Eastern equine encephalitis (EEE) is a potentially fatal neurologic condition caused by infection with the arthropod-borne virus Alphavirus togaviridae. Signs and symptoms range from febrile illness to encephalitis (i.e., inflammation of the brain parenchyma that causes neurologic dysfunction). EEE is most often fatal in horses and, although rare in humans, is associated with a high rate of morbidity and mortality in humans as well. The incubation period is about 5-15 days from time of exposure to A. togaviridae infection.
In the northeastern United States, EEE is spread by the mosquito Culiseta melanura, which breeds in freshwater swamps and feeds on passerine birds that serve as a reservoir for further viral dissemination. In the southeastern U.S., EEE is spread by the mosquito Culex erraticus, which is found primarily in the wetlands. Humans are infected incidentally; the mosquito injects the virus into the host's subcutaneous and cutaneous tissues where it replicates and causes a prodrome of nonspecific manifestations. Viral migration to the central nervous system (CNS) and the resulting influx of immunologically active cells into the brain parenchyma and perivascular areas cause neuronal destruction, focal necrosis, and spotty demyelination. The initial signs and symptoms of CNS involvement can progress rapidly to confusion, somnolence or even coma. Long-term sequelae include mental retardation, behavioral changes, paralysis, permanent focal neurologic deficits, seizure disorders, emotional lability and adjustment disorders.
There is no specific treatment for EEE. Initial medical care focuses on early diagnosis and differentiation of EEE from other potentially treatable causes of encephalitis. The lack of specific signs and symptoms along with the numerous organisms that cause similar signs and symptoms, make EEE difficult to diagnose.
Diagnosis of EEE should be suspected in patients with certain clinical manifestations (e.g., fever, headache, and/or altered mental status), a history of living in or traveling to an area where the virus is present (particularly during summer or early fall), and a history of exposure to mosquitoes, such as through occupation or recreational activities. Diagnosis is confirmed by either serology, viral culture or viral antigen detection in brain tissue or cerebrospinal fluid (CSF). Management is supportive and may include respiratory maintenance with ventilator support, nutritional support, and pharmacologic therapy with antipyretics, anticonvulsants, and/or anti-inflammatories (e.g., corticosteroids). Patients who survive EEE typically require extensive rehabilitation, in some cases including physical, occupational and/or speech therapy.
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