Equine encephalosis virus

The name equine encephalosis is misleading as the disease is not primarily a neurological disorder. Although the majority of infections result only in mild clinical signs, in more severe cases clinical signs include a short period (typically two to five days) of fluctuating fever, accompanied by varying degrees of inappetence.[4] Elevated heart and respiratory rates are also common, and occasionally as a result of nasal congestion, a red-brown discolouration of the mucous membranes may be observed.[4]

Although rare, more severe clinical signs may occur including facial swelling (lips and eyelids), respiratory distress, and petechial haemorrhages of the conjunctivae.[4] Pregnant mares may also abort during their first 5 months of gestation.[5]

Neurological signs are atypical, but in certain cases hindquarter ataxia, convulsions, hyperexcitability, and depression have been reported.[5] The mortality rate is normally low, accounting for only 5% of infected animals.[4]

Equine encephalosis virus is an Orbivirus, and as such encodes 4 non-structural and 7 structural proteins derived from 10 linear dsRNA genome segments.[6] The smallest of those genome segments, segment-10, encodes the NS3 protein, which allows the release of the viral particles from the infected cell.[4] The second largest of those segments in turn codes for one of the outer capsid proteins, VP(2).[4]

By analogy with Bluetongue virus, both these proteins may then be used to determine the serotype of EEV, of which seven have been identified to date.[4] This is achieved by analysing the interaction between VP(2), and the antibodies generated by the host during infection.[7] The sequence variation between the proteins is then associated with various viral serotypes.

First isolated in 1967, Equine encephalosis virus appeared until recently to be unique to the South African equidae.[5] As of 2008 however, evidence seems to suggest the virus has circulated beyond southern Africa, and outbreaks have been reported in a number of other countries including Israel, Ethiopia, Ghana, and Gambia.[5] Intriguingly, Morocco remains free of the epidemic, suggesting the Sahara desert may be acting as a natural barrier to the progression of the disease.[5] Such a progression is of major concern to the worldwide livestock industry, primarily due to the similarity between EEV and other more devastating equid pathogens, such as the African horse sickness virus.

As with all vector-borne diseases, EEV is not transmissible from host-to-host, rather infection requires another intermediate organism that will transmit the pathogen. In the case of Equine encephalosis virus, the transmission occurs via the Culicoides midges during a blood meal.[4]

Several studies have shown that between 50 and 75% of South African equids (notably horses, donkeys and zebras) are seropositive for EEV or have anti-EEV antibodies indicating a prior infection, with serotype 1 being the most prevalent.[3] Antibodies have also occasionally been reported in elephants.[3]