Pathphysiology

Streptococcal upper respiratory infection leads to production of antibodies. An abnormal immunological response to the upper respiratory infection with Beta- hemolytic streprococci resulting in acute rheumatic fever. This affects the heart and joints. Rheumatic fever episodes are marked by carditis involving all layers of the heart i.e. the endocardium, myocardium and pericardium. Rheumatic endocarditis is found in the valves with the thickening and erosion of valve leaflets. This may further lead to formation of vegetation, fibrous thickening of valve leaflets, fusion of commissures and chordae tendinae and fibrosis of papillary muscles. Valve leaflets may fuse and become thickened or even calcified resulting in stenosis. Reduction of mobility of valve leaflets may result in regurgitation as there is failure of the leaflets to oppose. Myocardial involvement is characterized by Aschoffs bodies-nodules formed by a reaction to inflammation with accompanying swelling an fragmentation of collagen fibers. Aschofl's bodies become more fibrous and scar tissue is formed in the myocardium. Rheumatic pericarditis affects both layers of pericardium. The pathophysiologic changes in the heart may occur as a result of an initial attack of Rh fever. Recurrent infection cause further damage.

Rheumatic fever lesions are systemic involving joints, skin, CNS and may be lungs.