IT鈥橲 an idea that will challenge and provoke the medical establishment. BSE
and multiple sclerosis have the same underlying cause, say a team of
immunologists in London.
They have evidence that BSE is triggered, not by rogue prions, but by common
soil bacteria. They also claim to have found a link between exposure to the bug
and MS in people. Although their radical theory has been published in a
reputable peer-reviewed journal, many experts are far from convinced.
In 1997, Alan Ebringer at King鈥檚 College London showed that cows with BSE
have unusually high levels of antibodies against Acinetobacter. He was also able
to differentiate between 29 samples of BSE-infected cow brain and 18 BSE-free
samples by screening for the antibodies in a blind trial. And he says he has got
similar results, as yet unpublished, from hundreds more cow brain samples.
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Now, Ebringer and his team are also claiming that patients with MS make more
antibodies than healthy people to Acinetobacter鈥攂acteria which
lurk under people鈥檚 fingernails. What makes the bug so unusual, says Ebringer,
is that it has biochemical markers on its surface which match those on brain and
nerve cells from humans, cows and other animals. The result, he believes, is
that antibodies mistake brain and nerve tissue for bacteria and home in on it,
causing BSE in cows, and vCJD and MS in humans.
Working with MS investigators at London鈥檚 Institute of Neurology, Ebringer
screened blood from 26 patients with MS, 20 with severe brain injuries caused by
accidents, 10 with viral encephalitis and 25 healthy volunteers. Their tests
showed that the MS patients made many more antibodies to Acinetobacter
than the other subjects. This fits with what they found in cows with BSE.
But Ebringer faces scepticism from BSE and MS researchers. 鈥淢any bacteria
have been [unsuccessfully] linked with MS before,鈥 says a spokesman for
Britain鈥檚 MS Society. 鈥淭he relevance of the antibodies deserves further
evaluation, but an association does not indicate cause.鈥
The spokesman also dismisses the idea that MS and BSE are the same. He says
that the brain damage is 鈥渃ompletely different鈥. Brains from cows with BSE and
humans with vCJD are spongy. Tissue from MS patients doesn鈥檛 have holes: the
myelin sheaths protecting nerves and the brain are covered with scars.
Last year, the Phillips inquiry on BSE rejected the 鈥渁utoimmune theory鈥 on
the grounds that mice incapable of making antibodies still caught BSE or scrapie
if injected with infected brain tissue. Ebringer says that the mice only died
when injected in the brain, probably because of trauma, not BSE or scrapie. He
thinks that, rather than being the cause of BSE, rogue prions are generated in
the fallout from the antibody attacks.
But Moira Bruce, a prion specialist at the Institute for Animal Health鈥檚
Neuropathogenesis Unit in Edinburgh, says that the brain damage is different
depending on whether scrapie or BSE prions are injected. If it was trauma, it
would always look the same, she says.
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More at:
Clinical and Diagnostic Laboratory Immunology (vol 8, p 1181)