Eastern Encephalitis

Eastern equine encephalomyelitis (EEE) virus is quite active in the United States, and many cases have been reported in Southeastern horses this year. The Florida state veterinarian expects levels close to 2003, when 200 horses were reported to have this disease. Most of the equine cases in 2003 and this year were not vaccinated and tend to be young, less than three years of age. Recent arrivals to the Southeast are another high-risk group.

What we generally see--EEE signs can vary from mild febrile (with fever) infection to the more common severe, fatal encephalomyelitis. About five days after exposure, horses get a high fever with depression and inappetence. These horses often have elevated heart rates, even with the depression. There might be an insidious onset of lameness or neurologic signs, but horses usually progress with rapidly deteriorating brain signs. Death can occur in three days. Horses with EEE frequently show signs of coma, dementia, head pressing, and seizure. They also might become blind. A rapid change in the horse's personality typically occurs with depression, somnolence (sleepiness), hyperexcitability, mania, and/or self-mutilation, although the latter is more common with rabies.

Cranial nerve signs do occur; the most common include nystagmus (involuntary rapid eye movement), facial nerve paralysis, and weakness of the tongue and pharynx. At least 75-95% of EEE horses die. If horses survive, they are rarely normal mentally and can have residual spinal cord abnormalities.

A less severe form of neurological disease rarely occurs. These horses usually have had some vaccination and develop mild to moderate forebrain signs with spinal ataxia (incoordination). An even less common syndrome of generalized febrile disease can occur and is associated with anorexia (lack of appetite), severe depression, and high fever. With subclinical exposure, horses can seroconvert (develop antibodies against the virus) with mild lymphopenia (decrease in the proportion of lymphocytes in the blood). This primarily has been seen with experimental infection.

Once most horses succumb to mentation changes or become recumbent, a comatose condition usually ensues. While some veterinarians have reported temporary waning of signs, usually death or conditions requiring humane destruction is the result. If there is a question of outcome even at this point, cerebrospinal fluid (CSF) evaluation is helpful in prognostication (more on this shortly).

Clinicopathologic findings--Very limited hemogram (blood count) and serum biochemical abnormalities occur in horses with EEE. Cerebrospinal fluid is a more valuable diagnostic aid than basic bloodwork, although bloodwork is important for ruling out systemic diseases like hepatoencephalopathy. In acute fulminate (sudden, severe) forms, an increased number of cells in the cerebrospinal fluid is common. This is characterized by white blood cell counts well above the normal of 5-10 cells/ul, with the predominant cell type being neutrophils. When the CSF is composed of neutrophils and the horse is down, it will rarely survive.

Testing--During the West Nile virus (WNV) outbreak, the National Veterinary Services Laboratory in Ames, Iowa, developed the IgM capture ELISA for diagnostic testing. This protocol was actually based on testing for EEE. Since 2001, the most efficient means of EEE confirmatory testing has once again proved to be the IgM capture ELISA because of its rapid turnaround time. However, most results are obtained after the horse is euthanatized even with this test.

Therapy and prevention--Given the high case fatality rate of EEE, there is obviously no proven therapy for EEE and other alphaviruses. Little is known regarding intervention with specific antibody therapy or interferon, which has been anecdotally reported effective in WNV treatment. Early intervention with corticoster-oids has been advocated once high levels of cells in the CSF are identified.

This disease can be prevented by vaccination. Since killed vaccines are the only products available, short but effective immunity is expected. The primary caveat is vaccination of young horses. Weanlings must be given three monthly vaccine injections, then boostering before mosquito season is a must after 12 months of age in endemic regions. Boosters at four-month intervals are highly recommended in the Southeastern region. In temperate regions, if EEE is identified early in the season by mosquito testing or reporting of clinical disease in mammals, six-month boostering after primary immunization is necessary to prevent outbreaks in horses. Otherwise, most Northern climates require yearly boosters.

While WNV has stolen the viral encephalitis spotlight over the past several years, EEE is here to stay and might actually prove just as active in the long run. Continued attention to preventive measures by horse owners is important, and future preventive strategies might incorporate longer-acting modified live virus vaccines and chimera vaccines. In addition, development of therapeutic strategies is also a priority for equine patients.

About the Author

Maureen Long, DVM, PhD, Dipl. ACVIM

Dr. Maureen Long is Associate Professor in the Department of Infectious Diseases and Pathology at the University of Florida and teachings microbiology and immunology. Her research focus is infectious disease of horses.

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