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PubMed2001

Characterization of consecutive Streptococcus pyogenes isolates from patients with pharyngitis and bacteriological treatment failure: special reference to prtF1 and sic / drs.

To analyze bacteriological treatment failure in streptococcal pharyngitis, 40 consecutive Streptococcus pyogenes isolates from 18 patients were characterized. For 17 patients, isolates were indistinguishable with respect to emm type, random amplified polymorphic DNA pattern, and presence of prtF1 encoding the fibronectin-binding protein F1. prtF1 was detected only in the 11 isolates (4 patients) with emm12 and in the single isolate with emm6. Further analysis by vir(mga) regulon typing, sequencing of sic encoding the streptococcal inhibitor of complement from 19 isolates with emm1 (9 patients), and sequencing of drs (distantly related sic) from 11 isolates with emm12 revealed distinct sic alleles with insertions and/or deletions in sic that corresponded to differences in restriction patterns of the vir(mga) regulon only for paired isolates of 2 patients. Among isolates with emm12, 2 novel drs alleles were found. Analysis of these data suggests that neither the presence of prtF1 nor the diversification of sic / drs is required for the persistence of S. pyogenes in pharyngitis.

Adhesins, Bacterial↗
PubMed1988

Investigations on the binding of erythrogenic toxin A of Streptococcus pyogenes on human peripheral blood lymphocytes. II. Identification of toxin-binding lymphocytes and characterization of the receptor.

Gold complexes of erythrogenic toxin A (ETA) of Streptococcus pyogenes (strain NY-5) were bound to human lymphocytes that could be characterized as T cells by rosetting or labelling with OKT 3 antibody and anti-mouse-IgG-gold. Using OKT 4 and OKT 8 antibodies, respectively, it was demonstrated that binding of ETA was confined to the T helper/inducer cell subpopulation. Treatment of lymphocytes with neuraminidase enhanced the binding of ETA-gold, whereas trypsin treatment resulted in its reduction. Gangliosides of type II or type III and D-galactose only slightly decreased the ETA-gold binding. Preincubation of living lymphocytes with the mitogens concanavalin A or the Lens culinaris-lectin enhanced the binding of ETA-gold.

Bacterial Proteins↗
PubMed1992

Antibacterial activity of cefixime against Streptococcus pneumoniae, Streptococcus pyogenes, and Haemophilus influenzae in the presence of Moraxella (Branhamella) catarrhalis.

We measured the sizes of the inhibition zones of oral beta-lactam antibiotics for Streptococcus pneumoniae, Streptococcus pyogenes and Haemophilus influenzae in the presence of beta-lactamase-producing-Moraxella (Branhamella) catarrhalis by the agar double-layer method. The sizes of the zones of amoxicillin for S. pneumoniae alone were the largest, followed in a descending order by those of cefixime and cefaclor. In the presence of 10(7) CFU/ml of M.(B.) catarrhalis, however, significant reduction of the sizes of the zones was seen with amoxicillin and cefaclor; inhibition with cefixime was nearly unchanged. Similar results were observed in those for S. pyogenes. These variable findings were attributed to the difference in stability of these drugs to the beta-lactamase produced by M.(B.) catarrhalis. When the susceptibility of H. influenzae in the presence of 10(8) CFU/ml of M.(B.) catarrhalis to cefixime, cefoteram, cefpodoxime, cefotiam and cefuroxime was examined, the sizes of the inhibition zones of all the drugs were reduced by the presence of 10(8) CFU/ml of M.(B.) catarrhalis, but those of cefixime were the largest of all the drugs tested. Our agar double-layer method is simple and useful for evaluating the influence of beta-lactamase-producing organism, as M.(B.) catarrhalis, on the disk susceptibility of other pathogens to antibiotics.

Cefixime↗
PubMed1986

Scrum kidney: epidemic pyoderma caused by a nephritogenic Streptococcus pyogenes in a rugby team.

In December, 1984, an outbreak of pyoderma affected five scrum players in the St Thomas' Hospital rugby team. The causative organism, Streptococcus pyogenes, was acquired during a match against a team experiencing an outbreak of impetigo, and was transmitted to two front row players of another team a week later, and to two girlfriends of affected St Thomas' players a month later. The strain was M-type 49, tetracycline-resistant, and virulent. It caused salpingitis in a girlfriend and acute glomerulonephritis in one rugby player. No case of subclinical glomerulonephritis was detected in eight patients with pyoderma. Screening of the St Thomas' Hospital team revealed four further cases of non-streptococcal skin infection, with evidence for contemporaneous spread of Staphylococcus aureus. Teams should not field players with sepsis, and it may be advisable to apply a skin antiseptic to traumatised skin after the match.

Acute Disease↗
PubMed1980

Interaction of streptolysin O from Streptococcus pyogenes and theta-toxin from Clostridium perfringens with human fibroblasts.

The membrane-damaging properties on human diploid embryonic lung fibroblasts of streptolysin O (from Streptococcus pyogenes) and theta-toxin (from Clostridium perfringens) were compared. The results are consistent with the suggested mechanism for hemolysis by streptolysin O involving one fixation site and one lytic site of this cytolysin. However, the membrane-damaging activity of the two toxins differed with respect to (i) relative cytolytic activity on human diploid lung fibroblasts compared with that on sheep erythrocytes, (ii) binding to the fibroblast membrane, (iii) activity at 0 degrees C, (iv) membrane repair after more than 30 min, and (v) effect on influx of amino acids. It is concluded that the mechanism of membrane damage caused by theta-toxin differs from that of cytoplasmic membrane. These results question the current concept that all thiol-activated, cholesterol-inactivated bacterial toxins are similar both structurally and functionally.

Binding Sites↗
PubMed1990

Conjugative mobilization of the cloned M6 protein gene from Streptococcus pneumoniae to Streptococcus pyogenes.

The host-vector system omega 6001-pDP36 was used to transfer the M6 protein gene (emm-6.1) of Streptococcus pyogenes to other S. pyogenes strains, isogenic and nonisogenic to D471, the strain from which emm-6.1 was originally cloned. The first step was to subclone emm-6.1 into the insertion vector pDP36. The resulting plasmid, pRMB20, was used as donor in transformation to insert emm-6.1 into the conjugative transposon omega 6001. Streptococcus pneumoniae DP1322, carrying omega 6001 integrated into the chromosome, was the recipient in the transformation experiment. omega 6001 containing emm-6.1 was then transferred by conjugation from S. pneumoniae to the chromosomes of M+ and M- S. pyogenes strains. S. pyogenes transconjugants contained one intact copy of emm-6.1 integrated into the chromosome, but no expression of M6 protein could be detected by Western blot analysis. We found no evidence of the positive transacting regulation of emm gene expression postulated by other authors. In fact, the cloned emm-6.1 was not expressed in three strains expressing their own M proteins (M5, M17 and a shorter M6). In these partial diploids M protein genes were expressed only when present in the original chromosomal locus.

Antigens, Bacterial↗
PubMed2004

Detection of multiple macrolide- and lincosamide-resistant strains of Streptococcus pyogenes from patients in the Boston area.

Macrolide (including erythromycin and azithromycin) and lincosamide (including clindamycin) antibiotics are recommended for treatment of penicillin-allergic patients with Streptococcus pyogenes pharyngitis. Resistance to erythromycin in S. pyogenes can be as high as 48% in specific populations in the United States. Macrolide and lincosamide resistance in S. pyogenes is mediated by several different genes. Expression of the erm(A) or erm(B) genes causes resistance to erythromycin and inducible or constitutive resistance to clindamycin, respectively, whereas expression of the mef(A) gene leads to resistance to erythromycin but not clindamycin. We studied the resistance of S. pyogenes to erythromycin and clindamycin at an urban tertiary-care hospital. Of 196 sequential isolates from throat cultures, 15 (7.7%) were resistant to erythromycin. Three of these were also constitutively resistant to clindamycin and had the erm(B) gene. Five of the erythromycin-resistant isolates were resistant to clindamycin upon induction with erythromycin and had the erm(A) gene. The remaining seven erythromycin-resistant isolates were susceptible to clindamycin even upon induction with erythromycin and had the mef(A) gene. Pulsed-field gel electrophoresis analysis and emm typing demonstrated that the erythromycin-resistant S. pyogenes comprised multiple strains. These results demonstrate that multiple mechanisms of resistance to macrolide and lincosamide antibiotics are present in S. pyogenes strains in the United States.

Anti-Bacterial Agents↗
PubMed2001

H(2)O(2)-nonproducing Streptococcus pyogenes strains: survival in stationary phase and virulence in chronic granulomatous disease.

The production of hydrogen peroxide (H(2)O(2)) and related phenotypes were studied with Streptococcus pyogenes strains isolated from cases of pharyngitis or severe group A streptococcal infections. Of the 46 strains examined (34 from severe infections and 12 from pharyngitis cases), 25 strains accumulated H(2)O(2) in the culture medium when grown under glucose-limited, aerobic conditions, whereas the rest of the strains did not. There was no correlation between these traits and the type of disease from which each strain had been isolated. The H(2)O(2)-nonproducing strains tested in this study belonged to T type 3 or T type 12. The accumulation of H(2)O(2) started when the culture reached the late exponential phase. A rapid loss of cell viability accompanied H(2)O(2) accumulation but was completely prevented by the addition of a catalase, indicating that the lethality was actually caused by H(2)O(2). Cells of H(2)O(2)-nonproducing strains were resistant to killing by phagocytes from patients with chronic granulomatous disease (CGD), whereas those of H(2)O(2)-producing strains were subject to killing. Subcutaneous inoculation of 10(5) c.f.u. H(2)O(2)-nonproducing S. pyogenes strains into the hind footpads of CGD mice provoked more prominent swelling of the footpad than did H(2)O(2)-producing strains. The mortality rate in the CGD mice infected with the H(2)O(2)-nonproducing strains was higher than that produced by the H(2)O(2)-producing strains. It is suggested that H(2)O(2)-nonproducing S. pyogenes strains are prevalent in humans and that they may be a potential threat to the health of CGD patients.

Animals↗
PubMed1993

Geographic and temporal distribution and molecular characterization of two highly pathogenic clones of Streptococcus pyogenes expressing allelic variants of pyrogenic exotoxin A (Scarlet fever toxin).

The molecular population genetics and pathogenic potential of North American and European invasive strains of Streptococcus pyogenes were assessed. Isolates from recent invasive infections and from infections in the 1920s and 1930s were characterized for multilocus enzyme genotype and allelic variation in the gene (speA) that encodes streptococcal pyrogenic exotoxin (SPE) A (scarlet fever toxin). A subset of strains was studied for allelic variation in genes that encode SPE B and streptokinase. All contemporary strains assigned to electrophoretic types (ETs) 1 and 2 that synthesize SPE A have the speA2 and speA3 allelic variants, respectively, and their relative virulence in two mouse models is similar to that of strains of the same ET and M protein types recovered earlier. In contrast, ET 1 and 2 isolates from disease episodes in the 1920s and 1930s contain the speA1 allele. The data suggest there may be temporal and geographic variation in the occurrence of clone--virulence factor allele combinations, an observation that may in part explain fluctuations in disease frequency, severity, and character.

Alleles↗
PubMed2006

The Rgg regulator of Streptococcus pyogenes influences utilization of nonglucose carbohydrates, prophage induction, and expression of the NAD-glycohydrolase virulence operon.

The expression of many virulence-associated genes in Streptococcus pyogenes is controlled in a growth phase-dependent manner. Unlike the model organisms Escherichia coli and Bacillus subtilis, such regulation is apparently not dependent upon alternative sigma factors but appears to rely on complex interactions among several transcriptional regulators, including Rgg. The purpose of this study was to identify changes in gene expression associated with inactivation of the rgg gene in S. pyogenes strain NZ131 (serotype M49). To this end, the transcriptomes of wild-type and rgg mutant strains were analyzed during both the exponential and postexponential phases of growth using Affymetrix NimbleExpress gene chips. Genomewide differences in transcript levels were identified in both phases of growth. Inactivation of rgg disrupted coordinate expression of genes associated with the metabolism of nonglucose carbon sources, such as fructose, mannose, and sucrose. The changes were associated with an inability of the mutant strain to grow using these compounds as the primary carbon source. Bacteriophage transcript levels were also altered in the mutant strain and were associated with decreased induction of at least one prophage. Finally, transcripts encoding virulence factors involved in cytolysin-mediated translocation of NAD-glycohydrolase, including the immunity factor IFS and the cytolysin (streptolysin O [SLO]), were more abundant in the mutant strain, which correlated with the amount of NADase and SLO activities in culture supernatant fluids. The results provide further evidence that Rgg contributes to growth phase-dependent gene regulation in strain NZ131.

Bacterial Proteins↗
PubMed2001

Severe impairment of anti-cancer effect of lipoteichoic acid-related molecule isolated from a penicillin-killed Streptococcus pyogenes in toll-like receptor 4-deficient mice.

A lipoteichoic acid-related molecule (OK-PSA) isolated from OK-432, a penicillin-killed Streptococcus pyogenes, is a potent inducer of Th1 cytokines, and elicits anti-cancer effect in tumor-bearing mice. Toll-like receptor (TLR) 4 is a member of the recently identified toll-like receptor family of proteins that has been implicated in lipopolysaccharide-induced cell signaling. In the present study, we have examined the role of TLR4 for OK-PSA-induced Th1-cytokine production and anti-tumor effect by using C3H/HeJ mice in which TLR4 function is impaired. Although OK-PSA strikingly induced Th1 cytokines [interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, interleukin (IL)-2, IL-12 and IL-18] in the splenocytes derived from control animals (C3H/HeN), OK-PSA did not induce the cytokines in the splenocytes from C3H/HeJ. Furthermore, C3H/HeJ-derived splenocytes acquired the responsiveness to OK-PSA stimulation by overexpression of TLR4 gene. Finally, OK-PSA administration significantly inhibited the tumor growth and lung metastasis of syngeneic squamous cell carcinoma cells in C3H/HeN; however, no effect of OK-PSA was observed in C3H/HeJ. These findings strongly suggest that TLR4 signaling is involved in regulating OK-PSA-induced anti-cancer immunity.

Animals↗
PubMed2002

Zinc binding and dimerization of Streptococcus pyogenes pyrogenic exotoxin C are not essential for T-cell stimulation.

Streptococcal pyrogenic enterotoxin C (Spe-C) is a superantigen virulence factor produced by Streptococcus pyogenes that activates T-cells polyclonally. The biologically active form of Spe-C is thought to be a homodimer containing an essential zinc coordination site on each subunit, consisting of the residues His(167), His(201), and Asp(203). Crystallographic data suggested that receptor specificity is dependent on contacts between the zinc coordination site of Spe-C and the beta-chain of the major histocompatibility complex type II (MHCII) molecule. Our results indicate that only a minor fraction of dimer is present at T-cell stimulatory concentrations of Spe-C following mutation of the unpaired side chain of cysteine at residue 27 to serine. Mutations of amino acid residues His(167), His(201), or Asp(203) had only minor effects on protein stability but resulted in greatly diminished MHCII binding, as measured by surface plasmon resonance with isolated receptor/ligand pairs and flow cytometry with MHCII-expressing cells. However, with the exception of the mutants D203A and D203N, mutation of the zinc-binding site of Spe-C did not significantly impact T-cell activation. The mutation Y76A, located in a polar pocket conserved among most superantigens, resulted in significant loss of T-cell stimulation, although no effect was observed on the overall binding to human MHCII molecules, perhaps because of the masking of this lower affinity interaction by the dominant zinc-dependent binding. To a lesser extent, mutations of side chains found in a second conserved MHCII alpha-chain-binding site consisting of a hydrophobic surface loop decreased T-cell stimulation. Our results demonstrate that dimerization and zinc coordination are not essential for biological activity of Spe-C and suggest the contribution of an alternative MHCII binding mode to T-cell activation.

Amino Acid Sequence↗
PubMed1995

Structure and stability of protein H and the M1 protein from Streptococcus pyogenes. Implications for other surface proteins of gram-positive bacteria.

M proteins and other members of the M protein family, expressed on the surface of Streptococcus pyogenes, bind host proteins such as immunoglobulins, albumin, and fibrinogen. Protein H and the M1 protein are expressed by adjacent genes and both belong to the M protein family. In this work, the structure and stability of these two proteins have been investigated. As judged from sequence analysis and circular dichroism spectroscopy, the proteins are almost entirely in an alpha-helix conformation. The amino acids are arranged in a seven-residue (heptad) repeat pattern along the greater part of the proteins. These observations support the previously accepted model of M proteins as coiled-coil dimers. However, it was also found that the structures of both proteins were thermally unstable; i.e., the content of helix conformation was greatly reduced at 37 degrees C as compared to 25 degrees C or below. Together with previous findings that these proteins appear as monomers at 37 degrees C and dimers at low temperatures, the results suggest that the coiled-coil dimers are unfolded at 37 degrees C. The heptad patterns of protein H and the M1 protein showed a nonoptimal distribution of residues expected for a coiled-coil conformation. This is a possible explanation for the low thermal stability of the proteins. It was also demonstrated that the proteins were stabilized in the presence of the ligands IgG and/or albumin. Protein H and M1 protein show a high degree of sequence similarity in their C-terminal regions, and a fragment from this region displayed a high content of helix conformation, whereas fragments from the nonsimilar N-terminal parts did not adopt any stable folded structure. Thus, the C-terminal parts, which are conserved within the M protein family, may constitute a framework for the formation of the parallel helical coiled-coil structure, and we propose that the less stable N-terminal part may also participate in antiparallel interaction with M proteins on adjacent bacteria. The results suggest that temperature fluctuations in the environment could change the properties of bacterial surface proteins, thereby affecting the molecular interactions between the bacterium and its host.

Amino Acid Sequence↗
PubMed1997

Molecular epidemiology of Streptococcus pyogenes in an area where acute pharyngotonsillitis is endemic.

During an open clinical trial in an area where streptococcal infections are hyperendemic, we studied the genetic polymorphism of Streptococcus pyogenes isolates collected from patients and from healthy carriers living in close contact with them. The clonal diversity of isolates was analyzed by pulsed-field gel electrophoresis with three restriction enzymes (SmaI, ApaI, and SacII). The pharynx of each patient and healthy carrier was colonized by a single clone, suggesting the clonal nature of streptococcal colonization in individuals. Among 52 isolates obtained from patients with acute pharyngotonsillitis, we found 14 genetically unrelated clones, showing the genetic diversity of S. pyogenes. However, two clones belonging to the M1 and M12 serotypes represented about 70% of isolates in carriers and patients. Pharyngeal colonization in cured patients was monitored for 3 to 4 months. After the initial elimination of S. pyogenes following antibiotic therapy, the rate of recolonization was high by day 30 (about 20%) and was also at that level between days 90 and 120; this was similar to the carriage rate in family contacts. Thus, cured patients can be recontaminated by unrelated clones, suggesting that colonization of healthy carriers might be a potential source of spread and redistribution of S. pyogenes isolates.

Acute Disease↗
PubMed1976

Membrane lipoteichoic acid of Streptococcus pyogenes and its stabilized L-form and the effect of two antibiotics upon its cellular content.

Membrane lipoteichoic acid continues to be synthesized by an osmotically fragile, stabilized L-form of Streptococcus pyogenes. Chromatographic and electrophoretic comparisons indicate that the lipid componenent of lipoteichoic acid in this L-form and its parental streptococcus is glycerophosphoryldiglucosyl diglyceride and not phosphatidylkojibiosyl diglyceride. Based upon dry weight determinations, the yield of lipoteichoic acid from the L-form is 0.19%, as compared with 0.97% from the streptococcus. When grown with bacitracin the L-form contains the same amount of teichoic acid as when grown without this antibiotic; however, its lipoteichoic acid content is reduced by 85%. Similarly, the L-form grown with novobiocin for 10 h contains only 17% of the teichoic acid found in control cells.

Bacitracin↗
PubMed2000

Streptococcus pyogenes collected in Torino (northwest Italy) between 1983 and 1998: survey of macrolide resistance and trend of genotype by RAPD.

We surveyed macrolide resistance in 1,086 isolates of Streptococcus pyogenes, collected between 1983 and 1998, from throat swabs of children with untreated pharyngotonsillitis living in Torino (northwest Italy). In 1983 and 1985, the frequency of erythromycin resistance was 10%, and from 1990 to 1992 it was 4%. However, it rose to 16.6% in 1994 and reached 51% in 1996 before decreasing to 38.5% in 1998. Characterization of the phenotype of resistant isolates revealed the prevalence of constitutive resistance (CR) in 1996, whereas the M phenotype, characterized by resistance to 14- and 15-membered macrolides with susceptibility to clindamycin and streptogramin B, prevailed in 1998. Moreover, in 1997 we observed an increase in the frequency of autoagglutinating bacteria and, in 1998, of OF-negative S. pyogenes. Meanwhile, penicillin tolerance, assessed in the isolates collected from 1990 to 1996, decreased and disappeared. Random amplification of polymorphic DNA (RAPD) was used to obtain the genomic profile of 32 S. pyogenes strains. Four main DNA profiles were demonstrated, generally related to the macrolide-resistance phenotype and for the major part to the T serotype. These results indicate that RAPD is reliable as a first screening method in the epidemiological characterization of resistant S. pyogenes.

Anti-Bacterial Agents↗
PubMed1999

Molecular analysis of the role of streptococcal pyrogenic Exotoxin A (SPEA) in invasive soft-tissue infection resulting from Streptococcus pyogenes.

Epidemiological studies strongly implicate the bacterial superantigen, streptococcal pyrogenic exotoxin A (SPEA), in the pathogenesis of necrotizing soft-tissue infection and toxic shock syndrome resulting from Streptococcus pyogenes. SPEA can act as a superantigen and cellular toxin ex vivo, but its role during invasive streptococcal infection is unclear. We have disrupted the wild-type spea gene in an M1 streptococcal isolate. Supernatants from toxin-negative mutant bacteria demonstrated a 50% reduction in pro-mitogenic activity in HLA DQ-positive murine splenocyte culture, and up to 20% reduction in activity in human PBMC culture. Mutant and wild-type bacteria were then compared in mouse models of bacteraemia and streptococcal muscle infection. Disruption of spea was not associated with attenuation of virulence in either model. Indeed, a paradoxical increase in mutant strain-induced mortality was seen after intravenous infection. Intramuscular infection with the SPEA-negative mutant led to increased bacteraemia at 24 h and a reduction in neutrophils at the site of primary muscle infection. Purified SPEA led to a dose-dependent increase in peritoneal neutrophils 6 h after administration. SPEA is not a critical virulence factor in invasive soft-tissue infection or bacteraemia caused by S. pyogenes, and it could have a protective role in murine immunity to pyogenic infection. The role of this toxin may be different in hosts with augmented superantigen responsiveness.

Animals↗