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One of the most intriguing pathogenetic puzzles of the many illnesses with unsolved origins-even in this age of molecular biology-is rheumatic fever. Despite a half-century of intensive and productive, basic, epidemiological, and clinical research, the precise mechanism(s) remain unknown. Of equal importance is that the opportunity to employ research findings to benefit potentially affected patients and populations is extremely limited. In this issue of Clinical Infectious Diseases, McDonald et al. [1] report epidemiologic and microbiologic data from their household studies of cases of streptococcal infection among Aboriginal people in northern Australia, a population group that experiences an extraordinarily high incidence of acute rheumatic fever (ARF). On the basis of their observations, the authors raise critical questions regarding the nature of the antecedent streptococcal infections that give rise to ARF. For many years, it has been established dogma that ARF only follows upper respiratory tract infection with group A streptococci (GAS), in contrast to post-

Antecedent Streptococcal Infection in Acute Rheumatic Fever