Ajfbjcan Horsesickness

5—7 days following infection, with death ensuing 3—6 days later. The mortality is approximately 80%, intermediate between the pulmonary and cardiac forms. Horsesickness fever is the mildest form of AHS. Infected animals usually recover following a low-grade fever, congested mucous membranes, loss of appetite, and mild depression over a 1 -week period.

The principal vertebrate hosts of AHS virus are wild and domestic equids such as zebras, horses, and mules. Donkeys are largely resistant but occasionally develop clinical disease. In endemic areas, however, native breeds seldom exhibit overt signs of infection, apparently having developed a natural or acquired immunity. Most AHS outbreaks have occurred in European breeds of equids introduced to endemic areas or as a result of exposure of susceptible equids to infected animals imported from endemic areas in Africa and parts of the Middle East. Other animals in which the presence of antibodies indicates exposure to AHS virus are goats, sheep, domestic cattle, buffaloes, dromedaries, and elephants. None of these hosts develop more than mild clinical signs but may serve as potential reservoirs for the virus. Infected dogs, however, can develop clinical disease and are believed to be important reservoirs in urban areas. Six strains of AHS virus have been isolated from street dogs in Egypt, where a number of dogs have died after consuming uncooked meat of infected horse carcasses. The progression of the disease in dogs is similar to the pulmonary form in horses.

Until the mid 1900s, epizootics of AHS were largely confined to South Africa. Beginning in 1944, with an outbreak among horses in several Middle East countries, major epizootics have occurred in other parts of Africa, the Middle East, India, and Europe. The most devastating outbreak occurred in 1959—1960, in which over 300,000 horses died or had to be destroyed in six Middle East countries and Cyprus, Afghanistan, Pakistan, and India. Although cases of AHS were reported in Spain as early as 1965, the most severe epizootic to occur in Europe took place in Spain and Portugal in 1987-1990, in which more than 160 horses, mules, and donkeys died or had to be destroyed. Some of those animals were valuable thoroughbred horses participating in international equestrian competitions being held in Spain at the time. Ten zebras imported to a zoological park near Madrid, Spain, from Namibia in southern Africa are believed to have been the source of the infection. The virus was subsequently transmitted by indigenous Culicoides populations to Portugal and Morocco. Wind-borne midges, particularly C. imi-cola, are believed to have played a role in spreading the virus. Wind dispersal of Culicoides vectors may help to explain the spread of AHS virus from endemic areas of Africa, causing outbreaks in various parts of the Middle East, Cyprus and Turkey in the Mediterranean region, the point is that all 3 areas are in the Mediterranean region (i.e., the parts of the Middle East bordering the

Mediterranean and Cyprus and Turkey) and the Cape Verde Islands off the northwestern coast of Africa.

There presently is no cure for this disease, leaving supportive therapy as the only means of treatment. Commercially available vaccines, however, have been helpful in protecting equids from infection in areas of Africa where AHS is endemic. Annual vaccinations are effective in maintaining immunity, reflecting the natural and complete immunity acquired by animals chronically exposed to this virus over extended periods of time. Regular vaccination of susceptible equids and strict control of the movement of unvaccinated animals is currently the only practical means of containing this disease.

The major vectors of AHS virus are Culicoides species. C. imicola is believed to be the most important species involved in transmission of this virus in Africa and the Middle East. Since the first isolation from field-collected C. imicola during an outbreak in South Africa, other species have been implicated as vectors. A few species have been shown to support replication of AHS virus following experimental inoculation, with members of the C. variipennis complex, for example. The virus has been successfully transmitted 12—13 days after an infected blood meal. Some mosquitoes also are believed to be potential vectors even though the virus has not been isolated from them under field conditions. Cx. pipiens, Ae. aegypti, and Anopheles stephensi have been experimentally infected with the virus, but there is no strong evidence to indicate that these particular mosquitoes are natural vectors.

AHS virus has been isolated from naturally infected camel ticks (Hyalomma dromedarii) in Egypt, raising a question about possible involvement of this tick as a secondary vector. The brown dog tick Rhipicephalus sanguineus has been shown to be capable of biologically transmitting AHS virus between horses and dogs. However, the virus has not been isolated from naturally infected ticks of this species.

Blood Protozoans

Biting midges are biological vectors of a number of protozoans called haemosporidians, which are blood parasites of reptiles, birds, and mammals. Three genera which are transmitted by biting midges are Haemoproteus (Fig. 10.17), Hepatocystis, and Leucocytozoon. Most of the species are avian parasites which cause little or no apparent harm to their hosts. A few, however, such as Haemoproteus meleagridis of turkeys and L. caulleryi of chickens, can cause significant problems for poultry producers.

Haemosporidians transmitted by biting midges are related to malarial parasites (Plasmodium species) with which they share a similar life cycle and developmental stages. While feeding on an infected vertebrate host, female midges ingest red blood cells containing

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