"The most controversial candidates for RA inflammatory triggers are the mycoplasmas. . . . Because mycoplasmas lack cell walls, they can camouflage themselves in their hosts's own histocompatability antigens. Thus, they're extremely difficult to culture from synovial fluid."
In the same article, Dr. Paul Plotz, chief of connective tissue diseases in NIADDK's arthritis and rheumatism branch, says:
"Though no convincing evidence, direct or indirect, implicates a particular infectious agent in RA, most of us share a conviction with Dr. Brown that RA will turn out to have a connection to infection."
Dr. GAW Rook et al. in A reappraisal of the evidence that rheumatoid arthritis and several idiopathic diseases are slow bacterial infections (Annals of the Rheumatic Diseases 1993;52:S30-S38) has this to say:
"If the infection 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 the proliferation of the organism, and so in the long term lead to more severe disease. Instead we will need to devise antibiotic regimens and immuno-therapeutic protocols."
Dr. Pnina Langevitz, et al in Minocycline in Rheumatoid Arthritis (Isr J Med Sci 1996;32:327-330), says at the end of the article, which is a followup to her first one:
"Based on our more than 5 years' experience with this drug and on the three double-blind studies, it seems minocycline is an effective and adequately tolerated drug in patients with rheumatoid arthritis, including those who did not respond to previous DMARD therapy."