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Necessity for Treatment
Another Part of the Recipe
A Rationale for Using Antibiotics to Treat Rheumatic Disease
One of the keys to antibiotic therapy is the concept of an infectious etiology and the focus on reducing or eliminating the antigen. Physicians who use antibiotic therapy to "treat an infection" get a better result than those who do not. Compared to the success rates of other therapies, this one shows comparable or better results to other DMARDs, and its long term safety has been demonstrated with acne.
The volume of published medical litera-ture on this topic is enormous, spans decades and comes from all over the world. Although the infectious etiology is not considered proven, the current volume of evidence precludes its dismissal.
The following paragraphs are quotes from published medical journals, dictionaries and textbooks. These are not our words, but those of your colleagues.
"Scientists don't know the cause, but they believe (RA) results from a combination of genetic factors that make a person susceptible to the disease and some type of environmental trigger-possibly an infectious agent such as a virus or bacterium." (1997-NIH-USA)1
"Candidate bacteria (for RA) include mycoplasma, mycobacteria, and various enteric organisms. It should be pointed out that failure to culture an organism from a joint does not exclude its involvement in RA." (1993-Arthritis Foundation-USA)2
"The occurrence of various Mycoplasma and Ureaplasma species in joint tissues of patients with rheumatoid arthritis, sexually transmitted reactive arthritis, and other human arthritides can no longer be ignored...M. fermentans has been detected by PCR in the synovial fluid of patients with inflammatory arthritis...M. genitalium has been implicated as an etiologic agent in certain human joint diseases... an association with U. urealyticum, M. pneumoniae, M. salivarium, and M. hominis that localized in joint tissue, frequently with destructive arthritis...In the absence of suitable mycoplasmacidal chemotherapeutic agents, vigorous and sustained chemotherapy with the most active antibiotic is the current method of choice." (1997-CDC-USA)3
"It has been suggested that related superantigen-like molecules may exist in mycoplasmas of human origin triggering autoimmune and other inflammatory pathologies." (1997-CDC-USA)3
"If the infectious hypothesis proves to be correct the treatment of RA will need to be completely revised, and the consequences for the pharmaceutical industry will be enormous. It could become unethical to use steroids, or agents which block prostaglandin synthesis, as we cannot be sure they do not promote proliferation of the organism, and so in the long term lead to more severe disease. Instead we will need to devise antibiotic regimens and immunotherapeutic protocols." (1993-Annals of Rheumatic Diseases-England)4
"Identification of antibodies to M. arthritidis and M. fermentans in the sera of patients with rheumatoid arthritis have been established." (1985-Russian Jour.)5
"Both mycoplasma and chlamydia are capable of inducing arthritis in animal models and human beings." (1995-Lancet-Canada)6
"The presence of M. fermentans in the joint is associated with inflammatory rheumatic disorders of unknown cause, including rheumatoid arthritis." (1996 - J Clinical Pathology-England)7
"It is speculated that there is an initial response to a particular antigen, followed by an infiltration of inflammatory cells with subsequent proliferation in the synovium...These results suggest that the immune response in RA is not random, but rather is driven by common stimuli." (1996-Arthritis & Rheumatism-Japan)8
"M fermentans is often present in affected joints in rheumatoid arthritis, and it is postulated that the chronic course of the inflammatory process is due to a hypersensitivity response to the organism." (1970-Lancet-England)9
"Mycoplasma was recovered from the synovial fluid in an active phase of the disease even when no antibodies could be detected by conventional methods." (1971-Annals of Rheumatic Diseases-Finland) 10
"It is clear that the issue of the role of mycoplasmas in inflammatory rheumatic disorders of unknown cause, including rheumatoid arthritis, can no longer be ignored." (1996-J Clinical Pathology-England, France)11
"2 recent editorials in the Journal of Rheumatology reflect that the dominant view among rheumatology investigators that RA is caused by a microbial agent. Future research must be freed from the constraints of postulates inherited from a previous era." (1992-Journal of Rheu-matology-New Zealand) 12
"Since the autoimmune manifestations of RA are virtually identical to those seen in chronic mycobacterial infections, it has been proposed that RA is, like Whipples Disease or the Spirochaetoses, a slow bacterial infection... We would also expect that immunosuppressive drug regimens would prevent the resolution of the triggering infection and thus enable continued joint damage." (1992 Clinical Experimental Immunology-England)13
"A spirochete is the etiologic agent of Lyme disease, a condition that occasionally mimics rheumatoid arthritis, indicat(ing) that infectious agents must still be considered as possible exogenous agents that can induce the inflammatory process in rheumatoid arthritis." (1984-Annals of Internal Medicine-USA)14
"There are interesting parallels concerning DNA-antibodies and DNA-repair between experimental mycoplasma arthritis and human systemic lupus erythematosus and rheumatoid arthritis." 1977-Fortscher Med-Germany)15
Ed: Testing for mycoplasma takes special skills and specialized laboratory methods. A lab unskilled in mycoplasma testing can lead to a false negative result.
1 E Ben-Ari, B Weldon, Nationwide Hunt for RA Genes Launched, NIH News Release, Sept 4, 1997.
2 RL Wilder, Etiology of RA, Primer on Rheu Dis, 10th ed, 1993, 87.
3 J Baseman, J Tully, Mycoplasmas: Sophisticated, Re-emerging and Burdened by Their Notoriety, Emerg Infect Dis, 3:1, 1997.
4 GAW Rook et al, A reappraisal of the evidence that RA and several other idiopathic diseases are slow bacterial infections, Ann Rhu Dis, 1993; 52:S30-S38.
5 LG Gorina, Detection of Mycoplasma arthritidis and Mycoplasma fermentans antibodies in RA patients by an immunoenzyme method, Zh Mikro Epi Immunobiol, 1985, 6: 48-52.
6 RJR McKendry, Is RA caused by an infection? Lancet, 1995, 345:5, 1319-1320.
7 T Schaeverbeke, Mycoplasma fermentans, but not M penetrans, detected by PCR assays in synovium from patients with RA and other rheumatic disorders, J Clin Path, 1996; 49:10, 824-828.
8 Y Ikeda et al, High frequencies of identical T cell clonotypes in synovial tissues of RA patients suggest the occurrence of common antigen-driven immune responses, Arth & Rhu, 1996; 39:3, 446-453.
9 MH Williams et al, Possible Role of Mycoplasma fermentans in Pathogenesis of RA, Lancet, Aug 8, 1970, 277-280.
10 E Jansson et al, An 8-yr Study on Mycoplasma in RA, Ann Rhu Dis, 1971, 30: 506-508.
11 D Taylor-Robinson, T Schaeverbeke, Mycoplasmas in RA and Other Human Arthritides, J Clin Path, 1996; 49, 781-782.
12 PLJ Tan, MA Skinner, Microbial Cause of RA: Time to Dump Koch's Postulates, J Rhu, 1992; 19:8, 1170-71.
13 J McCulloch et al, Rheumatoid Arthritis: how well do the theories fit the evidence? Clin Exp Immunol, 1993; 92:1-6.
14 NIH Conference, Rheumatoid Arthritis: Evolving concepts of pathogenesis and treatment, Ann Int Med; 1984, 101:810-824.
15 G Klein, Pathogenic concept of experimental mycoplasma arthritis, Fortscher Med, 1977; 95:7, 408-413.
Current thought stresses the process of rheumatoid disease rather than the origin or responsible trigger. This treatment focuses on the theory that the initial trigger is an infectious organism and treatment cannot be completely effective, even with antibiotic therapy, if the trigger is ignored in favor of the process.
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