Antelopes have form of 'mad cow' disease

Susan Watts,Technology Correspondent
Thursday 21 January 1993 00:02 GMT
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THREE greater kudu at London Zoo have contracted an antelope form of 'mad cow' disease.

Government scientists who examined the kudu believe that they picked up the disease (bovine spongiform encephalopathy) through contact with other animals in the herd, rather than through contaminated feed - the main transmission route in cattle.

Until these latest cases, contaminated feed was thought to be the most likely source of infection for other species. However, in a paper in the latest Veterinary Record, the scientists say 'horizontal transmission' from other animals is much more likely. This usually occurs after animals eat or lick placentae in fields shortly after births. It is a recognised route for scrapie infection in sheep, but so far there has been no evidence of the same process in cattle.

Kudu are 'exotic bovids', closely related to cattle. It does not follow, however, that horizontal transmission, once spotted in kudu, is any more likely in cattle. Dr Gerald Wells, an animal pathologist at the Central Veterinary Laboratory (CVL) in Weybridge, Surrey, and co-author of the latest paper, said that husbandry practices for cattle also decreased the opportunities for such transmission within herds.

The scientists say that six cases of spongiform encephalopathy have been seen in exotic bovids in British zoos, two of which were in greater kudu at London Zoo. The pattern of transmission of spongiform encephalopathies within species is far from clear, although these latest cases may help scientists to understand the mechanisms involved.

One of the kudu at London Zoo is thought to have contracted the disease through 'maternal transmission' - probably at the time of its birth, rather than through any genetic route. Maternal transmission is very unlikely in the latest cases, Dr Wells said. The first of the three new cases was a male, born in May 1988. This was a few weeks before the government ban on feeding protein derived from ruminants to other ruminants. However, the authors are almost certain that the animal ate no infected feed.

The animal developed the tell- tale nervous signs of the disease at 37 months. It was killed on humane grounds and the classic thread-like structures were found in microscope sections of its brain and spinal cord.

The second and third kudu, born after the feed ban, were both killed because only one male can be kept in a kudu herd. Neither showed any clinical signs of the disease but, on examination, recognisable changes were found in their brain matter.

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