Several possible mechanisms of chronic inflammatory arthritis that might be initiated by infectious agents are discussed. Some recent information on mycoplasma infections, long-term virus infections, and shed bacterial components provides the bases for new experimental approaches. Currently, evidence of involvement of mycoplasma or viral agents in rheumatoid arthritis is tenuous. Chronic peptidoglycan-immune-complex formation is a consideration that has been discussed, but only recently pursued in depth. It may well be that experimental studies on the infectious etiology of rheumatoid arthritis will be revitalized through an appreciation of the bacterial antigen load in the gastrointestinal tract. The perimental vehicles for testing this possibility are available and should be directly applicable at the clinical level.