7 April 2000



On March 20, 1996, health

secretary Stephen Dorrell

made a simple statement

that shook the world and

changed forever the way

farmers are viewed by the

public and the media.

He told the House of Commons

that the most likely

explanation for the 10 new

cases of Creutzfeldt-Jakob

disease (CJD) was exposure

to bovine spongiform

encephalopathy (BSE) before

the specified bovine offal ban

was introduced in 1989.

The subsequent cull of UK

cattle and introduction of new

rules designed to improve

meat safety are widely

accepted as the right course

of action, given the possible

risk to human life. Yet, four

years on, much remains

unresolved about the cause

of BSE and its link with what

is often termed "the human

form of mad cow disease".

SEAC, the governments

advisory body on BSE, says

evidence points to meat

and bonemeal in feed as

the most likely cause of

the disease and to a link

between the human

and cattle diseases.

But not everyone

agrees with this.

Alistair Driver reports

on two people who

want the government

and the scientific

community to listen

to their versions of

the BSE story –

both of which have

huge implications

for the safety

of British beef

EATING beef does not cause vCJD in humans, the cattle cull in the UK was unnecessary and there will be no vCJD epidemic in the human population.

If Professor Alan Ebringers radical theory that BSE and vCJD are both the result of an out-of-control immune reaction set off by bacteria that "mimic" the brain is correct, these are the dramatic implications. There is a lot at stake with much of the world still not eating British beef, an estimated £4.6 billion of UK taxpayers to be spent by 2001/2 in an effort to make British beef safer and over four million cattle already having been culled for the sake of BSE. Numerous farm businesses have been forced to close and farming suicides have been linked with these failures.

But, as with any revolutionary new scientific theory, it will take a lot of time, money and intense debate before the prevailing hypothesis is displaced. Most scientists believe the mysterious rogue prion causes BSE.

"There is very little support within the scientific community for my work," said Prof Ebringer, who is an immunologist at Kings College, London.

He believes he has identified acinetobacter – a common microbe found in large quantities in the soil, sewage and water supplies – as the culprit in BSE, vCJD and multiple sclerosis. In fact, he believes vCJD is an extreme manifestation of MS, while BSE is the bovine manifestation of the disease.

"When I first saw a cow suffering from BSE on television I recognised the symptoms of MS," he said.

He suspects transmission to cattle occurred primarily through "winter feed" as a result of changes in the way it was rendered in 1982, although he has no evidence to back this up. Subsequent tightening of the rules governing the rendering process would explain the gradual decline in BSE cases in the 1990s.

Connected to sinusitis

He believes, in humans, vCJD and MS are connected to sinusitis. "The bacteria can get under fingernails and infect people when they put their finger up their nose," he said.

"When cattle or humans are infected with acinetobacter, antibodies are stimulated into attacking it. But because of its similarity with brain cells, the antibodies also attack healthy brain tissue and keep on doing so once the bacteria is defeated," he explained.

His research has already revealed that two other diseases, rheumatoid arthritis and ankylosing spondylitis, result from this process of "molecular mimicry". Certain individual humans and animals may be more genetically susceptible to it than others, he says.

His interest in Transmissible Spongiform Encephalopathy diseases was aroused in 1996 by a paper showing scrapie, a similar disease to BSE, could not be introduced in immuno-deficient mice, but was readily introduced in animals with a normal immune system. He was further encouraged by earlier research from 1969 showing the injection of brain tissue into another animal causes a neurological disorder known as "experimental allergic encephalomyelitis" (EAE), which has similar features to BSE.

This encouraged him and Kings College microbiologist Professor Pirt to embark on a search to find bacteria that resembled the brain tissues in cattle. By 1997, a computer programme came up with acinetobacter.

"The next question was whether cattle affected by BSE had been exposed to acinetobacter microbes," he said.

MAFF became interested and provided a £15,000 grant and sera from 29 BSE-infected animals. Sera from 76 more cattle that had been BSE-free were provided as controls.

Tests showed significantly high levels of antibodies to acinetobacter in the 29 BSE infected cattle, compared with the 76 controls.

Experiments involving 58 MS patients and two vCJD patients also showed high levels of antibodies to acinetobacter relative to patients with other neurological diseases.

For Prof Ebringer, these results are hugely encouraging but not conclusive. Thanks to a further MAFF grant of £230,000 he has the opportunity to examine sera from more cattle – he wants to test 1,000 – which may provide more scientifically robust results. He also hopes to persuade the industry to accept a test for BSE in live animals based on the detection of the bacteria .

Prion theory

Supporters of the prion theory are generally dismissive of Prof Ebringers theory claiming that the antibodies he has found in cattle and humans are there as a result of the breakdown of proteins caused by prions.

"The main problem with Ebringers theory is that he does not identify what came first – infection by the bacteria which creates the antibodies and causes the disease or the disease which causes the presence of the antibodies," said David Brown, an expert in prion diseases at the University of Cambridge. "His theory is based on very thin results, which he is trying to make a great show of."

Prof Ebringer acknowledges he has no proof that acinetobacter causes the diseases but says he wants to test this by injecting animals with the bacteria. He claims the presence of a high level of prions in BSE infected cattle is the result of the breakdown of nervous tissue as a result of the auto-immune reaction at the centre of his theory.

"It is a chicken and egg argument that needs more research."

He also claims the prion theory does not conform to current concepts of molecular biology because of the way prions are supposed to replicate without containing genetic material.

"I do not think the decision to implement the cattle cull was wrong given the knowledge available at the time," he said. "All I want is the opportunity to carry out more research and get closer to the truth."

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