Congenital bovine epizootic arthrogryposis and hydranencephaly in Australia. Distribution of antibodies to Akabane virus in Australian Cattle after the 1974 epizootic.

At the end of the 1974 epizootic of bovine congenital arthrogryposis and hydranencephaly in south-eastern New South Wales, an Australia-wide serological survey (about 4,000 serums) was made to determine the ditribution of cattle possessing serum neutralising antibodies against Akabane virus. Eighty per cent of the serums from cattle in northern Australia (Western Australia, Northern Territory, and Queensland) were positive. A detailed study in the epizootic area in New South Wales (particularly around Bega) showed that 80 to 100% of serums from cows in herds in this area possessed neutralising antibodies. The animals possessing antibodies extended as far south as Genoa in north-eastern Victoria, and as far west as Darlington Point on the Murrumbidgee River. There were no positive herds along the Murray River, where an outbreak of the mosquito-borne disease Murray Valley encephalitis occurred in 1974. Serums tested from cows in the rest of Victoria, South Australia, south-western Western Australia, and Tasmania were negative. Arthrogrypotic calves born in Tasmania and south-western Western Australia were not associated with the presence of Akabane virus. In Papua New Guinea, serums collected from cattle at Boroka, Lae, and Goroka did not possess neutralising antibodies. The distribution of cattle possessing antibodies in Australia would fit a spread of the virus by Culicoides brevitarsis, a biting midge from which Akabane virus had been isolated on three occasions. The possibility of other vectors, as well as C. brevitarsis, was suggested by the presence of cows possessing antibodies at Alice Springs, where this biting midge has not been found. Possibly most cattle in northern Australia become infected early in life. The epizootics in New South Wales could occur when seasonal conditions allow a southerly extension of virus-infected C. brevitarsis which feed on susceptible pregnant animals. C. brevitarsis also bites sheep, and both neutralising antibodies to Akabane virus and congenitally deformed lambs have been observed in the epizootic area. An understanding of the distribtuion of Akabane virus and C. brevitarsis, a possible Australian vector for bluetongue virus, may prove useful if bluetongue should enter Australia.

Serologic evidence for etiologic role of Akabane virus in epizootic abortion-arthrogryposis-hydranencephaly in cattle in Japan, 1972-1974.

In the outbreak of abortions, premature births, stillbirths and congenital arthrogryposis-hydranencephaly (AH) syndrome in Japan during the summer through winter of 1972-73 and 1973-74, precolostral sera from calves with congenital AH syndrome and normal calves were tested for neutralizing antibodies against some arboviruses, i.e. Akabane, Aino, Getah and Japanese encephalitis (JE) viruses. The incidence of antibody for Akabane virus was very high in calves with AH syndrome (49/59 or 83 per cent) as compared with normal calves (3/11 or 27 per cent), indicating an intimate correlation between the AH syndrome and precolostral anti-Akabane antibody. Three stillborn fetuses also had anti-Akabane antibody. On the other hand, no precolostral serum antibody for the other viruses was detected in any of the calves tested. The mothers of these calves, normal and with AH syndrome, had anti-Akabane antibody in high percentages (44/52 or 85 per cent and 7/8 or 88 per cent), whereas a few of the mothers had antibodies for the other viruses. Serological surveys indicate a wide dissemination of Akabane virus in epizootic areas during the summer months of 1972 and 1973. Thus, 8 groups of cattle in epizootic areas showed high rates of seroconversion for Akabane virus during the 1972 or 1973 summer. Very high incidences of Akabane antibody were shown among cattle in epizootic areas but extremely low incidences in near-by non-epizootic areas. The geographic distribution of anti-Akabane antibody among cattle throughout the country in the 1973 spring generally agrees with the pattern of case distribution in the 1972--73 outbreak. All these findings strongly suggest that Akabane virus is the etiological agent of the outbreaks. Further studies are needed, particularly isolation of the virus, demonstration of infection with the virus in lesions by immunofluroescence and production of intrauterine infection by experimental infection of pregnant cows.