Acute rheumatic fever is a noncontagious disease characterized by febrile, nonsuppurative inflammation, primarily of articular and cardiac tissues, less frequently affecting the skin and brain. The cerebral manifestation – Sydenham’s chorea – and the superficial manifestations – subcutaneous nodules and erythema marginatum – are limited to children and young adults.

Etiology and Treatment

The disease is caused by infection, most often of the throat, with type A beta-hemolytic strains of streptococcus. Fever, migratory joint pains and tachycardia, the most frequent symptoms, typically begin 1 to 3 weeks after the onset of untreated streptococcal pharyngitis. However, only 0.1 to 3.0 percent of untreated bouts of this infection result in a first attack of rheumatic fever. Consequently, various largely unidentified permissive factors must participate in initiating the immunologic pathogenesis of the disease.

First attacks of acute rheumatic fever can be prevented by timely treatment of the streptococcal infection with penicillin or another appropriate antibiotic, but such treatment does not influence the course of the disease once it has begun. Rheumatic fever recurs only as a result of a new infection with a pathogenic strain of streptococcus. Prophylactic antibiotic treatment diminishes, but does not eradicate recurrences (Taranta et al. 1964). The shorter the interval since the previous bout of rheumatic fever, the greater is the likelihood that a new attack will be elicited. An infection that occurs within 2 years of an attack has a 20 to 25 percent chance of inducing a recurrence. If the first attack does not affect the heart, a recurrence usually spares it as well, but if the heart has been involved, a second bout it likely to result in greater damage (Spagnuolo, Pasternack, and Taranta 1971).