Overview of Wesselsbron Disease

Wesselsbron disease is caused by a flavivirus, which is an enveloped, positive-sense RNA virus. It has not been well characterized but has properties typical of a hemagglutinating flavivirus. It has been isolated from vertebrates and arthropods from many sub-Saharan African countries, and serologic surveys provide evidence of its occurrence in other countries. Evidence of infection has been reported in cattle, sheep, goats, camels, pigs, donkeys, horses, ostriches, and wild ruminants. Based on the distribution of aedine mosquitoes associated with Wesselsbron disease, the incidence of infection is likely greater than is generally realized. The high prevalence of antibodies in warmer and moister coastal areas of southern and eastern Africa 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, seroprevalence is generally lower, with irregular disease outbreaks occurring, usually in conjunction with Rift Valley fever (see Rift Valley Fever) when abnormally heavy rains lead to an abundance of floodwater-breeding mosquitoes. People may become infected by mosquitoes or by handling organs from infected animals.

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. Death may occur within 72 hr. In calves and adult sheep, goats, and cattle, nonfatal febrile or inapparent infection occurs. Occasional abortion, congenital CNS malformations with arthrogryposis, and hydrops amnii are seen in ewes. Wesselsbron disease and Rift Valley fever share many clinical and pathologic features. However, Wesselsbron disease is usually milder, producing much lower mortality, fewer abortions, and less destructive liver lesions. The virus appears to be more neurotropic than that of Rift Valley fever, and severe fetal teratology of the CNS is seen after experimental infection. Use of the attenuated vaccine in pregnant ewes may result in early embryonic death, severe teratology of the CNS, arthrogryposis, hydrops amnii, abortion, or fetal mummification. In people, mild to severe, nonfatal influenza-like symptoms are seen.

The clinical signs and epidemiology, together with a relatively high mortality in lambs, are an indication of Wesselsbron disease. It should, however, be distinguished from Rift Valley fever, and the two diseases may occur together. 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 but less so in complement fixation, a test that is specific in cattle sera. Nevertheless, homologous Wesselsbron titers greatly exceed heterologous flavivirus titers.

Production of an attenuated vaccine was discontinued shortly before 2000. Incidence of disease is low in sheep, but 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.