ABSTRACT
This chapter reviews some of the evidence that continues to make concepts of autoimmunity an attractive hypothesis to explain at least some of the clinical and pathological expressions of rheumatic fever (RF). Despite the elusiveness of the pathogenesis of RF, there are a few well-established requirements for its development: the presence of the group A streptococcus, the streptococcal antibody response indicative of actual recent infection, the persistence of the organism in the pharynx for a sufficient period of time, and the location of the infection in the throat. The environmental, bacterial, and host factors which appear to play a role in the development of RF are important primarily because they are related to the incidence of streptococcal infection. Perhaps the most convincing evidence is the prevention of both initial and recurrent attacks of RF by, in the former case, penicillin therapy and, in the latter, continuous prophylaxis of streptococcal infections.
