Overview of African Horse Sickness

AHS is caused by African horse sickness virus (AHSV), which is 55–70 nm in diameter and of the genus Orbivirus in the family Reoviridae. There are nine immunologically distinct serotypes of AHSV. The virus is inactivated at a pH of <6 (but is stable at higher pH), or by formalin, β-propiolactone, acetylethyleneimine derivatives, or radiation.

In endemic regions of Africa, the appearance of AHS may be preceded by seasons of heavy rain that alternate with hot and dry climatic conditions, which favor transmission by the insect (biting midge) vector. Outbreaks in central and east Africa have occasionally extended to Egypt, the Middle East, and southern Arabia. In 1959–1961, a major epidemic, caused by AHSV 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 1965–1966 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 AHSV 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, Portugal, and Morocco in subsequent years before its elimination in 1991. AHS outbreaks continue to occur in endemic regions of southern and eastern Africa, and in 2007, AHS serotype 2 was reported in West Africa (Nigeria and Senegal), and serotype 7 in Senegal. Outbreaks of AHS caused by any one of several serotypes have recently been reported in Ethiopia.

Culicoides spp are the principal vectors of all nine serotypes of AHSV, with C imicola usually considered to be 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 the winter in southern Egypt, where the disease is endemic. AHSV has apparently been transmitted between dogs by infected mosquitoes. Furthermore, dogs, and possibly large African carnivores such as lions and leopards, can be infected by ingestion of meat from AHSV-infected equids. However, it is generally considered that dogs and other large carnivores, ticks, and mosquitoes play little part in the epidemiology of AHS.

Mortality depends on the virulence of the particular AHSV 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%.

Subclinical AHSV infection occurs in partially immune equids, such as those previously vaccinated against the disease, or in equids naturally infected with live-attenuated vaccine strains of AHSV. Subclinical infections are also characteristic in zebras and certain other equids.

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. Anticoagulated blood should be obtained at the peak of fever and transported (at 4°C) to the laboratory. Spleen samples collected from freshly dead animals should be kept on ice. Presence of virus is best detected by group-specific reverse-transcriptase polymerase chain reaction (RT-PCR). AHSV also can be isolated by intracerebral inoculation of suckling mice or in mammalian or insect cell cultures. Although not widely available, indirect sandwich ELISA is also useful for rapid identification of AHSV antigen in tissues from animals that have died from acute infection.

Serotyping of AHSV previously relied on virus neutralization tests using type-specific antisera, which take ≥5 days. The recent development of type-specific RT-PCR can now confirm the serotype of an AHSV 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. AHSV is typically noncontagious and spread exclusively via the bites of infected Culicoides spp or by the direct inoculation of infectious material (via blood-feeding insects, needles, etc). 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). It is rarely possible to completely eliminate populations of vector Culicoides, especially in extensive pasture systems.

Live-attenuated virus vaccines are available for immunization of equids against AHS. These are typically based on cell culture–attenuated viruses and generally provide good, but not absolute, protection. Annual revaccination is recommended in regions where these vaccines are used. However, there are increasing concerns regarding use of live-attenuated AHSV vaccines because of their potential reversion to virulence, capacity for transmission by vector Culicoides midges, and reassortment of their gene segments with other vaccine and field strains of virus, leading to the creation of novel virus progeny. Inactivated and subunit vaccines avoid these potential drawbacks and, assuming they are commercially available, would likely be used after incursion of AHSV into previously unaffected regions.

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