OPHEPR; Eastern Equine Encephalitis - Profile for Healthcare Workers

Infective Dose & Infectivity: The infective dose is unknown. All people are considered susceptible though children are more likely to be severely affected.

Incubation Period: The incubation period is varies from 5-15 days.

Clinical Effects: The illness is characterized by rapid onset of high fever, vomiting, stiff neck, and drowsiness. Children frequently manifest generalized, facial, or periorbital edema. Motor involvement with paresis is common during the acute phase of the illness. Major disturbances of autonomic function, such as impaired respiratory regulation or excess salivation may dominate the clinical picture. Adults typically exhibit a febrile prodrome for up to 11 days before the onset of neurological disease; however, illness in children exhibits a more sudden onset. Up to 30% of survivors are left with neurological sequelae such as seizures, spastic paralysis, and cranial neuropathies. Cognitive impairment ranges from minimal brain dysfunction to severe dementia.

Lethality: Fatality rates for EEE are estimated to be from 50% to 75%. Mortality rates are highest among young children and the elderly.

Transmissibility: EEE infection occurs when a person is bitten by an infected mosquito. The virus is not directly transmitted from person-to-person.

Primary contaminations & Methods of Dissemination: As a bioterrorism weapon, EEE would most likely be delivered via aerosolization.

Secondary Contamination & Persistence of organism: Secondary transmission does not occur and EEE particles are not considered to be stable in the environment.

Decontamination & Isolation:

Patients – Standard precautions should be practiced and enteric precautions are appropriate until enterovirus meningoencephalitis is ruled out. Specific isolation procedures are not indicated.
Equipment, clothing & other objects – 0.5% hypochlorite solution (one part household bleach and 9 parts water = 0.5% solution) is effective for environmental decontamination.

Laboratory testing: Clinical laboratory findings in patients with EEE often demonstrate an early leukopenia followed by a leukocytosis. Elevated opening pressure is commonly noted on lumbar puncture, and in children, especially, the CSF lymphocytic pleocytosis may reach a cell count of thousands of mononuclear cells per microliter. Specific diagnosis of EEE depends on virus isolation or serologic testing in which rising titers of HI, CF, or neutralizing antibodies are observed. IgM antibodies are usually detectable in acute-phase sera.

Therapeutic Treatment: There is no specific therapy. Patients who develop severe illness may require anticonvulsant and intensive supportive care to maintain fluid and electrolyte balance, adequate ventilation, and to avoid complicating secondary bacterial infections.

Prophylactic Treatment: An investigational formalin-inactivated vaccine is available, but it is poorly immunogenic.

Differential Diagnosis: The differential diagnosis includes a number of infections including cytomegalovirus, herpes simplex encephalitis, St. Louis encephalitis, West Nile encephalitis, Western equine encephalitis, Venezuelan encephalitis, malaria, Naegleria infection, leptospirosis, lyme disease, cat scratch disease, bacterial meningitis, tuberculosis, and fungal meningitis.

References:

Chin J. Control of Communicable Diseases Manual, Seventeenth Edition, American Public Health Association; 2000.
Smith JF, Davis K, Hart MK, et al. Viral Encephalitides. In: Zajtchuk R, Bellamy RF, eds. Medical Aspects of Chemical and Biological Warfare. Washington, DC: Office of the Surgeon General, U.S. Department of the Army; 1997:561-589.

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