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PubMed1997

Genetic diversity in temperate bacteriophages of Streptococcus pyogenes: identification of a second attachment site for phages carrying the erythrogenic toxin A gene.

Bacteriophage T12, the prototypic bacteriophage of Streptococcus pyogenes carrying the erythrogenic toxin A gene (speA), integrates into the bacterial chromosome at a gene for a serine tRNA (W. M. McShan, Y.-F. Tang, and J. J. Ferretti, Mol. Microbiol. 23:719-728, 1997). This phage is a member of a group of related temperate phages, and we show here that not all speA-carrying phages in this group use the same attachment site for integration into the bacterial chromosome. Additionally, other phages in the group use the same serine tRNA gene attachment site as phage T12 and yet do not carry speA. The evidence suggests that recombination between phage genomes has been an important means of generating diversity and disseminating virulence-associated genes like speA.

Attachment Sites, Microbiological↗

PubMed1998

Resistance of Streptococcus pyogenes to erythromycin and related antibiotics in Italy. The Italian Surveillance Group for Antimicrobial Resistance.

A survey of antimicrobial resistance in Streptococcus pyogenes, performed within the framework of a national surveillance program, has revealed a dramatic increase in resistance of S. pyogenes to erythromycin in most areas of Italy. In virtually all the centers that provided data for 3 consecutive years, the incidence of erythromycin-resistant strains increased twofold to 20-fold from 1993 to 1995 and was greater than 30% in five of the 14 centers participating in the study. The clonality of erythromycin-resistant isolates was studied in 15 strains isolated from different patients at the Institute of Microbiology of Verona University (Verona). The features of the Verona isolates and the substantially different rates of erythromycin and clindamycin resistance observed in most centers suggest that the spread of different resistance genes in multiple clones might be occurring throughout the country.

Anti-Bacterial Agents↗

PubMed2000

Genomic differences in Streptococcus pyogenes serotype M3 between recent isolates associated with toxic shock-like syndrome and past clinical isolates.

Genomic differences among past Streptococcus pyogenes serotype M3 strains isolated in 1973 and before from patients with streptococcal pharyngitis, recent (1990s) serotype M3 clinical isolates from patients with pharyngitis, and recent M3 isolates from patients with toxic shock-like syndrome were investigated by restriction landmark genomic scanning and by modified random-amplified polymorphic DNA-polymerase chain reaction. Similar polymorphic DNA fragments were identified between the older M3 isolates and the recent isolates; also, the recent M3 clinical isolates from patients with pharyngitis were genetically indistinguishable, by the methods used, from the M3 isolates of patients with toxic shock-like syndrome. Although nucleotide sequences of these regions showed no apparent homology with known virulence factors, the DNA fragments could distinguish the recent M3 strains from the past strains. These results suggested that the recent strains have emerged because of genetic divergence.

Humans↗

PubMed1994

The gene encoding a new mitogenic factor in a Streptococcus pyogenes strain is distributed only in group A streptococci.

We recently cloned a gene encoding a new mitogenic factor (MF) from Streptococcus pyogenes NY-5. In the present study, we determined the distribution of this MF gene (mf) by PCR based upon its sequence. Of 371 streptococcal group A strains isolated from clinical specimens, 370 (99.7%) were positive for mf. The strain that was negative for the MF gene was also negative for the streptolysin O gene (slo). Some streptococcal strains belonging to groups C and G were negative for mf but positive for slo. Group B strains were negative for both. Furthermore, we examined the presence of mf in 54 strains belonging to 28 families and found mf only in group A streptococci. These results indicate that mf is distributed specifically in group A streptococci and the presence of mf in clinical samples strongly suggests infection with group A streptococci.

Bacterial Proteins↗

PubMed1996

Comparison of M-serotypes of Streptococcus pyogenes isolated from healthy elementary school children in two rural areas.

Serotypings have been used as markers for epidemiological surveys of Streptococcus pyogenes infections. Seventy-seven strains of S. pyogenes isolated from the throats of elementary school children in Kangwon Province in Korea in March and April 1992 were serotyped with M and/or opacity factor (OF) antisera. Sixty-eight strains of S. pyogenes from healthy school children in Chungnam Province in March 1993 were also serotyped and the distribution of serotype was compared with the isolates from those living in Kangwon Province. The distributions of M types were quite different between the two areas. M-78 (46.8%) and M-28 (22.1%) were most frequently encountered in Kangwon Province, while M-5 (20.6%), M-12 (16.2%), M-3 (13.2%), M-1 (11.8%) and M-62 (11.8%) were frequently isolated in Chungnam Province. Eighty-seven percent of strains in Kangwon produced OF while 33.2% of those in Chungnam produced OF (P < 0.0001). The difference in the distribution of serotypes and of OF production in the isolates from the children in the two provinces may be responsible for differences in the epidemiology of group A streptococcal infections and their sequelae.

Child↗

PubMed2000

Analysis of expression of a cytosolic enzyme on the surface of Streptococcus pyogenes.

The normally cytosolic glycolytic enzyme, glyceraldehyde-3-phosphate dehydrogenase, (GAPDH) has been reported to be expressed on the surface of Streptococcus pyogenes, group A, where it can act as a plasmin binding protein (Plr), and potentially a signaling molecule. In studies of wild-type and isogenic mutants, an association between surface expression of antigenic GAPDH/Plr and M and M-related fibrinogen-binding proteins was identified. Inactivation of the mga gene, whose product controls expression of M and M-related proteins also influenced expression of surface GAPDH/Plr. Revertants or pseudorevertants of mga mutants led to concomitant re-expression of surface GAPDH/Plr and M and M-related proteins. Using surface enhanced laser desorption ionization (SELDI) mass spectroscopy, a physical association between GAPDH/Plr and streptococcal fibrinogen-binding proteins was demonstrated. These studies support the hypothesis that surface M and M-related proteins are involved in anchoring GAPDH/Plr on the surface of group A streptococci.

Bacterial Proteins↗

PubMed1993

Purification of the beta product encoded by the Streptococcus pyogenes plasmid pSM19035. A putative DNA recombinase required to resolve plasmid oligomers.

Genetic evidence suggests that the gene beta product of Streptococcus pyogenes plasmid pSM19035 is required for converting plasmid multimers into monomers. The beta protein was purified from cells overexpressing the cloned gene. N-terminal protein sequence analysis demonstrated that the purified protein had the predicted sequence, except that the N-terminal initiator methionine was not present. Native beta protein consists of a dimer of two identical subunits with a molecular mass of 23.8 kDa (25 kDa in SDS-PAGE). The beta protein (isoelectric point of 9.7) binds specifically to a DNA fragment (312 bp in length) which contains the promoter region of the orf alpha-gene beta operon and two regions (sites I and II) that show dyad axes of symmetry. It is proposed that protein beta binds to sites I and II to mediate resolution of plasmid oligomers.

Bacterial Proteins↗

PubMed1993

Studies on binding of glycosaminoglycans to Streptococcus pyogenes by using 125I-heparan sulphate as a probe.

Binding of 125I-heparan sulphate to the cell surface of Streptococcus pyogenes is mediated by proteins, that could be released from the streptococcal cell wall by using alkaline buffer. SDS-electrophoresis revealed two bands with molecular weights of 63 and 58 kDa. Binding of the 125I-labelled heparan sulphate probe to streptococci seems to be due to charge interactions, as the same probe was displaced by unlabelled heparan sulphate, other negatively charged molecules such as heparin, dextran sulphate, dermatan sulphate or by high ionic strength. The interaction was also strongly influenced by pH. The binding constant at pH 7.2 was estimated to be 9.8 x 10(6) mol/l, suggesting a moderate affinity. The presence of collagen of different types enhanced binding of 125I-labelled heparan sulphate to streptococci, whereas fibronectin and vitronectin had an inhibitory effect. The cooperation between heparan sulphate and collagen could be important for the adhesion of streptococci to connective tissue.

Bacterial Outer Membrane Proteins↗

PubMed1998

Sulfonamide resistance in Streptococcus pyogenes is associated with differences in the amino acid sequence of its chromosomal dihydropteroate synthase.

Sulfonamide resistance in recent isolates of Streptococcus pyogenes was found to be associated with alterations of the chromosomally encoded dihydropteroate synthase (DHPS). There were 111 different nucleotides (13.8%) in the genes found in susceptible and resistant isolates, respectively, resulting in 30 amino acid changes (11.3%). These substantial changes suggested the possibility of a foreign origin of the resistance gene, in parallel to what has already been found for sulfonamide resistance in Neisseria meningitidis. The gene encoding DHPS was linked to at least three other genes encoding enzymes of the folate pathway. These genes were in the order GTP cyclohydrolase, dihydropteroate synthase, dihydroneopterin aldolase, and hydroxymethyldihydropterin pyrophosphokinase. The nucleotide differences in genes from resistant and susceptible strains extended from the beginning of the GTP cyclohydrolase gene to the end of the gene encoding DHPS, an additional indication for gene transfer in the development of resistance. Kinetic measurements established different affinities for sulfathiazole for DHPS enzymes isolated from resistant and susceptible strains.

Amino Acid Sequence↗

PubMed1994

M12 protein from Streptococcus pyogenes is a receptor for immunoglobulin G3 and human albumin.

We previously showed that M12 protein from opacity factor-negative Streptococcus pyogenes (group A streptococci) CS24 is responsible for immunoglobulin G3 (IgG3) binding activity. Here, we report that this M protein binds human serum albumin (HSA). Deletion analysis showed that the C repeats are sufficient for binding HSA, although upstream regions may be required for optimal binding. Like protein G, IgG3 and HSA bind to independent domains in the M protein. Experiments showed that bound IgG3 did not inhibit HSA binding to the M protein. The interaction between M12 protein and HSA is specific. M12 protein does not bind chicken egg and bovine serum albumins. Alignments of C1 and C2 repeats of M12 protein to sequences at the carboxy termini of other M proteins and Ig receptors revealed highly homologous sequences in the FcRV, M5, M6, ML2.1, and M57 proteins, suggesting that all could bind HSA. As predicted from the alignment, M5 protein and M6+ streptococci bound HSA, whereas an isogenic M6- mutant did not bind HSA. Furthermore, M2 protein from an opacity factor-positive strain also bound HSA.

Amino Acid Sequence↗

PubMed1988

Inducer expulsion in Streptococcus pyogenes: properties and mechanism of the efflux reaction.

Expulsion of preaccumulated methyl-beta-D-thiogalactoside-phosphate (TMG-P) from Streptococcus pyogenes is a two-step process comprising intracellular dephosphorylation of TMG-P followed by rapid efflux of the intracellularly formed free galactoside (J. Reizer, M.J. Novotny, C. Panos, and M.H. Saier, Jr., J. Bacteriol. 156:354-361, 1983). The present study identifies the mechanism and the order and characterizes the temperature dependency of the efflux step. Unidirectional efflux of the intracellularly formed [14C]TMG was only slightly affected when measured in the presence of unlabeled TMG (25 to 400 mM) in the extracellular medium. In contrast, pronounced inhibition of net efflux was observed in the presence of relatively low concentrations (1 to 16 mM) of extracellular [14C]TMG. Since net efflux was nearly arrested when the external concentration of [14C]TMG approached the intracellular concentration of this sugar, we propose that a facilitated diffusion mechanism is responsible for efflux and equilibration of TMG between the intracellular and extracellular milieus. The exit reaction was markedly dependent upon temperature, exhibited a high energy of activation (23 kcal [ca. 96 kJ] per mol), and followed first-order kinetics, indicating that the permease mediating this efflux was not saturated under the conditions of expulsion employed.

Diffusion↗

PubMed1994

The Streptococcus pyogenes hyaluronan synthase: sequence comparison and conservation among various group A strains.

We recently cloned the hyaluronan synthase gene (hasA) from Streptococcus pyogenes (DeAngelis et al., J. Biol. Chem. 268, 19181, 1993). Since this is the first glycosaminoglycan synthase gene to be cloned and these enzymes have also not been purified, nothing is yet known at the molecular level about the similarity or relatedness of hyaluronan synthase to other gene products. We found several proteins in the sequence database with substantial similarities to hyaluronan synthase (HasA), including NodC from Rhizobium, DG42 from Xenopus, and the three chitin synthases (Chs) from Saccharomyces. Like HasA, NodC and the Chs proteins all have at least an N-acetylglucosaminyl transferase activity in common and are membrane-associated. The polymerase chain reaction was also used to show that HasA, and probably the two gene operon for hyaluronan biosynthesis (hasA/hasB), is highly conserved among Group A streptococcal strains. In nine strains, isolated from 1917 through 1993, only five silent mutations were detected. The results show that hyaluronan synthase is highly conserved within Group A strains, although another virulence factor, the M protein, varies considerably in these same strains.

Amino Acid Sequence↗

PubMed2005

[Drug susceptibility and analysis using pulsed-field gel electrophoresis of Streptococcus pyogenes strains isolated from the patients with streptococcal toxic shock syndrome (STSS) in Japan].

Previously, we have performed T typing of Streptococcus pyogenes strains isolated from patients with streptococcal toxic shock syndrome (STSS) in Japan, and streptococcal pyrogenic exotoxin (SPE) typing for epidemiological examination. In this study, we conducted a drug sensitivity test using these strains, and investigated the results of gene analysis by pulse-field gel electrophoresis (PFGE) of S. pyogenes strains derived from patients with STSS, the patient's family, and patients other than those with STSS. To clarify the relationship between the host and bacterial factors, we investigated the association between clinical symptoms and T typing of the isolated strains/production of streptococcal pyrogenic exotoxin. There were no strains resistant to beta-lactams, and only 1 strain was resistant to multiple agents other than beta-lactams. The PFGE pattern of T1 type strains was classified into 2 ; the pattern was consistent between the strains derived from patients with STSS and those derived from the patient's family. The PFGE pattern of T3 type strains was classified into 5 (IV) ; Pattern I, which was most frequently observed, was detected in both the strains derived from patients with STSS/non-STSS. However, Patterns II and III were detected only in the strains derived from patients with non-STSS. Patterns IV and V were detected only in the strains derived from patients with STSS. When examining the association between clinical symptoms and bacterial factors, disseminated intravascular coagulation (DIC) was associated with T1-SPE B-producing strains, and pharyngitis was associated with T3-SPE A-producing strains. In the future, the relationship between the host and bacterial factors should be further investigated.

Anti-Bacterial Agents↗

PubMed2001

[Severe cutaneous Streptococcus pyogenes infections in the child: results of a multicenter survey].

UNLABELLED: To assess pediatric cases of severe cutaneous infections due to Streptococcus pyogenes. Since the beginning of 1980, the incidence of cellulitis and necrotizing fasciitis due to S. pyogenes has increased in adults. Serotyping of obtained isolates are in most cases M1, M3 or M5 protein. PATIENTS AND METHOD: A retrospective (1990-2000) survey was carried out in pediatric hospital centers. RESULTS: Three cases of necrotizing fasciitis and 15 of cellulitis were observed. In 30% of the cases, vancella lesions were associated; in the other cases, minor wounds were the site of the infection. Bacteriologic diagnosis was made by local samples in 14 cases; blood cultures were positive in four cases. In 11 cases, initial intravenous treatment consisted of third generation cephalosporin, in six cases of penicillin M or G and in one case of fusidic acid. In the second time, penicillin M was perfused in the majority of the cases. Mean duration of intravenous antibiotics perfusion was 15 days. There were no sequelae or death in this survey. CONCLUSIONS: Despite this study had limited epidemiological characteristics, it confirms that these two infections are rare. The frequency is probably underestimated, due to the difficulty in performing a diagnosis. The major site of infection was the varicella lesion. These two infections are so similar that it is frequent to mistake one infection for the other. Nonsteroidal anti-inflammatory drugs and site of infections did not influence prognosis. The treatment of cellulitis is penicillinotherapy whereas in necrotizing fasciitis early major surgery is often correlated with the rate of survival.

Cellulitis↗

PubMed1978

Regulation of the synthesis of M protein by sugars, Todd Hewitt broth, and horse serum, in growing cells of Streptococcus pyogenes.

Various sugars were tested for their effect on the differential rate of synthesis of M protein during the growth of Streptococcus pyogenes strain 0055 M12T12. In a semisynthetic medium alone, a high rate of M protein synthesis occurred with glucose as a substrate; decreasing rates of synthesis occurred with sucrose and trehalose, in that order, although the rates of growth were approximately equal with all sugars. A period of derepressed synthesis of M protein occurred in the lag phase of growth and in the stationary period as the substrates were being depleted. Although glucose inhibited the utilization of other sugars, diauxie was not apparent from the growth curves. However, synthesis of M protein followed strong diauxie curves with a reduction in rate of synthesis during the utilization of the second sugar. With glucose as a substrate, 2-deoxyglucose showed a strong permanent repression of M protein synthesis, whereas both glucose and 2-deoxyglucose caused temporary repression when sucrose was the substrate. Horse serum increased the rate of synthesis of M protein in a manner very similar to that caused by adding cyclic AMP, although quantitative analyses suggested that cyclic AMP, per se, was not the effector in horse serum. Addition of Todd Hewitt broth permitted the organisms to grow on phosphorylated sugars. Although the rates of growth on phosphorylated sugars were similar to that obtained with glucose, M protein was not synthesized when a phosphorylated sugar was the sole substrate. The addition of phosphorylated sugars with glucose or sucrose as substrates strongly repressed the synthesis of M protein with glucose-1-phosphate and with fructose 1,6-diphosphate repressing M protein synthesis the most. Clearly, M protein synthesis, which was not required for growth, was preferentially induced by glucose as compared to the other sugars and was dependent upon the metabolic route by which glucose was utilized.

Animals↗

PubMed2002

Molecular characterization of macrolide resistance mechanisms among Streptococcus pneumoniae and Streptococcus pyogenes isolated from the PROTEKT 1999-2000 study.

In this study, the distribution of macrolide resistance mechanisms was determined for isolates of Streptococcus pneumoniae and Streptococcus pyogenes obtained from the PROTEKT 1999-2000 study (a global, longitudinal study of the antibacterial susceptibility of bacterial pathogens associated with community-acquired lower respiratory tract infections). The global macrolide resistance mechanism distribution results for 1043 macrolide-resistant S. pneumoniae isolates collected from 25 countries were as follows: 35.3% mef(A), 56.2% erm(B), 6.8% both mef(A) and erm(B), 0.2% erm(A) subclass erm(TR) and 1.5% negative for mechanisms tested. Mechanisms of macrolide resistance were found to vary widely between countries and different geographical regions with mef(A) predominating in North America and erm(B) in Europe. Approximation of genotype from macrolide MIC without molecular determination of the mechanism of resistance resulted in an error of 10.2% (106 isolates). Overall, for 143 macrolide-resistant S. pyogenes isolates, 46.1% of the isolates tested were mef(A), 30.8% were erm(B), 23.1% were erm(A) subclass erm(TR) and no isolates were negative for all the genetic markers tested. Again, the distribution varied widely between countries and geographical regions. This study provides valuable baseline data for the continued monitoring of the evolution of macrolide resistance development in these important respiratory tract pathogens. The ketolide telithromycin retained excellent anti-pneumococcal activity irrespective of macrolide resistance mechanism, having a MIC(90) of 0.25, 0.5 and 0.5 mg/L against mef(A), erm(B) and mef(A)+erm(B) macrolide-resistant S. pneumoniae, respectively. It also exhibited potent activity against S. pyogenes that had become resistant to macrolides via either mef(A), (MIC(90 )0.5 mg/L) or erm(TR), (MIC(90) 0.03 mg/L).

Anti-Bacterial Agents↗

PubMed2000

Atypical behaviour and survival of Streptococcus pyogenes L forms during intraperitoneal infection in rats.

Groups of rats were injected intraperitoneally with cell wall-deficient (L) forms of Streptococcus pyogenes, with their parental (S) forms, as well as with a combined inoculum of both forms (S+L). Peritoneal exudate samples were harvested on days 1, 3, 7, 15 and 30 after challenge and were investigated by microbiological, electron microscopic, cytometric and biochemical methods. Parental S forms were isolated from peritoneal exudate samples up to day 15 post infection, while L form cultures were isolated until the end of the examined interval. Electron microscopic examination revealed continuous adhesion of L forms on the macrophage surface as well as intracellular persistence inside them. It was demonstrated that the intraperitoneal inflammatory response to L form infection was higher than to the other infections and the monocyte-macrophage populations were predominant. The established atypical behaviour and long survival of S. pyogenes L forms in the rat's peritoneum could explain some of the mechanisms of the pathogens' persistence as well as the reasons for chronic streptococcal infections.

Animals↗

PubMed2006

In vitro induction of resistance by tissue concentrations of azithromycin, clarithromycin, cefixime and amoxicillin/clavulanate in clinical isolates of Streptococcus pyogenes.

This study evaluated the effects of exposure to serum, tonsils and breakpoint drug concentrations of clarithromycin, azithromycin, cefixime and amoxicillin/clavulanate on Streptococcus pyogenes susceptibility. Frequency of mutation and development of resistance after ten passages on antibiotic gradient plates, followed by ten passages without antibiotic, were determined. Phenotypes of macrolide-resistant strains grown at the end of multi-step selection were also determined. Azithromycin induced a surge of resistant strains more rapidly and frequently than clarithromycin, particularly at tonsils concentrations. With amoxicillin/clavulanate no strains showed minimum inhibitory concentrations (MICs) higher than the susceptibility breakpoint. Mutational frequencies were higher for azithromycin, at serum and breakpoint drug concentrations, than for the other drugs. Most of the macrolide resistant strains showed an MLS(B) phenotype. In conclusion, the ability to prevent the occurrence of resistance in clinical isolates of S. pyogenes was similar for amoxicillin/clavulanate and clarithromycin followed by cefixime > azithromycin when tonsil drug concentrations were considered, and greater for amoxicillin/clavulanate followed by clarithromycin > cefixime> azithromycin, at breakpoint and serum concentrations.

Amoxicillin-Potassium Clavulanate Combination↗