Bacteriologic and Immunologic Studies on Patients With Hemolytic Streptococcic Infections as Related to Rheumatic Fever

Bacterial determinants of persistent throat colonization and the associated immune response in a primate model of human group A streptococcal pharyngeal infection

“…Indeed, to the extent that persistence in the throat and the consequent acquired immune responses are critical events leading to acute rheumatic fever, the model accurately reproduces important features of human disease. In this respect, the striking similarities to human illness include: (1) in the absence of therapy, recovery of wild-type GAS from the throat for extended periods of time after exposure (Rothbard et al, 1948;Siegel et al, 1961); (2) the early appearance of anti-SLO and slightly delayed appearance of anti-M protein antibody; (3) the inconsistent development of opsonic antibody and the ineffectiveness of the immune response in clearance of the organism from the pharynx (Mote and Jones, 1941;Rothbard et al, 1948;Stollerman et al, 1956;Denny et al, 1957); and (4) the stimulation of typespecific immunity by prolonged throat colonization (Wannamaker et al, 1953;Lancefield, 1959).…”

“…Untreated GAS pharyngitis leads to a humoral immune response with the development of antibodies to a variety of streptococcal components including streptokinase, streptolysin O (SLO), DNAase, hyaluronidase and the major surface protein, M protein (Rothbard et al, 1948;Stollerman et al, 1956;Denny et al, 1957;Siegel et al, 1961). The kinetics and specificity of many of the antibody responses have been characterized in human infection (Mote and Jones, 1941;Rothbard et al, 1948;Stollerman et al, 1956;Denny et al, 1957).…”

“…The kinetics and specificity of many of the antibody responses have been characterized in human infection (Mote and Jones, 1941;Rothbard et al, 1948;Stollerman et al, 1956;Denny et al, 1957). In the susceptible host, autoreactivity of this response (in particular crossreacting anti-M protein antibody) may contribute to the pathogenesis of acute rheumatic fever (Kaplan and Svec, 1964;Zabriskie et al, 1970;Krisher and Cunningham, 1985;Cunningham et al, 1989).…”

Studies on the Bacteriophages of Hemolytic Streptococci

“…Experiments are now in progress to demonstrate that the protein isolated here is antigenic, inducing the formation in rabbits of type-specific precipitins and protective antibodies. The need for elucidating the characteristics of M protein is obvious, since the evidence strongly suggests that it contributes to the virulence of Group A hemolytic streptococci in natural infections of man (28)(29)(30)(31), and in experimental infections of animals (32)(33)(34)(35).…”

The Determination of Antibody to Group a Streptococcal Polysaccharide in Human Sera by Hemagglutination

“…Since Lancefield described the C carbohydrate antigen of hemolytic streptococci (7), a number of investigators have reported finding precipitating antibody to A polysaccharide in sera from normal persons, patients convalescent from streptococcal infection, and patients with rheumatoid arthritis, rheumatic fever, and glomerulonephritis (8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18). In all but two of these investigations, crude acid extracts of Group A streptococci were used as antigen and it is likely that the precipitating antibody detected was a composite, representative of multiple streptococcal cellular antigens.…”