Eastern Equine Encephalitis Antibody, IgG and IgM, Serum
Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test
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.
Aiding in the diagnosis of Eastern 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 Western equine encephalitis and Eastern equine encephalitis 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.
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.
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 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.
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.
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.
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. 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