African horse sickness
|African horse sickness virus|
|Group:||Group III (dsRNA)|
|Species:||African horse sickness virus|
African horse sickness (AHS) is a highly infectious and deadly disease. It commonly affects horses, mules, and donkeys. It is caused by a virus of the genus Orbivirus belonging to the family Reoviridae. This disease can be caused by any of the nine serotypes of this virus. AHS is not directly contagious, but is known to be spread by insect vectors.
AHSV was first recorded south of the Sahara Desert in the mid-1600s with the introduction of horses to southern Africa. The virus is considered endemic to the equatorial, eastern, and southern regions of Africa. Several outbreaks have occurred in Equidaes throughout Africa and elsewhere. AHS is known to be endemic in Sub-Saharan Africa, and has spread to Morocco, the Middle East, India, and Pakistan. More recently, outbreaks have been reported in the Iberian Peninsula. AHS has never been reported in the Americas, eastern Asia or Australasia. Epidemiology is dependent on host-vector interaction, where cyclic disease outbreaks coincide with high numbers of competent vectors. The most important vector for AHS in endemic areas is the biting midge Culicoides imicola, which prefers warm, humid conditions. Larvae do not carry the virus and long, cold winters are sufficient to break epidemics in non-endemic areas.
The common hosts of this disease are horses, mules, donkeys and zebra. However, elephants, camels and dogs can be infected as well, but often show no signs of the disease. Dogs usually contract the disease after eating infected horse meat, but there has been a recent report of the diseases occurring in dogs with no known horse meat ingestion.
This disease is spread by insect vectors. The biological vector of the virus is the Culicoides (midges) species. However, this disease can also be transmitted by species of mosquitoes including Culex, Anopheles, and Aedes, and species of ticks such as Hyalomma and Rhipicephalus.
Horses are the most susceptible host with close to 90% mortality of those affected, followed by mules (50%) and donkeys (10%). African donkeys and zebras very rarely display clinical symptoms, despite high virus titres in blood, and are thought to be the natural reservoir of the virus. AHS manifests itself in four different forms: the pulmonary form, the cardiac form, a mild (horse sickness fever) form, and a mixed form.
The peracute form of the disease is characterized by high fever, depression, and respiratory symptoms. The clinically affected animal has trouble breathing, starts coughing frothy fluid from nostril and mouth, and shows signs of pulmonary edema within four days. Serious lung congestion causes respiratory failure and results in death in under 24 hours. This form of the disease has the highest mortality rate.
This subacute form of the disease has an incubation period longer than that of the pulmonary form. Signs of disease start at day 7–12 after infection. High fever is a common symptom. The disease also manifests as conjunctivitis, with abdominal pain and progressive dyspnea. Additionally, edema is presented under the skin of the head and neck, most notably in swelling of the supra-orbital fossae, palpebral conjunctiva, and intermandibular space. Mortality rate is between 50–70% and survivors recover in 7 days.
Mild or horse sickness fever form
Diagnosis is made at necropsy. Affected horses show signs of both the pulmonary and cardiac forms of AHS.
Presumptive diagnosis is made by characteristic clinical signs, post mortem lesions, and presence of competent vectors. Laboratory confirmation is by viral isolation, with such techniques as quantitative PCR for detecting viral RNA, antigen capture (ELISA), and immunofluorescence of infected tissues. Serological tests are only useful for detecting recovered animals, as sick animals die before they are able to mount effective immune responses.
Treatment and prevention
There is currently no treatment for AHS.
Control of an outbreak in an endemic region involves quarantine, vector control and vaccination. To prevent this disease, the affected horses are usually slaughtered, and the uninfected horses are vaccinated against the virus. Three vaccines currently exist, which include a polyvalent vaccine, a monovalent vaccine, and a monovalent inactivated vaccine. This disease can also be prevented by destroying the insect vector habitats using insecticides.
African horse sickness was diagnosed in Spain in 1987–90 and in Portugal in 1989, but was eradicated using slaughter policies, movement restrictions, vector eradication, and vaccination.
AHS is related to bluetongue disease and is spread by the same midge (Culicoides species).
Notes and references
- CIDRAP >> African Horse Sickness
- Van Sittert et al. (2013). "Occurrence of African horse sickness in a domestic dog without apparent ingestion of horse meat". Journal of the South African Veterinary Association 84 (1): 5. doi:10.4102/jsava.v84i1.948.
- "Lethal horse disease knocking on Europe's door" (Press release). Unknown. 2007-03-28. Retrieved 2007-03-27.
- The Merck Veterinary Manual – African Horse Sickness – Clinical Findings and Lesions
- Disease card from the World Organisation for Animal Health (OIE)
- Current status of African Horse Sickness worldwide at World Organisation for Animal Health (OIE). WAHID Interface – OIE World Animal Health Information Database
- CIDRAP Overview on African Horse Sickness
- 3D electron microscopy structures of the African horse sickness virus from the EM Data Bank(EMDB)
- The role of conserved residues in African horsesickness virus protein NS3 in intracellular localisation and cytotoxicity