Abstract
Rheumatic fever (RF) is the prototype of postinfectious autoimmune diseases. Similarities of structure and/or spatial conformation between Streptococcus pyogenes and human tissue proteins lead to autoimmune reactions due to molecular mimicry. The activation of T and B lymphocytes involves several genetically controlled molecules that act in both the innate and adaptive immune response. In this chapter, we describe the strains of bacteria that are more commonly involved in the development of RF worldwide as well as the genetic predisposition of diverse ethnic groups. The disease manifests in susceptible children and teenagers, usually starting as polyarthritis or Sydenham's chorea. This condition generally occurs several months after streptococcal infection. Erythema marginatum and subcutaneous nodules are rare cutaneous manifestation, and carditis is the most serious sequelae and can lead to severe valve damage and rheumatic heart disease (RHD). The immune mechanisms that lead to the diverse manifestations mentioned above are discussed. The diagnosis and treatment, particularly the revision of Jones Criteria in the era of Doppler echocardiography, as well as the perspective of vaccine development, are also presented.
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