretic phase, urine output increases to several litres per day. Convalescence is protracted and it maybe months before full strength and function are regained.
Not all the phases are seen in the less severe forms of the disease. The milder forms of HFRS, such as nephropathia epidemica due to Puumala virus, follow a similar but less severe course, with abrupt onset of fever of 38 to 40°C, headache, malaise, backache, and generalized abdominal pain. Back or loin pain is especially common. Signs of renal failure are usually not as pronounced, and the need for renal dialysis varies. Transient blurred vision occurs in about 10% of cases. Infection due to Seoul virus follows a similar course, but may present with more evidence of liver involvement. There is no evidence of person-to-person transmission.
Treatment and prognosis
Admission to hospital, avoidance of trauma and unnecessary movement, close observation, and careful supportive care are essential for patient survival. Treatment is phase specific, with special attention to fluid balance and volume, and control of hypotension and shock. Renal dialysis may be required. Antiviral therapy using ribavirin has been shown to be effective if started early in disease. Recovery is protracted but complete, with the exception of Seoul virus infection which carries the risk of chronic renal disease, hypertension, or stroke.
Hantavirus pulmonary syndrome
Hantavirus pulmonary syndrome, first reported from the United States of America in 1993, also occurs in Canada, Central and South America. The initial cases had a mortality of more than 50%, but rates have declined to 20 to 40% as clinical experience has increased. Most disease was reported from the western United States of America and Canada, and more recently from Argentina, Chile, Brazil, and other Central and South American countries. Sin Nombre virus was first associated with HPS, but many additional hantaviruses have now been recognized as likely causes of this syndrome (Table 1). As Old World hantaviruses are generally associated with specific microtine rodents (Microtinae: voles, lemmings, muskrats, and their allies, distributed worldwide), so each American hantavirus appears to be associated with a specific sigmodontine host (Sigmodontinae: cotton rats and their allies found in the western hemisphere). Apparent human-to-human transmission of Andes virus occurred during an outbreak in southern Argentina, including transmission to medical staff. Protective precautions are recommended when treating suspected cases of HPS.
Symptoms are primarily those of acute unexplained adult respiratory distress syndrome, rather than the expected renal disease. Nonspecific prodromal features of fever, myalgia, and malaise may last 4 to 6 days, with nausea, vomiting, and abdominal pain, often accompanied by dizziness. On admission, physical examination of patients with confirmed infection reveals fever (more than 38°C), tachycardia (more than 100 beats/min), tachypnoea (more than 20 breaths/min), and often hypotension (systolic pressure less than 100 mmHg), with audible rales in the chest. Laboratory findings include hypoxia, leukocytosis, haemoconcentration, thrombocytopenia, atypical lymphocytosis, elevated transaminases, and prolonged prothrombin time. Chest radiography shows progression from subtle interstitial findings to bilateral frank pulmonary oedema; pleural effusions are usually present. Thrombocytopenia and haemoconcentration are independent statistical predictors of HPS, although not infallible. In a patient with rapidly progressive pulmonary oedema, a blood smear showing four of the following five characteristics is a highly sensitive and specific means of establishing the diagnosis of HPS:
- lack of toxic granulation in neutrophils,
- more than 10% immunoblasts, and
Disease progresses rapidly once the lungs begin to fill, and death is commonly seen 24 to 48 h after admission, or sooner if there is hypoxia or circulatory failure. The severity of disease correlates with the degree of pulmonary oedema on chest radiography. Hypotension and shock may occur independently in patients whose hypoxaemia is medically controlled.
Treatment and prognosis
Treatment is supportive, ideally in a modern intensive care unit, with careful management of hypoxia, fluid balance, and shock. About two-thirds of patients require intubation and mechanical ventilation. Fluid loss into the lungs leads to haemoconcentration, but infusion of fluids exacerbates pulmonary oedema; therefore fluids should be administered cautiously with careful monitoring. Limited experience suggests that intravenous ribavirin has little effect on the course of HPS, perhaps because of the speed with which the disease progresses.
Prevention involves avoidance of infected rodents either through efficient rodent control programmes in cities, for Seoul virus, or maintenance of clean campsites so that waste food is not allowed to accumulate and attract rodents. Nationally approved inactivated vaccines, reported to be safe and effective against hantaviruses, are available for use in Asia.
The genus Nairovirus, named after Nairobi sheep disease, is an acute haemorrhagic gastroenteritis affecting sheep and goats in East Africa, with transmission by the sheep tick Rhipicephalus appendiculatus. It has caused laboratory infections, but the genus includes Crimean–Congo haemorrhagic fever virus and several other viruses known to infect humans, e.g. Ganjam virus, almost indistinguishable from Nairobi sheep disease virus but first isolated in India from Haemaphysalis intermedia ticks collected from healthy goats; Hazara virus, recovered from Ixodes redkorzevi ticks collected from the vole Alticola roylei in a subarctic habitat at an altitude of 3660 m in the Kaghan valley of Hazara district, Pakistan; Dugbe virus, isolated in Nigeria from Amblyomma variegatum ticks collected from healthy cattle; and Soldado virus, repeatedly isolated from a variety of bird ticks but recently linked to a mild illness in humans.
Crimean–Congo haemorrhagic fever virus
This was first recognized as a cause of an acute febrile haemorrhagic disease affecting humans in the Crimean region of the former Union of Soviet Socialist Republics, transmitted by ticks and carrying a mortality of 5 to 30%. In Africa, Congo virus was first isolated in the then Belgian Congo (now Democratic Republic of the Congo) from the blood of a local 13-year-old boy, and it caused a moderately severe laboratory infection. Related viruses were isolated in Uganda where more laboratory infections occurred, one of which ended fatally after a severe haematemesis. In Asia, a virus indistinguishable from Congo virus was isolated from pools of ticks collected from a variety of wild and domestic animals in western Pakistan. Crimean haemorrhagic fever virus was later proved to be serologically indistinguishable from Congo virus, hence the use of the term Crimean–Congo haemorrhagic fever virus. Different strains of this virus have been associated with outbreaks of severe and sometimes fatal disease in the Crimea, Rostov, and Astrakhan regions of Russia, in Albania, Bulgaria, and the Balkans, in East, West, and South Africa, in Iran, Iraq, and western Pakistan, and in China. From 2002 to 2008, ~2500 cases were reported in Turkey, although it was virtually unknown there previously. Most infections are seen among farmers or abattoir workers and acquired by tick bites or exposure to viraemic animal blood, but infections have occurred in both hospitals and laboratories.
The incubation period is 3 to 7 days. Fever usually starts suddenly and is normally continuous, although occasionally it is remittent or biphasic. Other clinical features are headache, nausea, vomiting, joint pains, backache, photophobia, circulatory disorders, thrombocytopenia, and leukopenia. Haemorrhagic manifestations are common. Patients show cutaneous petechiae and extensive ecchymoses, and bleed from nasal, gastric, intestinal, uterine, and urinary tract mucosae. Patients may present with acute abdominal pain, mimicking an acute surgical emergency, and operating-theatre staff have become infected and died through exposure to infected blood or secretions at operation. The mortality is about 5 to 30%, but may be up to 40% or higher in hospital or nosocomial outbreaks. Transient hair loss has been reported.
Control, treatment, and prognosis
No vaccine is available. Avoidance of tick bites may reduce the risk of infection. In hospital outbreaks, meticulous attention to the containment of infected secretions is essential and barrier nursing should be used. Overt disseminated intravascular coagulation usually indicates a poor prognosis, and haematemesis, melaena, and somnolence are significantly more common in fatal cases. Supportive therapy is essential, with monitoring of fluid and electrolyte balance. The antiviral ribavirin is recommended for severe cases based on observational studies. Limiting injections and avoidance of aspirin or other drugs affecting coagulation may reduce bleeding. Patients who recover may have residual polyneuritis persisting for months, but eventual recovery is to be expected. Laboratory investigations with live virus require biological safety level 4 containment.
At least nine different phleboviruses are known to infect humans (see Table 1). Pappataci fever, sandfly fever, or phlebotomus fever was recognized as a clinical entity in the Mediterranean area during the 19th century, and the association with Phlebotomus papatasi sandflies was demonstrated by showing that filtrates of human blood reproduced the disease in human volunteers. It was thought that humans were the only vertebrate host, but antibody studies indicate that gerbils, cattle, and sheep may also be infected. Naples virus was isolated from human serum collected during an outbreak of sandfly fever in Naples, and the Sicilian virus was isolated from American troops with a similar disease in Palermo, Sicily. The two viruses have many common properties, but are serologically quite distinct. Sandfly fever is widespread throughout the Mediterranean area, and also occurs in Egypt, Greece, Iran, Turkey, the former Yugoslavia, Bangladesh, India, Pakistan, and the southern states of Russia. Toscana virus, serologically related to the Naples virus, is found in countries bordering the Mediterranean; it is notable for its ability to infect the central nervous system, especially in central Italy where it is thought to be responsible for at least 80% of acute summertime infections of the central nervous system in children. The viruses that cause sandfly fever do not occur in the New World, but in South and Central America a similar clinical condition follows infection with Alenquer, Candiru, Chagres, and Punta Toro viruses.
Rift Valley fever has long been known as a disease of domestic animals, mainly sheep, in East Africa, which occasionally spreads to farm workers and others handling infected animals. The infection is endemic, but seldom recognized, in many wild game animals in Africa. Rift Valley fever virus differs from the sandfly fever viruses, Punta Toro virus, and most other members of the genus in being normally transmitted by mosquitoes rather than sandflies. Uukuniemi and Zaliv-Terpeniya viruses are tick-transmitted; the only evidence that Uukuniemi virus can infect humans is the finding of specific antibodies in some human sera collected in Estonia and in former Czechoslovakia. Zaliv-Terpeniya virus was isolated from bird ticks collected on an island in the Sea of Okhotsk, Sakhalin region, and there is some evidence that it may be pathogenic to humans.
Sandfly fever, Naples, and Sicilian viruses
After an incubation period of 2 to 6 days, fever starts abruptly with chills, nausea and vomiting, epigastric pain, and often severe generalized headache leading to incapacitating prostration. Fever of 38 to 40°C usually resolves after 2 to 3 days, but may be biphasic and persist for a week. There is no rash, but small haemorrhages into the skin and mucous membranes may be seen. Photophobia and eye pain occur, lymphadenopathy is often seen, and the liver may be tender although jaundice is rare. The disease is self-limiting, with complete recovery. No deaths have been attributed to either sandfly fever, Naples, or Sicilian viruses.
Rift Valley fever virus
Following its initial isolation in 1930 as the agent of enzootic hepatitis of domestic animals in Kenya, Rift Valley fever virus was recognized as the cause of sporadic human infections in East, Central, and West Africa, with a particular tendency to infect laboratory workers handling the virus. In East and Central Africa the virus has been isolated from a variety of mosquito species and it is capable of persisting in mosquito eggs during the dry season, emerging when larvae hatch in the rainy season. From 1951 to 1956 there were severe epizootics in lambs in southern Africa, and many human cases occurred. Further human cases with several deaths were seen in South Africa in 1975, and a major outbreak occurred in East Africa following El Niño flooding in 1997 to 1998, apparently seeding a ‘virgin soil’ outbreak in Saudi Arabia and Yemen in 2000. In 1997–8 and 2006–7 there were epizootics in Kenya, Tanzania, Burundi, and Somalia. In the recent epidemic, 684 cases with 155 deaths were reported in Kenya (case fatality 23%), 264 cases with 109 deaths in Tanzania (case fatality 41%), and 114 cases with 51 deaths in Somalia (case fatality 45%). Heavy rains in East Africa during 2006–7 triggered another outbreak with many human and animal cases.
In the Central African Republic in 1969, a virus isolated from Mansonia africana mosquitoes and named Zinga virus was associated with several cases of haemorrhagic fever; Zinga virus was later shown to be a strain of Rift Valley fever virus. In West Africa, Rift Valley fever virus was isolated from mosquitoes in Nigeria and from bats in Guinea, but despite the presence of antibodies in human sera collected in Nigeria and Senegal, human disease was unrecognized until 1987 when a substantial epidemic occurred in Mauritania, with further epidemics in following years. In 1977 the virus spread, apparently for the first time, into Egypt, producing a major epizootic in domestic animals, principally sheep and goats but also cattle, and causing about 600 human deaths within 3 months. The virus has been detected intermittently since then in Egypt. The principal known vector is the mosquito Culex pipiens. Both the Egyptian and the Mauritanian epidemics appeared to be linked to major ecological changes following the construction of the Aswan Dam on the Nile and dams on the Senegal River.
After an incubation period of 3 to 6 days, fever starts abruptly with shivering, nausea and vomiting, epigastric pain, arthralgia, and often severe generalized headache. The fever may be biphasic, with temperatures between 38 and 40°C, and may remain elevated for at least a week. There is no rash, but small haemorrhages appear on mucous membranes. Photophobia and eye pains occur. There may be conjunctival inflammation, and a central serous retinitis leading to central scotoma and sometimes to retinal detachment can occur late in disease. The fundus may show macular exudates that are slow to disappear. There is often a lymphadenopathy and although the liver is frequently involved and may be tender, jaundice is rare. Convalescence may be protracted but is usually uncomplicated.
A few patients develop severe disease with haemorrhage, encephalitis, or eye lesions. Haemorrhagic disease presents as above but progresses with cutaneous and mucous membrane petechiae, ecchymoses, gastrointestinal haemorrhage, and jaundice with severe liver and renal dysfunction often progressing to disseminated intravascular coagulation, hepatorenal syndrome, and death. Patients with encephalitis usually recover from acute febrile disease only to present within a few days to 2 weeks later with headache, meningism, confusion, and fever, often leading to residual defects or ending in death. Ocular complications are characterized by rapid onset of decreased visual acuity with scotomas due to retinal haemorrhage, exudates, and macular oedema. These are also seen after apparent recovery from the initial disease. About one-half of these patients have some degree of permanent visual loss. Death from Rift Valley fever was rarely recognized before the 1977 outbreak in Egypt, but the Mauritanian epidemics with mortality due to jaundice and haemorrhagic manifestations, and the recent East African and Arabian Peninsula outbreaks with several hundred suspect fatalities establish it as a life-threatening infection.
Control, treatment, and prognosis
Veterinary vaccines have been used for some years, and formalin-inactivated vaccines have also had limited use for the prevention of disease in laboratory workers and others exposed to high risk of infection. Improved vaccines based on molecular techniques are under development. Treatment is supportive. Although there are no reports of nosocomial transmission, barrier nursing would be a sensible precaution.
Unassigned viruses and viruses causing only minor disease in humans
The great majority of the viruses listed in Table 2 cause only a mild febrile illness, but the following show certain additional features.
Bhanja virus (unassigned)
This virus was first isolated from Haemaphysalis intermedia ticks collected from healthy goats in India, but has since been isolated in Sri Lanka, Africa, and Europe. Infection of goats is widespread in Italy and the Balkans where there have been several reported human cases, including some with severe neurological disease and at least two deaths. Laboratory infections have also occurred.
Bwamba virus (Orthobunyavirus)
This was first isolated in Uganda in 1941 and is very widespread throughout sub-Saharan Africa. More than 75% of adult human sera collected in Nigeria and over 95% of human sera collected in Uganda and Tanzania have antibodies against Bwamba virus. The original cases showed fever, headache, generalized pain, and conjunctivitis but no rash, although a rash has been described in the Central African Republic. No fatalities have been reported.
Nyando virus (Orthobunyavirus)
This virus was first isolated from mosquitoes in Kenya. It has since been isolated from humans in the Central African Republic where it caused fever, myalgia, and encephalitis.
Tataguine virus (unassigned)
This causes fever, rash, and joint pains in at least five African countries (Cameroon, Central African Republic, Ethiopia, Nigeria, and Senegal).
Wanowrie virus (unassigned)
This virus was first isolated in India from Hyalomma marginatum ticks collected from sheep. It has also been isolated in Egypt and Iran, and in Sri Lanka where it was recovered from the brain of a 17-year-old girl who died following a 2-day fever with abdominal pain and vomiting.
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Monath TP (ed) (1989). The arboviruses: epidemiology and ecology. CRC Press, Boca Raton.
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In the nineteenth century, Philadelphia banks and entrepreneurs played a pivotal role in facilitating the emergence of coal as the nation’s principal energy source for industry, transportation, and heating, by creating and financing the firms that first brought to market anthracite coal, mined exclusively in rugged eastern Pennsylvania.
To mine anthracite, or “hard coal,” on a large scale required extensive access to capital, much of which was drawn from Philadelphia. Before the Civil War, transportation firms led the way. The Lehigh Coal & Navigation Company, founded in 1822 by Josiah White (1781-1850) and Erskine Hazard (1789-1865), by 1840 had constructed thirty-six miles of canal, joining ten miles of navigable river down the Lehigh River to Philadelphia. In 1825, investors led by Philadelphia bankers and merchants founded the Schuylkill Navigation Company, which by the 1840s boasted a transportation network of 108 miles of canal and passable river, along with 450 tunnels and 120 locks for a capitalization of $2.2 million, all fed by annual coal shipments of 500,000 tons. In 1828 the North Branch Canal opened, reaching all the way to Nanticoke, and in 1831 it was extended to Pittston, connecting Luzerne County to the Philadelphia market. In 1829 the northern field opened to the New York market with the completion of the Delaware & Hudson Canal, which equaled the Erie Canal in capital outlay. This transportation artery included an inclined-plane railroad and a 110-lock canal system linking Honesdale, Pennsylvania, to Rondout, New York, on the Hudson.[caption id="attachment_21690" align="alignright" width="300"] Pennsylvanian railways played an integral role in transporting coal and other commodities like iron and steel to markets. Here, Pennsylvanian Railroad cars loaded with coal rest on tracks along the Schuylkill River in 1980. (Special Collections Research Center, Temple University Libraries)[/caption]
The emergence of the railroad system connecting Philadelphia and other eastern cities to the anthracite region soon eclipsed canal building. Frederick List (1789-1846), a leading early-nineteenth-century German economist and political refugee in Philadelphia in the 1820s, purchased a mine in the Little Schuylkill Valley in Tamaqua and recruited one of the nation’s richest men, Stephen Girard (1750-1831) of Philadelphia, as an investor to develop railroad links connecting mines to market. The railroad eventually became the powerful Philadelphia & Reading Railroad, which opened in 1833. Philadelphian Henry Charles Carey (1793-1879), the leading American economist of the nineteenth century and a close adviser to Abraham Lincoln, and like List an advocate of protective tariffs, also held anthracite mining interests. The Lehigh Valley Railroad (LVRR) opened in 1855 connecting Mauch Chunk (now Jim Thorpe) to Easton and then north through the Wyoming Valley into New York state and east into New Jersey and New York City. To the north, George Scranton’s Delaware, Lackawanna, & Western Railroad opened up the Northern Field to New York City and, via the Erie Canal, the Great Lakes. Everywhere railroads used their control of access to the market as leverage to dominate coal production.
Anthracite Boosts Steel Production
Railroads tied together the critical ingredients of the industrial economy of the nineteenth century: coal, iron, and steel. Once accessed, anthracite coal began to play an indispensable role in the industrial revolution. Prior to the use of anthracite in the smelting of iron, American industry lagged far behind its British counterpart, continuing to use charcoal through the 1830s that resulted in an inferior product unsuitable for rail manufacture. The intense heat unleashed in the burning of anthracite closed the gap. By the 1850s anthracite was fueling half of all iron production in the United States, much of it destined for rail building, much of the rest bound for the emerging field of metal machine making, an important industry in Greater Philadelphia. The city’s central entrepôt for the coal was the Reading Railroad’s massive Port Richmond Terminal, a sprawling complex of twenty-one wharfs on the Delaware River capable of loading scores of vessels. From here coal was shipped up and down the East Coast.
Growing demand before, during, and after the Civil War accelerated anthracite production. Regional coal production went from 910,000 tons in 1840 to 3,700,000 tons in 1850, to 9,200,000 tons in 1860, to 11,000,000 in 1865. Over the corresponding period, value of output increased from $1.3 million to $5.5 million in 1850, to $14 million in 1860, to $65 million in 1865, the final statistic suggestive of the enormous inflation and profits gained as a result of the Civil War. The anthracite region’s population—comprising Luzerne, Northumberland, Schuylkill, and what would become Carbon and Lackawanna Counties—grew rapidly, from 46,790 in 1820, to 66,256 in 1830, to 93,086 in 1840, to 155,743 in 1850, and to 248,655 in 1860. As the basis of the regional economy, mine employment went from 3,000 in 1840, to 10,000 in 1850, to 27,000 in 1860, to 39,000 in 1865. From the Civil War until 1900, anthracite production increased fivefold, from 10 million tons to 60 million tons annually. Tens of thousands of immigrants poured into the region, arriving first from Wales, England, and Scotland, then from Ireland, and finally Poland, Italy, Lithuania, Slovakia, Ukraine, Hungary, and many other lands. Workers unionized in bitter struggle against the mine owners in the United Mine Workers of America (UMWA) by the first decade of the twentieth century.
In the late nineteenth century coke processed from bituminous coal began to displace anthracite coal for industrial use, especially in steel production. Drawn from the nation’s vast deposits stretching from western Pennsylvania and West Virginia through Illinois, bituminous, or “soft coal,” was considerably cheaper to extract than anthracite coal. The coking industry developed first in western Pennsylvania, and with it the center of the American iron industry shifted from eastern Pennsylvania to the Pittsburgh region, eventually following the development of the iron mining industry in the Lake Superior region to the major cities of the Great Lakes. By 1905, the Pittsburgh area was producing 18 million tons of coke per year. Bituminous production in Pennsylvania alone reached 80 million tons by the turn of the century.[caption id="attachment_21692" align="alignright" width="205"] A propaganda poster produced by the United States Fuel Administration in 1917, in the midst of World War I, encourages American citizens to order coal. A worker can be seen unloading coal from the back of a horse-drawn wagon. (Special Collections Research Center, Temple University Libraries)[/caption]
Oil Displaces Anthracite
Another development from western Pennsylvania in the late nineteenth century ultimately contributed to the displacement of anthracite for home heating use, a long decline that accelerated after World War II. This was the discovery of consumer and industrial uses for oil and then natural gas. An industry dominated by John D. Rockefeller (1839-1937), oil was first shipped to Philadelphia via the Philadelphia and Erie Railroad, connecting with the Reading in Harrisburg. Beginning in the late nineteenth century oil and natural gas were shipped to refineries via pipelines from northwestern Pennsylvania. With the development of the internal combustion engine in the late nineteenth century, petroleum began to displace both coke and anthracite in industrial production.
The Susquehanna River, whose canals provided the original mode of transportation of anthracite to Philadelphia, contributed to the ultimate decline of the anthracite coal industry. The completion of the Holtwood Dam on the lower Susquehanna in 1910 greatly increased the market for electricity consumption in Philadelphia and Baltimore. The introduction of electricity in industrial production allowed for the rapid development of light industry dependent upon small machines, as well as the development of continuous production methods like the assembly line. By 1930 electricity had become the leading energy source in American industry, and most Philadelphia homes had abandoned carbon-burning appliances. In the years after World War II, the burning of coal as a home heating source declined.
Coal nonetheless continued to play an important role in the production of electricity in the region for many decades. Coal-powered plants generated substantial environmental pollution, and according to 2010 research carried out by the nonprofit Clean Air Task Force investigating the remaining Pennsylvania and New Jersey power plants using coal for generation, fine particle air contamination consisting of soot, heavy metals, sulfur dioxide, and nitrogen oxides was associated with dozens of deaths. Most of these plants were slated to close by the end of 2015.[caption id="attachment_21689" align="alignright" width="300"] John Wondolski, a former miner and the mayor of Centralia, a town in Columbia County, Pennsylvania, stands amid smoke venting from the Centralia mine fire in May 1981. Since 1962, the fire has continued to burn underground, fueled by coal. (Special Collections Research Center, Temple University Libraries)[/caption]
From the beginning, coal contributed to workplace and environmental problems. Tens of thousands of Pennsylvania workers died in the state’s mines, and tens of thousands more suffered and died from coal workers' pneumoconiosis, or black lung. The rivers and soils near mines and beehive coke ovens were damaged. Air pollution, coal ash deposits, and one ongoing underground coal fire, at Centralia, Pennsylvania, continued to present environmental problems to the state into the twenty-first century. One of the prices of coal, despite its central role in boosting area industry, has been these long-term effects.
Thomas Mackaman is Assistant Professor of History, at King’s College, Wilkes-Barre. He is author of the forthcoming book, New Immigrants and American Industry, 1914-1924.


Willis Eugene Lamb, Jr.
Willis Eugene Lamb, Jr. was born on July 12, 1913 in Los Angeles, California. He attended Los Angeles public schools and in 1930 entered the University of California at Berkeley. He received a B.S. in chemistry in 1934. His graduate work in theoretical physics at the same university led to a Ph.D. in 1938. J.R. Oppenheimer directed his thesis research on the electromagnetic properties of nuclear systems.
Lamb began his teaching career at Columbia University as an instructor in physics in 1938. Within a decade he became a full professor. From 1943 to 1951, he was associated with the Columbia Radiation Laboratory where his Nobel-prize winning research was performed. In 1951 he went to Stanford University as a professor of physics. Over the next decade Lamb held positions at Harvard University, Oxford University, England, and Yale University. He also taught at the University of Arizona.
Lamb’s research covered many topics including: theory of the interactions of neutrons and matter, field theories of nuclear structure, theories of beta decay, range of fission fragments, fluctuations in cosmic ray showers, pair production, order-disorder problems, ejection of electrons by metastable atoms, quadrupole interactions in molecules, diamagnetic corrections for nuclear resonance experiments; theory and design of magneton oscillators, theory of a microwave spectroscope, study of the fine structure of hydrogen, deuterium and helium; theory of electrodynamic energy level displacements.
Among his many honors are the 1955 Nobel Prize in Physics, the Rumford Premium of the American Academy of Arts and Sciences and the Research Corporation Award. Lamb also received an honorary degree from The University of Pennsylvania. He was a member of the National Academy of Sciences, and a fellow of the American Physical Society.
Lamb died May 15, 2008.
OSA Awards Won


1913 10¢ Panama-Pacific Exposition Commemorative
Issue Date: January 1, 1913
Quantity issued: 16,968,325
Printed by: Bureau of Engraving and Printing
Method: Flat plate
Watermark: Single line
Color: Orange yellow
This 1913 commemorative stamp series was issued to publicize the upcoming 1915 Panama-Pacific Exposition that was held in San Francisco. The exposition commemorated the discovery of the Pacific Ocean as well as the construction of the Panama Canal.
This issue commemorates the discovery of San Francisco Bay. The design is taken from a painting by Charles F. Mathews.
Many great navigators, such as Juan Rodriguez Cabrillo, Sir Francis Drake and Sebastián Cermeño explored the coastline near San Francisco Bay, but failed to discover this precious waterway. All failed for the same reason – the fog.
That’s why the first European explorer to see this scenic bay traveled overland. Members of an expedition led by the Spanish explorer Gaspar de Portola became the first Europeans to see San Francisco Bay in 1769.
The design on this stamp captures the magical moment when the expedition reached the peak of one of the hills surrounding the bay and beheld its breathtaking beauty.
How two common postal changes
led to one scarce stamp
The first Panama-Pacific commemorative series was issued in 1913, to publicize the upcoming 1915 Panama-Pacific Exposition, a World’s Fair commemorating the completion of the Panama Canal and 400th anniversary of the discovery of the Pacific Ocean. The new stamps were popular with the public.
Scott #400 “Discovery of San Francisco Bay” – the 10¢ Panama-Pacific stamp was the fourth stamp in the series – issued January 1, 1913. It was the first of three stamps from this series to bear the same design.
Shortly after the stamp’s issue, it was determined that its orange-yellow color was much too light – it was so weak that it destroyed the elegance of the stamp’s design. As complaints continued to mount about this color, plans were made to change it to a darker shade.
On August 25, 1913 – just over seven months after it went on sale – #400 was removed from sale and all remaining quantities were destroyed. A darker version was issued in its place, and given the number 400A. This stamp’s color was listed as orange.
Then a second problem occurred. The Postal Service received a great many complaints, particularly from high-volume mailers, that sheets perforated 12 (like #400 and #400A) were too brittle and fell apart at the slightest touch. Thus, to strengthen the sheets, perforating machines were altered to 10 perforations per two centimeters. The stamps of the Panama-Pacific Exposition were among the first to be changed to perforated 10 – which resulted in the third stamp bearing this attractive “Discovery of San Francisco Bay” design – U.S. #404.
On February 20, 1915, the Panama-Pacific Exposition opened in San Francisco, California.
As early as 1891, businessmen from San Francisco had wanted to host a world’s fair in their city. They wanted to show the rest of the nation the progress they had made in transforming the small frontier town into a growing city complete with the world’s most active mint.
Businessman Rueben Hale first submitted a proposal for the fair in 1904. He proposed that it honor the completion of the Panama Canal, which was not yet done. Congress put off the decision. But then in April 1906, San Francisco was hit with one of the worst earthquakes in US history, destroying about 80 percent of the city. The fair’s organizers rebuilt their businesses but were still set on hosting the fair, now determined to show the world how they would recover from this natural disaster. In 1911, President Taft signed a resolution naming San Francisco the home of the Panama Pacific Exposition.
In just four years, the fair’s organizers would purchase land, demolish over 200 buildings, fill in marshland, and build up the 635-acre fair. Opening day finally came on February 20, 1915. The state’s governor at the time declared the day a legal holiday. Despite the rainy weather, a parade of 150,000 residents and visitors marched through the streets leading up to the fairgrounds. The group stretched about two and a half miles. The gates opened at 10 am, followed by speeches and prayers at the Tower of Jewels. Then at noon, President Woodrow Wilson pressed a gold telegraph key in Washington, DC. That sent a signal to the antenna at the Tower of Jewels that opened the doors of the exhibition palaces and sent water rushing from the Fountain of Energy.
The fair included a number of fascinating attractions. In the Palace of Transportation, the Ford Motor Company had a working assembly line on display that produced a new automobile every 10 minutes. Many people had their first opportunity to see a plane in action with the Loughead (later changed to Lockheed) brothers taking fairgoers on 10-minute flights and Lincoln Beachey and Art Smith performing aerial stunts.
Alexander Graham Bell also had a transatlantic telephone set up. Just a month after he’d made the first transatlantic call, he had a phone set up at the fair connected to one in New York where a person on the other end read newspaper headlines and played music. Visitors were also treated to a 5-acre working model of the Panama Canal Zone.
The fair ran until December 4, 1915. During that time, over 18 million visitors attended the fair.
As early as 1904, the Post Office Department began planning a set of commemoratives to advertise the exposition to celebrate both the discovery of the Pacific Ocean and the completion of the Panama Canal. By 1912, the designs for the 1¢, 2¢, and 5¢ stamps had been prepared and approved. However, the design for the 10c issue posed a problem. Originally, the stamp was to depict Juan Rodriguez Cabrillo, who discovered the California mainland in 1542. But efforts to find a portrait of him proved unsuccessful. Eventually, a painting of the discovery of San Francisco Bay was unearthed. Found to be an acceptable design, it was adopted by the Post Office Department, and work on the stamp progressed rapidly. Six short months later, the Panama-Pacific Commemoratives were placed on sale.
Due to the fact that the exposition didn’t open until February 1915, the series remained current for nearly three years – longer than any other commemorative! However, the Post Office began to receive complaints that regular issue stamps were too brittle, so they started issuing stamps with 10 perforations per two centimeters, instead of the previous 12. The Panama-Pacific set was reissued with the new perforation size. However, since collectors had already purchased the perf. 12 stamps, the newer issues were mostly ignored. This makes them scarcer today.


Here’s a brief overview of six hints of dark matter — signals (two in the sky, and four underground) that just might be from dark matter particles doing something interesting — that are being explored, as of April 2013. One or two of them might turn out to be true, but not all six can be, since they contradict each other. And this shouldn’t worry you, because this situation is perfectly normal with forefront science; research is difficult, and most hints of something exciting turn out to be mirages — statistical flukes, previously unknown quirks of a measurement technique, or even pure mistakes. With the Higgs particle, for instance, we had several false alarms (one as recent as July 2011) before the alarms finally rang true in July 2012. So we have to be patient and cautious, yet hopeful; discoveries are rare, but they do happen.
Dark Matter Overhead
First, there is a hint from the Fermi satellite (pointed out by Christoph Weniger) that photons [particles of light] of a particular energy (about 135 GeV, i.e. about 143 times the mass-energy [i.e., the E=mc2 energy] of a proton) are streaming out of the center of our galaxy. This could potentially be a signal of dark matter particles (which, moving slowly around our galaxy, would be especially numerous at the galactic center) in the process of colliding, annihilating, and turning into photons.
Click here for more detailed explanation of how this works. Briefly: Energy conservation assures that the energy in two annihilating dark matter particles (which is mostly in mass-energy, since dark matter particles move slowly inside a galaxy) is converted into the motion-energy of two photons — and thus the energy of each photon is equal to the mass of the dark matter particle times c².
Should we worry that this signal isn’t what it seems to be? A minor issue is that a standard “WIMP” (a Massive Particle that Interacts with matter via the Weak nuclear force — roughly speaking) couldn’t produce this signal without giving other signals that we would also see (such as lots of photons at lower energy.) But WIMPs are more popular than they deserve to be (see, for example, this paper), and other types of dark matter particles, ones that various particle theorists have imagined over the years, could potentially do the job.
A much more serious concern is that not only is the signal coming from the galactic center, it also appears to be coming from the limb of the earth and maybe from the sun. You wouldn’t expect that from dark matter annihilation. And the fact that this signal shows up in strange places where it isn’t expected might mean that the whole business actually reflects a subtle problem with Fermi’s photon detector. Nobody knows for sure at this point.
Here’s another example. The AMS experiment attached to the International Space Station recently claimed to have made a big “discovery” (though actually, as most press articles forgot to mention, what they really did was confirm something that the PAMELA experiment already discovered back in 2008 — indeed I don’t know why Dennis Overbye didn’t emphasize this more in his New York Times article on AMS, given that he himself had written about the PAMELA experiment’s discovery back in 2008.) What PAMELA discovered, and AMS confirmed and explored in much greater detail, is that in outer space, one finds an excess, compared to what one would have expected, of high-energy positrons (the anti-particles of electrons). The extra positrons are observed to have energies from 10 GeV on up to at least 350 GeV, where AMS’s data currently fades out.
Now maybe — maybe — those positrons are from the annihilation of dark matter particles! But if so, they can’t be the same type of dark matter particles that FERMI might be seeing from the galactic center. Any dark matter particles responsible for AMS’s signal would have to have mass above 350 GeV/c², in order to produce positrons of 350 GeV, while if there are dark matter particles making FERMI’s photons, they’d never give positrons with energies above 135 GeV. [Again this is just energy conservation; if your two annihilating dark matter particles have mass of 135 GeV/c² each, and are moving slowly enough that their motion-energy is small, electrons and positrons produced in the annihilation can’t have energy above 135 GeV each.] So FERMI and AMS can’t both be seeing effects of dark matter; at least one of them is seeing something else.
As was suggested all the way back in 2008 (and as the AMS people were careful to admit), the positrons PAMELA saw then, and that AMS sees now, might be created by an astrophysical effect, such as a nearby pulsar (a rapidly spinning star with a powerful magnetic field, which can serve as a natural particle accelerator and become a source for extra electron-positron pairs.) And as everyone has known since 2008 (and as the AMS people were careful not to admit), a simple garden-variety neutralino from supersymmetry (or any other WIMP) could never give you such a big signal unless there was a previously unknown force able to enhance the annihilation rate. And even then, you wouldn’t get these positrons without getting other signals we also should have seen, unless you imagine this is from a very non-garden-variety type of dark matter — let’s call it a “jungle-variety” type of dark matter, not a bad name, because a whole host of particles are hidden away and hard to see. Jungle-variety theories are really cool, but the dark matter particles in such theories are not the simple supersymmetry WIMPs that the press articles about AMS all mentioned. (Talk about mixing your applets and your orangoutangs...)
Dark Matter Underfoot
Let’s move on! Anyone remember DAMA (now DAMA/LIBRA)? They’ve been claiming evidence of dark matter for over ten years! And they definitely have a real signal of something! Maybe it’s dark matter, and maybe it’s not.
You see, one clever way to look for dark matter is to let it find you. Just put a chunk or a vat of a carefully chosen and purified material in a mine deep underground. (Going deep underground drastically reduces effects from cosmic rays, high-energy particles from outer space.) Since dark matter must go right through ordinary matter, rarely leaving any trace, dark matter particles stream right through the rock and down into the mine and into the chunk or the vat. And if you’re very very patient, one of those dark matter particles might hit an atomic nucleus inside your material, and that little love tap may be just loud enough for you to detect it, if you’ve designed a very clever experiment. This is what DAMA, XENON, CoGeNT, CRESST, CDMS, and a host of other experiments are doing and have been doing for a long while now.
This is harder than it sounds. Radioactivity — the process by which an atomic nucleus changes from one type to another, spitting off a high energy particle or two along the way — can mimic the effects of a dark matter particle. [A process that mimics your “signal” — the thing you’re trying to detect — is called a “background”. For some conceptual discussion of signals and backgrounds, you can read the first part of this otherwise outdated article.] Backgrounds in this dark matter detection business are often much larger than the signals, and the experimenters need to understand all of the possible backgrounds very, very well if they’re going to detect something so small.
But now — getting back to DAMA specifically — here’s something you can do that’s diabolically clever. As the earth moves round the sun during the year, its velocity relative to the average velocity of the dark matter particles is changing. It’s similar to how, if you bike around a circular track on a windy day, sometimes the wind is brutally in your face, and sometimes it is comfortably at your back. So just as the strength of the wind changes as you circle the track, the speed of any dark matter “wind” changes strength during the year. And if the probability that a dark matter particle interacts with a nucleus depends on the relative velocity between the two (as is true in many examples of what dark matter might be), then the number of dark matter collisions that an experiment will measure will vary up and down, cycling once a year. So rather than just looking for signs of a few collisions, which might just be radioactivity that you’ve misinterpreted, perhaps you should look for variations of the number of collisions during the year! If you can convince yourself that radioactivity and other backgrounds themselves can’t cycle during the year, then any oscillation of this type is a smoking gun for dark matter.
Unfortunately, although this sounds great, the backgrounds can in fact cycle during the year after all, perhaps because minor temperature changes cause more or less radioactive gas to float around inside the mine, or something like that. So although DAMA/LIBRA’s data definitely shows an oscillating number of candidate dark-matter/nucleus collisions, it’s still not entirely clear this is due to dark matter. So far no one’s been able to verify their signal, but no one’s been able to show it’s a false alarm either.
DAMA/LIBRA is not alone. Over the past year or so, the CoGeNT experiment reported that they see an excess of possible collisions too, which, like DAMA/LIBRA, have a rate that oscillates up and down during the year.
That’s not all. Last year, the CRESST experiment also reported seeing a bunch of candidates for dark-matter particles hitting an atomic nucleus inside their detectors. There are several possible effects that could give candidates of this type, but — they say — when they add up all of those effects, they should see something like 42 candidates; but in fact they see 67, an excess of about 4 standard deviations, which is very strong evidence that something’s amiss.
Finally, the newest hint: the CDMS experiment has reported that they have seen three candidates for dark matter collisions in their chunks of silicon. [They have both silicon and germanium detectors; the new result is for data taken some years ago in the silicon chunks. Since a silicon nucleus is much lighter than a germanium nucleus, silicon is more responsive than germanium to a collision with a light-weight dark matter particle.] This is really very interesting! But, as they themselves are careful to say, hardly definitive yet. What’s almost certain is that it’s not from a background they expected. It’s not so obvious at first glance; the backgrounds they know about should only have generated about half an event on average, and the probability of getting these three events is about 5% — not very unlikely at all, when you consider how many different unlikely things can happen in an experiment. But when they account for the energies of these candidate collisions, the probability drops to 0.2%. Now that’s starting to get serious! But remember: all this means is that either (a) they’ve discovered dark matter, or (b) they’ve discovered a previously unknown background that gives them a false signal.
Now when we take these last four experiments all together, the news is both good and bad. The good news is that all four of these experiments — DAMA/LIBRA, CRESST, CoGeNT and CDMS — are consistent with a dark matter particle that is somewhere in the vicinity of 10 GeV/c², more or less.
The minor bad news is that the four measurements are inconsistent with each other; the interaction probabilities the experiments infer, for a given dark matter particle’s mass, aren’t all the same, and differ by as much as a factor of ten. This is illustrated in the figure below (taken from the CDMS paper), showing that the four allowed bands associated with the four experiments’ observations don’t generally overlap with one another. So this would suggest that at least two of the experiments must be false alarms.
The major bad news is that there’s another experiment which should (naively) be more sensitive to this type of dark matter particle than any of these four experiments. I refer to XENON100. For most of these signals, XENON100 should have seen lots of candidate events, typically tens or more. But they see only two. And so, nominally at least, all of these signals are ruled out by XENON100, and/or by a special analysis of the data from its predecessor, XENON10. Perhaps it can be argued that the CoGeNT and CDMS experiments’ signals are just barely ruled out, and so perhaps they’re still really worth taking seriously.
Yet one more sobering fact (NYU’s Neal Weiner emphasized this in his talk last week in Princeton) is that in all of these underground experiments, a failure to account for a small background will typically show up as a few extra low-energy collision candidates, which will then closely resemble what you’d expect for a low-mass dark matter particle. In other words, lightweight dark matter is what an oops! will look like.
As University of Chicago professor Juan Collar himself (leader of the CoGeNT experiment) said at a conference at CUNY’s graduate center in New York City about two years ago, the saga of dark matter searches is likely to be a long story of discovering one unexpected background after another — and it’s a story which could go on quite a while before dark matter is actually found, if ever, by one of these experiments. Indeed, this is reflected in the many false alarms that we’ve seen in recent years. [Interestingly, Collar stopped talking this way when CoGeNT started seeing a signal that could be interpreted as dark matter. But we remember what you said, Juan. We remember.]
Meanwhile, this type of puzzle is what theoretical physicists live for. A conundrum! A challenge! Invent a theory of dark matter that is such that CDMS and CoGeNT can easily observe its effects but XENON100 cannot! The experiments work differently — CDMS and CoGeNT are made from chunks of silicon and germanium respectively, while XENON100 uses — surprise! — a vat of xenon. There are already many papers on the matter. The most likely outcome is that XENON100 is right and CDMS and CoGeNT are seeing backgrounds of some type. But perhaps it will turn out otherwise.
To sum up: we have at least six hints of dark matter, mostly inconsistent with one another. The new CDMS hint is roughly consistent with CoGeNT; but if they’re both really seeing dark matter, why didn’t XENON100 see a big signal? Well… all of these experiments are working hard to improve their methods and their measurements, so if any of these hints are really signs of dark matter, we should start seeing more impressive evidence within a year or so.


Last updated: November 7, 2014
Synonyms: Polyangiitis, periarteritis nodosa, systemic necrotizing vasculitis
(PAN is part of this larger disease spectrum).
ICD-9 Code: 446.0.
ICD-10 Code: M30.0
Definition: PAN is a systemic necrotizing vasculitis that affects medium and small muscular arteries of the skin, kidneys, muscle, GI tract, and peripheral nerves. Microscopic polyangiitis is also described because it is a PAN variant and affects smaller sized arteries. Microscopic polyangiitis is distinguished from PAN by manifesting pulmonary capillaritis, alveolar hemorrhage, and P- ANCA positivity.
Etiology: PAN is systemic vasculitis of uncertain etiology. Although there is no consistent infectious cause; PAN has been associated with hepatitis B antigenemia, especially in intravenous substance abusers. Hepatitis C has been described in both PAN and microscopic polyangiitis.
Pathology: Immune complexes deposited in the vascular endothelium activate complement, attracting inflammatory cells. The cellular infiltrate contains both neutrophils and mononuclear cells. Release of proteolytic enzymes and oxygen free radicals results in destruction of the entire vessel wall with fibrinoid necrosis. Eosinophils and granuloma are very rare.
Demographics: PAN and microscopic polyangiitis are uncommon disorders. Median onset age is 40 to 60 years, with a 2:1 male predominance.
Cardinal Findings: Significant constitutional symptoms may predominate early and include fever, weight loss, and severe malaise. Arthralgias/myalgias (50%) and severe abdominal pain often herald disease onset. In PAN, visceral organ manifestations (in order of decreasing frequency) include (Fig. 7):
—Renal (70%–80%): Impaired renal function, proteinuria, and hypertension are secondary to renal artery involvement.
—Nerve (50%–70%): Peripheral neuropathy is common and often manifests early in the disease as mononeuritis multiplex (vasculitis of the vasa nervorum) and may present as foot drop. Distal sensorimotor polyneuropathy and late CNS involvement leading to encephalopathy also occur.
—GI (25%–70%): Severe abdominal pain with intestinal angina is common. GI hemorrhage, perforation, cholecystitis, pancreatitis, intrahepatic aneurysm rupture, and appendicitis have all been reported.
—Cardiac (<10%): Although coronary vasculitis is common at postmortem, symptomatic coronary vasculitis and cardiac disease are uncommon in PAN.
—Skin (40%): Livedo reticularis, nodules, nonspecific maculopapular eruptions, and ulcerations are seen. Subcutaneous skin lesions are typical in the more limited form, cutaneous PAN.
Uncommon Findings: PAN seldom involves the cerebral or pulmonary vasculature. Palpable purpura is also uncommon. In contrast, microscopic polyangiitis often involves the lung and heart.
Complications: Infarction of the bowel leading to hemorrhage and/or perforation is one of the most feared complications. Congestive heart failure and myocardial infarction are occasionally seen. Microscopic polyangiitis can be accompanied by rapidly progressive glomerulonephritis.
Microscopic polyangiitis: Microscopic polyangiitis and PAN share a similar onset and range of signs and symptoms. Microscopic polyangiitis commonly manifests with palpable purpura, alveolar hemorrhage, symptomatic cardiac involvement but is less likely to have hypertension, neuropathy, or hepatitis B. Distinctive pathology includes pulmonary capillaritis, necrotizing segmental glomerulonephritis, and P-ANCA serologies (Table 31). Although the prognosis is good, those with alveolar hemorrhage are at risk of early death.
Diagnostic Testing: Nonspecific inflammatory markers include elevated ESR or CRP, leukocytosis, anemia of chronic disease, and thrombocytosis. In the setting of renal disease, an abnormal urinalysis with proteinuria, granular or red blood cell casts, and declining creatinine clearance is frequently seen. Hypocomplementemia (low C4, C3) and circulating immune complexes are inconsistently detected; the latter are not recommended because of their poor sensitivity and specificity. Evidence of HBV or HCV infection should be sought. An angiogram of the mesenteric or renal arteries may strongly suggest PAN if vascular tapering, microaneurysms, and beading are noted. A histologic diagnosis is made by biopsy of a medium-sized muscular artery. Biopsies are best performed in clinically involved tissues and may include a sural nerve (with foot drop or neuropathy), a muscle (with myopathy or myalgia), or, less preferably, a symptomatic testicle. Renal biopsy is not helpful because specimens seldom exhibit characteristic abnormalities. Microscopic polyangiitis is associated with P-ANCA.
Keys to Diagnosis: PAN may be a diagnostic challenge. Histopathologic evidence of medium-vessel vasculitis or a pathognomonic angiogram in the appropriate clinical setting confirms a clinical diagnosis.
Diagnostic Criteria: The 1990 ACR criteria include (a) weight loss of at least 4 kg; (b) livedo reticularis; (c) testicular pain or tenderness; (d) myalgias, weakness, or leg tenderness; (e) mononeuropathy or polyneuropathy; (f) diastolic blood pressure >90 mm Hg; (g) BUN >40 mg/dL or creatinine >1.5 mg/dL; (h) HBV antigen or antibodies in serum; (i) arteriographic abnormalities (e.g., occlusions or aneurysms); and (j) small- or medium-sized artery biopsy specimen demonstrating PMN leukocytes. The presence of at least three of these features yields an 82% sensitivity and 87% specificity for the diagnosis of PAN.
Comparison if polyarteritis Nodosa and Microscopic Polyangiitis
|NeuropathyHypertensionAlveolar hemorrhageGlomerular diseaseHepatitis BP-ANCA||50%-70%CommonAbsentAbsent (vascular nephropathy)Uncommon10%||<35%Uncommon20%-30%Segmental necrotizing glomerulonephritisAbsent80%|
Differential Diagnosis: Alternative forms of systemic vasculitis with overlapping features include granulomatosis with polyangiitis, microscopic polyangiitis, Churg-Strauss angiitis, hypersensitivity vasculitis, and angiitis secondary to amphetamine or cocaine abuse. The vasculitides are compared in Vasculitis: Comparison Table. Medium-vessel arteritis may be a feature of many connective tissue and idiopathic inflammatory disorders (RA, SLE, cryoglobulinemia, Behçet’s syndrome). Occult malignancy, infective endocarditis, cholesterol emboli syndrome, and left atrial myxoma are also in the differential diagnosis. Hairy cell leukemia has been associated with PAN-like picture.
Therapy: In PAN, high-dose corticosteroids are the first line of treatment and are generally begun with at least 1 mg/kg in divided doses. Addition of such cytotoxic agents as cyclophosphamide and less commonly azathioprine is often justified, both for steroid sparing and for disease refractory to steroids alone. Some studies suggest improved survival with the use of cyclophosphamide. MTX has not been studied. Although trials are in progress, TNF inhibitors (infliximab, etanercept) have nonetheless been used with success in some patients with refractory PAN and granulomatosis with polyangiitis. The aggressiveness of therapy is based on the tempo of the disease and the extent of visceral involvement. Addition of plasma exchange to the therapeutic regimen is not of proven benefit. Antiviral therapy with interferon alpha should be considered in patients with PAN with evidence of active HBV infections. The benign course of limited cutaneous PAN supports conservative therapy for this variant.
Prognosis: PAN is associated with very high morbidity and substantial mortality. Untreated, mortality is >90%, but with corticosteroids, it decreases to 50%. The survival advantages of cytotoxic therapy are controversial. Most mortality is owing to renal failure, GI perforation/hemorrhage, and cardiac involvement. Patients who survive the initial manifestations of PAN are at high risk of infectious complications because of the potent immunosuppressive therapy necessary to control the disease. Chronic cardiac and/or renal disease are other long-term sequelae.
Langford CA. Treatment of polyarteritis nodosa, microscopic polyangiitis, and Churg-Strauss syndrome: where do we stand? Arthritis Rheum 2001;44:508–512. PMID:11263763
Langford CA. Vasculitis. J Allergy Clin Immunol 2003;111(suppl):S602–S612. PMID:12592306
Lhote F, Guillevin L. Polyarteritis nodosa, microscopic polyangiitis and Churg Strauss syndrome: clinical aspects and treatment. Rheum DisClin North Am 1995;21:911–948. PMID:8592743
Lightfoot RW, Michel BA, Bloch DA, et al. The American College of Rheumatology 1990 criteria for the classification of polyarteritis nodosa. Arthritis Rheum 1990;33:1088–1093. PMID:1975174
Soto O, Conn DL. Polyarteritis nodosa and microscopic polyangiitis. In: Hochberg MC, Silman AJ, Smolen JS, et al., eds. Rheumatology, 3rd ed. Edinburgh: Mosby, 2003:1611–1621.


This takes patience and the effect may seem too subtle. It is not an optical illusion proper, but it does show that we have a sense to immediately appreciate amounts, or “numerosity”.
What to see
In the experiment on the right there are two large light-grey discs. They are filled with a number of blobs, colored or grey. When the blobs are colored, there are many on the left, few on the right. When the blobs are grey, they are more equally distributed.
What to do
Your task is to look at the central down-counting digit and with your inner eye(!) compare the number of grey dots, whenever they briefly appear. If you feel the number of grey blobs differs between left and right, press one of the two bottom buttons to increase one side (the other decreases; the effect will only be apparent when the grey blobs appear again; internal accounting keeps track). Do this for a number of cycles, you may need to press the bottom left button repeatedly. At all times try to steadily fixate the central down-counter. When you're satisfied, press the “stop” button on the top left and you will see wether the adaptation had an effect on you.
The number of grey dots (now visible above the “increase” buttons) initially is set to 30:30. However, after looking at the display for a number of cycles, and increasing the left grey blob count, for me they appear equal at around 40:20.
There is a rule in psychophysics: “what is adaptable, exists”. Thus this experiment suggests that we actually have specific perception units for “numerosity”. Trivial explanations do not explain the rather strong effect: the position of the dots changes every cycle, thus precluding afterimages, and the effect even generalises across color.
The experiment allows to set the number of blobs for the adaptors and the test. Setting the adaptors to, say, 100:100 cancels any effect. You can also try 20:400 to convince yourself that it's not a trivial left field (or right hemisphere) effect.
If you want to know more: The sources below go into scientific depth. The present experiment was inspired by Burr & Ross’s demonstration, adding the “sawtooth” adaptation technique (Bach & Ulrich 1994) to drive into deep adaptation.
Burr DC, Ross J (2008) A visual sense of number. Current Biology 18:425–442
Ross J, Burr DC (2010) Vision senses number directly. JOV 10(2):10, 1–8
Tanya Lewis (2013) Is 'Numerosity' Humans' Sixth Sense? liveScience


Biological Quality Elements (BQE)
The ecological status of a river can be assessed by evaluating indicators for the composition, abundance, species diversity or absence of various groups of organisms known as “biological quality elements”. Four biological quality elements are used for rivers: algae (phytobenthos), macrophytes, macroinvertebrates and fish.
|Phytoplankton||Macrophytes and phytobenthos||Benthic invertebrates||Fish|
Using biological quality elements as indicators of hydromorphological degradation turns out to remain difficult. Improvements might be possible when using trait-based metrics Trait-based metrics instead of metrics based on species identity. Monitoring needs to be improved too. Nonetheless, unclear relationships between hydromorphological degradation and biota seem inevitable. Therefore REFORM recommends, with the current level of knowledge, using the hydromorphological method directly for ecological class assessment, circumventing the use of biological indicators.
Further reading: REFORM deliverables D3.1, D3.2, D3.3 and D3.4
Images taken from:


Lundi 29 Mars 2021 10:00 via Teams
Norms have proven to be useful mechanisms to coordinate societies. However, when choosing the norms to enact, we should also consider their ethical implications, since the selected norms may promote or demote moral values. Therefore, this selection process must consider how norms relate to moral values as well as the society's value preferences, so that the chosen norms (the so-called norm system) are those that align best with these preferences. Knowing how norms relate to values, we can use ranking functions to transform the moral value preferences to norm preferences. In the obtained norm ranking, more preferred norms are the ones that better align with the moral value preferences. Thus, we can use these norm preferences to compose the most value-aligned norm system. Interestingly, the generality of these methods allows to adapt them to many other ethical reasoning and decision making problems.


WHO IS THIS COURSE FOR?
This course is suitable for teachers working with young learners from 6 to 11 years old. It is for teachers that may be teaching English as a separate subject (ELT) or combining English with other subjects.
The course encourages participants to try out new classroom activities and discover the principles and methodologies used for teaching young learners.
- Ways of introducing and practising a new language
- Developing skills
- Using story books
- Different types of materials to use and adapt.
WHAT WILL YOU ACHIEVE?
Take this course to:
- Evaluate teaching activities, materials and media
- Understand how content and language are integrated in primary ELT and CLIL
- Consider classroom management, behaviour and motivation
- Share experiences with peers
1. Getting to know each other
2. Speak up! Helping learners with their oral communication skills
3. Vocabulary games with aims
1. Fun with flashcards! Exploit flashcards for vocabulary, grammar and pronunciation
2. Content and language integrated learning. CLIL v. ELT
3. Song, chants and drama in the classroom
1. Guided writing. Getting over the fear of the blank page
2. Different writing techniques for younger learners
3. Getting arty. Creative ideas for the classroom
1. Story-telling. Looking at popular children’s story books
2. Grammar Giggles. Games to recycle grammar
1. Managing behaviour. The use of praise in the classroom
2. Useful error correction techniques
3. Using technology in the classroom. Ideas and useful websites
4. End of course quiz and certificates
Przykładowe zajęcia dodatkowe:
bilard *, bowling *, cycling *, fitness *, ice scating *, sport in park, sports tournament, tennis *
bicycle tours *, boat cruises *, city tour/walk, concerts *, conversation practice, cultural activities, cultural events and festivals, guided city tours *, international evenings, museum visits, orientation tour, sightseeng, theatre or cinema visit *, walking tour
The London Eye *, British Museum, National Gallery, Victoria and Albert Museum, Royal Academy of Arts, Science Museum, Brighton *, Cambridge *, Oxford *
* zajęcia dodatkowo płatne


This week was Healthy Eating week and the children in Year 4 partook in various activities to think about staying hydrated, consuming more fruit and vegetables, incorporating more fibre in their diet and also considering ways to reduce food waste. Throughout the week, they researched fruits and vegetables and identified which parts of the plant we actually eat. They designed a healthy meal whilst grouping their ingredients according to food groups. They tasted 4 wholemeal items: morning cereal, tortilla, rice and wholemeal oat biscuits. They also sampled exotic fruits, evaluating not only the taste but the look, smell and texture. After creating a class database, they plotted their results on a graph. The class also had a chance to taste different infused water during the week, thinking about the importance of hydration, especially in the current heat. Thank you for all of you who kindly supported our learning by sending in fruit and veg; the children had a lovely time. It has been lovely to see them so open to new flavours and I am proud to announce we have 5 new wholemeal enthusiasts!
A huge well done to the class who sat their MTC tests this Tuesday. They worked very hard on their multiplication facts all year and tackled this rigorous exam with composure and confidence.
In English, the children used expanded noun phrases to describe characters whilst in Maths, we revised our formal written methods for the 4 calculations and consolidated long division. In RE, we deepened our understanding of Matthew’s parables further whilst in Art the children looked at artists from the 1960s to understanding how abstract art creates effect. In PE, we practiced our running and throwing skills when completing sprints, javelin throwing long jumping and obstacle drills.
A quick reminder that next Friday (23rd June) is non-uniform day in return for a hamper item (bottles, chocolates, raffle prizes, etc).
Have a lovely weekend,
Please see below your Home Learning:
|Home Learning||Due in by Tuesday, 20th June 2023|
|Spelling||Words with the prefix ‘bi-’ meaning ‘two’|
Please complete 2 activities and update reading log
Please complete the activities in your assigned pod, all Maths revision tasks.


GREENLAND POPULATION: 57,600
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|Greenland, the world's largest island, is about 81% ice-capped. Vikings reached the island in the 10th century from Iceland; Danish colonization began in the 18th century, and Greenland was made an integral part of Denmark in 1953. It joined the European Community (now the EU) with Denmark in 1973, but withdrew in 1985 over a dispute centered on stringent fishing quotas. Greenland was granted self-government in 1979 by the Danish parliament; the law went into effect the following year. Greenland voted in favor of increased self-rule in November 2008 and acquired greater responsibilty for internal affairs in June 2009. Denmark, however, continues to exercise control of Greenland's foreign affairs, security, and financial policy in consultation with Greenland's Home Rule Government.|
Map data ©2011 Geocentre Consulting, Tele Atlas -
1. Largest island.
2. Least dense population.
3. Given self-governance by Denmark in 1979.
4. Highest suicide rate (with teens in particular vulnerable): twice that of the next highest, Japan. Why? Guns are generally available (hunting mentality) and it really gets depressing in the winter.
5. Richie Cunningham--that character from Happy Days-- spent two winters here. No, not Ron Howard, he was smart enough not to be sent there.
6. If all the Greenland ice melted, our seas would rise by around 24 feet.