Rheumatic fever is a multisystem inflammatory disease that occurs as a dela
yed sequelae to group A streptococcal pharyngitis, The important clinical m
anifestations are migratory polyarthritis, carditis, chorea, subcutaneous n
odules and erythema marginatum occurring in varying combinations. The patho
genesis of this disorder remains elusive: an antigenic mimicry hypothesis b
est explains the affliction of various organ systems after a lag period fol
lowing pharyngeal infection. In its classic milder form, the disorder is la
rgely self-limited and resolves without sequelae, but carditis may be fatal
in severe forms of the disease. Chronic and progressive damage to the hear
t valves leads to the most important public health manifestations of the di
sease. Anti-inflammatory agents provide dramatic clinical improvement, but
do not prevent the subsequent development of rheumatic heart disease. The r
ole of corticosteroids in treatment of carditis is uncertain and controlled
studies have failed to demonstrate improved long term prognosis, Chorea, o
nce considered a benign self-limited disease, is now felt to require more a
ggressive treatment, in particular with sedatives. Prevention of first and
subsequent attacks of rheumatic fever is the mainstay in the limited arsena
l available to alter the natural history of this disease.