African horse sickness (AHS) is a life-threatening hemorrhagic disease of equids characterized by respiratory and circulatory impairment. The disease is caused by the AHS virus (AHSV), genus Orbivirus, family Sedoreoviridae. AHSV is transmitted by midges (Culicoides spp) and endemic to sub-Saharan Africa. Diagnosis is by real-time PCR assay. Control is centered around vaccination.
African horse sickness (AHS) is a noncontagious, nonzoonotic, arthropod-borne viral disease of equids and is endemic to sub-Saharan Africa. AHS can be acute, subacute, or subclinical and is characterized by clinical signs and lesions associated with respiratory and circulatory impairment.
AHS is a notifiable disease listed by WOAH because of its high mortality rate and potential for rapid spread. Treatment is largely supportive, with the main focus on preventive medicine aimed at vector control and vaccination to prevent further disease transmission. Diagnosis relies on antigen detection, with real-time PCR assays being the tests of choice in endemic countries.
Etiology and Epidemiology of African Horse Sickness
African horse sickness is caused by the AHS virus (AHSV), Orbivirus alphaequi, in the family Sedoreoviridae. O alphaequi is a segmented, nonenveloped double-stranded RNA virus 55–70 nm in diameter. Horses are the most susceptible equids, with AHSV infection potentially leading to case fatality rates of up to 95% in naive populations (1). Donkeys and mules are also susceptible but generally develop a milder form of disease. Zebras are highly resistant to disease.
Given its importance with regard to international trade and movement of horses, AHS is one of the few animal diseases for which the WOAH has introduced guidelines for members to be able to apply for official recognition of disease-free status.
There are nine immunologically distinct serotypes of AHSV (serotypes 1 to 9).
The virus is transmitted by midges, hematophagous arthropods ofCulicoides spp. The virus is most prevalent where the vector is most abundant, namely late summer rainfall areas of sub-Saharan Africa. Heavy rainfall followed by hot, dry weather contributes to the occurrence.
AHS is considered endemic to tropical and subtropical areas of Africa south of the Sahara, from Senegal in the west to Ethiopia and Somalia in the east and extending in the south to South Africa.
Epidemics of AHS have extended into new territories in the past (2):
1943–1944: Egypt, Syria, Jordan, Lebanon, and Palestine
1959–1960: Cyprus, Turkey, Lebanon, Iran, Iraq, Syria, Jordan, Palestine, Pakistan, and India (with the death of over 300,000 equids)
1965–1966: North Africa and Spain. In 1965, AHS was reported in Morocco, spread to Algeria and Tunisia, and crossed the Strait of Gibraltar into Spain in 1966.
The above outbreaks were all caused by AHSV serotype 9.
In 1987, a second AHS epizootic, due to serotype 4 virus in Spain, was caused by the importation of subclinically affected zebras from Namibia. Although extensive control measures were taken, AHSV successfully spread in 1988 to southern Spain and in 1989 to Portugal and Morocco. Spain and Portugal were finally cleared from AHSV in 1991, with the last clinical cases reported in 1990 (3).
In 2020, AHS was reported in Southeast Asia when an outbreak due to serotype 1 occurred in Thailand (4). The outbreak was traced to the legal import of subclinically affected zebras from South Africa and led to the deaths of more than 500 horses.
Outbreaks continue to occur in endemic regions of southern and eastern Africa, and, since 2007, AHSV serotypes 2 and 7 have become prevalent in central and western Africa as well, where, historically, outbreaks were predominantly due to serotype 9. In South Africa, with the exception of the AHS-controlled area of the southern Cape, outbreaks occur every year throughout the year with all 9 known serotypes.
Transmission of African Horse Sickness
Culicoides spp are the principal vectors of all 9 known serotypes of AHSV. C imicola is considered the most important species involved, with C bolitinos to a lesser extent.
The virus has also 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; however, the relevance of these two tick species to transmission must still be investigated.
Direct transmission has been shown in dogs after ingestion of infected horse meat, but it has further been shown that vector transmission to dogs is likely to also occur (5). However, it is generally considered that dogs and other large carnivores, ticks, and mosquitoes play a small role in the epidemiology of AHS.
Clinical Findings and Lesions of African Horse Sickness
African horse sickness is primarily characterized by pyrexia; edema of the lungs, pleura, and subcutaneous tissues; and petechiae and widespread hemorrhage. The incubation period is, on average, between 5 and 7 days. The viremic period generally corresponds with the onset of fever and can persist for anywhere between 2 and 14 days, but possibly longer. Clinical forms of AHS include peracute pulmonary, subacute cardiac, and mixed, as well as subclinical (horse sickness fever).
The pulmonary form of AHS is known colloquially in South Africa as "dunkop," meaning thin head. This form is a peracute infection, with clinical signs of pyrexia, congestion, dyspnea, and death due to severe pulmonary edema. Large amounts of frothy, serofibrinous fluid often flow from the nostrils. The case fatality rate for these cases is approximately 95% (1). The pulmonary form of AHS occurs predominantly in naive animals that are infected, such as foals that have lost colostral immunity or unvaccinated animals (see images of and in pulmonary AHS).
Characteristic frothy, blood-tinged fluid from the nostril of a horse that died of the peracute pulmonary (dunkop) form of African horse sickness.
Courtesy of Dr. Camilla Weyer.
Postmortem image showing the large amount of fluid found in the pleural cavity of a horse that died of peracute African horse sickness.
Courtesy of Dr. Camilla Weyer.
The cardiac form of AHS, also known as "dikkop," meaning thick head, is characterized by subcutaneous edema and consequent swelling of the supraorbital fossae, giving the appearance of a swollen head. Fever and mucous membrane congestion are generally the initial clinical signs, followed a few days later by supraorbital swelling and subcutaneous edema of the head and neck (see images of horses with and swelling in AHS). These clinical signs can be fairly severe and dramatic in appearance.
The presence of petechiae on mucous membranes is normally a poor prognostic indicator;the case fatality rate is approximately 50% (1).
Pearls & Pitfalls
|
Characteristic supraorbital swelling of a horse with African horse sickness, most commonly occurring in cardiac (dikkop) or mixed forms.
Courtesy of Dr. Camilla Weyer.
Horse with confirmed African horse sickness, showing swelling of the conjunctivae and periorbital swelling that occur in cardiac (dikkop) or mixed forms.
Courtesy of Dr. Camilla Weyer.
The acute, or mixed, form of AHS is therefore a mixture of the pulmonary and cardiac forms, and consequently both lung involvement and externally visible subcutaneous edema and supraorbital swelling typically occur. Severe colic, due to the fluid shift and hemorrhage in abdominal organs and mesenteric tissues, is often observed. The acute form of AHS is also frequently nonresponsive to pain medication. This form is probably the more common form in endemic regions.
Horse sickness fever is a milder form of disease and is normally characterized by a fever for a few days, together with depression only, followed by full recovery. This syndrome usually occurs in immunized animals as well as occasionally in donkeys and zebras.
Mortality rate depends on the virulence of the particular AHSV strain and susceptibility of the host. In naive populations of horses, mortality rates can reach 90% in epidemics (1).
Subclinical AHSV infection has occurred in endemic countries in zebras and donkeys but with the advent of more sensitive testing methods, it has been confirmed in horses as well. Subclinical infection is mostly likely to occur in previously well-immunized animals but has also occurred in naive animals suspected to have some innate resistance. This discovery has important implications for movement and disease control.
Diagnosis of African Horse Sickness
Provisional diagnosis: clinicopathological findings
Definitive diagnosis: agent identification
EDTA-anticoagulated whole blood or fresh organs (spleen and lung)
WOAH-validated real-time PCR assay
In endemic areas, clinical signs and postmortem lesions can lead to a presumptive diagnosis; however, they are not specific for AHS. Laboratory confirmation by agent identification is therefore essential for definitive diagnosis. Determination of the serotype is also advised and is important for control measures.
Historically, viral isolation with serotyping was used to provide a definitive diagnosis; however, this technique has been replaced with real-time PCR assays that are much faster and more sensitive. WOAH has validated and published the procedure for two group-specific PCR assays: the Aquero (2008) and Guthrie (2013) methods. Whole blood should be collected in EDTA tubes at the peak of fever, if possible, and transported (at 4°C [39°F]) to the laboratory. Spleen and lung samples collected from recently dead animals should be transported on ice (also at 4°C [39°F]).
Serotyping of AHSV previously relied on virus neutralization tests using type-specific antisera, which can take longer than 5 days to process and require a viral isolate. Type-specific RT-PCR assays can confirm the serotype of an AHSV within a few hours (6).
Serological analysis is rarely used for diagnostic purposes in endemic areas because many horses have not mounted an immune response at the time of sample collection or death. Furthermore, in areas where vaccination is routinely used or endemic circulation of the virus is present, results of serological testing can be difficult or impossible to interpret. Serological analysis, therefore, remains an aid in surveillance and screening methods in naive populations or nonendemic countries, where the virus is not present, as well as for immunological research purposes. Serological tests most commonly used include serum neutralization tests and ELISA.
Differential diagnoses include the following:
equine encephalosis virus (also in the Orbivirus genus, with similar, although normally milder, clinical signs)
snakebite (eg, certain cobra bites)
severe helminthiasis leading to hypoproteinemia
Prevention and Control of African Horse Sickness
Approaches vary for endemic versus AHS-free areas
Vaccination to prevent disease in endemic areas
Controlling equine movement to limit disease spread
Vector control through management practices and insecticide use
Currently, no specific curative treatment exists for animals with AHS. Supportive treatment is aimed at cardiac and pulmonary support, rest, and good, general husbandry. Colloidal fluid therapy, high-dose corticosteroids, and NSAIDs are regularly used in clinical cases with some small success.
Infected animals should be strictly confined for at least 4 weeks after clinical signs appear, because exertion can lead to pulmonary and cardiovascular collapse. Most efforts are aimed at preventing infection and preventing the introduction of infected equids from AHS risk areas to AHS-free areas or countries. To this end, the WOAH Terrestrial Animal Health Code includes published recommendations on control measures that should be implemented by AHS-infected exporting countries. Control measures include, in brief, vector-protected quarantine, vaccination control, and testing prior to exporting horses.
Vaccination remains the main form of AHS control in endemic countries. Currently the only commercially available registered vaccine remains the live attenuated virus vaccine. This vaccine consists of two polyvalent vaccine bottles with AHSV 1, 3, and 4 in bottle 1 and AHSV 2, 6, 7, and 8 in bottle 2. This vaccine generally provides good, but not absolute, protection. Annual revaccination is recommended in regions where AHS is considered endemic.
However, concerns regarding use of live attenuated AHSV vaccines are increasing because of their proven potential for reversion to virulence, their capacity for transmission by vector Culicoides midges, and the reassortment of their gene segments with other vaccine and field strains of virus, leading to the creation of novel virus progeny and outbreaks. Furthermore, existing diagnostic testslack the capability to differentiate between vaccine and field virus infection, leading to diagnostic complications in outbreaks in endemic areas where vaccination has occurred.
Inactivated or recombinant vaccines (eg, subunit, vectored, or viruslike particle–based vaccines) could avoid these potential complications and would likely be used after incursion of AHSV into previously unaffected regions. However, they are not currently commercially available, and more development and research is needed regarding the efficacy and longevity of immunity to take the concept forward.
In endemic areas, vaccination alone is not fully effective in the control of AHS, and management precautions need to be implemented:
Stabling during peak vector activity periods (especially from before sunset to after sunrise) would decrease the risk of transmission because the main Culicoides spp responsible (primarily C imicola) do not readily enter buildings.
Stables can further be protected by covering all stable openings with a fine-gauge shade cloth impregnated with insecticides and repellents.
Double-door systems, positive pressure ventilation, and automatic insecticide dispensers are all used in endemic areas to isolate horses from the vector.
See photographs of , , , and .
Topical insect repellents and insecticides applied in combination to the horse and to stable buildings are also effective in preventing insects from biting. Permethrin products are effective as insecticides, and repellents with 15% DEET are effective against the responsible Culicoides spp.
Photograph of a vector-protected stabling facility. All openings are covered with 80% shade cloth, which is then impregnated with a registered insecticide suitable for midge control or treated with a coarse spray daily. A positive-pressure ventilation system is used, with air inlets at a low level and extractor fans above.
Photograph of a vector-protected stabling facility. All openings are covered with 80% shade cloth, which is then impreg
Courtesy of Dr. Camilla Weyer.
Photograph of a double door system for a vector-protected stabling facility, allowing stepwise access into a facility to decrease the chance of the vector entering with staff.
Photograph of a double door system for a vector-protected stabling facility, allowing stepwise access into a facility t
Courtesy of Dr. Camilla Weyer.
Automatic insecticide dispensers are often installed within stable blocks to aid vector control.
Automatic insecticide dispensers are often installed within stable blocks to aid vector control.
Courtesy of Dr. Camilla Weyer.
Vector protected transport can be accomplished with the use of positive pressure ventilation, topical application of insecticides to the inside of the vehicle, and closing all openings with appropriate gauge netting. Air cooling and active circulation are normally also needed to decrease the risk of travel sickness during transport.
Vector protected transport can be accomplished with the use of positive pressure ventilation, topical application of in
Courtesy of Dr. Camilla Weyer.
Photograph of a vector-protected stabling facility. All openings are covered with 80% shade cloth, which is then impregnated with a registered insecticide suitable for midge control or treated with a coarse spray daily. A positive-pressure ventilation system is used, with air inlets at a low level and extractor fans above.
Photograph of a vector-protected stabling facility. All openings are covered with 80% shade cloth, which is then impreg
Courtesy of Dr. Camilla Weyer.
Photograph of a double door system for a vector-protected stabling facility, allowing stepwise access into a facility to decrease the chance of the vector entering with staff.
Photograph of a double door system for a vector-protected stabling facility, allowing stepwise access into a facility t
Courtesy of Dr. Camilla Weyer.
Automatic insecticide dispensers are often installed within stable blocks to aid vector control.
Automatic insecticide dispensers are often installed within stable blocks to aid vector control.
Courtesy of Dr. Camilla Weyer.
Vector protected transport can be accomplished with the use of positive pressure ventilation, topical application of insecticides to the inside of the vehicle, and closing all openings with appropriate gauge netting. Air cooling and active circulation are normally also needed to decrease the risk of travel sickness during transport.
Vector protected transport can be accomplished with the use of positive pressure ventilation, topical application of in
Courtesy of Dr. Camilla Weyer.
Key Points
African horse sickness, a hemorrhagic disease of equids, involves life-threatening respiratory and circulatory impairment.
AHS is caused by AHSV, genus Orbivirus, family Sedoreoviridae, and transmitted by midges (Culicoides spp).
Horses are most susceptible, but donkeys and mules can also contract disease.
AHSV is diagnosed by use of real-time PCR assay.
Control is based on vaccination and vector elimination.
For More Information
African horse sickness. Manual of Diagnostic Tests and Vaccines for Terrestrial Animals (Terrestrial Manual) of the World Organisation for Animal Health 2024.
Infection with African horse sickness virus. WOAH Terrestrial Animal Health Code, Adopted 2025.
Grewar J, Weyer C. African horse sickness: OIE guidelines for the practical control of viral transmission by reducing vector–host contact in the Asian context. WOAH; 2021.
African horse sickness: controlling the vector to stop the spread (infographic). WOAH; 2021.
Also see pet owner content regarding African horse sickness.
References
USDA Animal and Plant Inspection Service. Case definition: African horse sickness. 2024. https://www.aphis.usda.gov/sites/default/files/african-horse-sickness-case-definition.pdf
Lubroth J. The complete epidemiologic cycle of African horse sickness: our incomplete knowledge. In: Walton TE, Osburn BI, eds. Bluetongue, African horse sickness virus and related orbiviruses. CRC Press; 1992:197-204.
Rodriguez M, Hooghuis H, Castaño M. African horse sickness in Spain. Vet Microbiol. 1992;33(1-4):129-142. doi:10.1016/0378-1135(92)90041-q
King S, Rajko-Nenow P, Ashby M, Frost L, Carpenter S, Batten C. Outbreak of African horse sickness in Thailand, 2020. Transbound Emerg Dis. 2020;67(5):1764-1767. doi:10.1111/tbed.13701
van Sittert SJ, Drew TM, Kotze JL, Strydom T, Weyer CT, Guthrie AJ. Occurrence of African horse sickness in a domestic dog without apparent ingestion of horse meat. J S Afr Vet Assoc. 2013;84(1). doi:10.4102/jsava.v84i1.948
Morales J, Ruano MJ, Tena-Tomás C, et al. Modification and validation of a reference real-time RT-PCR method for the detection of a new African horse sickness virus variant. Microorganisms. 2025;13(12):2684. doi:10.3390/microorganisms13122684
