Eastern Equine Encephalitis

Eastern Equine Encephalitis Virus

Eastern equine encephalitis (EEE) is caused by infection with eastern equine encephalitis virus (EEEV). The natural reservoir for EEEV is tree-perching birds found in forested wetlands. The virus is spread between these birds and other small mammals, reptiles and amphibians by Culiseta melanura mosquitoes. Occasionally, humans and horses become infected with EEEV after being bitten by Aedes or Culex mosquitos that have taken blood meals from these birds.

In the United States, EEEV infections typically occur in late summer and early fall, before colder temperatures kill mosquitoes. The virus is most commonly found along the Gulf Coast, in the Atlantic States, and around the Great Lakes. The number of cases varies by year. In 2019, a record 38 cases were reported to the CDC. So far in 2024, CDC has been informed of 8 cases of neuroinvasive disease in Massachusetts, New Hampshire, New Jersey, Wisconsin, and Vermont. The patient in New Hampshire expired. 

After mosquitos inject their infected saliva into perivascular dermal tissue, EEEV infects Langerhans and dendritic cells. The infected cells migrate to regional lymphoid nodes, where EEEV replicates and can lead to systemic viremia. 

Approximately 95% of individuals remain asymptomatic after infection. A minority of patients develop nonspecific symptoms after an incubation period of 3 to 10 days. Symptoms include fever, malaise, intense headache, muscle aches, and nausea and vomiting. They may last as long as two weeks. Most patients recover uneventfully, but some progress to encephalitis. Imaging typically shows involvement of the basal ganglia and thalami. Approximately 30% of encephalitis cases are fatal.Survivors often have long-term neurological problems. 

Serologic testing remains the primary method for diagnosing eastern equine encephalitis. However, RT-PCR might be needed for patients who are immunocompromised. 

IgG and IgM antibodies to EEEV can be serum or cerebrospinal fluid. IgM antibodies are reliably detected within 1 to 3 weeks of symptom onset. IgM peaks rapidly and declines to undetectable levels by 3 months. IgG antibodies peaks within 1 to 2 months and then begins to slowly decline. The presence of IgM antibodies indicates an acute infection.  

No antiviral drug has been demonstrated to have efficacy against EEEV. The mainstay of treatment is supportive care, usually in an intensive care unit. Patients do not need to be isolated. 

EEE is a nationally notifiable condition. All cases should be reported to local or state public health authorities. 

Reference

Morens DM, Eastern Equine Encephalitis Virus — Another Emergent Arbovirus in the United States. New Engl J Med 2019;381:1989-92.