RF is an acute inflammatory disease which follows group A b hemolytic streptococcal infection of the throat. Its most common manifestation is arthritis, most serious- carditis, most curious- chorea and most rare and inconsequential- subcutaneous nodule and erythema marginatum.

Age : Peak occurrence is between 5-15 years. It is lower in developing countries. It is rare in adults.

Poor socioeconomic status: Poor health care, non-treatment or late treatment of streptococcal throat infection, over-crowding, industrialization, urbanization.

Familial predisposition: It is 7 times more common in monozygotic twins than dizygotic twins. There are increased chances in blood relatives.

Recurrence : It may occur after subsequent streptococcal infection.

RF is a non-suppurative, post-streptococcal event. It occurs following streptococcal infection of throat, but never after skin infection. Streptococci attach to the receptor on the epithelium of the throat with the help of the lipoteichoic acid on the fimbria. M Protein of the fimbria makes ingestion by phagocytes difficult and thus increase the virulence. Rheumatogenicity of the infecting strain of streptococci decides the chances of RF or its recurrences. Streptococci remain localized to the throat but their products diffuse out- some of these products are cardiotoxic.

Some theories for pathogenesis of RF, postulated are: -

Theory of autoimmunity: Several antigens of streptococci cross react with human tissue antigen and therefore are recognized as "self". Erroneous recognition as "foreign" lead to - auto immune mechanism.

Theory of mimicry: - Mimicking antigens to avoid detection. Lymphocytes at site of infection activate the "Forbidden Clone" - with autoimmune activity. Streptococcal antigen transforms local lymphocytes into blast cells, which cause the damage.

Arthus like reaction: Decreased quantities of C1q, C3 & C4 in the synovial fluid suggest that complement fixing with antigen antibody damage the tissues.

Probably more than one mechanism is involved.