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Although rheumatoid arthritis (RA) has been widely suspected to have an infectious etiology, this hypothesis has remained difficult to prove. Epstein-Barr virus, parvoviruses, and retroviruses are considered by some investigators to be the primary candidates. An increasing body of data, on the other hand, appears to implicate bacteria or their products in the syndrome. Important evidence has surfaced in support of this view.
Lyme arthritis, a
disease caused by a bacterium, can mimic RA. Bacteria and their products have been conclusively linked to many forms of inflammatory “reactive” arthropathies. RA-like diseases can be induced in certain inbred strains of rats with bacterial cell-wall fragments, e.g., streptococcal and other bacterial peptidoglycans. Immunologic relationships between host and bacterial peptidoglycans, relevant to RA, have been well documented, e.g., heat shock proteins, bacterial IgG Fc binding proteins, and rheumatoid factors. These data not only support the hypothesis that bacteria may play an important role in RA but also indicate that current concepts of infection and autoimmune
disease are broadening and overlapping.