Overview of Viral Encephalitides in Poultry
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 (See also West Nile Virus Infection in Poultry). 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.
Eastern equine encephalitis (EEE) is most commonly a disease of horses (see 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, and subsequently spreading within the flock 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 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.
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 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.
Western equine encephalitis (WEE) virus has many characteristics in common with EEE virus; however, it is rarely associated with disease in avian species. WEE virus was identified as the cause of encephalitis and high mortality in turkeys; affected turkeys exhibited somnolence, tremors, and leg paralysis. WEE virus also has been identified as a cause of decreased egg production in turkeys.
WEE is seen 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.
Highlands J (HJ) virus is a cause of encephalitis in chukar partridges. Chukars exhibit somnolence, ruffled feathers, and recumbency before death. HJ virus infection in this species is associated with high mortality. Microscopic lesions primarily consist of nonpurulent meningoencephalitis and focal myocardial necrosis. HJ virus can cause decreased egg production in turkeys. The virus has been identified only in eastern parts of the USA.
Israel turkey meningoencephalitis has been reported only in turkeys. It generally occurs only in birds >10 wk old. 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 mosquitoes and Culicoides. Turkeys exhibit neurologic dysfunction characterized by progressive paresis and paralysis, with variable mortality. Morbidity and mortality rates average 15%–30% but may be as high as 80%. In turkey breeder hens, egg production drops severely. Gross lesions in affected turkeys include splenomegaly or atrophy of the spleen, catarrhal enteritis, and myocarditis. The principal microscopic lesions are nonpurulent meningoencephalitis characterized by submeningeal and perivascular lymphocytic infiltration and focal myocardial necrosis.
Diagnosis of EEE, WEE, and HJ virus infection or Israel turkey meningoencephalitis may be confirmed by isolation and identification of the virus, detection of viral antigens in tissues by ELISA, detection of viral RNA in tissues using reverse transcriptase PCR procedures, 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.
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 is highly efficacious and commercially available.
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 people 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.