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Unit Code 83156:
Western Equine Encephalitis Antibody, IgG and IgM, Serum

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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

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.

Reference Values

IgG: <1:10

IgM: <1:10

 

See "Virology" in Special Instructions for additional

interpretive information.

Interpretation

In patients infected with this virus, IgG antibody is generally

detectable within 1-3 weeks of onset, peaking within 1-2 months,

and declining slowly thereafter.

 

IgM class antibody is also reliably detected within 1-3 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 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.

Cautions

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 10-21 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.

 

EEE and WEE 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.

Special Instructions and Forms

• Virology 

Clinical Reference

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 Microbiolgy. 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

Key