Occurrence of R Antigen Specific for Group a Type 3 Streptococci

Abstract

Three different protein antigens, designated by the letters M, T, and R, have been shown to be present on the surface of Group A streptococci (1). With respect to streptococcal infections the M antigens are the most important, since they are essential to the virulence of the microorganisms and stimulate the production of protective antibodies in the infected or immunized animal. Accordingly, the M antigens were selected as the basis for classification of Group A streptococci into serological types.The serological type of a given Group A streptococcus is usually determined by specific precipitin tests for M antigen. Other immunological reactions dependent upon this antigen-antibody system can also be used for identification of either M antigen or its antibody. Thus, under appropriate conditions the following procedures have been used to obtain information about the type-specific reactions of M antigens and their antibodies: agglutination reactions, active and passive protection tests, anaphylaxis experiments, bactericidal tests dependent upon phagocytosis of sensitized streptococci, and occasionally complement fixation tests (2).In those cases in which precipitin or agglutination tests give equivocal results in attempted identification of the M antigen, definitive information can be derived from the more biological mouse protection and bactericidal tests. Thus, T antigens, which cause confusion in agglutination tests for type specificity, can be clearly differentiated from M antigens by protection or bactericidal tests. Similarly, these procedures serve to establish the fact that 28 R antigen is not one of the M proteins.The present report concerns a newly identified antigen found in certain Type 3 strains. The experiments reported in this paper show that it is not an M antigen. So far it has not been found in any other type or group of streptococci, but only in Group A streptococci, Type 3. Since this antigen, like the 28 R antigen, appears to represent another protein antigen which can interfere

To harm or not to harm? On the evolution and expression of virulence in group A streptococci

“…These systems may therefore allow GAS to switch between phenotypes appropriate for asymptomatic colonization and superficial symptomatic infection, respectively, without genetic changes. The existence, heritability, and reversibility of such alternative phenotypic states are supported by data from several studies on GAS [29,[50][51][52][53]. (In contrast, the CovRS mutations often found in GAS isolated from invasive infections (discussed earlier), in virtue of being mutations are not part of the epigenetic phenotypic switch described here).…”

Interactions Between Rabbit Polymorphonuclear Leucocytes and Staphylococci

“…The two strains of Group A were poorly ingested as evidenced by the large number of extraceUular organisms at 180 minutes and showed no net reduction in viable counts. Strain D58Xll contains M protein whereas D58X contains little or no M protein (15). Strain 090R of Group B behaved in a similar fashion but appeared to be capable of more rapid proliferation in the presence of leucocytes.…”

Conserved DegP Protease in Gram-Positive Bacteria Is Essential for Thermal and Oxidative Tolerance and Full Virulence in Streptococcus pyogenes

“…Whether the reduction in virulence is due to a growth defect in the mouse (body temperature 36.5 to 38°C) or due to oxidative stress is unclear at present. Previous investigations indicate that in vitro passage of S. pyogenes may result in the loss of certain virulence factors, including M protein, and that in vivo mouse passage of these strains results in the restoration of these factors (21). Therefore, under the current nonpassaged conditions, it is surmised that the 35-fold increase in the LD 50 for the degP null mutant can be considered a conservative estimate of this mutation's effect.…”