The demonstration of secondary antigens and antibodies in rheumatic fever recently reported by Coburn and Pauli1 of Columbia University is clinical confirmation of a speculative hypothesis proposed a decade or more ago by immunologists.2 If confirmed, this renaissance of the speculative theory of secondary anaphylaxis and immunity may lead to practical diagnostic and therapeutic methods in numerous infectious diseases.
The New York clinicians picture the evolution of rheumatic attacks in three distinct phases. Phase 1 is an acute pharyngeal infection usually of not more than three days' duration, hemolytic streptococci being the causative agent. This is followed by an afebrile, symptom-free period (phase 2) commonly lasting about fourteen days. Phase 3, the period of acute rheumatic symptoms, often shows one or more cycles of activity.
From their point of view the second period (phase 2) is the crucial stage in the genesis of rheumatic symptoms. Only one serologic