Aiding in the diagnosis of EEE

Eastern equine encephalitis (EEE) is within the alphavirus group.

It is a low prevalence cause of human disease in the eastern and

Gulf Coast states. EEE is maintained by a cycle of mosquito/wild

bird transmission, peaking in the summer and early fall, when man

may become an adventitious host. The most common clinically

apparent manifestation is a mild undifferentiated febrile illness,

usually with headache. Central nervous system involvement is

demonstrated in only a minority of infected individuals, it is more

abrupt and more severe with EEE than other arboviruses, with

children being more susceptible to severe disease. Fatality rates

are approximately 70% for EEE.

IgG: <1:10

IgM: <1:10

See "Virology" in Special Instructions for additional

interpretive information.

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

western equine encephalitis (WEE) and EEE antigens will show a

noticeable cross-reactivity.

Infections 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. Infection among males is primarily due to work

conditions and sports activity taking place where the vector is

present.

All results must be correlated with 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 antigen 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.

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2.     Donat JF, Hable-Rhodes KH, Groover RV, Smith TF: Etiology

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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

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