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PubMed1987

In vivo Streptococcus pyogenes C5a peptidase activity: analysis using transposon- and nitrosoguanidine-induced mutants.

The streptococcal C5a peptidase removes a six-amino-acid fragment from human C5a and thereby inactivates this chemotaxin. We used transposon and chemical mutagenesis to generate mutants of Streptococcus pyogenes that did not produce C5a peptidase. These mutants showed no alteration in expression of capsule, M protein, streptolysins O and S, or pyrogenic exotoxin C. Serial passage of a peptidase-producing strain in vivo resulted in a 100-fold increase in production of C5a peptidase. The presence of C5a peptidase delayed the accumulation of polymorphonuclear leukocytes (PMNLs) in the peritoneal cavities of mice after intraperitoneal challenge. However, there was no difference in virulence (as evaluated by LD50) between strains that produced and those that lacked C5a peptidase. Although C5a peptidase is expressed on the cell surface, antibody to this enzyme did not opsonize streptococci for phagocytosis in vitro. These studies show that C5a peptidase alters the normal host inflammatory response by delaying the accumulation of PMNLs at the foci of streptococcal infection.

Adhesins, Bacterial↗
PubMed2001

Lactobacillus casei acquires the binding activity to fibronectin by the expression of the fibronectin binding domain of Streptococcus pyogenes on the cell surface.

Fibronectin binding domain was expressed on the cell surface of Lactobacillus casei strain Shirota which hardly adheres to fibronectin. DNA for the fibronectin binding domain of the sfbl gene, which encodes a fibronectin binding protein of Streptococcus pyogenes ATCC 21059, was amplified with polymerase chain reaction, cloned into a surface display vector pSAK332, and introduced into L. casei. The fibronectin binding domain was expressed as a fusion protein consisting of staphylokinase of Staphylococcus aureus and the anchor sequence of cell wall-associated 763 proteinase of Lactococcus lactis NCDO 763. The fibronectin binding ability of the resulting L. casei was confirmed with Western blot analysis, immunoelectron microscopic analysis, and adherence to fibroblast cells. These results indicate that L. casei has acquired a new phenotype to bind fibronectin upon the expression of the fibronectin binding domain on the cell surface. This L. casei also shows binding affinity to fibrinogen, indicating that fibronectin binding domain is involved in the binding to fibrinogen as well.

Adhesins, Bacterial↗
PubMed2005

Establishment of a superficial skin infection model in mice by using Staphylococcus aureus and Streptococcus pyogenes.

A new animal model for the purpose of studying superficial infections is presented. In this model an infection is established by disruption of the skin barrier by partial removal of the epidermal layer by tape stripping and subsequent application of the pathogens Staphylococcus aureus and Streptococcus pyogenes. The infection and the infection route are purely topical, in contrast to those used in previously described animal models in mice, such as the skin suture-wound model, where the infection is introduced into the deeper layers of the skin. Thus, the present model is considered more biologically relevant for the study of superficial skin infections in mice and humans. Established topical antibiotic treatments are shown to be effective. The procedures involved in the model are simple, a feature that increases throughput and reproducibility. This new model should be applicable to the evaluation of novel antimicrobial treatments of superficial infections caused by S. aureus and S. pyogenes.

Animals↗
PubMed2003

In vivo lysogenic conversion of Tox(-) Streptococcus pyogenes to Tox(+) with Lysogenic Streptococci or free phage.

Temperate bacteriophage can transfer toxin-encoding genes between bacteria, often resulting in acquired pathogenicity. However, little is known regarding the effects of the eukaryotic host on the phage-pathogen interaction. Using Streptococcus pyogenes as a model, we demonstrate, both in vitro and in vivo, that the eukaryote mediates the efficient induction of toxin-encoding temperate phage and the resultant conversion of Tox(-) flora to Tox(+). Furthermore, we show that both phage induction and subsequent conversion need not happen in the same mammalian host, as host-to-host phage transmission can result in toxigenic conversion within the secondary host. Ultimately, our findings demonstrate that the eukaryotic host serves as an essential component in the phage-mediated evolution of virulence within the microbial population.

Animals↗
PubMed1998

Initial events in the pathogenesis of acute tonsillitis caused by Streptococcus pyogenes.

Bacterial and epithelial cell samples were obtained, within 24 h of onset of pharyngeal symptoms, from the palatine tonsils of nine patients (four female and five male; age range 10-40 years, median age 23) with acute tonsillitis, culture-positive for Streptococcus pyogenes. The specimens were examined using fluorescein isothiocyanate- (FITC) and gold-labelled antiserum to S. pyogenes and fluorescence, scanning electron and transmission electron microscopy. S. pyogenes could be identified both in the mucous layer covering the tonsils and attached to the surface epithelial cells. Long chains of coccus-shaped bacteria could be seen encroaching on the epithelial cell borders. S. pyogenes can apparently penetrate the mucous barrier, attach to the epithelial cells, spread from cell to cell and possibly penetrate into the outermost layer of the epithelial cells. These events in turn provoke cytokine production and/or complement activation, which induce inflammatory reaction in the tonsillar tissue.

Acute Disease↗
PubMed1978

Complex surveillance of Streptococcus pyogenes. IV. The phenomenon of interference of human serum under the conditions of the bactericidal test.

The phenomenon of interference of human sera under the conditions of the bactericidal test was described. In the presence of these sera, secondarily non-resistant strains of Streptococcus pyogenes were capable of vigorous growth and anti M 12 bactericidal activity was impaired. The factor was found in the albumin fraction and has probably the character of a blocking cytophilic lymphokin. It can markedly distort the interpretation of the bactericidal test.

Adult↗
PubMed2002

Self epitopes shared between human skeletal myosin and Streptococcus pyogenes M5 protein are targets of immune responses in active juvenile dermatomyositis.

OBJECTIVE: To identify self T cell epitopes associated with proinflammatory immune responses and clinically active juvenile dermatomyositis (juvenile DM). The target of our search for relevant epitopes was represented by amino acid sequences shared between human skeletal myosin and Streptococcus pyogenes M5 protein. The long-term objective of the project is to identify suitable targets for immunotherapy of the disease. METHODS: We used computerized algorithms to identify putative agretopes on both the human myosin and Streptococcus M5 proteins. Direct binding assays for homolog peptides were used to confirm such predictions. Antigenicity and functional cross-reactivity were evaluated by cytotoxicity assays and by measurement of cytokine levels. Specific T cells were isolated by T cell capture, and T cell receptor (TCR) V(beta) gene usage was identified by reverse transcriptase-polymerase chain reaction. RESULTS: We identified peptides that are targets of disease-specific cytotoxic T cell responses. T cell reactivity against the self peptides correlates with clinical signs of early, active myositis. Such reactivity is accompanied by production of proinflammatory cytokines, which may contribute to the damage. T cell cross-recognition of bacterial and human homologs was shown functionally as well as by sorting peptide-specific T cells and identifying oligoclonal and largely overlapping TCR V(beta) gene usage. CONCLUSION: These findings represent the first identification of a self epitope in juvenile DM, providing a potential candidate for antigen-specific immune therapy.

Bacterial Proteins↗
PubMed1993

Contributions of post-antibiotic lag and repair-recovery to the post-antibiotic effects of ciprofloxacin on Escherichia coli, Klebsiella pneumoniae, Staphylococcus aureus and Streptococcus pyogenes.

A viable counting technique was used to determine the post-antibiotic effect (PAE) of ciprofloxacin against four bacterial species, treated with either one or four times the minimum inhibitory concentration for 1 or 3 h. PAE were demonstrated with Escherichia coli, Staphylococcus aureus or Streptococcus pyogenes after exposure to either concentration for both times. No clear PAE was demonstrated for Klebsiella pneumoniae after any treatment. In some cases, PAE was due to an increased post-treatment lag phase, which was followed by nearly normal multiplication, whereas in other cases a long lag was followed by abnormally rapid cell division, with the generation times of treated cultures being much less than those of the corresponding drug-free controls. This is evidence of recovery of cells that have completed DNA repair. S. aureus, E. coli and K. pneumoniae all exhibited evidence of this type of repair even though K. pneumoniae gave no significant PAE. However, the post-treatment generation times of S. pyogenes, which produced the greatest PAE, gave no evidence of such repair. It is concluded that PAEs may result from a variety of factors.

Ciprofloxacin↗
PubMed2000

High prevalence of erythromycin-resistant, clindamycin/miocamycin-susceptible (M phenotype) Streptococcus pyogenes: results of a Spanish multicentre study in 1998. Spanish Group for the Study of Infection in the Primary Health Care Setting.

Using the standard agar dilution method we studied the prevalence of susceptibility to 14-, 15- and 16-membered ring macrolides and clindamycin in Streptococcus pyogenes isolated in 1998 from 21 laboratories in Spain. The number of strains admitted to the study was proportional to the numbers of inhabitants in each geographical area. We also determined the susceptibility phenotypes and the genetic basis for the antibiotic resistance. A total of 486 unduplicated isolates of S. pyogenes were used. Throat swab samples provided 359 (73.9%) isolates, and the remaining 127 isolates were from other sources. One hundred and fourteen (23.5%) isolates were resistant to erythromycin, a 14-membered ring macrolide, and azithromycin, a 15-membered macrolide, whereas only 1% of isolates were resistant to miocamycin, a 16-membered macrolide and 0.8% were resistant to clindamycin. Of the 114 erythromycin-resistant strains, 109 (95.6%) were susceptible to clindamycin and miocamycin. Since induction with erythromycin did not modify susceptibility to the latter antibiotics, these 109 strains were considered to have the M phenotype. Twenty strains with the M phenotype, one per laboratory, were assayed by PCR and showed the presence of the mef gene, which is responsible for antibiotic resistance by an efflux system. Among comparable studies covering entire countries, ours demonstrates one of the highest rates of S. pyogenes erythromycin resistance and clindamycin and miocamycin susceptibility in the world. Strains with the M phenotype account for the great majority of these isolates.

Adult↗
PubMedDate not supplied

[Investigation of bactericidal effect and cytokine response of the oral epithelial cells against different antigenic doses of Streptococcus pyogenes].

Epithelial cells (EC) have an important role in the constitution of both innate and acquired immune responses. The aim of this study was to investigate the alterations of bactericidal effects and cytokine production patterns of human oral epithelial cells (OEC) against different doses of Streptococcus pyogenes. For this purpose, OEC have been stimulated with S. pyogenes with an effector/target (E/T) cell ratio of 1/1, 1/100, 1/1.000 and 1/10.000, and bactericidal effects and interleukin (IL)-6, IL-8 and IL-10 levels were detected in the first and sixth hours of incubation. The mean rates of bactericidal effect detected in the first and sixth hours were 38.7% and 54.5%, respectively. The bactericidal effects observed at 1/1 E/T cell ratio in the first hour, and at 1/1 and 1/100 E/T cell ratio in the the sixth hour were found significantly higher then the other cells ratios (p<0.05). Time- and dose-depended differences were detected in the cytokine responses of OEC for different S. pyogenes concentrations. IL-6 levels produced by stimulated OEC were found higher, and IL-8 levels were found lower then the levels which were produced by unstimulated OEC (p<0.05, p<0.001, respectively) in the first hour, while there were no change in IL-10 levels after stimulation with different bacterial concentrations (p>0.05). At the sixth hour there were no differences in the IL-6 levels produced by stimulated and unstimulated cells, while the levels of IL-8 produced by stimulated cells were found lower then the levels produced by unstimulated cells in the E/T cell ratio of 1/100, 1/1000 and 1/10.000 (p<0.05, p<0.01, p<0.01, respectively). Nevertheless IL-10 levels in the E/T cell ratio of 1/100 and 1/1.000 were statistically higher then the levels produced by unstimulated cells (p<0.05, p<0.05). As a result OEC stimulated with S. pyogenes showed dose dependent manner in bactericidal effect and cytokine production. It is suggested that epithelial cells stimulation with different doses of antigen contributed to the immune system activation or tolerance.

Antigens, Bacterial↗
PubMed1993

Analysis of Streptococcus pyogenes promoters by using novel Tn916-based shuttle vectors for the construction of transcriptional fusions to chloramphenicol acetyltransferase.

We have developed a series of shuttle vectors based on the conjugative transposon Tn916 that have been designed for the analysis of transcriptional regulation in Streptococcus pyogenes and other gram-positive bacteria. Designated the pVIT vectors (vectors for integration into Tn916), the vectors are small, stable plasmids in Escherichia coli to facilitate the fusion of promoters from cloned S. pyogenes genes to a promoterless gene which encodes chloramphenicol acetyltransferase. The vectors each contain one or more small regions of Tn916 to direct the integration of the transcriptional fusion into the transposon via homologous recombination following transformation of S. pyogenes or other suitable gram-positive hosts. Integration can be monitored by the inactivation or replacement of an antibiotic resistance determinant in modified derivatives of Tn916. Promoter activity can then be quantitated by the determination of chloramphenicol acetyltransferase-specific activity. In addition, since integration is into loci that do not disrupt the conjugative transpositional functions of Tn916, the vectors are useful for analysis of regulation in strains that are difficult or impossible to transform and can be introduced into these strains by conjugation following transformation of an intermediate host. The promoters for the genes which encode both the M protein and protein F of S. pyogenes were active in pVIT vectors, as was the region which controls transcription of mry, a trans-acting positive regulator of M protein expression. However, neither of the two characterized promoters for mry demonstrated activity when independently analyzed in pVIT-generated partial diploid strains, suggesting that regulation of mry is more complex than predicted by current models. The broad host range of Tn916 should make the pVIT vectors useful for analysis of regulation in numerous other bacterial species.

Antigens, Bacterial↗
PubMed1996

[Toxic shock-like syndrome with Streptococcus pyogenes in a pleural effusion].

A 58-year-old woman was admitted to the hospital because of fever and hypotension. That night, shock developed. On the second hospital day, a chest roentgenogram showed retention of pleural fluid and the group A-beta hemolytic organism Streptococcus pyogenes was detected in the effusion. The toxic shock-like syndrome was diagnosed. The patient recovered with artificial ventilation, administration of antibiotics, and blood purification. In this patient, the type of pyrogenic exotoxin was B + C.

Female↗
PubMed1998

A novel erythromycin resistance methylase gene (ermTR) in Streptococcus pyogenes.

Erythromycin resistance among streptococci is commonly due to target site modification by an rRNA-methylating enzyme, which results in coresistance to macrolide, lincosamide, and streptogramin B antibiotics (MLSB resistance). Genes belonging to the ermAM (ermB) gene class are the only erythromycin resistance methylase (erm) genes in Streptococcus pyogenes with MLSB resistance that have been sequenced so far. We identified a novel erm gene, designated ermTR, from an erythromycin-resistant clinical strain of S. pyogenes (strain A200) with an inducible type of MLSB resistance. The nucleotide sequence of ermTR is 82.5% identical to ermA, previously found, for example, in Staphylococcus aureus and coagulase-negative staphylococci. Our finding provides the first sequence of an erm gene other than ermAM that mediates MLSB resistance in S. pyogenes.

Amino Acid Sequence↗
PubMed2005

Impact of the SpeB protease on binding of the complement regulatory proteins factor H and factor H-like protein 1 by Streptococcus pyogenes.

Microbial pathogens often exploit human complement regulatory proteins such as factor H (FH) and factor H-like protein 1 (FHL-1) for immune evasion. Fba is an FH and FHL-1 binding protein expressed on the surface of the human pathogenic bacterium Streptococcus pyogenes, a common agent of pharyngeal, skin, and soft-tissue infections. Fba has been shown to contribute to phagocytosis resistance, intracellular invasion, and virulence in mice. Here, we look at the role of Fba in recruitment of FH and FHL-1 by five serotype M1 isolates of streptococci. Inactivation of fba greatly inhibited binding of FH and FHL-1 by all isolates, indicating that Fba is a major FH and FHL-1 binding factor of serotype M1 streptococci. For three isolates, FH binding was significantly reduced in stationary-phase cultures and correlated with high levels of protease activity and SpeB (an extracellular cysteine protease) protein in culture supernatants. Analysis of a speB mutant confirmed that SpeB accounts for the loss of Fba from the cell surface, suggesting that the protease may modulate FH and FHL-1 recruitment during infection. Comparisons of fba DNA sequences revealed that the FH and FHL-1 binding site in Fba is conserved among the M1 isolates. Although the ligand binding site is not strictly conserved in Fba from a serotype M49 isolate, the M49 Fba protein was found to bind both FH and FHL-1. Collectively, these data indicate that binding of FH and FHL-1 is a conserved function of Fba while modulation of Fba function by SpeB is variable.

Amino Acid Sequence↗
PubMed1998

Fibronectin-binding protein I of Streptococcus pyogenes is a promising adjuvant for antigens delivered by mucosal route.

A common problem in human vaccinology is the limited availability of efficient and non-toxic adjuvants capable of promoting mucosal responses. The potential usefulness of fibronectin-binding protein I (Sfbl) of Streptococcus pyogenes as immunological adjuvant was assessed using ovalbumin (OVA) as a model antigen. Mice were immunized by intranasal route, either with soluble OVA or OVA covalently coupled to Sfbl. Immunization with OVA-Sfbl resulted in the elicitation of about 100-fold higher titers of anti-OVA serum IgG than using OVA alone. The anti-OVA IgG subclass pattern was dominated in both groups of mice by IgG1, followed by IgG2b, IgG2a, and IgG3. Immunization with OVA-Sfbl also resulted in the elicitation of OVA-specific IgA in lung washes (24% of the total IgA), which was absent in mice immunized with OVA alone. Spleen cells from OVA-Sfbl-immunized mice also gave a much stronger proliferative response to restimulation with soluble OVA in vitro. Phenotypic analysis of proliferating cells showed an enrichment in CD4+ T cells, producing a pattern of cytokines (IL-4, IL-5, IL-6 and IL-10) characteristic of Th2-type cells. In contrast to immunization with soluble OVA alone, OVA-Sfbl induced the generation of CD8+ OVA-specific cytotoxic cells. These results demonstrate that Sfbl represents a promising mucosal adjuvant able to substantially improve cellular, humoral and mucosal responses when coupled to an antigen administered by intranasal route.

Adhesins, Bacterial↗
PubMed2003

Presence of D-alanine in an endopeptidase from Streptococcus pyogenes.

D-amino acids are commonly found in peptide antibiotics and the cell wall peptidoglycan of bacterial cell walls but have not been identified in proteins or enzymes. Here we report the presence of 6-7 A-alanine residues in an endopeptidase of Streptococcus pyogenes, a unique enzyme involved in surface protein attachment that we term LPXTGase. Using D-amino acid oxidase coupled with catalase for the deamination of D-alanine to pyruvic acid (a conversion unique to D-alanine), we were able to identify [14C]pyruvic acid in a [14C]alanine-labeled preparation of purified LPXTGase, which represents 27% of the amino acid composition. Because D-amino acids are not accommodated in ribosomal peptide synthesis, these results suggest that the same process used in assembling peptide antibiotics or a yet unidentified mechanism may synthesize the core protein of this endopeptidase.

Alanine↗
PubMed1995

Occult Streptococcus pyogenes in cellulitis: demonstration by immunofluorescence.

A 23-year-old man developed cellulitis and ascending lymphangitis of the right leg. Blood cultures and skin saline aspirates were sterile. Gram stain of the aspirate did not show any bacteria. Direct and indirect immunofluorescent staining with polyclonal and monoclonal antibodies to Streptococcus pyogenes revealed streptococci in the reticular dermis. The cellulitis resolved following treatment with intravenous cefazoline.

Adult↗
PubMed2002

Fluoride exposure attenuates expression of Streptococcus pyogenes virulence factors.

Fluoridation causes an obvious reduction of dental caries by interference with cariogenic streptococci. However, the effect of fluoride on group A streptococci that causes rheumatic fever and acute poststreptococcal glomerulonephritis is not known. We have used proteomic analysis to create a reference proteome map for Streptococcus pyogenes and to determine fluoride-induced protein changes in the streptococci. Cellular and extracellular proteins were resolved by two-dimensional polyacrylamide gel electrophoresis and identified by matrix-assisted laser desorption ionization mass spectrometry. 183 protein spots were visualized, and 74 spots representing 60 unique proteins were identified. A 16-h exposure to sodium fluoride caused decreased expression of proteins required to respond to cellular stress, including anti-oxidants, glycolytic enzymes, transcriptional and translational regulators, and protein folding. Fluoride caused decreased cellular expression of two well-characterized S. pyogenes virulence factors. Fluoride decreased expression of glyceraldehyde-3-phosphate dehydrogenase, which acts to bind fibronectin and promote bacterial adherence. We also performed proteomic analysis of protein released by S. pyogenes into the culture supernatant and observed decreased expression of M proteins following fluoride exposure. These data provide evidence that fluoride causes decreased expression by S. pyogenes proteins used to respond to stress, virulence factors, and implicated in non-suppurative complications of S. pyogenes, including glomerulonephritis and rheumatic fever.

Antioxidants↗