Alan J. Guthrie, Camilla T. Weyer
African Horse Sickness
African horse sickness (AHS) is an infectious but noncontagious viral disease of equids transmitted by Culicoides spp midges. African horse sickness has an extremely high mortality rate (>70%) in horses. The disease is manifested by pyrexia and clinical signs and lesions compatible with impaired circulatory and respiratory function that are characterized by subcutaneous, intramuscular, and pulmonary edema; transudation into the body cavities; and hemorrhages on serosal and mucosal surfaces.
African horse sickness virus (AHSV) has an icosahedral configuration, with 10 double-stranded RNA genome segments encapsulated in a double-layered capsid composed of seven structural proteins with a diameter of approximately 70 nm. The virus is classified in genus Orbivirus in the family Reoviridae. It has similar morphology and shares many properties with other Culicoides-transmitted orbiviruses, such as bluetongue virus (BTV), equine encephalosis virus (EEV), and epizootic hemorrhagic disease virus (EHDV). There are nine serotypes of AHSV.
Epidemiology
African horse sickness is endemic in sub-Saharan Africa. In subtropical regions, including South Africa, AHS is strictly seasonal, with the first cases historically occurring in late summer and then abruptly disappearing following the onset of colder weather in the fall. Epidemics of AHS have occurred in North African countries on a number of occasions following spread of the disease up the west coast of Africa or up the Nile valley. Epidemics have also occurred in the Middle and Near East (in 1944 and 1959 through 1963) and southern Europe (1966 and 1987 through 1990). The disease is transmitted biologically by midges (Culicoides spp), which are most active at dawn and dusk. In endemic areas, the most important vectors are Culicoides imicola and Culicoides bolitinos. Other species, including Culicoides sonorensis in the Americas and Culicoides brevitarsis in Australasia, should also be considered as potential vectors. Windborne spread of infected midges may play a role in local spread of AHS. Long-distance spread of AHS is usually the result of inadvertent movement of equids infected with AHSV. The 1987 AHS epidemic in southern Europe was associated with the introduction of infected zebra from Namibia to a safari park in Spain.
The incubation period in horses following natural infection with AHSV is from 5 to 9 days. In experimentally induced AHS, the incubation period usually varies from 5 to 7 days, but may be as short as 3 days. In susceptible horses, the mortality rate ranges from 70% to 95%, and the prognosis is extremely poor. In mules, the death rate is approximately 50%, and in European and Asian donkeys, it is 5% to 10%. The mortality rate is very low in African donkeys and in zebra.
Recent changes in the global distribution and nature of BTV infection have been especially dramatic, with spread of multiple serotypes of the virus throughout extensive portions of Europe and invasion of the southeastern United States with previously exotic virus serotypes. Although climate change has been incriminated in the emergence of BTV infection of ungulates, the precise role of anthropogenic factors is less certain. Similarly, recent alterations in the distribution of other Culicoides-transmitted orbiviruses have been seen, including EHDV, AHSV, and EEV, and therefore horse industries and veterinary administrative bodies in many countries have developed contingency plans for AHS.
Clinical Signs
In affected horses, AHS elicits a wide range of clinical presentations, which are generally classified into four clinical forms. The dunkop or “pulmonary” form is the peracute form of the disease, from which recovery is exceptional. The incubation period is short, usually 5 to 6 days, and is followed by a rapid rise in body temperature that may reach 104° to 106 °F (40° to 41° C). This form of the disease is characterized by marked and rapidly progressive respiratory failure, and the respiratory rate may exceed 50 breaths/minute. The animal tends to stand with its forelimbs spread, head extended, and nostrils dilated. Expiration is frequently forced in character and is accompanied by abdominal heave lines. Profuse sweating is common, and paroxysmal coughing may be observed terminally, often with frothy, serofibrinous fluid exuding from the nostrils. The onset of respiratory distress is usually very sudden, and death occurs within 30 minutes to a few hours of its appearance.
The dikkop or “cardiac” form of AHS has an incubation period of 7 days or more, followed by a febrile reaction of 102° to 106° F (39° to 41° C) that persists for 3 to 4 days. The more typical clinical signs often do not appear until the fever has begun to decline. Initially, the supraorbital fossae fill as the underlying adipose tissue becomes edematous and raises the skin above the level of the zygomatic arch. This can later extend to the eyelids, lips, cheeks, tongue, intermandibular space, and laryngeal region. Subcutaneous edema may extend a variable distance down the neck toward the chest, often obliterating the jugular groove. However, ventral edema and edema of the lower limbs are not observed. Terminally, petechial and ecchymotic hemorrhages develop on the conjunctivae and on the ventral surface of the tongue. The animal becomes very depressed and may lie down frequently, but for very short periods only. Occasionally, signs of colic develop that may be unresponsive to analgesics. Finally, the animal remains prostrate and dies from cardiac failure about 4 to 8 days after the onset of the febrile reaction. In animals that recover, swellings gradually subside over a period of 3 to 8 days.
The “mixed” form of AHS is seen at necropsy in most fatal cases of AHS in horses and mules. Initial pulmonary signs of a mild nature that do not progress may be preceded, or followed, by development of edematous swellings and effusions, and death resulting from cardiac failure. In most cases, however, the subclinical cardiac form is suddenly followed by marked dyspnea and other signs typical of the pulmonary form. Horse sickness fever is the mildest form and is frequently overlooked in natural outbreaks of AHS. The incubation period is up to 9 days, after which the body temperature gradually rises over a period of 4 to 5 days to 104° F (40° C). Apart from the febrile reaction, other clinical signs are rare and inconspicuous. The conjunctivae may be slightly congested and the pulse rate may be increased. This form of the disease is usually observed in previously immunized horses.
