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Overview of African Horse Sickness


African horse sickness (AHS) is an acute or subacute, insectborne, viral disease of equids that is endemic to Africa. It is characterized by clinical signs and lesions associated with respiratory and circulatory impairment.

AHS is caused by an orbivirus, 55–70 nm in diameter, of the family Reoviridae. There are 9 immunologically distinct types. The virus is inactivated at a pH of <6 or ≥12, or by formalin, β-propiolactone, acetylethyleneimine derivatives, or radiation.

Appearance of AHS may be preceded by seasons of heavy rain that alternate with hot and dry climatic conditions, which favor transmission. Outbreaks in central and east Africa have occasionally extended to Egypt, the Middle East, or southern Arabia. In 1959–1961, a major epidemic of serotype 9 extended from Africa through the Near East and Arabia as far as Pakistan and India, causing the deaths of an estimated 300,000 equids. A further epidemic of the same serotype in 1965–66 centered on northwest Africa (Morocco, Algeria, and Tunisia) but also extended briefly into southern Spain. This outbreak in Spain was eliminated by a vigorous vaccination and slaughter campaign. In July 1987, AHS caused by serotype 4 was reported in central Spain, due to the importation of infected zebra from Namibia. The outbreak lasted until the cold weather started in October 1987; however the virus survived the winter and caused disease in southern Spain in 1988. Again the outbreak ended with the advent of cold weather, but further recrudescences occurred in 1989 and 1990. The virus also extended into Portugal and Morocco in 1989; although quickly eliminated from Portugal, it continued through much of Morocco until late 1991. More recently, AHS outbreaks have been reported from several locations within sub-Saharan Africa, including western Botswana (1999–2001), Namibia (2000 and 2001), South Africa (2006), and Swaziland (2006). In 2007, for the first time, AHS serotype 2 was reported in West Africa (Nigeria and Senegal) and serotype 7 in Senegal. Serotype 4 was also isolated from equids in Kenya. In 2008 a severe outbreak of serotype 2 was recorded in southwest Ethiopia.

Culicoides spp are the principal vectors of all 9 serotypes of AHS virus, with C imicola being the most important. Consequently, AHS is seen during warm, rainy, seasons, which favor propagation of the vectors, and disappears when cold weather stops or significantly reduces vector activity. The virus also has been isolated from the dog tick Rhipicephalus sanguineus sanguineus, and the camel tick Hyalomma dromedarii during winter in the southern Egypt where the disease is endemic. AHS virus has apparently been experimentally transmitted between dogs by infected mosquitoes. However, these studies have not been confirmed elsewhere and at present most authorities believe that dogs, ticks, and mosquitoes play little part in the epidemiology of AHS.

Mortality depends on virulence of the viral strain and susceptibility of the host. In naive populations of horses, which are the most susceptible equids, mortality may reach 90% in epidemics. The acute respiratory form is characterized by an incubation period of 3–5 days, interlobular edema, and hydropericardium; death occurs in ∼1 wk. A fever of 40–40.5°C (104–105°F) for 1–2 days is followed by dyspnea, spasmodic coughing, and dilated nostrils; the animal stands with its legs apart and head extended. The conjunctivae are congested and the supraorbital fossae may be edematous. Recovery is rare, and the animal dies of anoxia, congestive heart failure, or both. At necropsy, pulmonary edema is especially visible in the intralobular spaces. The lungs are distended and heavy, and frothy fluid may be found in the trachea, bronchi, and bronchioles. There may be pleural effusion. Thoracic lymph nodes may be edematous, and the gastric fundus may be congested. Petechiae are found in the pericardium, and there is an increase in pericardial fluid; however, cardiac lesions usually are not outstanding. The abdominal viscera may be congested. A frothy exudate may ooze from the nostrils. The pulmonary form is the predominant form in dogs, which are usually infected by ingesting virus-contaminated meat.

The cardiac form of AHS is subacute with an incubation period of 1–2 wk. A fever of <1 wk is followed by edema of the supraorbital fossae. Swelling may extend to the eyelids, facial tissues, neck, thorax, brisket, and shoulders. Death usually occurs within 1 wk and may be preceded by colic. The mortality rate is ~50%. Petechiae and ecchymoses on the epicardium and endocardium are prominent. The lungs are usually flaccid or slightly edematous. There are yellow, gelatinous infiltrations of the subcutaneous and intramuscular tissues, especially along the jugular veins and ligamentum nuchae. Other lesions include hydropericardium, myocarditis, hemorrhagic gastritis, and petechiae on the ventral surface of the tongue and peritoneum. A mixed pulmonary and cardiac form is most commonly seen in outbreaks, with a mortality rate in horses of ∼80%.

In endemic areas, clinical signs and lesions may lead to a presumptive diagnosis. However, laboratory confirmation is essential for definitive diagnosis and determination of the serotype; the latter is important for control measures. Blood specimens should be obtained at the peak of fever, preserved in OCG solution (50% glycerol, 0.5% potassium oxalate, 0.5% phenol), and transported (at 4°C) to the laboratory. Spleen samples collected from freshly dead animals should be preserved in 10% buffered glycerin at 4°C. For virus isolation, intracerebral inoculation of suckling mice is best, mammalian or insect cell cultures may also be used. The more isolation systems employed, the greater the likelihood of success. Infected mice may develop nervous and paralytic signs and should be observed for 3 wk; mammalian tissue culture systems may show cytopathic effects within 3–7 days.

AHS virus can be identified directly from whole blood, other tissues, and infected cell culture supernatant using molecular probes and reverse transcriptase-PCR group-specific primers. The indirect sandwich ELISA is also useful for the rapid identification of AHS virus antigen in solid tissues taken from animals that have died from acute infection. In addition, isolated viruses can be identified by group-specific tests such as complement fixation and direct and indirect fluorescence.

Serotyping of AHS virus previously relied on virus neutralization tests using type-specific antisera, which take ≥5 days. The recent development of type-specific reverse transcriptase-PCR has now provided a method of confirming the serotype of an AHS virus within 24 hr.

There is no specific treatment for animals with AHS apart from rest and good husbandry. Complicating and secondary infections should be treated appropriately during recovery. AHS virus is noncontagious and can only be spread via the bites of infected Culicoides spp. Various methods of control may be attempted, such as introducing animal movement restrictions to prevent infected animals initiating new foci of infection, and husbandry modification to deny or reduce vector access to susceptible or infected animals (eg, stabling in vector-proof housing); slaughter of viremic animals in certain circumstances (eg, for welfare reasons or very early in an epidemic) can prevent them from acting as a source of virus for vector insects. It is rarely possible to completely eliminate populations of vector Culicoides; however, it may be feasible to reduce the number of potentially infecting bites that susceptible animals receive to levels at which maintenance of an epidemic becomes unsustainable.

Live-virus vaccines are available for all 9 serotypes. These are generally based on cell culture-attenuated viruses and apparently provide good protection, although annual revaccination is recommended. However, some authorities may be reluctant to use live-virus vaccines because of concerns about their possible reversion to virulence, transmission by vector Culicoides, and reassortment with field strains of virus. Inactivated and subunit vaccines without these potential drawbacks are under development, but these are not at present commercially available.

Transport of equids from countries where AHS virus occurs to virus-free areas is subject to strict regimens of testing and quarantine, although the precise requirements may vary from country to country. Presence of antibodies alone should not preclude such movements as long as infectious virus is not present.

Last full review/revision March 2012 by Phillip S. Mellor, OBE, DSc, FRES, FHEA

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