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Wesselsbron Disease: Introduction |  |
| Wesselsbron disease is an acute, arthropodborne flavivirus infection of sheep, cattle, and goats. Infection is common but clinical disease is infrequent. Mortality in newborn animals may reach 27% in lambs and 18% in goat kids. Infection in adults is usually subclinical, but disease may be severe in the presence of pre-existing liver pathology. Occasional abortion in ewes, together with congenital malformation of the CNS with arthrogryposis of the ovine fetus and hydrops amnii in
ewes, is also seen. In humans, it causes a nonfatal influenza-like disease. |
| Etiology and Epidemiology: |
| The virus, with properties typical of a hemagglutinating flavivirus, has not been well characterized. It has been isolated from vertebrates and arthropods from several African countries, and serologic surveys provide evidence of its occurrence in others. From the distribution of aedine mosquitos associated with Wesselsbron disease, it can be surmised that the incidence is greater than is generally realized. The high prevalence of antibodies
in warmer and moister areas suggests that domestic herbivores may play a significant role in maintenance of the virus, and activity appears to occur year round. In drier areas, however, disease outbreaks are irregular and tend to occur in conjunction with Rift Valley fever (
Rift Valley Fever: Introduction) when abnormally heavy rains favor floodwater-breeding mosquitos. |
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| Clinical Findings: |
| After an incubation period of 1-3 days in newborn lambs, nonspecific signs of illness, including fever, anorexia, listlessness, weakness, and increased respiration, become evident. Wesselsbron disease and Rift Valley fever share many clinical and pathologic features. However, Wesselsbron disease is usually mild, producing much lower mortality and abortion and less destructive liver lesions. The virus appears to be more neurotropic than that of Rift Valley fever because severe
fetal teratology of the CNS is seen after experimental infection. |
Lesions:
| In newborn and young animals, a moderate to severe icterus and hepatomegaly are seen; the liver is yellowish to orange brown. Petechiae and ecchymoses are commonly found in the mucosa of the abomasum, the contents of which are chocolate-brown in color. Histopathology reveals mild to extensive necrosis of the parenchyma and individual or small, scattered groups of necrotic hepatocytes. Lesions in adult animals are usually much milder. |
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| Diagnosis: |
| The clinical signs and epidemiology, together with a relative high mortality in lambs, are an indication of the disease. The virus can be isolated from almost all organs of lambs that have died during the clinical stage of the disease. Intracerebral inoculation of newborn mice is the best method of isolation. The virus can be distinguished from that of Rift Valley fever by intraperitoneal inoculation of weaned mice; Wesselsbron disease virus will not kill such mice whereas Rift
Valley fever virus will. Confirmation of the viral identity can be accomplished by virus neutralization. |
| Serodiagnosis has been based on hemagglutination-inhibition, complement fixation, and virus neutralization. Flavivirus cross-reactivity is marked in hemagglutination-inhibition tests. Nevertheless, homologous Wesselsbron titers greatly exceed heterologous flavivirus titers. |
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| Control: |
| Production of an attenuated vaccine was discontinued shortly before 2000. Incidence of disease is low in sheep, and injudicious use of the vaccine in pregnant ewes resulted in severe economic losses in the past due to abortion and fetal malformations. Attempts to control mosquito vectors are of little value as a preventive measure. |
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