ANKYLOSING SPONDYLITIS MEETING
SAN ANTONIO - TEXAS
Sat. 29 - Sunday 30th JULY 2000.
Speaker: Professor Alan EBRINGER
King's College, University of London
&
Department of Rheumatology, Middlesex Hospital,
LONDON, England, U.K.
Organizer: Mr. George McCaffery,
10801 Hammerly Boulevard, Suite 114
Houston, Texas.
Phone: 713-464-3311
Fax: 713-464-6111
e-mail: 105057.2332@compuserv.com
SAN ANTONIO MEETING -- AGENDA
Saturday morning: Ankylosing spondylitis (AS).
Definitions.
HLA-B27 and molecular mimicry.
Klebsiella microbe.
Countries with anti-Klebsiella antibodies.
"Early" AS.
Saturday afternoon: LOW STARCH DIET.
Origins of diet.
Diet is really "Low starch/High protein"
Diet and salazopyrin-EN.
EXERCISE.
Sunday morning: General discussion with audience.
Sunday afternoon: Other diseases involving molecular mimicry.
Rheumatic fever.
Rheumatoid arthritis.
Diet for rheumatoid arthritis.
Neurological diseases: Multiple sclerosis.
Bovine spongiform encephalopathy.
.
Professsor Alan EBRINGER B.Sc, MD, FRCP, FRACP, FRCPath
Professor of Immunology, King's College London & Honorary
Consultant Rheumatologist, University College School of Medicine,
Middlesex Hospital, LONDON, U.K.
WORDS USED
ANTIBODY is a specific substance produced by the body as a reaction to
the presence of an antigen.
ANTIGEN is something that evokes an immune response, it may be a
foreign particle or a microorganism.
AS is an abbreviation for the disease "ankylosing spondylitis".
COMPLEMENT is a substance in normal blood, which can cause the
destruction of bacteria.
DIGESTION is the process of breakdown of food in the stomach and
small intestine. Undigested food, including starch enters the
large bowel or colon.
Simple sugars are absorbed in the small intestine.
Starch is broken down in the large inestine to simple sugars.
Klebsiella lives and multiplies in the large intestine.
HLA-B27 stands for "human lymphocyte antigen", and are molecules
present on most cells, especially in AS patients. Such
people are referred to as being: "HLA-B27 positive".
IMMUNE RESPONSE is the body's response to an antigen.
INFLAMMATION is the response of living tissue to injury, characterised
by redness, pain, heat or swelling around a foreign body which
may be a specific micro-organism.
KLEBSIELLA is a bacterium. Its structure very closely resembles that of
HLA-B27. It feeds on sugars derived from STARCH.
SACRO-ILIITIS is inflammation of the sacro-iliac joints.
STARCH is a complex carbohydrate, made up of long molecules of
sugars and present in bread, potatoes, cakes and pasta.
(1) Ankylosing spondylitis:
Ankylosing spondylitis (AS) was first described by Connor in 1692 but the clinical features have only been characterized in some detail over the last one hundred years.
The disease affects approximately 1 - 2% of the U.K and American population - therefore it is not a rare disease.
However one of the greatest problems is that it takes 5 - 10, or even 20 years to make the diagnosis, during which time the patient suffers from recurrent bouts of backache, muscle stiffness and is often accused of being "neurotic" or malingering .
The main reason for "delay to diagnosis" is that one of the definitions for the disease is "presence of sacro-iliitis" on X-ray examination of sacro-iliac joints: - However it takes 5 to 10 years for sacro-iliitis to develop.
Therefore the patients are told "YOU CANNOT HAVE "AS" BECAUSE YOU DO NOT HAVE SACRO-ILIITIS".
(2) Discovery of the link between HLA-B27 and AS.
In 1973 one of the greatest discoveries in "AS" was made by 2 groups - Brewerton's group from the Westminster Hospital in London and Terasaki's group from Los Angeles: They showed that 96% of AS patients carried the "white cell blood group" HLA-B27 (=Human lymphocyte antigen-B27) which is present in all nucleated cells including the bone and cartilage cells of the lumbar spine, whilst the frequency of this blood group marker in the Caucasian populations of the USA or U.K. is 8%.
Furthermore, the remaining 4% who are HLA-B27 NEGATIVE, usually
suffer from psoriasis or bowel disease or the diagnosis is WRONG.
Clearly, possessing HLA-B27 has something to do with the disease.
In 1975, we set up the "Ankylosing Spondylitis Research Clinic"at the
Middlesex Hospital in London, to answer the question: Why B-27 in AS ?
(3) HLA-B27: The size of the problem.
It is known that 8% of the US/U.K. populations are HLA-B27 POSITIVE.
Since the population of the U.S is 275 million, there are 22 million people in the U.S. who are HLA-B27 POSITIVE and in the U.K. there are 5 million who are also HLA-B27 POSITIVE.
It is agreed by many workers, that 20% of HLA-B27 POSITIVES have some symptopms of AS.
THUS: THERE ARE 5 MILLION AMERICANS with some symptoms of AS.
THERE ARE 1 MILLION ENGLISH SUBJECTS with some symptoms of AS.
MOST OF THESE ARE NOT BEING TREATED !!!
It is our suggestion that the discovery of the link between HLA-B27 and "AS", COULD RESOLVE THIS PROBLEM.
(4) Clinical features of "AS".
"AS" is a disease which affects 3-4 times as many males as females, it usually starts in the teens or twenties and is characterized by recurrent episodes of backache, large joints problems and muscle stiffness.
Often the diagnosis is elusive, despite many visits to the doctors.
NOTHING UPSETS PATIENTS MORE THAN TO BE TOLD: THERE IS "NOTHING WRONG WITH YOU", it is muscle strain, lumbago, stress, nerves or "you are just imagining it".
However a careful clinical history will elicit characteristic features of AS or pre-AS.
(5) Early "ankylosing spondylitis".
It has been suggested by Agarwal from Pittsburgh, that "pre-ankylosing spondylitis" (pre-AS) occurs in a patient who has symptoms of AS but has not yet developed X-ray evidence of sacro-iliitis.
In our "AS Research Clinic" at the Middlesex Hospital, we have identified 6 characteristic symptoms of AS which can be obtained by taking a careful clinical history from the patient.
If the patient happens to be also HLA-B27 POSITIVE, we then make a diagnosis of "Pre-AS" and proceed to treat the patient as if he had AS.
The 6 characteristic clinical features of AS are:
(1) Lumbar pain, on and off for 3 months.
(2) Buttocks pain.
(3) Pain "moves" from one side to the other, from right to left and
and vice-versa.
(4) "Morning stiffness" - sometimes it is so distressing that patient
cannot get out of bed and is worried that he/she has
developed some severe neurological disorder.
(5) The stiffness in the morning can be so severe that on careful
questioning the patient will actually say they
"ROLL OUT OF BED".
(6) The PAIN and MUSCLE STIFFNESS can be relieved by
EXERCISE.
Some patients will say that they have to "crawl on all fours"
to get to the toilet and then they get better.
IF 5 out of these 6 features are present in an HLA-B27 positive individual that patient has AS and should be treated.
(6) Ankylosing spondylitis, HLA-B27 and Klebsiella.
The model we used in 1975 to study "AS" in the "AS Research Clinic"
was based on the model of rheumatic fever.
Rheumatic fever is caused by an upper respiratory tract infection by the microbe Streptococcus, usually in the tonsils.
Zabriskie from New York has shown that this microbe has sequences resembling human heart tissue - the microbe shows molecular mimicry with cardiac tissues.
Three to six weeks after such an infection, the patient will develop a cardiac murmur because the patient's anti-Streptococcal antibodies not only attack the microbes but also the heart of the patient because of this
molecular mimicry.
In 1975, we proposed that there is a microbe which carries in its coat
or cell wall molecular sequences resembling HLA-B27.
A rabbit was duly injected with human HLA-B27 cells and the resultant
antiserum reacted with a microbe called Klebsiella, which is a normal component of the human bowel flora.
In 1976, we reported for the first time, at an "HLA and Disease" Congress held in Paris that ankylosing spondylitis was probably caused by
Klebsiella microbes, (See paper 1) because they showed molecular mimicry
with HLA-B27. (Paper 2)
(7) Anti-Klebsiella antibodies in AS patients:
Subsequently we showed that antibodies to Klebsiella were found in
AS patients in London (Papers 3 and 4), as well as in AS patients in
Spain (Paper 5), the Netherlands (Paper 6) and Japan (Paper 7).
Antibodies against Klebsiella in AS patients, have now been reported from 17 different countries, including the USA.
(8) Klebsiella microbes in AS patients:
Furthermore the Klebsiella microbes can be isolated from from the faeces of AS patients during the active phases of the disease (Paper 8),
when they have elevated levels of serum IgA (Paper 9).
The microbe Klebsiella contains the nitrogenase and pullulanase molecules which crossreact with HLA-B27, as well as with collagen
components found in the lumbar spine and muscle (Paper 10).
(9) AS as an autoimmune disease:
We have suggested that AS is an autoimmune disease caused by autoantibodies produced following ileo-caecal infection of the colon (See diagram or "Simple illustration") by Klebsiella microbes (Paper 11) and some of these autoantibodies will cause muscle damage, thereby explaining the frequent presence of "muscle stiffness" in AS patients (Paper 12).
(10) The LONDON "AS DIET"
The "LONDON "AS" DIET, involves a Low starch/High protein diet for ankylosing patients.
The Klebsiella bacteria in the large bowel feed on food stuffs consumed by the patient in the preceding 3 to 4 hours.
When one eats large amounts of starchy foods (BREAD,POTATOES, CAKES and PASTA), the Klebsiella bacteria feed on it, multiply and then the immune system of the patient makes antibodies against the microbe and some of these antibodies will also have activity against the collagens of the spine and uvea, since iritis or uveitis also occurs in AS patients.
Therefore these antibodies are acting as tissue damaging autoantibodies and CAUSE AS - hence the need to ABSTAIN from these foods (Paper 13, consist of the "Diet sheets" we give to our patients).
(11) The origins of the "Low-starch diet":
The use of this "LOW STARCH-HIGH PROTEIN DIET" for AS patients was first described at an AS meeting held in Dallas, Texas in 1985,
which was subsequently published in "Advances in Inflammation Research"
in New York - as this was a rather long article, only the pages dealing with the diet have been included (Paper 14).
Some patients have now been observed for a period of 15 years or more and their episodes of inflammation or disease activity, as measured by "ESR" (= erythrocyte sedfimentation rate) have significantly decreased over this period of time (Paper 15), and clinically it would appear the progression of their disease has been arrested.
(12) Other forms of treatment: SALAZOPYRIN and EXERCISE:
Numerous studies have demonstrated the efficacy of SALAZOPYRIN,
especially in its enteric-coated form as a useful drug in AS.
The usual dose we use with our patients is 1 to 4 tablets (0.5 G per day).
HOWEVER THE MOST IMPORTANT FORM OF THERAPY
IN "AS" PATIENTS IS REGULAR EXERCISE, ESPECIALLY OF THE "STRETCHING VARIETY".
I hope that these brief comments on "AS" will be of benefit to participants of the San Antonio Meeting.
With Best Wishes,
Yours sincerely,
Alan Ebringer B.Sc, MD, FRCP, FRACP, FRCPath.
Professor of Imunology, King's College London and
Honorary Consultant Rheumatologist, UCL School Medicine.
BY PROFESSOR ALAN EBRINGER
1. Crossreactivity between Klebsiella aerogenes species and B27 lymphocyte antigens as an aetiological factor in ankylosing spondylitis.
A. Ebringer, P. Cowling, N. Ngwa Suh, D.C.O. James and R.W. Ebringer
"HLA and Disease" Ed. Dausset and Svejgaard. Editions INSERM. 1976; 58:27
(First report of a link between HLA-B27 and Klebsiella)
2. Ankylosing spondylitis: Klebsiella and HLA-27.
R.W.Ebringer, D. Cook, D.R. Cawdell, P. Cowling and A. EbringerRheumatology and Rehabilitation. 1977; 16: 190-196.
(First report of increased fecal Klebsiella in patients with AS)
3. Sequential studies in ankylosing spondylitis: Association of Klebsiella pneumoniae with active disease.
R.W, Ebringer, D.R. Cawdell, P. Cowling and A. Ebringer.
Annals of the Rheumatic Diseases 1978; 37: 146 - 151.
4. Immune response inversion following hyperimmunisation: A possible mechanism in the pathogenesis of HLA linked diseases.
C.R. Young, A. Ebringer and J. Archer
Annals of the Rheumatic Diseases. 1978; 37: 152 - 158.
5. The link between genes and disease.
A. Ebringer.
New Scientist, 1978, 79: 865 -867.
6. Klebsiella pneumoniae and acute anterior uveitis in ankylosing spondylitis.
R.W. Ebringer, D.Cawdell and A. Ebringer.
British Medical Journal. 1979, 1: 383.
7. Ankylosing spondylitis, immune response genes and molecular. Mimicry.
A. Ebringer.
Lancet, 1979, I: 1186.
8. Ankylosing spondylitis, HLA-B27 and Klebsiella. I. Crossreactivity studies with rabbit antisera.
J. Welsh, H. Avakian, P. Cowling, A. Ebringer, P. Wooley, G. Panayi and R.Ebringer.
British Journal of Experimental Pathology, 1980, 61: 85 - 91.
9. Ankylosing spondylitis, HLA-B27 and Klebsiella. II. Crossreactivity studies with human tissue typing sera.
H. Avakian, J. Welsh, A. Ebringer and C. Entwistle.
British Journal of Experimental Pathology, 1980; 61: 92 - 96.
(First report of anti-HLA-B27 tissue typing sera binding to Klebsiella)
10. C-reactive protein, erythrocyte sedimentation rate and Klebsiella in ankylosing spondylitis.
P. Cowling, R. Ebringer, D. Cawdell, M. Ishii and A. Ebringer.
Annals of the Rheumatic Diseases, 1980; 39: 45 - 49.
11. Association of inflammation with elevated serum IgA in ankylosing spondylitis.
P. Cowling, R. Ebringer and A. Ebringer
Annals of the Rheumatic Diseases, 1980; 39: 545 - 549.
12. Ankylosing spondylitis: Host-parasite interaction in the production of rheumatological disease.
R. Ebringer and A. Ebringer.
Recent Advances of Rheumatology. Edited by W. Watson Buchanan and W. Carson Dick, Churchill Livingstone. Edinburgh, 1981; 2: 107 - 120.
13. Uveitis, vitreous humour and Klebsiella. I. Binding studies with rabbit antisera.
H. Avakian, R. Abuknesha, J. Welsh and A. Ebringer.
British Journal of Opthalmology, 1981; 65: 315 - 322.
14. Uveitis, vitreous humour and Klebsiella. II. Crossreactivity studies using radioimmunoassay.
J Welsh, H. Avakian and A. Ebringer.
British Journal of Opthalmology, 1981; 65: 323 - 328.
15. Spondylitis ankylopoietica und Klebsiella: Ein genetischer Zusammenhang.
A. Ebringer.
Munchener Medizinische Wochenschrift, 1982; 124: 120 - 122.
16. The crosstolerance hypothesis in IR-gene systems, rheumatic fever and ankylosing spondylitis.
A. Ebringer
Rivista di Biologia, 1982; 75: 197 - 229.
17. Yersinia enterocolitica biotype I, diarrhoea and episodes of HLA-B27 related ocular and rheumatic inflammatory disease in South-East England.
R. Ebringer, D. Colthorpe, G. Burden, C. Hindley and A. Ebringer.
Scandinavian Journal of Rheumatology, 1982; 11: 171 - 176.
18. An investigation into the properties of the Klebsiella strains isolated from ankylosing spondylitis patients.
P.E. Pease, R.A. Tyler, J.R. England, D. Colthorpe and A. Ebringer.
Journal of Hygiene, 1982; 89: 119 - 123.
19. Properties of Yersinia enterocolitica strains isolated from ankylosing spondylitis patients.
P. E. Pease, S.E. Palmer, R.L.Bartlett, D. Colthorpe, A. Ebringer and R. Ebringer.
European Journal of Clinical Microbiology, 1982; 1: 256 - 257.
20. Muscle changes in ankylosing spondylitis.
G.O. Hopkins, J. McDougald, K. Mills, D. Isenberg and A. Ebringer.
British Journal of Rheumatology, 1983; 22: 151 - 157.
( First report of changes in muscles of AS patients.)
21. The crosstolerance hypothesis, HLA-B27 and ankylosing spondylitis.
A. Ebringer
British Journal of Rheumatology 1983; 22 (suppl.2): 53 - 66.
22. Circulating immune complexes in ankylosing spondylitis.
H. Deicher, A. Ebringer, S. Hildebrand, A. Kemper and H. Zeidler
British Journal of Rheumatology, 1983; 22(suppl.2): 122 - 127.
23. IgA antibodies in ankylosing spondylitis.
A.K. Trull, R. Ebringer, G.S. Panayi, D. Colthorpe, A. Ebringer and D.C.O. James.
Scandinavian Journal of Rheumatology, 1983; 12: 249 - 253.
(First report of elevated levels of specific antibodies to Klebsiella in AS patients.)
24. La spondylarthrite ankylosante, HLA-B27 et la theorie de la tolerance croisee.
A. Ebringer.
Revue du Rhumatisme, 1983; 50: 763 - 769.
25. HLA-B27 and the immune response to enterobacterial antigens in ankylosing spondylitis.
A.K. Trull, A. Ebringer, G.S. Panayi, R. Ebringer and D.C.O. James.
Clinical and Experimental Immunology, 1984; 55: 74 - 80.
26. Etiopathogenesis of ankylosing spondylitis and the crosstolerance hypothesis.
A. Ebringer, M. Baines, M. Childerstone, M. Ghuloom and T. Ptaszynska.
"The spondyloarthropathies." Edited by M. Ziff and S.B. Cohen.
Raven Press New York, 1985
Advances in Inflammation Research, 1985; 9: 101 - 128.
( First report of "Low Starch Diet" in AS patients)
27. Spondyloarthritis, uveitis, HLA-B27 and Klebsiella.
A. Ebringer, M. Baines, T. PtaszynskaImmunological Review, 1985; 86: 103 - 118.
28. Antibodies to Proteus in Rheumatoid arthritis.
A. Ebringer, T. Ptaszynska, M. Corbett, C. Wilson, Y. Macafee, H. Avakian, P. Baron and D.C.O. James.
Lancet, 1985; ii: 305 - 307
( First report of elevated levels of anti-Proteus antibodies in rheumatoid arthritis patients, whilst AS patients, acting as disease controls, have elevated levels of antibodies to Klebsiella. )
29. Absence of antibodies to Yersinia enterocolitica in patients with ankylosing spondylitis in London.
A.Toivanen, T.H. Stahlberg, K. Granfors and A. Ebringer
Lancet, 1986; ii: 1400.
30. Role of micro-organisms in the pathogenesis of HLA-B27 diseases.
A. Ebringer, M. Ghuloom, T. Ptszynska and C Wilson.
In: " Spondyloarthropathies - Involvement of the gut" Ed. E. Veys and H. Mielants
Excerpta Medica, Elsevier Amsterdam. 1987; Pg 235 - 247.
31. A study of anti-polynucleotide antibodies, anti-Klebsiella (K 30) antibodies and anti-DNA antibody idiotypes in ankylosing spondylitis
D. Isenberg, R. Feldman, C. Dudeney, F. Konikoff, D. Jones, A. Ebringer and Y. Schoenfeld
British Journal of Rheumatology, 1987; 26: 168 - 171.
32. Klebsiella antibodies in ankylosing spondylitis and Proteus antibodies in rheumatoid arthritis.
A. Ebringer, N. Cox, I Abuljadayel, M. Ghuloom, S. Khalafpour, T. Ptaszynska, F. Shodjai-Moradi and C Wilson.
British Journal of Rheumatology, 1988; 27 (suppl. 2): 72 - 85
33. Antibodies to Klebsiella and Proteus microorganisms in ankylosing spondylitis and rheumatoid arthritis measured by ELISA.
S. Khalafpour, A. Ebringer, I. Abuljadayel and M. Corbett.
British Journal of Rheumatology, 1988; 27 (suppl 2): 86 - 89.
34. Ankylosing spondylitis and Klebsiella reactive arthritis.
A. Ebringer
Journal of Orthopaedic Rheumatology, 1988; 1: 243 - 250.
35. The relation between Klebsiella infection and ankylosing spondylitis.
A. Ebringer
In Balliere`s "Clinical Rheumatology": "The gut and rheumatic disease"
Ed. By P.J.Rooney, 1989 (August); 3: 321 - 338.
36. The use of enzyme immunoassay (EIA) and radiobinding assay to investigate the crossreactivity of Klebsiella antigens and HLA-B27 in ankylosing spondylitis patients and healthy controls.
M.G, Baines, A. Ebringer, H, Avakian, H. Samuel and D.C.O. James.
Scandinavian Journal of Rheumatology, 1990; 19: 341 - 349.
37. Theoretical models to explain the association of HLA-B27 with ankylosing spondylitis.
A. Ebringer
Scandinavian Journal of Rheumatology. 1990; suppl.87: 151 -163.
38. Ankylosing spondylitis and Klebsiella - the debate continues.
A. Ebringer.
The Journal of Rheumatology 1991; 18: 312 -313.
39. Ankylosing spondylitis is caused by Klebsiella: Evidence from immunogenetic, microbiologic and serologic studies.
A. Ebringer.
Rheumatic Disease Clinics of North America 1992; 18: 105 - 121.
40. Molecular Mimicry.
A. Ebringer
In "Encyclopedia of Immunology" Eds. I. Roitt and P.J. Delves.
W.B. Saunders: London 1992 Pgs:1084 - 1086.
41. IgA antibody response to Klebsiella in ankylosing spondylitis measured by immunoblotting.
F. Shodjai-Moradi, A. Ebringer and I. Abuljadayel.
Annals of Rheumatic Diseases 1992; 51: 151 - 163.
42. Ankylosing spondylitis and HLA-B27: Restriction fragment length polymorphism and sequencing of an HLA-B27 allele from an ankylosing spondylitis patient.
C.M. Higgins T. Lund, M.E. Shipley, A. Ebringer, M. Sadowska-Wroblewska and R.K. Craig.
Annals of Rheumatic Diseases 1992; 51: 855 - 862.
43. HLA and disease.
M. Baines and A. Ebringer.
Molecular aspects of Medicine 1992; 13: 263 - 378.
44. Serum IgA anti-Klebsiella antibodies in ankylosing spondylitis patients from Catalonia.
A. Collado, J. Gratacos, A. Ebringer, T. Rashid, A. Marti and J. Munoz-Gomez.
Scandinavian Journal of Rheumatology 1994; 23: 119 - 123.
45. Que va-t-il-se passer demain en ce qui concerne HLA-B27 et la spondylarthrite ankylosante?
A. Ebringer
Annales de Medicine Interne 1994; 145: 238 - 240 (Interview du moi)
46. Molecular mimicry: The geographical distribution of immune responses to Klebsiella in ankylosing spondylitis and its relevance to therapy.
Ebringer A, Ahmadi K, Fielder M, Rashid T, Tiwana H and Wilson C.
Clinical Rheumatology 1996; 15: Suppl 1, 57 - 61.
47. The use of a low starch diet in the treatment of patients suffering from ankylosing spondylitis.
Ebringer A, Wilson C.
Clinical Rheumatology 1996; 15: suppl 1, 62 - 66.
48. Antibodies to Klebsiella, Proteus and HLA-B27 peptides in Japanese patients with ankylosing spondylitis and rheumatoid arthritis.
Tani Y, Tiwana H, Hukuda S, Nishioka J, Fielder M, Wilson C, Bansal S and Ebringer A.
Journal of Rheumatology 1997; 24: 109 - 114.
49. Antibody responses to gut bacteria in ankylosing spondylitis, rheumatoid arthritis, Crohn`s disease and ulcerative colitis.
Tiwana H, Wilson C, Walmsley RS, Wakefield AJ, Smith MNS, Cox NL, Hudson MJ and Ebringer A.
Rheumatology International 1997; 17: 11 - 16.
50. Antibodies to Klebsiella pneumoniae in Dutch patients with ankylosing spondylitis and acute anterior uveitis and to Proteus mirabilis in rheumatoid arthritis.
Blankenberg-Sprenkels S, Fielder M, Feltkamp TEW, Tiwana H, Wilson C and Ebringer A.
Journal of Rheumatology 1998; 25: 743 - 747.
51. Molecular mimicry.
Ebringer A
In "Encyclopedia of Immunology - second edition"
Eds. IM Roitt and PJ Delves
Academic Press: London 1998 (pages 1736 - 1742)
52. Antibodies to Klebsiella pneumoniae nitrogenase reductase in patients with ankylosing spondylitis
Ahmadi K, Wilson C, Tiwana H, Shanmuganathan S, BinderA and Ebringer A.
Annals of Rheumatic Diseases 1998; 57: 441.
53. Antibodies to Klebsiella pneumoniae lipoposaccharide in patients with ankylosing spondylitis.
Ahmadi K, Wilson C, Tiwana H, Binder A and Ebringer A.
British Journal of Rheumatology 1998; 37: 1330 - 1333.
54. Characterization of the humoral immune response to Klebsiella species in inflammatory bowel disease and ankylosing spondylitis.
Tiwana H, Walmsley RS, Wilson C, Yiannakou JY, Ciclitira PJ, Wakefield AJ and Ebringer A.
British Journal of Rheumatology 1998; 37: 525 - 531.
55. Molecular mimicry, mad cows and arthritis: Is bovine spongiform disease due to bacteria?
Ebringer A
Science Spectra 2000; Issue 19: 46 - 53.
56. HLA molecules, bacteria and autoimmunity.
Ebringer A and Wilson C.
Journal of Medical Microbiology 2000; 49: 305 - 311.
57. Ankylosing spondylitis and diet.
Ebringer A and Wilson C.
In: "Food allergy and intolerance." Edited by Brostoff J and Challacombe C.
(Accepted for publication)
58. Correlation between the immune responses to collagen types I, III, IV, V and Klebsiella pneumoniae in patients with Crohn`s disease and ankylosing spondylitis.
Tiwana H, Natt RS, Benitez-Brito R, Shah S, Wilson C, Bridger S, Harbord M, Sarner M and Ebringer A.
Rheumatology; 2000 ( Accepted for Publication ).
