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%.