Last Update: March 2000
Author: F. A. Leighton
Reviewer: H. Artsob
WEE virus is a member of the Alphavirus genus within the family Togaviridae. The virus was first recognized in a horse in California in 1930. In is an enveloped, single-stranded RNA virus. WEE virus is one of a group of 6 closely related viruses that once were thought to represent a single WEE virus. North American members of this closely-related group of viruses include WEE itself, Highlands J virus and Fort Morgan virus. The group also includes Sinbis virus (Africa, Europe, Asia), Aura virus (South America) and Y62-33 virus (former USSR).
WEE virus has been reported across south-central Canada from approximately Lake Superior to the Rocky Mountains, but it also has occurred in British Columbia. Disease in humans and horses has occurred most often in Saskatchewan and Manitoba. In North America, the general distribution of WEE virus is west of the Mississippi River in agricultural landscapes. This distribution parallels that of the most important mosquito vector of WEE, Culex tarsalis.
WEE virus normally cycles among wild birds and mammals, and mosquitoes. In western Canada, Culex tarsalis is the mosquito host of greatest importance, but the virus has been found in a variety of mosquito species of five genera: Aedes, Anopheles, Coquillettidia, Culex and Culesita. Birds are thought to be the most important vertebrate hosts for WEE. The virus replicates very effectively in birds, and birds thus act as amplifiers of the virus and important sources of infection for mosquitoes. In Western Canada, the House Sparrow and the House Finch appear to be particularly important amplifying hosts. WEE virus, or antibodies against the virus, have been found in a wide range of wild bird species. Mammals also may play roles in the ecology of WEE. Virus has been isolated from Richardson's Ground Squirrel (Spermophilus richardsoni) and Snowshoe hares (Lepus americanus). The virus also has been isolated from Garter Snakes (Thamnophis sp.) and from Leopard Frogs (Rana pipiens).
WEE virus goes through an annual cycle of amplification and dissemination. Nestling birds are infected in the spring by virus-infected mosquitoes. The virus replicates readily in these birds and other mosquitoes that feed on the birds become infected. They, in turn, can infect more birds, and the amplification cycle is repeated. Over the summer, the prevalence of infection in vector species of mosquitoes increases. Cold weather in the fall ends these cycles as mosquitoes die or become dormant. It is not known precisely how WEE virus is maintained during winter. Mammals and reptiles or amphibians may play roles in over-winter survival and also in summer amplification. Outbreaks of disease in people and horses tend to occur in years when, due to a complex of ecological factors, the prevalence of infection in mosquitoes is particularly high. Infection in mosquitoes is highest at the end of summer - in August and September - and infections in people and horses are most common during these months.
Wildlife: It is not known if WEE is an important pathogen to its normal vertebrate or mosquito hosts, but in general this appears not to be the case. WEE virus has been isolated from nestling House Sparrows that were clinically ill or dead and from some rodents suspected of having rabies. However, it is not certain that WEE was the cause of disease in these animals. It seems likely that WEE may cause disease in wild animals from time to time, but there is no evidence to date that it is an important wild animal pathogen.
Domestic Animals: Horses can suffer severe, often fatal disease after infection with WEE. In 1937-38 in the prairie provinces, 52,500 horses suffered clinical disease and 15,000 died. Clinical disease develops 1-3 weeks after infection and ranges from a general fever followed by recovery to severe infection and inflammation of the brain leading to deranged behaviour and death. In reported outbreaks of WEE, from 10% to 50% of horses that became clinically ill died of the disease. One disease outbreak in turkeys in the United States was thought to have been caused by WEE.
Of the arboviruses that occur in Canada, WEE has been the most important cause of human disease. Sporadic outbreaks have been recognized in Canada each decade since the 1930's. An epidemic occurred in the prairie provinces in 1941 in which 1094 human cases were recorded, which is most of the total of cases (1500 or so) recorded in Canada up to 1990. However, most people infected with WEE suffer only mild disease or no disease at all. Children are more likely to suffer disease than are adults; approximately half of children under one year of age will become ill if infected while slightly less than one in 1,000 people aged 14 years or older will become ill if infected. The mortality rate from WEE is reported to range from 8 to 15% in people who develop clinical disease after infection.
Because of its annual cycle of amplification, risk of disease in people and horses varies greatly from year to year, depending on the prevalence of infected mosquitoes of species likely to feed on both birds and mammals. Surveillance programs of various kinds are in place or have been used in the past to monitor the prevalence of infected mosquitoes. When a high prevalence is detected, education programs to urge people to avoid exposure to mosquitoes and mosquito control programs can be undertaken. Earlier assessment of the magnitude of the amplification cycle is possible by surveys of nestling birds or use of sentinel bird flocks which are monitored for exposure to WEE virus. Since mosquito control generally is not very effective when undertaken late in the summer, early detection can trigger control efforts earlier in the season which are more likely to succeed. Television and air conditioning appear to have reduced the incidence of disease from WEE in people by modifying human behaviour in such a way as to reduce contact with infected mosquitoes.
Effective vaccines are available for use in horses but none is available for general use in humans. The small number of human cases of WEE is insufficient to justify a public vaccination program.
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