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THE beef industry in Canada was stunned this week to learn that BSE had been confirmed in a single cow in Alberta.
Quarantine was put in place and investigations begun to trace the cow and the disease, which was confirmed by a laboratory in the UK. The only previous BSE case in Canada, in 1993, was in a cow imported from Britain.
The news comes as the Government here has halted funding to a scientist conducting research into Mad Cow Disease and the deadly human disease with which it has been linked.
Professor Alan Ebringer believes the cause of BSE is a bug commonly found in the soil.
Further, he says that those listed as victims of vCJD (variant Creutzfeldt-Jacob disease) commonly linked to BSE, in fact died of a form of multiple sclerosis (MS).
The theory runs counter to the mainstream view that a prion causes BSE in cattle and vCJD in humans and that cattle contracted BSE (Mad Cow Disease) from a prion in feed that contained protein from other cattle and sheep (possibly from scrapie-infected sheep). People who contracted vCJD had consumed BSE-infected meat.
In 1997, Prof Ebringer and his researchers at King's College, London (KCL), reported that cows with BSE have unusually high levels of antibodies against Acinetobacter, a common soil bacteria. That microbe, he said, was in their feed.
More recently, the professor of immunology at the School of Health and Life Sciences at KCL said he made a similar finding in people with MS. Those patients were found to make more antibodies to Acinetobacter bacteria than do people without the disease (the bacteria is found under people's fingernails).
He believes BSE in cows, and vCJD and MS in humans, is caused when these antibodies mistake brain and nerve tissue for bacteria and home in on it.
His theory is dismissed by other researchers. A spokesperson for the MS Society said the brain damage that accompanies BSE and MS are "completely different".
Brains from cows with BSE and humans with vCJD are spongy. Tissue from MS patients doesn't have holes: the myelin sheaths protecting nerves and the brain are covered with scars.
Prof Ebringer is not the only researcher to question the link between BSE and vCJD. In 2001, George Venters, a consultant to Lanarkshire Health Authority, reported in the British Medical Journal that vCJD is not the human version of BSE. He said the cattle prion can't be found in human brains, that a 'species barrier' usually prevents prion diseases from jumping species and pointed out that although scrapie has existed in sheep for at least 250 years, it has never spread to humans.
However, mainstream CJD researchers dismissed his report. An epidemiologist at Imperial College, Roy Anderson, said the paper was "confused, confusing and misleading".
Prof Ebringer believes his theory - researched thanks to a £200,000 grant from DEFRA - deserves much further study. But he says DEFRA will not provide further funding because the committee established by the Government to investigate BSE/vCJD is dominated by researchers who are all funded for research into the prion theory.
He pointed out that when research commences on a new topic, it is common for more than one plausible theory to come forward, as it has with BSE. The Government is wrong, he says, to put all of its eggs in one basket by concentrating on the prion theory.
When asked why he made tests only on those with MS and not those with vCJD, he said he was blocked because of concerns relating to legal action by the families of those who had died in the aftermath of the BSE crisis.
If BSE is caused by a common soil bacteria, why didn't it occur long ago? Prof Ebringer says it probably did. George Venters supplied the likely explanation. If a cow began to show the unusual symptoms, it was slaughtered and ended up as the Sunday roast.
Updated: 12:41 Wednesday, May 21, 2003
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