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Eastern Equine Encephalitis (EEE) is an infectious, often fatal disease of horses, humans, and pigs. Wild ruminants (white-tailed deer) can also become infected. EEE is caused by an RNA virus in the family Togaviridae and is mosquito-borne (Arbovirus). Infection can cause abnormal neurological behavior and encephalitis in the affected animal. Most Arboviruses that infect wild mammals are not known to cause disease in their host. The virus is maintained in temperate areas by wild bird reservoirs and mosquito vectors.
EEE is found in a number of avian species from the eastern United States to Central and South America. This virus produces inapparent or subclinical infections in a wide range of wild birds, although wild birds can also become sick and die. Evidence of exposure (serology) to the virus has been reported in a variety of free-ranging wild birds and mammals in North America. Clinical disease and death has occurred in glossy ibis and several exotic avian species including pheasants, chukar partridge, rock doves, house sparrows, and emus.
Mortality attributed to EEE in white-tailed deer has only been reported in five states: Georgia (1 in 2001), Wisconsin (1 in 2004), and Michigan (8 in 2005, 1 in 2009, 2 in 2010, 3 in 2015, 1 in 2016, 1 in 2017, 3 in 2018, and 14 in 2019), Massachusetts (1 in 2019), and Rhode Island (3 in 2019). EEE was also diagnosed in one mute swan and two ruffed grouse in 2019, the first time the disease has been diagnosed as a cause of death in free-ranging birds in Michigan.
EEE virus is transmitted by mosquito vectors, especially Cutiseta melanura (which prefers to feed on birds). Other mosquito species that can be involved and are considered bridge vectors (mosquito species that feed on both birds and large mammals) are Coquillitidea perturbans, Aedes vexans, and Aedes canadensis. The virus replicates in the mosquitoes which transmit it to vertebrate hosts (usually birds). The virus replicates (amplifies) again in the infected vertebrate, which develops virus in the bloodstream and serves as a source of infectious blood meals for other mosquitoes, completing the transmission cycle. In native avian species most infections are inapparent.
When levels of the circulating virus are high, aberrant hosts (mammals, specifically horses, humans, and deer) can become infected when bitten by a mosquito that has fed on an infected bird. Mosquito habitat, the feeding habits of the different mosquito species, the abundance of the vectors, the activity patterns and abundance of vertebrate hosts, temperature, and humidity are all factors affecting the frequency of disease transmission.
Mammals are generally regarded as dead-end hosts for the virus because they do not produce enough virus in their blood to infect biting mosquitoes. There is no evidence that infected mammals are able to transmit the virus by direct contact. Under certain circumstances (a large vector population and a large population of nearby horses) horses may provide transient amplification of the virus and serve as a source of the virus to biting mosquitoes.
It is possible, although unlikely, that humans could become infected with the EEE virus through their eyes, open skin wounds, or lungs (aerosolized) when contacting brain or spinal cord matter from an infected deer.
Clinical signs in infected white-tailed deer (and horses) may include central nervous system disorders after a 1-3 week incubation period. Affected animals may lose awareness of their surroundings, walk in circles, exhibit muscle paralysis, stupor, lethargy, and incoordination.
No gross lesions are generally seen in EEE affected animals. Histopathological (microscopic) examination reveals lesions consistent with a viral caused meningoencephalitis or encephalitis.
A tentative diagnosis can be determined from a histopathological examination that reveals lesions consistent with a meningoencephalitis or encephalitis. However, additional testing is required to confirm the disease. Polymerase Chain Reaction (PCR) testing and virus isolation on fresh brain tissue are the accepted methods to confirm the diagnosis.
There is no specific therapy for viral encephalitis except supportive care. Supportive care includes fluids, anti-inflammatory agents, and anticonvulsants if necessary. For wild animals this type of care is unrealistic.
There is no vaccine for EEE that can be used on wild deer. There is a killed vaccine that has proven to be effective in horses. Mosquito control can reduce the likelihood of contact with the vector and the virus. Vector control can include eliminating breeding sites (water management), control of native insects (larvae and adults), and protection of the hosts from insect predators.
Precautions humans can take to reduce the risk of exposure are: use insect repellants for personal protection; keep tight screens on windows, doors, and porches; and use protective clothing. If a wild deer appears sick or acts abnormal, it should not be handled or consumed.
EEE is a zoonotic disease that can infect humans, horses, and deer. The disease appears to have a minimal impact on wild deer populations in North America. EEE is not likely to be a major mortality factor in deer but it is possible that it could impact a local population.
Because EEE can be transmitted to humans by mosquitoes, people should take the necessary precautions to avoid exposure to these insects. In humans there is a case fatality rate of 30 to 70% and EEE often causes severe permanent neurological disorders among survivors. It is unlikely but possible that humans could become infected with EEE by getting brain or spinal cord matter from an infected deer in their eyes, lungs, or skin wounds. Hunters should take precautions when field dressing harvested deer (see EEE - Addressing Hunter Concerns).
Although it occurs only rarely, EEE remains an important zoonotic disease in Michigan from public health and economic perspectives.
