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See also warmwell's fuller section on BSE/CJD

Related References:
Ebringer et al. (1997) BSE as an autoimmune disease. Immunology News Vol 4 Pg:149-150.
Ebringer et al. (1997) Bovine spongiform encephalopathy: Is it an autoimmune disease due to bacteria showing molecular mimicry with brain antigens ? Environmental Health Perspect Vol.105 Pg:1172-1174.
Ebringer et al. (1998) Bovine spongiform encephalopathy (BSE): Comparison between the "prion" hypothesis and the autoimmune theory. J Nut & Env. Med 8, 265-276.
1997 Tiwana H, Wilson C, Walmsley R S, Wakefield A J, Smith M N S, Cox N L, Hudson M J, Ebringer A Antibody responses to gut bacteria in ankylosing spondylitis, rheumatoid arthritis, Crohn's disease and ulcerative colitis Rheumatology International 17 11-16
Ebringer et al (1998) Autoantibodies to brain components in bovine spongiform encephalopathy (BSE) supports the autoimmune theory Abstract from NMHCCs 4th International "Transmissible Spongiform Encephalopathies" Meeting, Dec 7-8 Washington D.C.


BBC Report on May 17, 1999 - BSE 'may never have posed human danger'

Studies at King's College, London, under the supervision of Prof. Alan Ebringer B Sc, MD, FRCP,FRACP,FRCPath. into BSE have been deprived of further funding.

There are two main competing theories in trying to explain the origin of BSE; the "prion" theory and the "autoimmune" theory.
The prion theory has been widely accepted particularly by SEAC, the body closely allied to the Food Standards Agency and which shares a secretariat with DEFRA, which has been instrumental in depriving Prof Ebringer's team of further research funding.
The minutes of the meeting in February this year, at which Prof Ebringer was allowed precisely 25 minutes to present his work, do not, according to Prof Ebringer "correspond to what I had said at the meeting or correspond to the discussion after my presentation."

Our layman's very simplified understanding of the situation:

The "prion" theory: Stanley Prusiner, the scientist at the University of California in San Francisco won a Nobel Prize for discovering mutated "prions". These are the defective proteins believed to cause brain-wasting diseases like BSE, vCJD and scrapie. "Prions" are found in brains, spinal cords, spleens and other lymphoid tissue and these parts have long been banned for human consumption. Prion proteins exist in the brain but do not replicate since they have no nucleic acid ( as in DNA) However, an "infectious particle" - a rogue prion - can replicate in the brain, destroying its tissues and causing the sponge-like holes.

The autoimmune theory: a bacterium that attacks an animal is counter - attacked by the host's immune system. But if the bacterium itself closely resembles a cell structure within the host, then those cells, the hosts' own cells, will be attacked too. The Acinebacterbacterium closely resembles brain tissue in its molecular sequences. If an animal falls prey to this invasion it will use its immune system to attack its own brain tissue.
What we find particularly interesting in the work of Prof Ebringer that we have looked at is the fact that mice with little or no immune system remain impervious to infection when inoculated with affected brain tissue. If infectious "prions" were the cause of BSE such animals, unable to defend themselves with an immune system, would succumb. Yet it is precisely those with no immune system that do not. To the autoimmune theory "prions" are not "Infectious particles" but are breakdown products of damaged nervous tissue.
|the theory maintains that the BSE epidemic occurred as a result of producing animal feeds containing high concentrations of bacteria showing molecular mimicry with brain antigens. The cull of cattle was unnecessary and the disease can be prevented by simply removing the relevant microbes from the normal flora and the animal feeds.
Experiments are required to determine if immune responses to these bacteria have occurred in BSE or scrapie-affected animals.

Professor Alan Ebringer's five year government commissioned research into the autoimmune theory of "bovine spongiform encephalopathy" or BSE cost £234,260 and was carried out in two stages. The first involved a pilot study to determine whether BSE animals had antibodies to a soil bacterium called Acinetobacter calcoaceticus. The microbe has molecular sequences resembling bovine and human brain tissue.
The second, commissioned in 1999 involved an investigation of 128 BSE animals and 127 healthy controls.

The late Professor John Pirt (see his letter to SEAC) who appeared before the Phillips Inquiry on BSE strongly supported research into a microbiological link to autoimmune diseases.

The two main competing theories about the origin of BSE have been compared over ten different biological and medical criteria, and in each case they predict different experimental observation and veterinary or clinical outcomes which are relevant to policy decisions in the field of health, food, safety and the cattle industry

Ebringer A et al. "Journal of Nutritional Medicine" Sept 1998
PRION HYPOTHESIS AUTOIMMUNE THEORY
1. Biological activity of agent retained at 100°C Biological activity of bacterial myelin peptides retained at 100°C
2. Increased antibody levels to crossreacting bacteria in sera of affected animals not present Increased antibody levels to crossreacting bacteria in sera of affected animals present
3.Prion proteins are "Infectious particles" Prion proteins are not "Infectious particles" but are breakdown products of damaged nervous tissue
4. Autonomous "infectious prions" exist in the environment Autonomous "infectious prions" do not exist in the environment
5. Brain and muscle tissue are infected by "prions" in affected animals Brain and muscle tissue are infected but crossreacting autoantibodies binding to nervous tissue are present which cause neurological damage
6. The agent causing BSE is in the brain and spinal cord of offal material The agent causing BSE is not in the brain and spinal cord, but in the bacteria present in the "green offal" material
7. Consumption of BSE affected meat is dangerous Consumption of BSE affected meat is not dangerous
8. CJD epidemic is expected in the human population No CJD epidemic is expected in the human population since humans do not consume "green offal" material
9. "Growth Hormone Preparations" were contaminated with prions which caused "CJD" in some patients "Growth Hormone Preparations" were contaminated with denatured human brain tissue which caused an EAE-like syndrome in some patients.
10. The prion hypothesis is not compatible with current concepts of molecular biology and postulates the existence of novel particles which cause neurological damage The autoimmune hypothesis is compatible with current concepts of molecular biology and proposes BSE/scrapie are produced by a mechanism involving molecular mimicry between common bacteria and nervous tissue.
The conclusions reached by Prof Ebringer's team are as follows:

  1. If it can be confirmed that BSE is an autoimmune disease caused by Acinebacter then it cannot be transmitted by meat consumption, (as long as the meat is hygienically prepared) This conclusion would appear to be compatible with the extensive nutritional studies carried out by the "National CJD surveillance Unit" in Edinburgh, who in their yearly reports state that "...the link between meat consumption and vCJD is less than compelling."
  2. Therefore the public's fears about the safety of meat consumption could be allayed by publicising these new facts concerning BSE.
  3. The culling of healthy animals would appear to be unnecessary, thereby saving substantial amounts of taxpayers' money.
  4. The use of M.A.N. (Myelin-Acinetobacter-Neurofilament) assay provides a simple ante-mortem test of BSE. The test could determine whether a cow has BSE before it is sent to a slaughter house and thus prevent its entry into the human food chain.
  5. The M.A.N. test could also be used in ther diagnosis of M.S. In February 2002 Prof. Ebringer was allotted precisely 25 minutes to present his work to the SEAC committee.

SEAC has succeeded in stopping further research into the autoimmune theory of BSE. We can only speculate why.

Meanwhile, we see that measures to kill "TSE susceptible" animals continue apace. SI 843, to be discussed by Parliament on May 15th clearly shows that the prion theory of BSE is the only theory that is acceptable. Is it because the members of SEAC do not relish the thought of the prion theory being shot down in flames, taking with it many reputations and making the future existence of SEAC itself highly dubious?
If the autoimmune theory were to be accepted, the destructive legislation of panicky governments would be shown up as utterly misguided.
Perhaps Professor Ebringer's £234,260 worth of work is being discarded before it is finished because the prion theory is so useful? It permits further widespread and legalised killing of livestock, particularly sheep, in the UK - as the SI 843 so very quietly shows; (the slaughter of clinical BSE or scrapie suspects, the offspring of confirmed BSE cases, and animals, which may have been exposed to the BSE agent, is permitted.) The ever-accelerating reduction in small farms as a result of the crisis in farming means the land is more likely to come under central control.

Professor Ebringer was asking for only £2 million to set up a reference laboratory at King's College where further studies could take place The benefits of this research would be of enormous value it seems to us.

  1. It would be possible to determine whether antibodies to Acinetobacter species precede or follow the development of clinical disease in BSE affected cattle - a question that could be resolved if it could be shown in small experimental animals that exposure or immunization with Acinetobacter bacteria or antigens leads to a neurological disease., with development of auto antibodies and if post mortem studies show spongiform changes similar to those in BSE affected animals.
  2. The question also awaits further study whether Acinetobacter infections preceded or follow onset of the human disease MS, an autoimmune disease affecting 80,000 people in the UK. MS patients have high levels of antibodies to Acinetobacter.
  3. The experiments required to determine if immune responses to these bacteria have occurred in BSE or scrapie-affected animals can be carried out.
  4. Further work could proceed on the refinement of the BSE test that can be carried out on live animals. It already has 70% accuracy rate.
  5. It will be remembered perhaps that SEAC identified a "theoretical" risk of "catching vCJD" with the traditional surgical equipment used in removing tonsils. Consequently, on January 4 last year, the Department of Health ordered a ban on multiple-use surgical equipment for tonsil removal. The decision caused chaos as waiting lists for tonsillectomies grew ever longer and manufacturers were ordered to produce 60,000 disposable kits at a cost of £25 million. These cheap disposable instruments have already been linked to two deaths and scores of injuries

    Professor Smith admitted at the beginning of May this year, "It is a theoretical risk (of catching vCJD) and there has been no transmission by this route so far, so my guess is that (were it medically necessary) I would go ahead" (i.e. continue to use traditional surgical instruments.

    £25 million seems rather a lot for a risk that is considerably less than the one we take when we get out of bed in the morning. It is also £23 million more than Prof Ebringer was asking for.

    MC


    The real news here was the implications of their research. As one Times columnist put it, "If he [Ebringer] is right, there is no risk of human epidemic, no question of an infectious agent from mad cows crossing the species barrier, no need for the European ban on British beef, and no need for the cull. If he is right, there has been a multi-billion-pound blunder." Even Stanley Prusiner, whose competing "prion" theory earned him a Nobel prize, told the BSE inquiry earlier this month that he was not convinced that nvCJD is caused by BSE in cattle. Moreover, Prusiner believes that, "[D]espite the panic over British beef, CJD is not a major health problem -- it occurs in one person per million" http://www.stats.org/newsletters/9806/madcow.htm
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    La maladie de la vache folle est peut-jtre inoffensive Un chercheur britannique remet en cause la thiorie selon laquelle la viande contaminie par la maladie de la vache folle pourrait provoquer la maladie de Creutzfeldt-Jacob chez l'homme.
    Grande-Bretagne
    17/05/1999 - En 1996, le gouvernement britannique a dépensé sept milliards de dollars pour détruire tous les troupeaux bovins porteurs de la maladie de la vache folle. Certains indices, en effet, donnaient à penser que cette maladie pouvait se transmettre ` l'homme à travers des protiines spiciales nommies prions et y provoquer la maladie de Creutzfeldt-Jacob. Mais cet inorme effort d'iradication de la maladie de la vache folle n'était pas justifiie, selon Alan Ebringer, un spécialiste en immunologie du King's College de Londres. http://www.cybersciences.com/cyber/3.0/n1257.asp