BSE is not caused by prions but by a common bug, and so does not lead to CJD in humans, claim Alan Ebringer and John Pirt. If they are right, the government has wasted Pounds 3 billion and destroyed the British beef industry for nothing. Kathryn Jackson reports
A scientific hypothesis remains just that until it has been tested, reviewed and tested again to see whether or not the initial results can be duplicated. But when a hypothesis runs counter to a dominant point of view, it can be difficult to find funding for research or to publish results in peer-reviewed journals. The scientist can be left high and dry, with no means of proving his or her theory.
A team of researchers at King's College, London hold an extremely controversial hypothesis about the cause of BSE or so-called mad-cow disease. Headed by Alan Ebringer, professor of immunology, and John Pirt, emeritus professor of microbiology, the team believes that BSE is an auto-immune disease, like multiple sclerosis or rheumatoid arthritis, and that it is caused by a common bacterium, acinetobacter, that lives in water, soil and sewage.
In The THES last month, Ebringer said that when he first saw a BSE cow in 1989 he was struck by how similar its behaviour was to that of a multiple sclerosis sufferer. MS patients "can use their hands to eat but have difficulty walking". Likewise, said Ebringer, "Betsy stood on her front legs, but had no control over her backside."
If Ebringer and Pirt are right, then you cannot get the progressive dementia Creutzfeldt-Jakob disease by eating beef from cows affected by BSE. Not only does this hypothesis challenge scientific dogma, but it also calls into question a government policy that has cost more than Pounds 3 billion, has strained international relations and has caused worldwide fear and anxiety.
Ebringer has yet to test his theory fully. After much prompting, the Ministry of Agriculture, Fisheries and Food gave him 29 samples of blood from BSE-affected cattle. He found they all had high levels of antibodies to acinetobacter.
Then, last week, MAFF finally recognised the validity of his research. It awarded him a Pounds 200,000 grant and promised him more than 500 blood samples. "You can't expect the government to change its policy on the basis of 29 samples," says Ebringer. "But if we get positive results from 500 or 1,000 samples, and I am confident that we will, then the ministry will have to admit that it made a mistake."
At the public inquiry into the handling of the BSE crisis a few months ago, Ebringer's was a lone voice. Most scientists are convinced BSE is caused by an infectious form of protein-like particles called prions, even though infectious prions have never been isolated or seen under a microscope. "The prion theory is not compatible with current concepts of microbiology," says Ebringer.
His autoimmune theory is simpler. "Before 1988, cows were fed a 'green offal' that contained faecal material. Acinetobacter would have been in that feed," says Ebringer. "We have found that the molecular structure of acinetobacter mimics that of bovine brain tissue. In trying to fend off an infection from acinetobacter, the immune system mistakenly destroys its own healthy brain tissue." The result is a soft and spongy brain - the classic BSE symptom. Initially, the "green offal" was heated to a temperature high enough to kill any bugs. BSE appeared after 1982, when the temperature was lowered.
Ebringer believes that CJD is also caused by acinetobacter. He points out that a young vegetarian woman died of so-called new variant CJD. She worked in a pet store and would have been exposed to acinetobacter in the droppings of cats and dogs in the shop.
But Ebringer faces much opposition. Simon Cousens, an epidemiologist at the London School of Hygiene and Tropical Medicine and co-author of the paper that originally defined new-variant CJD, doubts whether the new theory can account for the fact that there have been 40 documented cases of nvCJD since 1995. Ebringer, however, sees no evidence to believe there is a new variant of CJD, and suspects greater vigilance is the reason for an increase in the number of documented cases of what he thinks is the old form of the disease.
Ebringer bases his autoimmune theory of BSE on his previous research. He has found that a gut-loving bacteria called klebsiella causes the autoimmune disease ankylosing spondylitis, and that Proteus mirabilis, a microbe that causes cystitis, mimics a protein that lives around the joints of the hands and feet, resulting in rheumatoid arthritis. While other rheumatologists deal with the symptoms of this disease, Ebringer finds that its female sufferers can be helped if they control their susceptibility to cystitis simply by drinking a lot of fluids.
For the next two years, Ebringer's team will be testing the blood samples sent by MAFF. The political implications of these experiments are vast. If he is right, he will show that the government wasted billions of pounds, destroyed an industry and caused unnecessary public panic. But Ebringer, a medical doctor who regularly treats patients, is more concerned with what this all means for patients. He has requested serum from US researchers who have studied kuru, a spongiform disease found in Papua New Guinea and is similar to CJD. And he looks forward to the time when he can test serum from CJD sufferers. "If we can establish a connection between CJD and acinetobacter, then we can find ways to locate the microbe and control the disease," he says.