Western Equine Encephalitis Antibody Panel, IgG and IgM, Spinal Fluid
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
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.
Aiding the diagnosis of Western equine encephalitis
Detection of organism-specific antibodies in the cerebrospinal fluid (CSF) may suggest central nervous system infection. However, these results are unable to distinguish between intrathecal antibodies and serum antibodies introduced into the CSF at the time of lumbar puncture or from a breakdown in the blood-brain barrier. The results should be interpreted with other laboratory and clinical data prior to a diagnosis of central nervous system infection.
Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances
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 cerebrospinal fluid at collection.
Western equine encephalitis and eastern equine encephalitis viruses show some cross-reactivity; however, antibody response to the infecting virus is typically at least 8-fold higher.
Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.
Reference values apply to all ages.
Clinical References Provides recommendations for further in-depth reading of a clinical nature
1. Gonzalez-Scarano F, Nathanson N: Bunyaviruses. In Fields Virology. Vol 1. Second 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. Seventh edition. Edited by PR Murray, EJ Baron, MA Pfaller, et al. Washington, DC, ASM Press, 1999, pp 1107-1124
4. Calisher CH: Medically important arboviruses of the United States and Canada. Clin Microbiol Rev 1994;7:89-116