Eastern equine encephalitis virus (family Togaviridae, genus Alphavirus) can cause disease in poultry, game birds, and wild birds. Neurological disease is the most common clinical outcome; however, this virus also may result in decreased egg production and myocarditis. Diagnosis is based on serological testing or detection of virus in serum or tissues using virus isolation, antigen-capture ELISA, immunohistochemical testing, or RT-PCR assay. No specific treatment is available; control is based primarily on decreasing contact with vector (ie, mosquito) populations.
Eastern equine encephalitis (EEE) is most commonly a disease of horses; however, many outbreaks of EEE in farm-raised ring-necked 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 can cause illness and death in some captive exotic birds, including African penguins and southern cassowaries. Although EEE virus infection typically is not believed to cause high fatality rates in native wild birds, illness and death occasionally occur in some species, notably in some wading birds (cranes, egrets), and sporadically in others (birds of prey, ruffed grouse).
EEE virus is found primarily in the eastern parts of North America, throughout Central America and the Caribbean, and in the eastern parts of South America. In the US, EEE activity has been identified in most states east of the Mississippi River as well as Louisiana, Arkansas, Minnesota, North Dakota, and Texas; it is observed most often along the Atlantic seaboard and in the Gulf Coast and Great Lakes states. Reported isolations of the virus in Europe and Asia have not been confirmed.
EEE virus outbreaks generally occur in late summer and fall in temperate latitudes as a consequence of increased seasonal activity of mosquito vectors:
Culiseta melanura, the principal mosquito vector, is likely responsible for transmission to 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 mosquito species.
Wild birds, primarily passerine species that frequent freshwater wetlands, 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 Findings in Eastern Equine Encephalitis Virus in Birds
Clinical signs of disease produced by eastern equine encephalitis virus in poultry, game birds, and wild birds are usually attributed to CNS infection with or without visceral involvement. However, EEE virus also may produce visceral infections with little or no involvement of CNS tissues.
Pheasants develop clinical signs of incoordination, listlessness, leg paralysis, torticollis, and tremors. The mortality rate may be as high as 80%. Gross lesions are not observed; however, microscopic changes in the CNS consist of vasculitis and fibrinoid change, patchy necrosis, neuronal degeneration, and meningeal inflammation.
Chukar partridges exhibit clinical signs of listlessness, somnolence, and high mortality rates (30%–80%). Pale, focal areas are often 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 rate (< 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 listlessness, hemorrhagic diarrhea, emesis of bloodstained ingesta, and high mortality rate (as much as 80%). Hemorrhagic enteritis is the principal lesion evident on postmortem examination. Microscopic lesions include necrosis of hepatocytes and intestinal mucosa.
Wild birds susceptible to disease exhibit similar clinical signs, including listlessness, ataxia, and progressive weakness, with variable mortality rates, depending on the species affected. Microscopic lesions in wild birds may include extensive necrosis, vascular changes (eg, fibrinoid change), and nonsuppurative inflammation in the CNS or in visceral organs (including heart) as well as vascular congestion and scattered hemorrhage.
Diagnosis of Eastern Equine Encephalitis Virus in Birds
Antemortem: clinical evaluation and serological testing
Postmortem: RT-PCR assay, immunohistochemical testing, or virus isolation from tissues
Diagnosis of eastern equine encephalitis may be confirmed by various means:
isolation and identification of the virus
detection of viral antigen using antigen-capture ELISA or immunohistochemical testing
detection of viral RNA using RT-PCR assay
serological testing
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 Vero (African green monkey kidney), 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 titers in serum collected soon after onset of clinical signs and 1–2 weeks later.
EEE virus must be distinguished from other causes of neurological disease in poultry and game birds, including the following:
avian paramyxovirus type 1 (cause of Newcastle disease)
highly pathogenic avian influenza viruses
Clostridium botulinum toxin (cause of botulism)
other encephalitic viruses
Listeria monocytogenes (cause of listeriosis)
bacteria such as Pasteurella multocida, Erysipelothrix rhusiopathiae, and others
In captive exotic and wild birds, including raptors, EEE virus infections are uncommonly documented and must be distinguished from other causes of neurological or severe systemic disease, such as the following:
West Nile virus
highly pathogenic avian influenza viruses
traumatic head injury
lead intoxication
Clostridium botulinum toxin
systemic bacterial infection (eg, Listeria monocytogenes, Pasteurella multocida, Escherichia coli, etc)
In the case of wild birds, environmental (field) data should be taken into consideration when determining differential diagnoses.
Due to the high case-fatality rate of EEE virus infection in humans, care must be taken when handling specimens that potentially contain this virus for diagnostic purposes. EEE virus is considered a select agent by the US Department of Health and Human Services. Permission and approved high-level containment procedures must be followed to work with live EEE virus, and detection of EEE virus must be reported to the appropriate authorities.
Prevention and Control of Eastern Equine Encephalitis Virus in Birds
No specific treatment for eastern equine encephalitis is available. EEE is best prevented by measures aimed at decreasing vector populations. Such measures include decreasing vector habitats by modifying the environment or by chemical spraying. If feasible, farms that raise susceptible species should be located away from wetlands and other areas that provide suitable conditions 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 in birds has been questioned, and protection should not be assumed. One-tenth of the equine dose is injected intramuscularly into the pectoral muscle, preferably when birds are released from the brooder house at 5–6 weeks old.
Zoonotic Risk of Eastern Equine Encephalitis Virus From Birds
Eastern equine encephalitis virus is a zoonotic agent and potential cause of severe neurological disease in humans; infections may progress to paralysis, convulsions, coma, and death. The case-fatality rate for EEE virus in humans is ~50%–75%. Infection in humans is usually acquired by mosquito bite; however, care should be taken to avoid contact or droplet exposure, including the use of appropriate personal protective equipment, when handling suspect infected birds and performing necropsies.
Key Points
EEE virus is a potential cause of disease in poultry, game birds, and captive exotic and wild birds. Neurological disease is the most common clinical outcome; however, the disease also may result in decreased egg production, myocarditis, and other visceral infections.
Diagnosis is based on detection of EEE virus in serum or tissues by virus isolation, detection of viral antigen using immunohistochemical testing, antigen-capture ELISA, or RT-PCR assay. Serological procedures also are commonly used.
No specific treatment for EEE is available. Prevention and control are based on decreasing vector populations and locating production facilities away from vector habitats.
EEE virus is a zoonotic threat. Appropriate biosafety precautions must be taken in suspected cases.
For More Information
Eastern equine encephalitis virus. Centers for Disease Control and Prevention. Updated June 13, 2023. Accessed October 13, 2023.
Equine encephalitis (EEE/WEE/VEE). Animal and Plant Health Inspection Service. US Department of Agriculture. Updated November 23, 2022. Accessed November 24, 2023.
Eastern equine encephalitis. Division of Disease Surveillance. Maine Center for Disease Control and Prevention. Accessed November 24, 2023.
Armstrong PM, Andreadis TG. Ecology and epidemiology of eastern equine encephalitis virus in the northeastern United States: an historical perspective. J Med Entomol. 2022;59(1):1-13. doi:10.1093/jme/tjab077
