Continued from page 2Eastern Equine Encephalitis
Key points: Seems to be an emu specific disease at present time; carried asymptomatically in the wild bird population of the eastern and southeastern United States; neuromuscular signs may include rapid onset ataxia or prostration; moderate morbidity and high mortality; gross lesions include hemorrhagic enteritis with petechial hemorrhages of serosal membranes; no CNS lesions seen; equine bi-or trivalent vaccine seems to be protective.
The causative agent of eastern equine encephalitis is a togavirus. Taxonomically, this virus is included in the group of alpha (Group A) arboviruses. Wild bird populations in cluding passerines and columbiformes have been found to be asymptomatic carriers of EEE. Disease has been documented in many avian species including emus, pheasants, whooping cranes, turkeys, chuckars, bobwhite quail, domestic chickens and domestic ducks. In ratite medicine, EEE has not been associated with disease in the ostrich, rhea or cassowary - and at present time is viewed as exclusively a disease of the emu.
Clinical signs of EEE infection that have been reported in the emu includes an acute onset of depression, profuse hemorrhagic diarrhea, anorexia and ataxia. Terminally, these birds show prostration, hemorrhagic diarrhea and emesis. This disease in emus is characterized as having moderate morbidity and high mortality.
Eastern equine encephalitis virus was isolated from a group of emus in south central Louisiana that were exhibiting clinical signs of hemorrhagic diarrhea and peracute mortality. The outbreak involved juvenile and adult breeding birds ranging in age from 20-36 months. Morbidity was 76%, and mortality was 87%. Recovered birds mounted high antibody titers. Post mortem examination revealed hemorrhagic enteritis and petechia of the viscera. Histopathology demonstrated severe necrosis of the hepatocytes, intestinal mucosa and a necrotizing vasculitis of the spleen and lamina propria of the intestine. No nervous system lesions were seen.
Diagnosis of EEE infection in emus is based on rising serologic titers in conjunction with clinical signs. Previously vaccinated birds, of course, cannot have serology utilized. Histopathology and virus at necropsy can also confirm a diagnosis. Treatment at this time remains suportive only. Clinically ill birds with EEE tend to demonstrate a low survivability rate.
Prevention of EEE in emus is in part based on the regional aspects of this disease. EEE remains a problem in the southeastern and sough central United States. Mosquitoes are believed to be the key vectors from the wild bird endemic population to the emu. Currently, equine bi-or trivalent vaccines are believed to produce some degree of immunity and protection. It is believed that the emu acts as as sentinel for this disease, rather than a reservoir.
Western Equine Encephalitis
Key points: WEE is a zoonotic pathogen, and the emu is believed to be a sentinel species; virus is endemic in the Western United States wild bird and reptile populations; disease is characterized as one of moderate morbidity and low mortality; gross lesions include vasculitis and serositis; use of a bi or trivalent equine vaccine is believed to be protective. The causative agent of WEE disease in emus is a togavirus. Taxonomically, this virus is included in the group of alpha (Group A) arboviruses, similar to EEE and VEE. WEE is comparatively a less understood pathogen than EEE in ratite species, but still is recognized as an emu specific disease at present time. WEE can be a significant zoonotic pathogen as well. In the 1950's, a California outbreak of WEE was associated with over 300 fatalities.
Clinical signs associated with WEE infection in emys have included depression, anorexia and ataxia. In advanced cases, paddling of the legs and death have been seen. Overall, this disease is characterized as one of moderate morbidity and low mortality. Young birds reportedly are more susceptible than yearlings or adults.
Diagnosis is established in the live bird by rising antibody titers and supportive clinical signs. Previously vaccinated birds, of course, exclude serologic diagnosis. In those bird that succomb to this disease, gross lesions may include serositis and vasculitis related lesions. Secondary bacterial lesions may mask primary lesions. Virus isolation from dead birds and suppportive histopathology establish the post mortem diagnosis of WEE infection.
Treatment is supportive, and protection against secondary bacterial invaiders is important. Fluids, analgesics, and antibiotics are commonly indicated. Survivability, unlike what is seen in EEE, is very good.
The epidemiology of WEE is actually quite unique, and can play a significant role in the preventative management of this disease. In California, WEE is endemic in wild bird species including the house finch and house sparrow. Ancillary reservoir hosts include the redwing blackbird and the gopher snake. An intermediary amplification cycle is known to occur in the blacktailed jackrabbit and an Aedes spp mosquito is known to transmit virus from the rabbit to dead end hosts such as man and horse. Squirrels and other rodents have also been implicated as "dead end hosts". WEE is vectored between bird species by the mosquito, Culex tarsalis. This mosquito is common in standing pools of water - classically rice fields. Because of the zoonotic concern pertinent to this virus, mosquito abatement districts as well as human health services have maintained surveillance of virus activity in the state of California since 1952. The data generated from these surveillance programs has allowed for accurate mapping of the status of WEE viral presence in harvested vector mosquito pools and sentinel chicken flock seroconversions. Relative risk of exposure and infection in emus can easily be gaged with this type of information. In an outbreak of WEE in California, Culex tarsalis pools first were tested positive, followed by the development of emus with clinical signs, followed by seroconversion of sentinel chicken flocks. This observation suggests strongly that the emu acts as a sentinel for this virus rather than a reservoir.
Western equine encephalitis caused widespread disease in emus throughout the Southwest United States in the summer of 1992. Clinical signs included anorexia, diarrhea, ataxia and abnormal neck motions. A limited number of birds progressed to lateral recumbency and death. Gross necropsies revealed serositis and pericardial fluid. Virus was isolated from necropsy specimens. Vaccination with a killed three-way equine product seemed to eliminate further problems.
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