Unit Code 83918:
Western Equine Encephalitis Antibody Panel, IgG and IgM, Spinal Fluid
Useful For
Aiding the diagnosis of WEE
Clinical Information
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 (CNS) disease from an endemic area. Infants are
highly susceptible to CNS 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 the acute disease, patients
may require from several months to 2 years to overcome the fatigue,
headache, and irritability. Infants and children are at a higher risk of
permanent brain damage after recovery than adults.
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, sex, and 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.
Reference Values
IgG: <1:10
IgM: <1:10
Reference values apply to all ages.
Interpretation
A positive result indicates intrathecal synthesis of antibody and is
indicative of neurological infection.
Cautions
All results must be correlated with clinical history and other data
available to the attending physician.
False-positive results may be caused by breakdown of the blood-
brain barrier, or by the introduction of blood into the CSF at collection.
WEE and eastern equine encephalitis viruses show some cross-
reactivity; however, antibody response to the infecting virus is typically
at least 8-fold higher.
Clinical Reference
1. Gonzalez-Scarano F, Nathanson N: Bunyaviruses. In Fields
Virology. Volume 1. 2nd Edition. Edited by BN Fields, DM Knipe.
New York, Raven Press, 1990, pp 1195-1228
2. Donat JF, Rhodes KH, Groover RV, Smith TF: Etiology and
outcome in 42 children with acute nonbacterial meningoencephalitits.
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


