| Viral Encephalitides: Introduction |  |
| Encephalitis in poultry and farm-reared gamebirds may be caused by several different arboviruses. These include eastern equine encephalitis (EEE) virus, western equine encephalitis (WEE) virus, Highlands J (HJ) virus, Israel turkey meningoencephalitis virus, and West Nile Virus (
West Nile Virus Infection in Poultry: Introduction). The term “arbovirus,” an abbreviation of arthropod-borne virus, is used to describe a virus that replicates in a hematophagous (bloodsucking) arthropod and is
transmitted by bite to a vertebrate host. |
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Eastern Equine Encephalitis: |
| Eastern equine encephalitis (EEE) is most commonly seen as a disease of horses (see
equine encephalomyelitis,
Dysautonomia); 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) and game birds (ratites). EEE virus exists primarily in the eastern and central 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. Reports of EEE 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
, an ornithophilic mosquito, is the principal vector; however, the virus also has been identified in a variety of other mosquitos.
C
melanura
is the likely vector responsible for transmission to poultry and game birds. 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 1 or more birds in a flock, with subsequent spread within the flock occurring as a result of feather picking and cannibalism. In ratites, the virus may be transmitted by the fecal-oral route. |
| Clinical disease produced by EEE virus in poultry and game birds usually is attributed to CNS infection with or without involvement of viscera. However, EEE also may produce visceral infections with little or no involvement of CNS tissues, especially in ratites. |
| Pheasants develop incoordination, depression, leg paralysis, torticollis, and tremors. Mortality may be as high as 80%. Gross lesions are not observed; however, microscopic changes in the CNS may include lymphocytic encephalitis, 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 in the brain consist of gliosis, satellitosis, and perivascular lymphocytic infiltration. Myocardial lesions include multifocal necrosis and lymphocytic infiltration. |
| EEE virus infection in turkeys is characterized by drownsiness, 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 2-60%. Microscopic lesions consist of edema of spinal cord white matter, lymphocytic meningitis, and microgliosis. |
| Ratites exhibit depression, hemorrhagic diarrhea, emesis of blood-stained ingesta, and high mortality (up to 80%). Hemorrhagic enteritis is the principal lesion observed at postmortem examination. Microscopic lesions include necrosis of hepatocytes and intestinal mucosa. |
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Western Equine Encephalitis (WEE): |
| This virus has many characteristics in common with EEE virus; however, it is rarely associated with diseases in avian species. WEE virus has been reported to cause encephalitis and high mortality in turkeys; affected turkeys exhibited somnolence, tremors, and leg paralysis. WEE virus may also cause decreased egg production in turkeys. |
| WEE is identified mainly in western parts of the USA and Canada, Central America, and South America. In the USA and Canada it is transmitted principally by
Culiseta
tarsalis
, a mosquito vector that is relatively common west of the Mississippi River. |
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|
Highlands J Virus: |
| Highlands J (HJ) virus is a cause of encephalitis in Chukar partridges. Chukars exhibit somnolence, ruffled feathers, and recumbency prior to death. HJ virus infection in this species is associated with high mortality. Microscopic lesions primarily consist of lymphocytic meningoencephalitis and focal myocardial necrosis. HJ virus has been shown to cause decreased egg production in turkeys. The virus has been identified only in eastern parts of the USA. |
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Israel Turkey Meningoencephalitis: |
| This disease has been reported only in turkeys and generally is seen only in birds >10 wk of age. It has been reported only in Israel and South Africa. While the specific vector has not been identified, the seasonal incidence and sporadic occurrence in flocks on the same farms strongly suggest that it is transmitted by insect vectors, most likely mosquitos and
Culicoides
spp
flies. Turkeys exhibit neurologic dysfunction characterized by progressive paresis and paralysis, with variable mortality. Morbidity and mortality rates generally average 15-30% but may be as high as 80% . Turkey breeder hens exhibit a severe drop in egg production. Gross lesions in affected turkeys include splenomegaly or atrophy of the spleen, catarrhal enteritis, and myocarditis. The principal microscopic lesions are meningoencephalitis characterized by submeningeal
and perivascular lymphocytic infiltration and focal myocardial necrosis. |
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| Diagnosis: |
| Diagnosis of EEE, WEE, and HJ virus or Israel turkey meningoencephalitis infection may be confirmed by isolation and identification of the virus, detection of viral antigens in tissues by immunohistochemistry, detection of viral RNA in tissues using reverse transcriptase PCR, and serologic testing. Virus can be isolated by inoculation of newborn mice, day-old chickens, embryonated chicken eggs, or a variety of cell cultures. Brain, spleen, liver, and serum are the preferred
materials for diagnostic analyses. |
| Arbovirus infections must be distinguished from other causes of neurologic disease in poultry and game birds such as Newcastle disease virus, avian encephalomyelitis virus, botulism, and listeriosis. |
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| Prevention and Control: |
| EEE, WEE, and HJ virus infection and Israel turkey meningoencephalitis are best prevented by measures aimed at reducing vector populations. Such measures include reduction of vector habitats by modifying the environment or by chemical spraying. If feasible, farms that raise susceptible avian species should be located away from swamps and other areas that provide habitat for vectors. |
| Formalin-inactivated EEE virus vaccines, prepared for use in horses, have been used to protect pheasants against EEE, although their efficacy has been questioned. One-tenth the equine dose of either an eastern or bivalent eastern and western vaccine is injected into the pectoral muscle, preferably at 5-6 wk of age or when birds are released from the brooder house. |
| Israel turkey meningoencephalitis also can be controlled by vaccination. A live attenuated vaccine has been prepared by serial passage of virus in Japanese quail kidney cells; this vaccine has been shown to be highly efficacious and is commercially available. |
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| Zoonotic Risk: |
| EEE and WEE viruses are zoonotic agents and potential causes of significant human disease. These viruses result in neurologic disease that may progress to paralysis, convulsions, coma, and death. The case fatality rate for EEE virus in humans is 50-75%, and survivors often have permanent neurologic sequelae. WEE virus is less severe, with a case-fatality rate of ~3-7%. Most infections are subclinical. Human infection usually is acquired by mosquito bite; laboratory and
clinically acquired infections are rare. However, care should be taken to avoid contact or droplet exposure when handling suspect infected birds or performing necropsies. |
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