Studies of Diphtheria Antitoxin in Rheumatic Fever

The importance of group A hemolytic streptococcal infections in the pathogenesis of rheumatic fever is widely recognized, but little is known of the mechanism by which the streptococcal infection gives rise to the disease. The concept that an antigen-antibody interaction may be involved in the origin of the pathologic processes has received increasing attention, and recent antibody studies (1, 2) provide suggestive evidence in support of this point of view. For example, studies in several laboratories dealing with a variety of streptococcal antigens have demonstrated that the mean antibody response of a group of rheumatic fever patients to these antigens is greater than that of a comparable group of patients with uncomplicated streptococcal disease (3-6). In view of these findings, it is of importance to determine whether the hyperreactivity of rheumatic subjects is limited to antigens derived from the streptococcus or is a reflection of a fundamental difference which would be demonstrable in an enhanced response to a variety of different antigens. Because it has been impossible in natural infections with the hemolytic streptococcus to obtain accurate quantitative information concerning the antigenic stimulus, one of the possible explanations of the relative enhancement of the immune response in rheumatic subjects is that these individuals may have been exposed to comparatively greater quantities of antigen. At the present time it is difficult to approach this problem experimentally using streptococcal antigens, but other antigens are available, some in highly purified