Many studies have been made of tissue alterations due to infections with Group A streptococci in laboratory animals. Cardiac lesions characterized by muscle necrosis, myocarditis, and giant-cell formation have been reported in a variety of laboratory animals following injections of living Group A streptococci and some of their products.1l Some of these lesions were described as quite similar to the Aschoff bodies of rheumatic carditis.4 The mechanism of formation of these cardiac lesions has been attributed to toxic effects of streptococcal products,6 7 to immune response to streptococcal components (hypersensitivity or autoimmunity) ,10 or to combinations of these processes. Among these studies, the pharyngeal cavity of animals was used as the portal of entry of streptococci only in that of Glaser et al.,11 who found cardiac lesions within 72 hr. of a single intratonsillar injection of virulent Group A streptococci. These lesions were focal, and showed muscle necrosis, infiltrations of mononuclear cells, and occasional giant cells. No streptococci could be isolated from such lesions, and it was concluded that the lesions were probably not caused by an immunologic process."' The present report describes the induction of lesions in cardiac and other tissues of rabbits following injection, by intratonsillar and other routes, of streptococcal extracellular products (SEP) obtained from Group A streptococci grown in steady-state culture. These lesions occured soon after single injections of these materials and probably reflect direct toxic effect on the cells of these tissues.

Various streptococcal species produce an haemosensitizing factor during the logarithmic phase of growth. A variety of mammalian cells sensitized with this factor become agglutinated following the addition of antistreptoccocal serum and also undergo cytopathic changes in the presence of complement. The haemosensitizing factor is thermostable and is unaltered by trypsin, papain, chymotrypsin, lipases or ribonucleases. Attempts to destroy the binding sites on the cell membrane by treatment with phospholipase C from Clostridium welchii or by neuraminidase failed. Treatment with trypsin or papain on the other hand markedly increased the binding capacity of red blood cell for the haemosensitizing factor. Studies on the nature of the binding sites on the erythrocyte membrane of the haemosensitizing factor suggest that cholesterol and phospholipids constitute some of the binding sites for this factor.