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PubMed1990

[Diseases caused by Streptococcus pyogenes in Norway, 1975-1989. A microbiologic and epidemiologic survey].

The article briefly surveys the epidemiology of Streptococcus pyogenes caused disease in Norway during the last 15 years based on notification data, with emphasis on the nation-wide outbreak in 1987-88 caused by mucoid M-1 organisms. During the season S. pyogenes infections was 60% higher than expected. The number of bacteraemia cases, many with fulminant septicaemia, showed an almost threefold increase compared with earlier years. Unusual clinical manifestations such as necrotising fasciitis, pneumonia with empyema, primary peritonitis and meningitis also occurred. We briefly review the known virulence factors of S. pyogenes in an attempt to improve our understanding of the shift in clinical manifestations and occurrence of the disease.

Adolescent↗

PubMed1990

A new heart-cross-reactive antigen in Streptococcus pyogenes is not M protein.

To identify tissue-cross-reactive antigens other than M protein in Streptococcus pyogenes, proteins of M-positive strains and an M-negative strain were probed in Western blots for reactivity with cross-reactive streptococcal monoclonal antibodies (MAbs) 36.2.2 and 54.2.8. A protein(s) near a molecular mass of 60 kDa in extracts of five group A streptococcal serotypes and the M-negative strain reacted with the MAbs. A study of human antibody responses to purified membranes of S. pyogenes indicated a hyperreactivity to a 60-kDa protein in acute rheumatic fever. Since MAbs 36.2.2 and 54.2.8 are known to cross-react with myosin or actin and streptococcal M protein, the data suggest that a homology or conformation is shared between the 60-kDa antigen and M protein. Therefore, the 60-kDa antigen is a new heart- or tissue-cross-reactive antigen of S. pyogenes that shares immunologic epitopes with but is distinct from M protein.

Acute Disease↗

PubMed2006

Regulation of SpeB in Streptococcus pyogenes by pH and NaCl: a model for in vivo gene expression.

For a pathogen such as Streptococcus pyogenes, ecological success is determined by its ability to sense the environment and mount an appropriate adaptive transcriptional response. Thus, determining conditions for analyses of gene expression in vitro that are representative of the in vivo environment is critical for understanding the contributions of transcriptional response pathways to pathogenesis. In this study, we determined that the gene encoding the SpeB cysteine protease is up-regulated over the course of infection in a murine soft-tissue model. Conditions were identified, including growth phase, acidic pH, and an NaCl concentration of <0.1 M, that were required for expression of speB in vitro. Analysis of global expression profiles in response to these conditions in vitro identified a set of coregulated genes whose expression patterns showed a significant correlation with that of speB when examined during infection of murine soft tissues. This analysis revealed that a culture medium that promotes high levels of SpeB expression in vitro produced an expression profile that showed significant correlation to the profile observed in vivo. Taken together, these studies establish culture conditions that mimic in vivo expression patterns; that growth phase, pH, and NaCl may mimic relevant cues sensed by S. pyogenes during infection; and that identification of other environmental cues that alter expression of speB in vitro may provide insight into the signals that direct global patterns of gene expression in vivo.

Animals↗

PubMed2003

Infection by Streptococcus pyogenes induces the receptor activator of NF-kappaB ligand expression in mouse osteoblastic cells.

Group A Streptococcus pyogenes is known to induce nongonococcal septic arthritis in addition to pharyngitis, scarlet fever, and poststreptococcal sequelae. However, little is known about the interaction between S. pyogenes and bone cells. We report here that S. pyogenes strain JRS4 (M6) attached to and invaded mouse primary osteoblasts. Reverse transcription-PCR demonstrated that S. pyogenes infection of osteoblasts stimulated expression of mRNA for the receptor activator of NF-kappaB ligand (RANKL). Western blot analysis followed by ligand precipitation with the receptor activator of NF-kappaB receptor showed that there was an increase in RANKL protein in infected osteoblasts. Production of interleukin-6 was also stimulated, but no production of interleukin-1beta or tumor necrosis factor alpha was observed. Stimulation of RANKL production was not observed in osteoblasts stimulated with heat-inactivated S. pyogenes, suggesting that an active interaction of S. pyogenes with osteoblasts is essential for this phenomenon. A Western blot analysis performed with antibodies specific for phosphorylated signal transduction proteins demonstrated that S. pyogenes infection induces phosphorylation of p38 mitogen-activated protein kinase. A specific inhibitor of this kinase, SB203580, inhibited RANKL production by infected osteoblasts. These results suggest that infection of osteoblasts by S. pyogenes stimulates RANKL production and may trigger bone destruction in infected bone tissue.

Animals↗

PubMed2003

Macrolide-resistant Streptococcus pneumoniae and Streptococcus pyogenes in the pediatric population in Germany during 2000-2001.

In a nationwide study in Germany covering 13 clinical microbiology laboratories, a total of 307 Streptococcus pyogenes (mainly pharyngitis) and 333 Streptococcus pneumoniae (respiratory tract infections) strains were collected from outpatients less than 16 years of age. The MICs of penicillin G, amoxicillin, cefotaxime, erythromycin A, clindamycin, levofloxacin, and telithromycin were determined by the microdilution method. In S. pyogenes isolates, resistance rates were as follows: penicillin, 0%; erythromycin A, 13.7%; and levofloxacin, 0%. Telithromycin showed good activity against S. pyogenes isolates (MIC(90) = 0.25 micro g/ml; MIC range, 0.016 to 16 micro g/ml). Three strains were found to be telithromycin-resistant (MIC >/= 4 micro g/ml). Erythromycin-resistant strains were characterized for the underlying resistance genotype, with 40.5% having the efflux type mef(A), 38.1% having the erm(A), and 9.5% having the erm(B) genotypes. emm typing of macrolide-resistant S. pyogenes isolates showed emm types 4 (45.2%), 77 (26.2%), and 12 (11.9%) to be predominant. In S. pneumoniae, resistance rates were as follows: penicillin intermediate, 7.5%; penicillin resistant, 0%; erythromycin A, 17.4%; and levofloxacin, 0%. Telithromycin was highly active against pneumococcal isolates (MIC(90) </= 0.016 micro g/ml; range, 0.016 to 0.5 micro g/ml). The overall resistance profile of streptococcal respiratory tract isolates is still favorable, but macrolide resistance is of growing concern in Germany.

Anti-Bacterial Agents↗

PubMed2002

Fatal case of pneumonia caused by a nonhemolytic strain of Streptococcus pyogenes.

We report a case of pneumonia with a fatal outcome caused by a nonhemolytic strain of Streptococcus pyogenes. This strain was isolated in pure growth from blood cultures and was fully identified biochemically. Such strains will be difficult to recognize and isolate from sites with heavy growth of normal flora. This phenomenon has been reported sporadically before, and it is unknown how common such strains may be in pharyngeal samples.

Aged↗

PubMed1991

Hyperendemic Streptococcus pyogenes infection despite prophylaxis with penicillin G benzathine.

BACKGROUND: In closely confined populations, in which epidemics of Streptococcus pyogenes infection are common, penicillin G benzathine has long been used prophylactically to reduce morbidity from this pathogen. We report on our investigations of the effectiveness of penicillin G benzathine prophylaxis at a military recruit camp. METHODS: We prospectively studied the rates of pharyngeal colonization and infection by S. pyogenes among 736 male U.S. Marine Corps recruits from January through March 1989. Throat swabs for culture, clinical data, and questionnaire data were obtained during six examinations at intervals of two weeks. Serum samples obtained before training, after training, and from acutely ill recruits were analyzed with use of an antistreptolysin O microtitration technique. RESULTS: Although 93 percent of the recruits received prophylaxis with two intramuscular injections of 1.2 million units of penicillin G benzathine each (administered 30 to 39 days apart), 33 percent of the recruits were colonized by S. pyogenes, and 42 percent had infection (as defined by a two-dilution increase in the antistreptolysin O titer). Thirty-seven percent of 265 recruits who reported a sore throat and were infected with S. pyogenes did not seek medical attention. The recruits who were allergic to penicillin (7 percent of the total), who received no prophylaxis, were more likely to be colonized; an increased risk of colonization and infection among the nonallergic recruits was associated with the presence of a higher percentage of allergic recruits in the platoon. After the study was completed, all recruits who were allergic to penicillin were prescribed 250 mg of oral erythromycin twice daily (a total daily dose of 500 mg) for 60 days. Subsequently, the average weekly rate of clinically evident S. pyogenes pharyngitis fell by more than 75 percent. CONCLUSIONS: If the prevention of S. pyogenes infection is to be effective in closely confined populations such as military recruits, prophylactic antibiotics must be administered to all members of the population. Exempting those who are allergic to penicillin may create a bacterial reservoir from which infection can be transmitted to nonallergic members of the population.

Drug Hypersensitivity↗

PubMed2000

[Invasive disease caused by Streptococcus pyogenes. Report of a case with cutaneous and kidney metastasis].

Few cases of invasive disease due to Streptococcus pyogenes in children have been described. Greater knowledge of this disease is needed due to its increasing incidence and seriousness. New serotypes have been discovered with greater virulence due to exotoxin production and to the development of resistance to phagocytosis. We present a case of invasive disease due to S. pyogenes with bacteremia and cutaneous and kidney metastasis, in a non-immunodeficient child. The case is of interest because kidney dissemination has not been described in the literature and because evolution was satisfactory with endovenous beta-lactamica treatment during 15 days for only 48 hours. The importance of ruling out multi-organ metastatic foci, including use of urine cultures to rule out kidney involvement are highlighted. The epidemiological, pathogenic, clinical and diagnostic aspects of this entity, as reported in recent literature, are described.

Female↗

PubMed1982

Glycoprotein inhibitors and iodophilic polysaccharide storage in group A Streptococcus pyogenes.

Inhibitors of glycoprotein synthesis in eucaryotic cells also inhibited iodophilic polysaccharide (IPS) storage in group A streptococcus pyogenes. Addition of bacitracin or amphomycin, known inhibitors of polyisoprenol phosphate metabolism or lipid-linked oligosaccharide synthesis, indicated that a key intermediate must be synthesized before IPS storage could be detected. Based on inhibitor action and energy requirements the intermediate was most likely an undecaprenol pyrophosphoryl maltosaccharide. Biosynthesis of the maltosaccharide had an ATP requirement as shown by arsenate action but IPS synthesis via amylomaltase was energy independent if the lipid-linked saccharides were preformed. Maltosaccharide acceptor site blockade with 2-deoxy-d-glucose immediately inhibited IPS storage, which demonstrated the need of acceptor glucose residues for transglycosylation activity of amylomaltase. Tunicamycin failed to inhibit IPS synthesis although it was added in lethal concentrations.

Anti-Bacterial Agents↗

PubMedDate not supplied

[Fast identification of Streptococcus pyogenes serotype M.12 in throat swabs by an improvised coagglutination technique].

A rapid procedure for identification of Streptococcus pyogenes serotype M. 12 directly in throat swabs, is reported and compared with standard culture method on blood agar plates and typing of group A Streptococci isolated, with double gel immuno-diffusion. This procedure consist of chlorhydric acid extraction of swabs and testing of the extract towards specific M. 12 protein serum using extemporaneous coagglutination technique. We have tested 1100 throat swabs, with this procedure and with standard culture procedure. Identification of group A Streptococci serotype M. 12 with reported method is obtainable within 30 to 45 minutes of receipt of the clinical specimen. This method is easy to perform, with a sensitivity and a specificity respectively: 89.7% and 98.8%.

Agglutination Tests↗

PubMed1992

Purification and characterization of a peptide essential for formation of streptolysin S by Streptococcus pyogenes.

Peptides in a pronase digest of bovine serum albumin were required for streptolysin S formation by Streptococcus pyogenes besides maltose and a carrier (the oligonucleotide fraction obtained by treatment of Saccharomyces cerevisiae RNA with RNase A). A peptide essential for streptolysin S formation was purified to homogeneity from a pronase digest of bovine serum albumin by Sephadex G-25 column chromatography, and anion-exchange, reverse-phase, and gel filtration high-performance liquid chromatography. The purified peptide was divided into more than two peptides by HCOOOH oxidation and was composed of four residues of cysteine, three of leucine, and one each of aspartic acid and glutamic acid. Leucine and cysteine were detected as amino-terminal residues, and leucine and glutamic acid were detected as carboxyl-terminal residues, suggesting that two or three peptides are linked by a disulfide bond(s). A disulfide bond structure in the peptide seemed to be required for streptolysin S formation.

Amino Acid Sequence↗

PubMed2003

Localization of peptide/MHC class II complexes in macrophages following antigen processing of viable Streptococcus pyogenes.

The subcellular localization of peptide/MHC complexes was investigated during processing of the surface M5 protein from Streptococcus pyogenes. Bone marrow-derived macrophages were pulsed with viable S. pyogenes for 20 min followed by various periods of chase. T hybridoma cells detected complexes of one epitope, M5(17-31) with E(d) on the surface of macrophages within 30 min of chase. In contrast, complexes with another epitope, M5(308-319) with A(d) peaked later. Intracellular localization of peptide/MHC-II complexes was studied by subcellular fractionation and detection of complexes in fractions by T hybridoma cells. M5(17-31)/E(d) complexes were detected in light membrane fractions containing plasma membrane and early endosomes by 10-30 min. M5(308-319)/A(d) complexes were detected in these light membranes after 3 h of chase. Thus, the time course of M5(308-319)/A(d) presentation was delayed relative to M5(17-31)/E(d). However, neither type of complex was detected at any time in fractions containing phagosomes. Both species of peptide/MHC complexes localized to endocytic compartments, indicating a role for endosomes in presentation of antigens from phagocytosed bacteria.

Animals↗

PubMedDate not supplied

[Antibiotic sensitivity of Streptococcus pyogenes in pediatrics].

BACKGROUND: The purpose of this study was to set up the current level of Streptococcus pyogenes sensitivity, in pediatric patients in our community, to penicillin, clindamycin, clarithromycin, erythromycin and azithromycin. MATERIAL AND METHODS: 100 strains were collected between October 1996 to July 1997. 79 were pharyngeal and 21 were non-pharyngeal strains. The MICs were obtained by the E-test method, and furthermore the results were compared by the Kirby-Bauer method. RESULTS: All strains were sensitive to penicillin and except one (inducible resistance) to clindamycin. 19% were resistant to macrolide, without differences among clarithromycin, erythromycin and azithromycin. From 13 strains (16.5%) of pharyngeal and 6 (28.5%) from non-pharyngeal samples, 4 of these from cutaneous samples, showed resistance. 18 of the resistance strains belonged to novel resistance fenotip and one to 10 inducible fenotip. Only minor discrepancies about erythromycin and clindamycin were observed between E-test and Kirby-Bauer methods. CONCLUSIONS: This study confirms a remarkable level of resistance to macrolides in pediatric patients, mainly in the cutaneous samples. Due to the reduced prevalence of macrolide-susceptible strains, in vitro susceptibility testing appears necessary in case of macrolide chemotherapy.

Adolescent↗

PubMed1996

Insertional inactivation of Streptococcus pyogenes sod suggests that prtF is regulated in response to a superoxide signal.

In establishing an infection, Streptococcus pyogenes has the capacity to bind to the host extracellular matrix protein fibronectin via its protein F adhesin. Previous studies have suggested that the expression of protein F is stimulated during aerobic growth or upon addition of superoxide-generating agents to the culture under O2-limited conditions. To further explore the role of superoxide, we have examined the transcription of the gene which encodes protein F (prtF), as well as the expression of superoxide dismutase (SOD) under conditions which promote or repress protein F expression. These studies show that prtF transcription is regulated in response to superoxide concentration and that SOD is regulated in different environments in a manner which directly parallels the expression of protein F. A mutant deficient in SOD activity was constructed by insertional mutation into the gene which encodes SOD (sod). The resulting mutant was sensitive to superoxide and aerobic conditions, showed hypersensitive induction of prtF in response to superoxide, and expressed prtF under normally unfavorable O2-limited conditions. These findings suggest that a streptococcal signal transduction system which senses superoxide may coordinately control expression of prtF and sod.

Adhesins, Bacterial↗

PubMed1984

[T-proteins of Streptococcus pyogenes. IV. Isolation of T1-protein using affinity chromatography on immobilized fibrinogen].

T-protein of Streptococcus pyogenes, type 1 (strain SF 130 Griffith) was extracted by enzymatic treatment of the cells with trypsin and partially purified by ion exchange chromatography on DEAE cellulose and gel chromatography on ultrogel ACA 44. The crude T protein still showing serologically type specific and cross reactions finally was applied to a fibrinogen sepharose column. Components eluted with the neutral buffer (0.05 M phosphate, 0.2 M NaCl, 0.02% NaN3, pH 7.0) reacted serologically in the same manner as the crude T protein. By using 0.1 M citrate, 6 M urea pH 3.0 buffer a type specifically reacting protein (T1-TRYP-F) was eluted from the fibrinogen column. T1-TRYP-F showed identical precipitation lines with the recently characterized T1-protein (T1-TRYP-I) purified by immunochromatography on type specific anti-T antibodies. Comparison of the SDS-patterns of T1-TRYP-F and T1-TRYP-I revealed a less complex molecular size subunit structure for the fibrinogen binding T1-TRYP-F (two bands of 60000 and 70000) as found for T1-TRYP-I, which showed serologically active peptides between 30000 to about 500000. It is discussed that T protein also may be linked covalently with fibrinogen receptors as it has been reported for M protein.

Amino Acids↗

PubMed1988

Changes in the pattern of infection caused by Streptococcus pyogenes.

The distribution of T- and M-protein antigens was determined in 12,469 cultures of Streptococcus pyogenes sent to a reference laboratory. Of these 7232 (58%) were isolates from hospital patients, 249 (2%) from hospital staff and 4988 (40%) from the community. The survey extended from January 1980 to June 1987. During this time the numbers of isolates of M-types 6, 49 and 81 rose then fell, being replaced by types 1, 3 and 28. The proportion of isolates of M-types 4 and 12 remained constant. Few strains were received from cases of nephritis or rheumatic fever but there has been an increase in the number of strains from serious infections and deaths. Forty-four of the 55 (80%) strains received since 1985 from fatal infections have belonged to M-type 1. All other strains, bar two, received from fatal infections in those years belonged to M-type 3. Representatives of M-type 1 were also associated with erysipelas. Types 3 and 4 predominated among the isolates from scarlet fever, types 1, 4, 12 and 49 from nephritis, types 49 and 81 from skin infections in meat workers and type 28 in cases of puerperal sepsis. The M-typability rate was 97% but new M antigens await definition among strains causing pyoderma.

Agglutination Tests↗

PubMed1997

Transcriptional analysis of mga, a regulatory gene in Streptococcus pyogenes: identification of monocistronic and bicistronic transcripts that phase vary.

Transcription of several surface virulence proteins of Streptococcus pyogenes is regulated by Mga, a protein that shows homology to response regulators of two-component signal-transducing systems. Two of these surface virulence proteins, M protein and C5a peptidase, undergo phase variation. To determine whether Mga itself undergoes phase variation and might allow the phasing switch to coordinate the activity of these genes, expression of the mga gene was analyzed. We show for the first time that there are two mga-specific transcripts: a 3.8-kb bicistronic message that includes both mga and emm12 genes and a monocistronic 1.6-kb mga message. Both transcripts phase vary and are present in higher amounts in M+ variants than in M- variants. Incubation of RNA with rifampicin indicates that the smaller 1.6-kb message is not a processed product. Two promoters were mapped upstream of mga: P1 at position 666 (-395) and P2 at position 978 (-83). In strain CS46 (delta mga), transcription initiation from the P1 promoter does not occur, and multiple start sites are found around the P2 promoter. Complementation experiments indicate that sequences upstream of the P2 promoter are required for activation of emm12 and scpA by Mga in trans.

Amino Acid Sequence↗

PubMed2002

Influence of recombination and niche separation on the population genetic structure of the pathogen Streptococcus pyogenes.

The throat and skin of the human host are the principal reservoirs for the bacterial pathogen Streptococcus pyogenes. The emm locus encodes structurally heterogeneous surface fibrils that play numerous roles in virulence, depending on the strain. Isolates harboring the emm pattern A-C marker exhibit a strong tendency to cause throat infection, whereas emm pattern D strains are usually recovered from impetigo lesions; as a group, emm pattern E organisms fail to display obvious tissue tropisms. The peak incidence for streptococcal pharyngitis and impetigo varies with season and locale, leading to wide spatial and temporal distances between throat and skin strains. To assess any impact of niche separation on genetic variation, the extent of recombinational exchange between emm pattern A-C, D, and E subpopulations was evaluated. Analysis of nucleotide sequence data for internal portions of seven housekeeping loci from 212 isolates provides evidence of extensive recombination between strains belonging to different emm pattern subpopulations. Furthermore, no fixed nucleotide differences were found between emm pattern A-C and D strains. Thus, despite some niche separation created by distinct epidemiological trends and innate tissue tropisms there is little evidence for neutral gene divergence between throat and skin strains. Maintenance of a relationship between emm pattern and tissue tropism in the face of underlying recombination suggests that tissue tropism is associated with emm or a closely linked gene.

Alleles↗