Western Equine Encephalitis (WEE)
The western equine encephalitis alphavirus (WEE) was first isolated in California in 1930 from the brain of a horse with encephalitis. WEE remains an important cause of encephalitis in horses and humans in North America, mainly in the Western USA and Canada. In the Western US, the enzootic cycle of WEE involves passerine birds, in which the infection is inapparent, and culicine mosquitoes, principally Cx. tarsalis, a species that is associated with irrigated agriculture and stream drainages. Other important mosquito vector species include Aedes melanimon in California, Ae. dorsalis in Utah and New Mexico and Ae. campestris in New Mexico.
Human WEE cases are usually first seen in June or July. Most WEE infections are asymptomatic or present as mild, nonspecific illness. Patients with clinically apparent illness usually have sudden onset of fever, headache, nausea, vomiting, anorexia and malaise, followed by altered mental status, weakness and signs of meningeal irritation. Children, especially those under 1 year of age, are affected more severely and 5-30% may be left with permanent sequelae. The overall mortality rate is about 3%.
Expansion of irrigated agriculture in the North Platte River Valley during the past several decades has created habitats and conditions favorable for increases in populations of granivorous birds such as the house sparrow and mosquitoes such as Cx. tarsalis, Ae. dorsalis and Ae. melanimon. All of these species may play a role in WEE virus transmission in irrigated areas.
No human vaccines are commercially available for this disease. Arboviral encephalitis can be prevented in two major ways: personal protective measures and public health measures to reduce the population of infected mosquitoes. Personal protective measures include reducing time outdoors, particularly in early evening hours; wearing long pants and long sleeved shirts, and applying mosquito repellent to exposed skin areas. Public health measures often require insecticide spraying.