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Chapter 20 - Eastern Equine Encephalomyelitis
Authors: Wallace Hansen and Douglas E. Docherty
EEE, eastern encephalitis, EE, eastern sleeping sickness of horses
Eastern equine encephalitis (EEE) is caused by infection with an RNA virus classified in the family Togaviridae. The virus is also referred to as an "arbovirus" because virus replication takes place within mosquitoes that then transmit the disease agent to vertebrate hosts such as birds and mammals, including humans. The term arbovirus is shortened nomenclature for arthropod (insect) borne (transmitted) viruses. Culiseta melanura is the most important mosquito vector; it silently (no disease) transmits and maintains the virus among birds. However, several other mosquito species can transmit this virus, including the introduced Asian tiger mosquito. New hosts become infected when they enter this endemic natural cycle and are fed upon by an infected mosquito. Therefore, the presence of mosquito habitat, the feeding habits of different mosquito species, and the activity patterns of vertebrate hosts are among the important factors for disease transmission.
This disease is primarily found in eastern North America especially along the Atlantic and Gulf Coasts, and the disease range extends into Central and South America. The causative virus has been isolated from eastern Canada to Argentina and Peru, and it is maintained in a mosquito-wild bird cycle as an endemic (enzootic) focus of infection in nature that is usually associated with freshwater marshes. Wild bird die-offs from EEE have been limited to captive-rearing situations. Die-offs have occurred in pheasants in coastal States from New Hampshire to Texas, where they have been raised, in chukar partridge and whooping cranes in Maryland, and in emus and ostriches in Louisiana, Georgia, Florida, and Texas.
EEE virus produces inapparent or subclinical infections in a wide range of wild birds (Fig. 20.1). However, EEE virus has caused mortality in glossy ibis and in several bird species that are exotic to the United States, including pigeon, house sparrow, pheasants, chukar partridge, white Peking ducklings, and emu. The infection rate in penned emus in the United States has reached 65 percent with a case mortality rate of 80 percent. In the past, extensive losses have occurred in ring-necked pheasant being reared in captivity for sporting purposes, including one outbreak in a South Dakota pheasant farm. Large-scale mortalities in captive pheasants are perpetuated by bird-to-bird disease spread through pecking and cannibalism after EEE has been introduced by mosquitoes, usually of the genus Culiseta. Outbreaks have not been reported during recent years.
In September and November of 1984, EEE virus was associated with the deaths of 7 of 39 captive whooping cranes at the Patuxent Wildlife Research Center in Laurel, Maryland. Sandhill cranes coexisting with the whooping cranes did not become clinically ill or die.
Passerines (perching songbirds), some small rodents, and bats are highly susceptible to infection and they often die from experimental infections. Horses are highly susceptible and they often die from natural infections.
EEE is associated with the early summer appearance of C. melanura mosquito populations (Fig. 20.2). Nestling birds, such as passerines and other perching birds, are the amplification hosts for the virus, producing high concentrations of virus in their blood or viremia following mosquito infection. New populations of emerging mosquitoes become infected when they feed on the viremic birds. C. melanura and other species of infected mosquitoes can transmit the virus to other species of birds susceptible to disease (Fig.20.3).
The summer-fall transmission cycle is followed by little virus transmission during the winter and spring months. The overwintering mechanism for virus survival is not known. Infected mosquitoes, other insects, cold-blooded vertebrate species, or low levels of virus transmission by mosquitoes are among current theories for virus cycle maintenance in milder climates. It is also believed that bird migration spreads the virus to higher latitudes in the spring.
Clinical signs do not develop in most native species of wild birds infected with EEE virus. Clinical signs for non-indigenous birds (including pheasants) include depression, tremors, paralysis of the legs, unnatural drowsiness, profuse diarrhea, voice changes, ataxia or loss of muscle coordination, and involuntary circular movements (Fig. 20.4). Some of the EEE-infected whooping cranes became lethargic and incoordinated or ataxic, with partial paralysis or paresis of the legs and neck 38 hours prior to death; other cranes did not develop clinical signs before they died.
Gross lesions in whooping cranes included fluid accumulation in the abdominal cavity or ascites, intestinal mucosal discoloration, fat depletion, enlarged liver or hepatomegaly, enlarged spleen or splenomegaly, and visceral gout (Fig. 20.5).
Because of human health hazards, field personnel should not dissect birds suspected of having died from EEE. Whole carcasses should be submitted to diagnostic laboratories capable of safely handling such specimens. EEE can be diagnosed by virus isolation from infected whole blood or brain and other tissues from dead birds. Diagnosis of virus activity can be made from surviving birds because they will have virus neutralizing antibodies in their blood serum. The rise and fall in serum antibodies that occurs after virus exposure can be used to assess infection rates and the relative timing of exposure before antibody levels reach nondetectible levels. Most native birds do not suffer clinical infections.
There are two approaches to protecting susceptible animals from infection from vector-borne diseases. The first approach includes separating mosquitoes from animals at risk. This requires eliminating mosquito breeding and resting sites in an endemic area or protecting animals from mosquito contact by maintaining them in an insect-proof enclosure. In the second approach, vaccination is used to render the animal immune. A killed-virus vaccine was used in captive whooping cranes to protect the rest of the breeding flock following the 1984 outbreak. Vaccination has also been used to protect whooping cranes released into an area where EEE is prevalent in mosquito populations. Field data suggest that immunity in those cranes is being boosted by natural infections after their release.
Humans are susceptible to EEE and human cases typically arise after the disease has appeared in horses. EEE is a significant disease in humans with a case fatality rate of between 3070 percent and it often causes severe permanent neurological disorders among survivors. Aerosol infection is possible but rare. Laboratory personnel have been infected with this virus. Human pre-exposure vaccination is recommended for people who may handle infected tissues.
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