African horse sickness (AHS) is a highly infectious and deadly disease caused by African horse sickness virus. 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.
This information is adapted from the current OIE Technical Disease Card for African Horse Sickness
Spread of AHS
AHS virus 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 the Equidae 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 (1987-1990) and Thailand (2020).
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 nonendemic areas.
The common hosts of this disease are horses, mules, donkeys, and zebras. However, elephants, camels, and dogs can be infected, as well, but often show no signs of the disease. Dogs usually contract the disease by eating infected horse meat, a recent report has been made of the disease occurring in dogs with no known horse-meat ingestion.
Transmission of AHS
This disease is spread by mosquitoes, midges and possibly biting flies, particularly by Culicoides spp. According to the World Organisation for Animal Health (OIE) The disease has both a seasonal (late summer/autumn) and an epizootic cyclical incidence, with disease associated with drought followed by heavy rain.
Clinical signs of AHS
Horses are the most susceptible host with a mortality rate of 50% to 95% of those affected, followed by mules (50%) and donkeys (5-10%). In African donkeys and zebras mortality is rare. They 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:
Mild or horse sickness fever form
- Fever (40–40.5°C/104°F–105°F)
- Mild form; general malaise for 1–2 days
- Very rarely results in death
Mild to subclinical disease is seen in zebras and African donkeys. Infected animals may have a low-grade fever and congested mucous membrane. The survival rate is 100%.
Subacute or cardiac form
- Fever (39–41°C/102–106°F)
- Swelling of the supraorbital fossa, eyelids, facial tissues, neck, thorax, brisket and shoulders
- Mortality usually 50% or higher; death usually within 1 week
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 supraorbital fossae, palpebral conjunctiva, and intermandibular space. Mortality rate is between 50 and 70%, and survivors recover in 7 days.
Acute respiratory or pulmonary form
- Fever (40–41°C/104–106°F)
- Dyspnoea, spasmodic coughing, dilated nostrils with frothy fluid oozing out
- Redness of conjunctivae
- Nearly always fatal; death from anoxia within 1 week
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.
- Occurs frequently
- Pulmonary signs of a mild nature that do not progress, oedematous swellings and effusions
- Mortality: about 70–80% or greater
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 & control of AHS
No treatment for AHS is known. Control of an outbreak in an endemic region involves:
- identifying the virus and serotype,
- establish quarantine and movement controls,
- consideration of euthanasia of exposed equines,
- establish vector (insect) control, e.g. stabling of horses from dusk to dawn, when culicoides are most active, destroy culicoides breeding areas, use insect repellents, insecticides and/or larvicides.
- Uninfected horses are vaccinated against the virus.
According to the OIE, at present, only the live attenuated AHS vaccines currently exist – a polyvalent vaccine, a monovalent vaccine. There was a monovalent inactivated vaccine, but it is no longer available. A serotype specific subunit vaccine is currently in development.
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