Etiology and Epidemiology

The equine encephalosis virus (EEV) is an insect-borne orbivirus that is transmitted by a variety of Culicoides spp.¹ and is closely related to bluetongue and epizootic hemorrhagic disease viruses.² EEV has characteristics in cell culture similar to African horse sickness virus³ (see Chapter 15). Seven serotypes^3–8 of EEV infect equids of southern Africa, including Kenya, Botswana, and South Africa.⁴

The virus replicates to varying degrees in midges depending on species of midge and strain of the virus. The genetic and phenotypic stability of EEV strains is unknown, and the potential exists for emergence of new strains or recognition of currently undetected strains. Variations in pathogenicity are not recognized but might exist. The observation of increased rates of seasonal seroconversion to a specific serotype, with ongoing low level of infection by other serotypes, suggests independent persistence of EEV serotypes in a maintenance cycle.⁴

Horses, donkeys, and zebra in southern Africa frequently have antibodies to a group epitope of EEV, indicating widespread infection of these equids. In South Africa, 77% of 1144 horses, 57% of 518 horses, 49% of 4875 donkeys, and up to 88% of zebra have antibody to EEV.^1,4–6 Elephant seldom have antibodies to EEV.⁶ Zebra foals develop antibodies to the virus within months of losing their maternally acquired passive immunity.⁸

Clinical Findings

The equine encephalosis virus acquired its name after original isolation from a horse with clinical signs of neurologic disease. The clinical importance of EEV is uncertain but appears to be limited. Seroconversion in closely managed horses without evidence of clinical disease suggests that infection by the virus is asymptomatic in most cases. However, the disease associated with infection by EEV is poorly documented, and given the high prevalence of infection, EEV might be falsely incriminated as the cause of disease in some situations. Most infections are subclinical based on the high seroprevalence rate and lack of reports of disease outbreaks.

Clinical signs typically attributed to EEV infection include fever, lassitude, edema of the lips, acute neurologic disease, and enteritis. Abortion has anecdotally been associated with infection by EEV. Disease associated with EEV has not been recorded in donkeys or zebra.¹

Diagnosis

Characteristic abnormalities in serum biochemistry or hematology are not reported. Antibodies to the virus are detected by serum neutralization assays (which are serotype specific) and enzyme-linked immunosorbent assay (ELISA), which is not serotype specific. A group-specific, indirect sandwich ELISA detects EEV antigen and does not cross react with African horse sickness virus, bluetongue virus, or epizootic hemorrhagic disease virus.⁷

Pathologic Findings

Necropsy examination of affected horses reveals cerebral edema, localized enteritis, degeneration of cardiac myofibers, and myocardial fibrosis, but whether these abnormalities are attributable to EEV is unclear.³ Definitive diagnosis is difficult, if not impossible, at present because of the high prevalence of seropositive animals and the poorly defined clinical and necropsy characteristics of the disease.

Treatment and Prevention

No recognized measures exist for treatment, control, or prevention of EEV infection, and there is no vaccine.

Public Health Considerations

The equine encephalosis virus does not appear to cause disease in humans.

Etiology

Getah virus and Ross River virus are classified in the Alphavirus genus within the Semliki Forest complex of the Togaviridae family. These are small, enveloped viruses with a single-stranded, positive-sense ribonucleic acid (RNA) genome. These viruses are discussed under the same heading because of the similarities in their cladistic classification, ecology, and clinical signs in horses. Getah virus causes disease in horses and pigs, whereas Ross River virus causes disease in humans and, arguably, horses.

Epidemiology

The geographic range of Getah and Ross River viruses is distinctive; Getah virus is reported from Japan, Hong Kong, Southeast Asia, Korea, and India, and Ross River virus is found in most areas of continental Australia, Tasmania, West Papua and Papua New Guinea, New Caledonia, Fiji, Samoa, and the Cook Islands.⁹ Reports from the 1960s document antibodies to Getah virus in animals in Australia, but the presence of this virus in Australia has not been confirmed using modern techniques that can differentiate antibodies to Getah virus from those of the related Ross River virus and other viruses in this complex. There are no reports of disease caused by Getah virus in Australia. Considerable sequence homology exists between Getah and Ross River virus genomes.¹⁰ There is geographic genetic variability among isolates of Ross River virus and temporal, but not geographic, variability among isolates of Getah virus from Southeast Asia and Japan.^11,12

Both viruses are arthropod borne, and infection is through the bite of an infected mosquito. The virus is maintained in the mosquito-vertebrate-mosquito host cycle typical of arboviruses. The definitive, amplifying vertebrate host for Getah virus is unknown, although a number of vertebrates, including horses, cattle, and pigs, can be infected by the virus. Horses and pigs become viremic and presumably can infect mosquitoes, although this does not appear to have been confirmed experimentally. The life cycle of Getah virus has not been explicated. The virus is assumed to be maintained in a mosquito-pig-mosquito cycle in those areas with year-round mosquito activity.¹³ Persistence of the virus in areas where mosquito activity is seasonal has not been explained, and whether transovarial or transtadial transmission occurs within the mosquito population is not reported. The vertebrate hosts of Ross River virus include a large number of eutherian, marsupial, and monotreme mammals and birds.⁹ Macropod species, including kangaroos and wallabies, are assumed to be the most important amplifying hosts, although this is debated.

During outbreaks of disease it is suspected that Getah virus is spread by horse-to-horse contact, based on the rapidity of spread among horses, the short duration of the outbreak, and the lack of mosquito activity at the time some horses developed the disease.^14,15 However, experimental evidence suggests that this route of spread is likely of limited importance in propagation of epidemics because of the low concentration of virus in nasal and oral secretions of infected horses and the large inoculum required to cause disease in horses by the intranasal route.¹⁶

The prevalence of serologic evidence of infection of horses by Getah virus in Japan ranges from 8% to 93%, depending on the region of the country in which the samples were collected and the disease history of the band or stable of horses.^14,17 Seroprevalence was 17% in India and 25% in Hong Kong.^16,18 These results confirm the widespread incidence of subclinical infection of horses by Getah virus in endemic areas.

There is a similarly high incidence of Ross River virus infection of horses in endemic regions of Australia. Prevalence of seropositive horses in Queensland, an area with likely year-round mosquito activity, was approximately 80%, whereas that of horses around the Gippsland lakes in southern Australia, a region with seasonal mosquito activity, was 50%.¹⁹

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