Signalment:  

A 4-year old Tennessee Walking horse (Equus caballus) gelding, was submitted.The horse was examined in late March for severe lethargy that rapidly progressed to recumbency later that same day. The animal was euthanized late that evening based on the poor prognosis. The horse had been purchased the previous day and transported to the farm in Tennessee from Kentucky. A killed tetanus Eastern/Western encephalitis flu vaccine was administered approximately 5 days before the purchase. The owner was unaware of any previous vaccinations having been given to the horse.

Gross Description:  

There were no significant gross findings.

Morphologic Diagnosis:  

Brain: meningoencephalitis, suppurative, subacute, severe, Tennessee Walking horse, equine

Lab Results:  

Rabies examination was negative utilizing fluorescent antibody methods. Eastern Equine Encephalitis virus was isolated in mice and cell culture from the brain. The sample was also negative for West Nile virus and positive for Eastern Equine Encephalitis viral RNA utilizing reverse transcriptase polymerase chain reaction testing.

Condition:  

Rabies

Contributor Comment:  

Multiple sections of brain from varying sites were submitted and feature a widespread meningoencephalitis with extensive perivascular cuffing consisting of neutrophils and mononuclear cells. Multiple suppurative foci were also relatively common within portions of gray matter with scattered neuronal degeneration and necrosis being evident. Intense inflammatory foci are sometimes associated with necrosis of neuropil. A few neutrophils and mononuclear cells are present within pia-arachnoid spaces.

Eastern equine encephalitis is an alphavirus in the togavirus family that causes encephalitis in both humans and horses. The reservoir host is wild birds, where virus replicates to sufficiently high titers to facilitate vector transmission of the disease. Mosquitoes serve as the biological vector for Eastern equine encephalitis. In contrast to birds, horses and humans are dead-end hosts since a sufficient viremia to allow transmission does not occur. Infected horses often present with fever, anorexia, and lethargy that ultimately progresses to a range of neurological signs that include paresis, seizures, paralysis, and death. Mortality due to Eastern equine encephalitis is quite high, often approaching 90%.

Eastern equine encephalitis is sporadically seen in Tennessee, primarily in western portion of the state during the months of August and September. The horse in this case was euthanized in late March due to the infection, and defies a simple explanation since the biological vector would not yet be available. Iatrogenic transmission has been suspected in another recent case of EEE and administration of a killed vaccine several days prior to onset of clinical signs warrants consideration in this case. Additionally, the rapid clinical progression and the severity of inflammation seen in the brain could reflect introduction of a much larger inoculum than would be seen in association with normal vector-borne disease.

JPC Diagnosis:  

Brain: Meningoencephalitis, necrotizing, neutrophilic, lymphoplasmacytic, and histiocytic, diffuse, moderate, Tennessee Walking horse (Equus caballus).

Conference Comment:  

The contributor gives an excellent review of the eastern equine encephalitis (EEE) virus. Other members of the Togaviridae family include Alphaviruses such as western equine encephalomyelitis (WEE), Venezuelan equine encephalomyelitis (VEE), Highlands J, and Semliki forest viruses, and Flaviviruses including Cache Valley virus, St. Louis encephalitis, and Japanese B encephalitis viruses.³

EEE, WEE, and VEE are caused by related but distinct alphaviruses. EEE and VEE are lethal in approximately 90% of cases, whereas WEE is less virulent with approximately 40% mortality in the horse. In endemically infected areas, EEE and WEE are maintained by a wild bird-mosquito (reservoir-vector) cycle, particularly in swampy or tropical areas. Avian reservoirs maintain sufficient viremia to permit infection of mosquitoes. The infection of domestic animals and humans occurs with the movement of virus from swampy areas carried by reservoirs, vectors, or both. Culiseta and Culex sp. of mosquitoes are most important in maintaining endemic infections.

References:

1 Del Piero F, Wilkins PA, Dubovi EJ, Biolatti B, Cantile C: Clinical, pathological, immunohistochemical, and virological findings of Eastern equine encephalomyelitis in two horses. Vet Pathol 38:451-456, 2001
2. Franklin RP, Kinde H, Jay MT, Kramer LD, Green EN, Chiles RE, Ostlund E, Husted S, Smith J, Parker MD: Eastern equine encephalomyelitis virus infection in a horse from California. Emerg Inf Dis 8:283-288, 2002
3. George, LW: Diseases producing cortical signs. In: Large Animal Internal Medicine, ed. Smith, BP, 2nd ed., pp. 1018-1021. Mosby, St. Louis, MO, 1996
4. Hahn CN, Mayhew IG, Mackay RJ: Disease of multiple or unknown sites. In: Equine Medicine and Surgery, eds. Colahan PT, Mayhew IG, Merritt AM, Moore JN, 5th ed., vol. 1, pp. 884-888. Mosby, St. Louis, MO, 1999
5. Maxie MG, Youssef S: Nervous system. In: Jubb, Kennedy, and Palmers Pathology of Domestic Animals, ed. Maxie MG, 4th ed., vol. 2, pp. 423-424. Elsevier Limited, St. Louis, MO, 2007
6. Rakich, PM, Latimer KS: Cytology. In: Duncan & Prasses Veterinary Laboratory Medicine Clinical Pathology, eds. Latimer KS, Mahaffey EA, Prasse KW, 4th ed., p. 322, Blackwell Publishing, Ames, IA, 2003
7. Summers BA, Cummings JF, de Lahunta A: Inflammatory diseases of the central nervous system, In: Veterinary Neuropathology, eds. Summers BA, Cummings JF, de Lahunta A, pp.144-146. Mosby, St. Louis, MO, 1995

A virtual slide is not available for this case.

---