scholarly journals Hyaluronic acid capsule is a virulence factor for mucoid group A streptococci.

1991 ◽  
Vol 88 (19) ◽  
pp. 8317-8321 ◽  
Author(s):  
M. R. Wessels ◽  
A. E. Moses ◽  
J. B. Goldberg ◽  
T. J. DiCesare
1959 ◽  
Vol 110 (4) ◽  
pp. 617-628 ◽  
Author(s):  
Marie Judith Foley ◽  
W. Barry Wood

A quantitative study of the combined antiphagocytic effects of the M protein and the hyaluronic acid capsules of four strains of Group A streptococci revealed the following facts relating to their intraperitoneal virulence in mice and rats: 1. The most virulent strain, S23M (matt), produced both a large hyaluronic acid capsule and a full complement of M protein, the combined effects of which rendered the organism highly resistant to surface phagocytosis. 2. The slightly less virulent strain, T14/46 (matt virulent) was somewhat more susceptible to surface phagocytosis owing to the fact that its smaller capsule was less antiphagocytic than that of the S23M organism. 3. The glossy variant of the S23 strain (S23G), which ranked third in virulence, was still more susceptible to surface phagocytosis because of its lack of detectable M substance. Its large hyaluronic acid capsule, however, was capable of protecting it against phagocytosis on glass. 4. The least virulent strain, T14 (matt avirulent), was the most susceptible of all to phagocytosis. Though it possessed both M substance and capsule, which together prevented its phagocytosis on glass, each of them was shown to be quantitatively and functionally deficient as compared to Strain S23M. The differences in phagocytability, which appear to be directly related to the pathogenicity of the organisms, could be adequately demonstrated in vitro only by phagocytic tests designed to measure surface phagocytosis in the absence of opsonins. This fact is in keeping with the observation, previously reported, that surface phagocytosis plays a critical role in the defense of the host, particularly during the earliest stages of experimental streptococcal infections. Its possible relation to suppuration during the later stages of infection is also discussed.


mBio ◽  
2012 ◽  
Vol 3 (6) ◽  
Author(s):  
Anthony R. Flores ◽  
Brittany E. Jewell ◽  
Nahuel Fittipaldi ◽  
Stephen B. Beres ◽  
James M. Musser

ABSTRACTGroup A streptococcus (GAS) causes human pharyngitis and invasive infections and frequently colonizes individuals asymptomatically. Many lines of evidence generated over decades have shown that the hyaluronic acid capsule is a major virulence factor contributing to these infections. While conducting a whole-genome analysis of thein vivomolecular genetic changes that occur in GAS during longitudinal human pharyngeal interaction, we discovered that serotypes M4 and M22 GAS strains lack thehasABCgenes necessary for hyaluronic acid capsule biosynthesis. Using targeted PCR, we found that all 491 temporally and geographically diverse disease isolates of these two serotypes studied lack thehasABCgenes. Consistent with the lack of capsule synthesis genes, none of the strains produced detectable hyaluronic acid. Despite the lack of a hyaluronic acid capsule, all strains tested multiplied extensivelyex vivoin human blood. Thus, counter to the prevailing concept in GAS pathogenesis research, strains of these two serotypes do not require hyaluronic acid to colonize the upper respiratory tract or cause abundant mucosal or invasive human infections. We speculate that serotype M4 and M22 GAS have alternative, compensatory mechanisms that promote virulence.IMPORTANCEA century of study of the antiphagocytic hyaluronic acid capsule made by group A streptococcus has led to the concept that it is a major virulence factor contributing to human pharyngeal and invasive infections. However, the discovery that some strains that cause abundant human infections lack hyaluronic acid biosynthetic genes and fail to produce this capsule provides a new stimulus for research designed to understand the group A streptococcus factors contributing to pharyngeal infection and invasive disease episodes.


2000 ◽  
Vol 28 (4) ◽  
pp. 221-226 ◽  
Author(s):  
Markus Woischnik ◽  
Bettina A (Leonard) Buttaro ◽  
Andreas Podbielski

1948 ◽  
Vol 88 (3) ◽  
pp. 325-342 ◽  
Author(s):  
Sidney Rothbard

Five strains of encapsulated group A streptococci of different serological types, each with a glossy and a matt variant, were studied to compare the rôles of the M substance and the hyaluronic acid capsule in virulence of these microorganisms. The results indicated that both contribute to the virulence of group A streptococci but that the M antigen is the more fundamental factor. Encapsulated variants, both glossy and matt, were slightly less susceptible to phagocytosis than those from which the capsule had been removed with hyaluronidase. Glossy variants, containing no M substance, were readily phagocyted; matt, M-containing variants were resistant to phagocytosis except in the presence of anti-M serum when they became fully susceptible. Only the M-containing, matt strains were mouse-virulent. Mice were protected against infections with these strains: (a) By removal of the capsule with hyaluronidase, which resulted in slight protection, but only against 10 M.L.D. Early and intensive treatment was required to produce this effect; i.e., simultaneous injection of enzyme and streptococci followed by prolonged enzyme therapy. (b) By a single injection of anti-M serum administered the day before inoculation of the streptococci, which resulted in protection against 100,000 M.L.D. (c) By combined use of enzyme and anti-M serum, an additive effect of the two protective agents occurred, which resulted in protection against 1,000,000 M.L.D.


1960 ◽  
Vol 111 (3) ◽  
pp. 309-322 ◽  
Author(s):  
James G. Hirsch ◽  
Alice B. Church

Studies have been made on phagocytosis and killing of Group A streptococci during mixing with suspensions of leucocytes in vitro. Under appropriate test conditions an anti-phagocytic effect can be demonstrated for the streptococcal hyaluronic acid capsule as well as for its M protein. The results obtained suggest an explanation for the suitability of human, but not rabbit, blood for opsonophagocytic tests designed to measure type-specific streptococcal antibodies. Human sera contain a factor which counteracts the anti-phagocytic effects of streptococcal hyaluronic acid capsules, and hence human blood serves well for detection of antibodies which combine with the only other phagocytosis-resisting component of this microorganism, namely M protein. In contrast, rabbit sera contain none of this factor, and addition of antibody to M protein to phagocytic test systems employing rabbit serum does not necessarily render the streptococci susceptible to engulfment by white cells, since the hyaluronic acid capsule may continue to interfere with phagocytosis. The nature of the human serum factor which opsonizes encapsulated streptococci is unknown. It does not appear to be an antibody or an enzyme capable of depolymerizing hyaluronic acid.


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