Saturday, October 18, 2008

HLA-B27 and Ebringer speech text

This is just a quickie as the RSPH website reshuffle (pretty well on the day of the last post) deleted Ebringer's text. It doesn't seem to be anywhere official on the net nowadays, so I feel OK to put it up here. I would just add that while I feel his work is very interesting, the pathology of MS and the pathology of BSE appear to be quite different. I've got a pdf of the BSE/acinetobacter work pre publication too, I'll probably stick that up in a few minutes and people can pick it over if they wish...


Here's the text:

Prof. Alan EBRINGER,
King’s College London

Your Royal Highnesses, Mr. Chairman, Ladies and Gentlemen.

I would like to thank The Royal Society for the Promotion of Health for the great honour it has bestowed on me in awarding the Donaldson Gold Medal to me for the work from our group,on “Bovine Spongiform Encephalopathy or BSE or more commonly known as mad cow disease. This work is a credit to the outstanding group of research workers in our Unit, especially Dr. Clyde Wilson, who recently was elected a Member of the Royal College of Pathologists, rather than to anything I may have done personally.

I graduated in Medicine from the University of Melbourne way back in 1962, obtained a Travelling Scholarship from the “Royal Australasian College of Physicians” to come to the U.K. and I have been working in the University of London since 1970. Over the last thirty years, our group has been studying the autoimmune diseases, ankylosing spondylitis, a chronic condition characterized by backache and also another arthritic disease rheumatoid arthritis. We have found that ankylosing spondylitis is triggered by the bowel microbe klebsiella and rheumatoid arthritis is produced following a urinary tract infection by the microbe proteus.

Prof. Feltkamp from Amsterdam in the Netherlands, asked us to cooperate in a joint study, which showed that Dutch patients with ankylosing spondylitis have antibodies to klebsiella and Dutch patients with rheumatoid arthritis have antibodies to proteus, as do English patients. These results have been published.

In auto immune diseases patients have antibodies which attack their own organs and these are called autoantibodies. Our model for studying autoimmune diseases was rheumatic fever, which is caused by the microbe streptococcus, which infects the tonsils and has components which resemble the human heart.

Following a streptococcal tonsillitis antibodies are produced which attack not only the microbe itself but also the human heart and cause rheumatic fever. Thus molecular mimicry or similarity between a microbe and a target organ produces an autoimmune disease.

Rheumatic fever is no longer a problem in the Western world because streptococcal tonsillitis responds to antibiotics but in countries of the Third World where access to such drugs is financially prohibitive, the disease remains a serious problem.

We have used this concept of molecular mimicry to identify the trigger factors in rheumatoid arthritis and ankylosing spondylitis.

Over the last seven years, our group has been studying “bovine spongiform encephalopathy” (BSE), also known as mad cow disease. A computer analysis showed that the soil and skin microbe acinetobacter has components which resemble brain tissues.

We approached MAFF (Ministry of Agriculture, Fisheries and Food) with the idea that we had an alternative theory, an autoimmune theory, to the prion hypothesis, which could explain the origin of BSE. Despite a few objections from some quarters, some funds were made available and access given to BSE material.

A study of BSE affected cattle showed that they have elevated levels of antibodies to the soil bacterium acinetobacter, a microbe which has components resembling brain tissues and to a lesser extent to the related microbe pseudomonas.

So far we have studied 508 animals; 218 with BSE and compared them to 290 controls.

These results are specific since the BSE animals do not show antibody elevations to five other microbes: klebsiella, proteus, serratia, E. coli, bacillus and agrobacterium.

The elevated levels of antibodies to acinetobacter found in BSE cattle lends itself to the development for an ante-mortem test for BSE, It has been proposed that BSE is caused by exposure to acinetobacter fragments, found in the “meat-and-bonemeal” flour meal fed to cattle.

The hypothesis is that antibodies against acinetobacter, attack the brain and cause mad cow disease.

The first time that a BSE cow was observed, it was found to be standing on its forelegs but falling down by its hindquarters and in this it resembles multiple sclerosis patients who have a greater incidence of lower limb paralysis.

Patients with multiple sclerosis were also found to have antibodies to acinetobacter and to the related microbe pseudomonas.

Over 50% of patients with multiple sclerosis suffer from sinusitis and thus could have become infected by the saprophytic microbe acinetobacter.

The general hypothesis is proposed that BSE is multiple sclerosis in cows and therefore it is an autoimmune disease which CANNOT BE TRANSMITTED BY THE CONSUMPTION OF “BSE” AFFECTED MEAT. If this theory can be confirmed then the following conclusions arise:

(1) Consumption of meat is safe and has always been safe.
(2) Culling of cattle was unnecessary.
(3) There will be no epidemic of CJD.
(4) An ante-mortem test for detecting BSE in live cattle is feasible.

Clearly the autoimmune theory of BSE requires further investigations but two months ago, DEFRA withdrew research funds for such studies.

We are currently cooperating with our Dutch colleagues in studying patients with multiple sclerosis. We hope that such Anglo-Dutch studies will continue in the future and serve not only international cooperation but also the aims and mission of the Royal Society for thePromotion of Health.

Thank you for your attention.


juliem said...

after reading your article i was interested in the findings that ankylosing spondylitis/rheumatoid arthritis are /can be triggered by other influences other than genetics??? i am confirmed coeliac disease from biopsy but HLA-B27 negative, i also have clinical ankylosing spondylitis but again all blood cultures suggest not, i have sacroillitis confirmed from isotope scan increased uptake of 5 on the left and 4.5 on the right no bone defects. i am currently undergoing investigation at the cardiology dept slow heart rate (possibly normal) slow electrical signal from top to bottom of heart (possibly normal) chest pain possible spinal nerve involvement.i have been very confused as to how i can have clinical issues but laboratory testing's are always negative. it is obvious from coeliac disease and sacroillitis that that my immune system is reacting inaproppriatly, i also have a puple patch of inflamation at the back of the left eye (episcleritis)apparently nothing to do with my eyes!! i would just like to say i found it very distressing that my problems were not taken seriously because of negative blood cultures to HLA B27,MY QUESTION WOULD HAVE TO BE IS IT ONLY THE HLA- B27 GENE THAT CAN CAUSE THE INFLAMATORY REACTION???? MY LOGIC SAYS NOT OR I WOULDNT HAVE COELIAC DISEASE???

Peter said...

Hi Juliem,

No I don't think you have to be HLA B27 positive or have active or confirmed coeliac disease. There will be other genes involved, B27 is the best known and commonest. All you need is to go fully paleo LC for a month and see what happens. I'd go minimal starch too, despite starches being pretty paleo in tropical regions.

You've got nothing to loose and I eat this way without the driving need to...