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The virus that causes western equine encephalitis (WEE) is widely distributed throughout the United States and Canada; disease occurs almost exclusively in the western states and Canadian provinces. The relative absence of the disease in the eastern United States probably reflects a paucity of the vector mosquito species, Culex tarsalis, and possibly a lower pathogenicity of local virus strains. The disease usually begins suddenly with malaise, fever, and headache, often with nausea and vomiting. Vertigo, photophobia, sore throat, respiratory symptoms, abdominal pain, and myalgia are also common. Over a few days, the headache intensifies; drowsiness and restlessness may merge into a coma in severe cases. In infants and children, the onset may be more abrupt than for adults. WEE should be suspected in any case of febrile central nervous system disease from an endemic area. Infants are highly susceptible to central nervous system disease and about 20% of cases are under 1 year of age. There is an excess of males with WEE clinical encephalitis, averaging about twice the number of infections detected in females. After recovery from acute disease, patients may require from several months to 2 years to overcome the fatigue, headache, and irritability. Infants and children are at higher risk of permanent brain damage after recovery than adults.
Aiding the diagnosis of Western equine encephalitis
In patients infected with this virus, IgG antibody is generally detectable within 1 to 3 weeks of onset, peaking within 1 to 2 months, and declining slowly thereafter.
IgM class antibody is also reliably detected within 1 to 3 weeks of onset, peaking and rapidly declining within 3 months.
Single serum specimen IgG > or =1:10 indicates exposure to the virus.
Results from a single serum specimen can differentiate early (acute) infection from past infection with immunity if IgM is positive (suggests acute infection).
A 4-fold or greater rise in IgG antibody titer in acute and convalescent sera indicate recent infection.
In the United States it is unusual for any patient to show positive reactions to more than 1 of the arboviral antigens, although Eastern equine encephalitis (WEE) and eastern equine encephalitis (EEE) antigens will show a noticeable cross-reactivity.
Infections with arboviruses can occur at any age. The age distribution depends on the degree of exposure to the particular transmitting arthropod relating to age and sex, as well as the occupational, vocational, and recreational habits of the individuals. Once humans have been infected, the severity of the host response may be influenced by age: WEE tends to produce the most severe clinical infections in young persons. Infection in males is primarily due to working conditions and sports activity taking place where the vector is present.
All results must be correlated with the clinical history and other data available to the attending physician.
Specimens drawn within the first 2 weeks after onset are variably negative for IgG antibody and should not be used to exclude the diagnosis of arboviral disease. If arboviral infection is suspected, a second specimen should be drawn and tested 10 to 21 days later.
Since cross-reactivity with dengue fever virus does occur with St. Louis encephalitis (SLE) antigens and, therefore, cannot be differentiated further. The specific virus responsible for such a titer may be deduced by the travel history of the patient, along with available medical and epidemiological data, unless the virus can be isolated.
Eastern equine encephalitis and Western equine encephalitis viruses show some cross-reactivity; however, antibody response to the infecting virus is typically at least 8-fold higher.
Usually, when an infection with an arbovirus is suspected, it is too late to isolate the virus or draw serum specimens to detect a rise of antibody titer.
1. Gonzalez-Scarano F, Nathanson N: Bunyaviruses. In Fields Virology. Vol 1. 2nd edition. Edited by BN Fields, DM Knipe. New York, Raven Press, 1990, pp 1195-1228
2. Donat JF, Hable-Rhodes KH, Groover RV, Smith TF: Etiology and outcome in 42 children with acute nonbacterial meningoencephalitis. Mayo Clin Proc 1980;55:156-160
3. Tsai TF: Arboviruses. In Manual of Clinical Microbiology. 7th edition. Edited by PR Murray, EJ Baron, MA Pfaller, et al. Washington, DC, American Society for Microbiology, 1999, pp 1107-1124
4. Calisher CH: Medically important arboviruses of the United States and Canada. Clin Microbiol Rev 1994;7:89-116