Eastern equine encephalitis (EEE) is most commonly a disease of horses Equine Arboviral Encephalomyelitis ; however, many outbreaks of EEE in farm-raised ringnecked pheasants and chukar partridges have been identified. EEE occurs only sporadically in other species of poultry (turkeys, ducks), game birds, and ratites (emus). EEE virus is found primarily in the eastern parts of North America, throughout Central America and the Caribbean, and in eastern parts of South America. In the USA, EEE has been identified in most states east of the Mississippi River as well as Louisiana and Texas; it is seen most often in Atlantic seaboard and Gulf Coast states. Reported isolations of the virus in Europe and Asia have not been confirmed.
EEE outbreaks generally occur in late summer and fall as a consequence of increasing numbers of mosquito vectors. Culiseta melanura, the principal mosquito vector, is likely responsible for transmission to poultry and game birds. Transmission to mammalian species most likely occurs by other mosquitoes such as Aedes and Coquillettidia spp, which feed on birds but also have a propensity to bite mammals. The virus has also been identified in a variety of other mosquitoes. Wild birds, primarily the smaller species of Passeriformes, are the principal vertebrate hosts of EEE virus. These birds rarely become ill but serve as maintenance and amplifying hosts for the virus in the transmission cycle.
Epornitics of EEE virus infection in pheasants are believed to be initiated by mosquito-borne infection of one or more birds in a flock, subsequently spreading within the flock as a result of feather picking and cannibalism. In ratites, the virus also may be transmitted by the fecal-oral route.
Clinical disease produced by eastern equine encephalitis virus in poultry and game birds is usually attributed to CNS infection with or without visceral involvement. However, EEE also may produce visceral infections with little or no involvement of CNS tissues.
Mortality may be as high as 80%. Gross lesions are not observed; however, microscopic changes in the CNS consist of vasculitis, patchy necrosis, neuronal degeneration, and meningeal inflammation.
Chukar partridges exhibit clinical signs of depression, somnolence, and high mortality (30%–80%). Pale, focal areas generally are present on hearts of affected birds, and spleens are mottled and enlarged. Microscopic lesions consist of gliosis, satellitosis, perivascular lymphocytic infiltration in the brain, and myocardial necrosis with lymphocytic infiltration in the heart.
Turkeys with EEE virus infection may exhibit drowsiness, incoordination, progressive weakness, paralysis of legs and wings, and low mortality (< 5%). In turkeys, EEE virus also has been identified as a cause of decreased egg production.
Ducklings infected with EEE virus develop a paralytic disease characterized by sudden onset, posterior paresis, and paralysis; mortality rates in affected flocks range from 2% to 60%. Microscopic lesions consist of edema of spinal cord white matter, lymphocytic meningitis, and microgliosis.
Ratites exhibit depression, hemorrhagic diarrhea, emesis of bloodstained ingesta, and high mortality (as much as 80%). Hemorrhagic enteritis is the principal lesion seen on postmortem examination. Microscopic lesions include necrosis of hepatocytes and intestinal mucosa.
Diagnosis of eastern equine encephalitis may be confirmed by isolation and identification of the virus, detection of viral antigen using antigen-capture ELISA or immunohistochemistry, detection of viral RNA using reverse-transcriptase PCR, and serology.
EEE virus can be readily isolated in newborn mice inoculated by the intracerebral route, day-old chickens by the intramuscular or subcutaneous route, and embryonated chicken eggs by the yolk sac route. The virus also may be isolated by inoculation of chicken or duck embryo cells. Preferred clinical samples include serum or tissues (brain, spleen, liver, heart).
Serological diagnosis may be accomplished using a variety of procedures, including virus-neutralization, hemagglutination-inhibition, ELISA, and complement fixation. A definitive diagnosis is based on demonstrating a rise in antibody in serum collected soon after onset of clinical signs and 1–2 weeks later.
EEE must be distinguished from other causes of neurologic disease in poultry and game birds, including Newcastle disease Newcastle Disease in Poultry Newcastle disease is a severe, systemic, and fatal viral disease of poultry due to virulent strains of avian paramyxovirus type 1. Clinical signs in unvaccinated birds include sudden death,... read more , avian encephalomyelitis Avian Encephalomyelitis Avian encephalomyelitis is a viral infection affecting the CNS of several species of birds. Signs include tremors, ataxia, and weakness that progresses to paralysis. Diagnosis is based on history... read more , botulism Botulism in Poultry Botulism is a toxic disorder resulting from ingestion of the exotoxin produced by Clostridium botulinum. It affects a wide variety of birds and mammals. Clinical signs include leg weakness... read more , and listeriosis Listeriosis in Poultry Listeriosis affects a wide range of bird species, but most infections do not cause clinical signs. Sporadic cases in backyard chickens may cause encephalitis or septicemia and sudden death.... read more .
Prevention and Control
No specific treatment for eastern equine encephalitis is available. EEE is best prevented by measures aimed at reducing vector populations. Such measures include reducing vector habitats by modifying the environment or by chemical spraying. If feasible, farms that raise susceptible species should be located away from swamps and other areas that provide habitat for vectors.
Commercial, inactivated EEE vaccines, prepared for use in horses, have been used for protection of pheasants against EEE outbreaks; however, the efficacy of these vaccines has been questioned. One-tenth the equine dose is injected intramuscularly into the pectoral muscle, preferably at 5–6 weeks of age when birds are released from the brooder house.
Eastern equine encephalitis virus is a zoonotic agent and potential cause of significant neurologic disease in people; these infections may progress to paralysis, convulsions, coma, and death. The case-fatality rate for EEE virus in humans is approximately 50%–75%. Human infection usually is acquired by mosquito bite; however, care should be taken to avoid contact or droplet exposure when handling suspect infected birds and performing necropsies.
EEE virus is a potential cause of disease in poultry and game birds. Neurological disease is the most common clinical outcome, but the disease also may result in decreased egg production or myocarditis.
EEE diagnosis is based on detection of EEE virus in serum or tissues by virus isolation, detection of viral antigen using immunohistochemistry or antigen-capture ELISA, and reverse-transcriptase PCR. Serologic procedures also are commonly used.
No specific treatment is available. Prevention and control are based on reducing vector populations and/or locating production facilities away from vector habitats.