Bluetongue was first reported in the United States in 1948 in sheep in Texas. The virus has now been isolated from sheep in 19 States. When the disease first occurs in a flock, the morbidity may reach 50 to 75% and mortality 20 to 50%. In subsequent years, the morbidity may be only 1 to 2% with very few deaths. Difference in breed susceptibility has not been observed. Natural bluetongue infection has not been observed in Angora or dairy goats. Bluetongue virus was first isolated from cattle, in Oregon, in 1959. The virus has now been isolated from cattle in 13 States. In cattle, the disease is usually inapparent but can cause mild to severe clinical disease and neonatal losses. Natural clinical bluetongue has also been reported in bighorn sheep, exotic ruminants in a zoo, mule deer, and white-tailed deer. Serological evidence of exposure to the virus has also been found in other species of ruminants in the wild. Inoculation of virulent bluetongue virus, vaccine virus, or natural disease can cause congenital deformities and neonatal losses in calves, lambs, and white-tailed deer fawns. Culicoides is considered the important insect vector of bluetongue. The virus has also been isolated from sheep keds and cattle lice. U.S. field strains of the virus fit into four serologic groups. No cross reactions were found between bluetongue and epizootic haemorrhagic disease of deer viruses. Cattle are considered significant virus reservoirs. It is necessary to use washed erythrocytes, rather than whole blood, and to inoculate susceptible sheep, rather than embryonated chicken eggs, to detect longer-term viraemia in cattle.
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