Expression of both M protein and hyaluronic acid capsule by group A streptococcal strains results in a high virulence for chicken embryos

1996 ◽  
Vol 184 (4) ◽  
pp. 169-173 ◽  
Author(s):  
Karl-Hermann Schmidt ◽  
Elisabeth Günther ◽  
Harry S. Courtney
Keyword(s):  
Hyaluronic Acid ◽  
M Protein ◽  
Chicken Embryos ◽  
High Virulence ◽  
Group A ◽  
Hyaluronic Acid Capsule

scholarly journals STUDIES ON THE PATHOGENICITY OF GROUP A STREPTOCOCCI

1959 ◽  
Vol 110 (4) ◽  
pp. 617-628 ◽  
Author(s):  
Marie Judith Foley ◽  
W. Barry Wood
Keyword(s):  
Hyaluronic Acid ◽  
Virulent Strain ◽  
Critical Role ◽  
M Protein ◽  
Group A Streptococci ◽  
Streptococcal Infections ◽  
Full Complement ◽  
Group A ◽  
Hyaluronic Acid Capsule

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.

scholarly journals STUDIES OF PHAGOCYTOSIS OF GROUP A STREPTOCOCCI BY POLYMORPHONUCLEAR LEUCOCYTES IN VITRO

1960 ◽  
Vol 111 (3) ◽  
pp. 309-322 ◽  
Author(s):  
James G. Hirsch ◽  
Alice B. Church
Keyword(s):  
Hyaluronic Acid ◽  
M Protein ◽  
Rabbit Serum ◽  
Polymorphonuclear Leucocytes ◽  
Group A Streptococci ◽  
Test Conditions ◽  
Human Sera ◽  
Group A ◽  
Hyaluronic Acid Capsule

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.

scholarly journals Relative contributions of hyaluronic acid capsule and M protein to virulence in a mucoid strain of the group A Streptococcus.

1997 ◽  
Vol 65 (1) ◽  
pp. 64-71 ◽  
Author(s):  
A E Moses ◽  
M R Wessels ◽  
K Zalcman ◽  
S Albertí ◽  
S Natanson-Yaron ◽  
...  
Keyword(s):  
Hyaluronic Acid ◽  
Group A Streptococcus ◽  
M Protein ◽  
Group A ◽  
Hyaluronic Acid Capsule

scholarly journals Role of Group A Streptococcal Virulence Factors in Adherence to Keratinocytes

2000 ◽  
Vol 68 (3) ◽  
pp. 1215-1221 ◽  
Author(s):  
Gary L. Darmstadt ◽  
Laurel Mentele ◽  
Andreas Podbielski ◽  
Craig E. Rubens
Keyword(s):  
Hyaluronic Acid ◽  
Mutant Strain ◽  
Virulence Factors ◽  
M Protein ◽  
Skin Infections ◽  
Wild Type ◽  
Group A ◽  
Hyaluronic Acid Capsule ◽  
Type Strains

ABSTRACT To evaluate the role of putative group A streptococcal virulence factors in the initiation of skin infections, we compared the adherence of a wild-type M49-protein skin-associated strain to that of a series of 16 isogenic mutants created by insertional inactivation of virulence genes. None of the mutants, including the M-protein-deficient (emm mutant) strain, displayed reduced adherence to early-passage cultured human keratinocytes, but adherence of the mutant lacking hyaluronic acid capsule expression (has mutant) was increased 13-fold. In contrast, elimination of capsule expression in M2-, M3-, and M18-protein has mutants increased adherence only slightly (1.3- to 2.3-fold) compared to their respective wild-type strains. A mutant with inactivation of both emm andhas displayed high-level adherence (34.9 ± 4.1%) equal to that of the has mutant strain (40.7 + 8.0%), confirming the lack of involvement of M49 protein in attachment. Moreover, adherence of the M49-protein-deficient (emmmutant) and wild-type strains was increased to the same level (57 and 55%, respectively) following enzymatic digestion of their hyaluronic acid capsule. Adherence of mutants lacking oligopeptide permease (Opp) expression was increased 3.8- to 5.5-fold, in association with decreased cell-associated hyaluronic acid capsule. Finally, soluble CD46 failed to inhibit adherence of M49- and M52-serotype skin strains. We conclude that (i) bacterial M protein and keratinocyte CD46 do not mediate adherence of M49 skin-associated Streptococcus pyogenes to epidermal keratinocytes, (ii) hyaluronic acid capsule impedes the interaction of bacterial adhesins with keratinocyte receptors, (iii) modulation of capsule expression may be important in the pathogenesis of skin infections, and (iv) the molecular interactions in attachment of skin strains of S. pyogenesto keratinocytes are unique and remain unidentified.

scholarly journals STUDIES ON BACTERIOPHAGES OF HEMOLYTIC STREPTOCOCCI

1957 ◽  
Vol 106 (3) ◽  
pp. 365-384 ◽  
Author(s):  
Richard M. Krause
Keyword(s):  
Cell Wall ◽  
Hyaluronic Acid ◽  
Cell Walls ◽  
Receptor Site ◽  
Surface Proteins ◽  
Phage Antibody ◽  
Group A ◽  
Phage Receptor ◽  
Hyaluronic Acid Capsule ◽  
Isolated Cell

The host ranges of bacteriophages for group A, types 1, 6, 12, and 25 and group C streptococci have been determined. The findings indicate that the susceptibility to these phages is primarily a group-specific phenomenon, although it is modified by several factors such as the hyaluronic acid capsule, lysogeny, and possibly the presence of surface proteins. Phage antibody studies indicate that while the group A phages are antigenically related, they are distinct from the group C phage. This is in agreement with the observation that group A phages are not specific for their homologous streptococcal types. The purified group C carbohydrate inactivates group C phage but not the group A phages, thus suggesting that the carbohydrate, a component of the cell wall, may serve as the phage receptor site. It has not been possible to inactivate the group A phages with group A carbohydrate. Phage lysis of groups A and C streptococci is accompanied by fragmentation of the cell wall since the C carbohydrate has been identified serologically and chemically in the supernate of centrifuged lysates. The immediate lysis of groups A and C hemolytic streptococci and their isolated cell walls by an accesory heat-labile lytic factor in fresh group C lysates is also described.

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
Keyword(s):  
Hyaluronic Acid ◽  
Virulence Factor ◽  
Group A Streptococci ◽  
Group A ◽  
Hyaluronic Acid Capsule

scholarly journals Emergence of a New Highly Successful Acapsular Group A Streptococcus Clade of Genotype emm89 in the United Kingdom

mBio ◽  
2015 ◽  
Vol 6 (4) ◽  
Author(s):  
Claire E. Turner ◽  
James Abbott ◽  
Theresa Lamagni ◽  
Matthew T. G. Holden ◽  
Sophia David ◽  
...  
Keyword(s):  
United Kingdom ◽  
Hyaluronic Acid ◽  
Genome Sequencing ◽  
Virulence Factors ◽  
Invasive Disease ◽  
Whole Genome ◽  
The United Kingdom ◽  
Streptolysin O ◽  
Group A ◽  
Hyaluronic Acid Capsule

ABSTRACTGroup AStreptococcus(GAS) genotypeemm89 is increasingly recognized as a leading cause of disease worldwide, yet factors that underlie the success of thisemmtype are unknown. Surveillance identified a sustained nationwide increase inemm89 invasive GAS disease in the United Kingdom, prompting longitudinal investigation of this genotype. Whole-genome sequencing revealed a recent dramatic shift in theemm89 population with the emergence of a new clade that increased to dominance over previousemm89 variants. Temporal analysis indicated that the clade arose in the early 1990s but abruptly increased in prevalence in 2008, coinciding with an increased incidence ofemm89 infections. Although standard variable typing regions (emmsubtype,teetype,softype, and multilocus sequence typing [MLST]) remained unchanged, uniquely the emergent clade had undergone six distinct regions of homologous recombination across the genome compared to the rest of the sequencedemm89 population. Two of these regions affected known virulence factors, the hyaluronic acid capsule and the toxins NADase and streptolysin O. Unexpectedly, and in contrast to the rest of the sequencedemm89 population, the emergent clade-associated strains were genetically acapsular, rendering them unable to produce the hyaluronic acid capsule. The emergent clade-associated strains had also acquired an NADase/streptolysin O locus nearly identical to that found inemm12 and modernemm1 strains but different from the rest of the sequencedemm89 population. The emergent clade-associated strains had enhanced expression of NADase and streptolysin O. The genome remodeling in the new clade variant and the resultant altered phenotype appear to have conferred a selective advantage over otheremm89 variants and may explain the changes observed inemm89 GAS epidemiology.IMPORTANCESudden upsurges or epidemic waves are common features of group A streptococcal disease. Although the mechanisms behind such changes are largely unknown, they are often associated with an expansion of a single genotype within the population. Using whole-genome sequencing, we investigated a nationwide increase in invasive disease caused by the genotypeemm89 in the United Kingdom. We identified a new clade variant that had recently emerged in theemm89 population after having undergone several core genomic recombination-related changes, two of which affected known virulence factors. An unusual finding of the new variant was the loss of the hyaluronic acid capsule, previously thought to be essential for causing invasive disease. A further genomic adaptation in the NADase/streptolysin O locus resulted in enhanced production of these toxins. Recombination-related genome remodeling is clearly an important mechanism in group AStreptococcusthat can give rise to more successful and potentially more pathogenic variants.

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