Equine Encephalitis Virus

Viral Family

Members of the Togaviridae are small, lipid- and protein-enveloped RNA viruses. Within this family are disease-causing arboviruses (insect-borne virsuses) of the Alphavirus genus.

Viral Genus

Alphaviruses are single-stranded, linear, positive-sense RNA viruses, 60-70nm in diameter.

Important Serotypes

During equine and human epidemics of encephalitis in the Western Hemisphere, the most frequently isolated alphaviruses have included:

• Eastern Equine Encephalitis virus (EEV)
• Western EEV
• Venezuelan EEV

EEE and WEE are specific and discrete species. There are North and South American antigenic variants of EEE. WEE is a recombinant between an EEE-like virus and a Sindbis-like virus. There are two antigenic subtypes of WEE virus: WEE and Highlands J viruses. Extensive geographical overlap occurs between the various strains which have equivocal differences in antigenic properties and biological behaviour. There are 6 distinct subtypes of VEE virus. Over the last 20 years, large outbreaks of equine encephalitis in the Western Hemisphere have been caused by subtypes IAB, IC and IE. ID and IF variants from Central America and Brazil respectively, type II (Everglades) virus in Florida and types II, IV, V ad VI viruses are considered endemic and are of low pathogenicity for horses under most circumstances.

Diseases

Equine Togaviral Encephalitis

Epizootiology

Reservoirs

Togaviridae generally persist by asymptomatically infecting wild animals (sylvatic hosts) such as birds, small mammals and reptiles. Viruses overwinter in sylvatic populations.

Vectors

The major disease vectors for each serotype of veterinary significance are:

• EEE: Aedes spp.
• WEE: Culex tarsalis
• VEE: Culex melanconium, Aedes spp., Phosphora spp.

Culiseta melanura is a vector for EEE. It is largely confined to freshwater swamps, feeds primarily on swamp birds and is rarely found in areas of increased horse density. This mosquito generally serves as a vector for the enzootic cycle involving swamp birds. Aedes spp. are more important in epizootics and epidemics.

Pathogenesis

After inoculation into an equine host, viruses multiply in the muscle, enter the lymphatic circulation and localize in lymph nodes. Viral replication occurs in macrophages and neutrophils with subsequent shedding and significant clearance of viral particles. No further clinical signs develop if clearance is successful but neutralizing Abs are still produced. Viral immunological avoidance mechanisms include erythrocyte and leukocyte absorption. After incomplete elimination, residual virus infects endothelial cells and concentrates in highly vascular organs such as the liver and spleen. In these organs, viral replication produces circulating virus. The second viraemic period is typically associated with early clinical signs. CNS infection occurs within 3-5 days.