Epizootic Hemorrhagic Disease

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FIGURE 10.12 White -tailed deer fawn infected with epizootic hemorrhagic disease virus. Note hanging head and protruding tongue. (Photo by G. R. Mullen.)

referred to as black tongue disease by deer hunters in the southeastern United States.

Clinical disease in white-tailed deer and other ruminants varies from sudden death without apparent signs of illness to mild infections from which animals fully recover, Typically the disease is characterized by rapid onset of fever, loss of appetite, disorientation and weakness, a hanging head, labored breathing with the tongue often protruding (Fig. 10.12), swelling of the head and

FIGURE 10.13 White-tailed deer buck in late stage of epizootic hemorrhagic disease, with characteristic tender hooves, difficult}' walking, arched back, laid-back ears, and general depression. (Photo by G. R. Mullen.)
FIGURE 10.14 Extensive hemorrhaging and edema of lung tissue in white-tailed deer that died of epizootic hemorrhagic disease. (Courtesy of Alabama Veterinary Diagnostic Laboratory, Auburn, AL.)

neck, arched back, and painful hooves (Fig. 10.13). As the virus multiplies in endothelial cells lining the blood vessels, it spreads to various organ systems, causing extensive internal hemorrhaging (Fig. 10.14), intravascular coagulation, and thrombosis. In acute cases, death usually occurs in 4—10 days following the initial infection. In those animals which survive, recovery can be prolonged and debilitating, resulting in permanent lameness due to deformed hooves (Fig. 10.15) and difficulty eating due to damage to the oral tissues.

EHD is the most important infectious disease in wild deer populations in the United States. It primarily affects white-tailed deer, causing sporadic die-offs. Mule deer, pronghorns, and domestic cattle also can develop fatal infections but do so less commonly. Other wild ruminants which have been found to be infected during EHD epizootics include elk, bison, bighorn sheep, Rocky Mountain goats, and several species of exotic animals, such as

FIGURE 10.15 Foot lesions, swelling, and deformed hooves in white-tailed deer with epizootic hemorrhagic disease. (Courtesy of Southeastern Cooperative Wildlife Disease Study, Athens, GA.)

yak and ibex. Wapiti and moose do not appear to be adversely affected by this virus.

Although this disease is endemic throughout the United States where white-tailed deer populations are established, it is more prevalent in the Southeast, Midwest, and Northwest and along the Pacific Coast. Epizootics, with sudden die-offs in local deer herds, tend to occur in more temperate areas, whereas asymptomatic and subclinical infections are more common in the coastal endemic areas of the southeastern states, where infection rates may be as high as 70% or more. Outbreaks of EHD have also been reported in the western provinces of Canada, notably in southeastern Alberta (1962), the Okanagan Valley of British Columbia (1975), and southern Saskatchewan (1986—1987). In each case, the source of infection has been attributed to Culicoides from adjacent endemic areas in the United States. The only serotype isolated in Canada has been EHD-2.

Cattle are commonly exposed to EHD virus. Based on serologic surveys, infections in cattle are widespread throughout the United States. In most cases these are silent infections or involve only mild clinical disease. Occasionally, however, epizootics do occur in cattle, as in central Oregon in 1969 and eastern Tennessee in 1972. Infections of cattle with EHD virus also have been reported in the South American countries of Guyana, Suriname, and Colombia and in Taiwan, Malaysia, and Indonesia.

Biting midges of the genus Culicoides are the only known vectors of EHD virus. The most important species and only proven vector in North America is C. sonoren-sis. Other species have been implicated as potential vectors based on isolations of the virus from field-collected midges and limited experimental studies. The high prevalence of seropositive deer for EHD virus in areas where members of the C. variipennis complex are uncommon or absent supports the belief that other Culicoides species are involved in transmission of this virus in the United States. The vectors in other parts of the world remain unknown.

AHS is a viral disease of horses, donkeys, and mules which can be highly fatal in susceptible animals (Fig. 10.16). It is known by various names, including la pesta equine (Spain), pesta ecvina (Romania), equine plague, and horse sickness fever. The disease was first recognized in South Africa in the early 1700s, with the etiologic agent being first isolated from infected horses nearly two centuries later, in 1899. It occurs throughout sub-Saharan Africa and the Arabian Peninsula, extending intermittently into southwestern Asia and southern Europe, where epizootics have occurred in recent years.

FIGURE 10.16 Horse that died with African horsesickness; death was attributed to pulmonary edema. (Courtesy of USDA-APHIS, Foreign Animal Disease Diagnostic Laboratory, Plum Island, NY.)

The etiotogic agent of AHS is an orbivirus in the family Reoviridae, closely related to the viruses that cause blue-tongue and EHD. Nine AHS serotypes are recognized, all nine of which occur in South Africa. Eight of the nine serotypes were recovered from just seven horses during an outbreak in Nigeria in 1974—1975. The occurrence of multiple serotypes in a given geographic region and simultaneous infections of animals with more than one serotype underscore the epizootic complexity of this disease.

Four clinical forms of AHS are recognized: pulmonary (peracute), cardiac (subacute), mixed pulmonary-cardiac (acute), and horse sickness fever. The pulmonary form is the most fatal, with mortality rates as high as 95%. Clinical signs develop within 3—5 days of the initial infection. The onset of symptoms is sudden, usually beginning with fever followed by congestion of the mucous membranes of the eyes, nose, and mouth. Animals sweat profusely, experience increased respiratory rates, and cough spasmodically due to the accumulation of fluids in the lungs. Froth is commonly emitted from the nostrils in the terminal stage. Death usually occurs within a few days of the onset of clinical signs.

The cardiac form is similarly characterized by initial fever and congestion of the mucous membranes following an incubation period of 7—14 days. Animals subsequently develop extensive subcutaneous edema which is often apparent in the neck and jugular area, in the muscles along the back and hips, around the eyes and eyelids, and in the jaws. Other signs include depression and petechial hemorrhages on the underside of the tongue. Infected animals continue to feed and drink throughout the course of the disease. Death usually occurs in 4—8 days following the onset of fever, with mortality rates approaching 50%. The mixed pulmonary-cardiac form of AHS is characterized by clinical signs associated with each of the previous two syndromes. The onset of symptoms typically occurs

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