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PubMedDate not supplied

Haemophilus influenzae and Streptococcus pyogenes group A challenge induce a Th1 type of cytokine response in cells obtained from tonsillar hypertrophy and recurrent tonsillitis.

We have previously shown that tonsil tissue both from children with tonsillar hypertrophy and recurrent tonsillitis is colonized and invaded by Haemophilus influenzae and Streptococcus pyogenes group A. In order to evaluate if these bacteria are involved in the immunopathogenesis of these two conditions, tonsillar cells from both groups were stimulated in vitro with intact, heat-inactivated H. influenzae or S. pyogenes A. The immunoreactivity was evaluated by assessing the induction of cytokine production (IL-1 alpha, IL-1 beta, TNF-alpha, IL-6, IL-8, IL-2, IFN-gamma, IL-4, TNF-beta and IL-10), which was detected at the single-cell level. All cytokines studied except IL-4 were induced in both groups after stimulation with H. influenzae or S. pyogenes A. The dominating cytokines were IL-1 beta, IFN-gamma and TNF-beta. No major differences in the cytokine pattern or number of cytokine-producing cells were noticed between the two patient cohorts after H. influenzae stimulation. Activation by S. pyogenes A bacteria gave rise to higher frequencies of IFN-gamma- and TNF-beta-synthesizing cells in the recurrent tonsillitis group. The incidence of CD4-, CD8-positive T cells and CD40-positive B cells was comparable between the two groups while the MAC-387-positive macrophages were significantly higher in the recurrent tonsillitis groups. In conclusion, a Th1 type of cytokine response was found in both groups following stimulation with H. influenzae or S. pyogenes A.

Antigens, Bacterial↗
PubMed1992

Expression of protein F, the fibronectin-binding protein of Streptococcus pyogenes JRS4, in heterologous streptococcal and enterococcal strains promotes their adherence to respiratory epithelial cells.

In a previous study we reported the identification of protein F, a fibronectin-binding protein that was essential to the ability of Streptococcus pyogenes JRS4 to adhere to respiratory epithelial cells (E. Hanski and M. Caparon, Proc. Natl. Acad. Sci. USA, 89:6172-6176, 1992). To further evaluate the role of protein F in the adherence of the group A streptococci, we screened other group A streptococcal strains, including six recent clinical isolates, and one strain of Enterococcus faecalis for their capacity to bind fibronectin and for the presence of the gene encoding protein F (prtF). Seven of eight group A streptococcal strains analyzed, including all recent clinical isolates, both bound fibronectin at high affinity and contained DNA sequences that hybridized with a prtF-specific probe. One group A streptococcal isolate and the strain of E. faecalis examined neither contained a prtF-related gene nor bound fibronectin. These two strains also could not efficiently adhere to respiratory epithelial cells. However, upon the introduction of the cloned prtF gene, both of these strains gained the capacity to bind fibronectin and to adhere to respiratory epithelial cells. These results suggest that protein F is an important adhesin, which may have a general role in the virulence of the group A streptococci.

Animals↗
PubMed1974

Incorporation of D-alanine into the membrane of Streptococcus pyogenes and its stabilized L-form.

A principal aim of this study was to explain our earlier finding of a lack of d-alanine in the glycerol teichoic acid from the membrane of a stabilized L-form of Streptococcus pyogenes (B. M. Slabyj and C. Panos, 1973. J. Bacteriol. 114:934-942). It was found that the incorporation of d-alanine into the membrane teichoic acid of S. pyogenes requires either supernatant fraction or two enzymes from supernatant fraction, stimulator (d-alanine activating enzyme) and d-alanine:membrane acceptor ligase, plus membrane fragments, ATP and Mg(2+). A similar system from the L-form is inoperative. Also, no incorporation is observed with L-form or coccal supernatant fractions when L-form membranes are used. However, d-alanine incorporation is observed when L-form enzymes are used with membrane fragments from the parental streptococcus. Thus, the L-form possesses the required soluble components for d-alanine incorporation but the L-form membrane cannot function as acceptor even though it contains d-alanine-deficient membrane teichoic acid. These results suggest that a defect has occurred in the membrane of this stabilized L-form for d-alanine incorporation into membrane teichoic acid.

Adenosine Triphosphate↗
PubMed1999

Tumor necrosis factor-alpha and interleukin-1alpha decrease the adherence of Streptococcus pyogenes to cultured keratinocytes.

We hypothesized that the primary epidermal cytokines, tumor necrosis factor (TNF)-alpha and interleukin (IL)-1alpha, which are produced after skin injury, modulate bacterial adherence and the initiation of group A streptococcal skin infections. Streptococcus pyogenes binds preferentially to highly differentiated keratinocytes in vitro, simulating the superficial human skin infection, impetigo, and providing a model system for testing this hypothesis. Exposure of keratinocytes to 10 ng/mL TNF-alpha for 20 h decreased adherence to undifferentiated and differentiated keratinocytes by 33% and 38%, respectively. Treatment with 1 ng/mL IL-1alpha decreased adherence to undifferentiated and differentiated keratinocytes by 23% and 18%, respectively. Exposure to both cytokines simultaneously produced an additive 50% reduction in adherence. These data suggest that TNF-alpha and IL-1alpha may play a role in cutaneous host defense by impeding streptococcal adherence and decreasing its ability to form a nidus of infection in the skin.

Bacterial Adhesion↗
PubMed1983

Adherence of streptococcus pyogenes, Escherichia coli, and Pseudomonas aeruginosa to fibronectin-coated and uncoated epithelial cells.

The relationship between the variability in the fibronectin (Fn) content on human buccal epithelial cells and the capacity of the cells to bind gram-positive (Streptococcus pyogenes) or gram-negative (Escherichia coli or Pseudomonas aeruginosa) bacteria was investigated. Adhesion experiments performed with mixtures of epithelial cells and mixed suspensions of either S. pyogenes and E. coli or S. pyogenes and P. aeruginosa exhibited three major populations of buccal cells: one of these was able to bind S. pyogenes (gram positive) but neither of the gram-negative bacteria; a second population was able to bind the gram-negative but not the gram-positive bacteria; and a third was able to bind various numbers of both types of organisms. Further adhesion experiments performed with a mixture of epithelial cells and a mixed suspension of S. pyrogens, E. coli, and fluoresceinconjugated methacrylate beads coated with immune immunoglobulin G directed against Fn revealed that the epithelial cells recognizing the gram-positive bacteria were rich in Fn, whereas those recognizing the gram-negative organisms were poor in Fn. Immunoelectron microscopy confirmed that cells of S. pyogenes bound to epithelial cells coated with Fn, whereas cells of E. coli bound to epithelial cells lacking Fn. These results suggest that Fn on the surfaces of epithelial cells may modulate the ecology of the human oropharyngeal cavity, especially with respect to the colonization of these surfaces by pathogenic gram-negative or gram-positive bacteria.

Adsorption↗
PubMed2004

Report of unusual clinical appearance in bacteraemia with nonhaemolytic M-type 58 Streptococcus pyogenes.

BACKGROUND & OBJECTIVES: The occurrence of haemolytic colonies on blood agar often provides the starting point for the laboratory diagnosis of pyogenic streptococci, while non-haemolytic variants could pass unrecognised, leading to a failure of diagnosis. We report the details of two epidemiologically unrelated patients with bacteraemia featuring M-type 58 Streptococcus pyogenes, a seemingly rare cause of human infection in the UK, and briefly review previous reports of infection with non-haemolytic strains of this species. METHODS: Case notes of the two patients were reviewed. Isolates obtained from clinical specimens were recovered and identified and cultured on horse blood agar to observe pattern of haemolysis. RESULTS: In the first case, of a 75 year-old man with leukaemia and a retropharyngeal abscess, the isolate was consistently non-haemolytic, probably due to a failure to produce streptolysin S as has been described before in a small number of reports involving various M-types. In the second case, of an 84 year-old woman with dermatitis and septicaemia, the organism was principally beta-haemolytic but with no haemolysis on aerobic culture where the colonies were well spaced, a phenomenon thought to be associated with abundant production of serum opacity factor (OF). INTERPRETATION & CONCLUSION: These cases are a reminder that misleading cultural appearances can occur with S. pyogenes and that OF positive strains can produce poor haemolysis on aerobic culture, or fail even to do so at all.

Aged↗
PubMed1993

[Toxic shock syndrome caused by Streptococcus pyogenes].

Four days after being bitten by an insect a 35-year-old woman without any serious underlying disease developed an extensive phlegmonous inflammation of the left eyelid which soon spread to the entire left half of her face. Streptococcus pyogenes serotype M1, which produced the erythrogenic toxin A in vitro, was isolated from two blood cultures. The course of the illness was characterized by high fever, diarrhoea, vomiting, circulatory failure, consumption coagulopathy, abnormal renal functions and a generalized exanthem with desquamation of the skin, exhibiting the full-blown picture of a toxic shock syndrome caused by S. pyogenes. She eventually recovered completely under intensive care involving administration of catecholamines, fresh frozen plasma and antithrombin III substitution, as well as antibiotic treatment with clindamycin (600 mg three times daily), ampicillin/sulbactam (4 g three times daily)--after 3 days replaced by imipenem (0.5 g four times daily)--and gentamycin (80 mg three times daily) for two weeks. Extensive necroses later required plastic surgery to the left eyelid, cheek and temporal region.

Adult↗
PubMed2002

Prevalence and characterization of macrolide resistance in clinical isolates of Streptococcus pneumoniae and Streptococcus pyogenes from North America.

Resistance to macrolides is not a new phenomenon but it deserves attention because of the widespread use of these agents and their inclusion in many clinical guidelines for respiratory tract infections. The most common mechanisms by which Streptococcus pneumoniae and Streptococcus pyogenes develop resistance to macrolides is by target site modification (erythromycin ribosome methylase, erm) and efflux of the drug out of the organisms (macrolide efflux, mef). Target site modification may be of greater concern because it confers high-level resistance to all antimicrobials in the macrolide-lincosamide-streptograminB (MLSB) group. The genotype profiles of macrolide-resistant S. pneumoniae and S. pyogenes differ somewhat across regions in the US and between the US and Canada and other countries. There is some evidence for an association between macrolide resistance and treatment failure but this must be researched more fully. S. pneumoniae and S. pyogenes isolates resistant to macrolides are generally susceptible to ketolide antimicrobials because these agents bind more strongly to the relevant domain of the ribosomal subunit (withstanding erm resistance) and are less vulnerable to efflux compared to the macrolides.

Anti-Bacterial Agents↗
PubMed2000

Bactericidal activity of moxifloxacin compared to grepafloxacin and clarithromycin against Streptococcus pneumoniae and Streptococcus pyogenes investigated using an in vitro pharmacodynamic model.

The aim of the present investigation was to study and compare the killing activity of two new fluoroquinolone compounds, moxifloxacin and grepafloxacin, and a new generation macrolide, clarithromycin, against three clinical isolates of Streptococcus pneumoniae (penicillin-susceptible, -intermediate and -resistant) and two Streptococcus pyogenes (erythromycin-susceptible and -resistant) strains by simulating their human pharmacokinetics in a pharmacodynamic model. Results were achieved by measuring the reduction in viable bacterial count during the 24-h experimental period. All three antimicrobials led to a continuous reduction in the bacterial counts of penicillin-susceptible S. pneumoniae and erythromycin-susceptible S. pyogenes strains, the maximal reduction observed after 8-10 hours being 5-6 logs for moxifloxacin and 3 logs for grepafloxacin; clarithromycin exhibited a similar reduction of 5 logs only after 24 h. No regrowth was observed for any strain after 24 h with any of the antibiotics. The bactericidal activity of both the fluoroquinolones was not affected by penicillin resistance of S. pneumoniae and erythromycin resistance of S. pyogenes. In contrast, clarithromycin was not able to reduce the bacterial count of penicillin-resistant S. pneumoniae and erythromycin-resistant S. pyogenes strains. Moxifloxacin exhibited, within 24 h, higher and faster bactericidal activity than grepafloxacin and clarithromycin against S. pneumoniae, and was not affected by penicillin resistance. These results suggest that moxifloxacin is a promising new agent for treatment of streptococcal infections.

Anti-Bacterial Agents↗
PubMed1992

[Detection of polymeric IgA antibody to herpes simplex virus by pretreatment of sera with Streptococcus pyogenes--its application to diagnosis of primary infection].

In 17 patients of genital herpes virus infections, herpes simplex virus (HSV)-specific IgA antibody responses were analyzed using an enzyme-linked immunosorbent assay (ELISA) and the absorption of sera with Streptococcus pyogenes, AW43 and AR1, which bind monomeric IgA (m-IgA) and IgG antibodies, respectively. The ratio of polymeric IgA (p-IgA) to total IgA was calculated from the formula, the p-IgA index = IgA activity after absorption/IgA activity before absorption. In early-convalescent-phase sera from primary cases, the p-IgA indices were 0.5-0.9, whereas in recurrent or provoked cases, they were lower than 0.2. There results indicate that the p-IgA index may be useful for rapid and simple differentiation of primary from non-primary HSV infections.

Antibodies, Viral↗
PubMed2000

Bacteriologic characteristics and serotypings of Streptococcus pyogenes isolated from throats of school children.

To determine the carrier rate of beta-hemolytic streptococci (BHS), throat cultures were taken from healthy elementary school children in four separate areas of Korea from 1992 to 1995, including Inje, Nonsan, Seoul and Chinju. The strains of Streptococcus pyogenes had been serotyped with anti-T, -OF and -M sera. The isolation rates of BHS and S. pyogenes ranged from 14.1-32.4% and 10.9-18.5% respectively. More than half of the carriers showed heavy growth of BHS. M78 (48.6%) and M28 (22.2%) were most common in Inje, M12 (23.6%) and M5 (20.3%) in Nonsan, M12 (48.8%) and M5 (14.6%) in Seoul, and M12 (26.3%) and M22 (14.5%) in Chinju, respectively. About 15% of school children were positive for S. pyogenes in throat cultures, and the distribution of serotypes varied according to geographical regions.

Carrier State↗
PubMed2001

Detection of macrolide resistance mechanisms in Streptococcus pneumoniae and Streptococcus pyogenes using a multiplex rapid cycle PCR with microwell-format probe hybridization.

In this study, a multiplex rapid cycle PCR with microwell-format probe hybridization method was developed to perform high-volume screening for macrolide resistance determinants in isolates of Streptococcus pneumoniae and Streptococcus pyogenes. The method was then utilized to determine the distribution of macrolide resistance mechanisms in recent isolates of S. pneumoniae and S. pyogenes from Great Britain and Ireland. For 83 strains of macrolide resistant S. pneumoniae tested, 51 (61.4%) were positive for mef(A), 29 (34.9%) erm(B), two (2.4%) double mechanisms mef(A) + erm(B), and one (1.2%) negative for all mechanisms tested. For 56 strains of macrolide-resistant S. pyogenes tested, 33 (58.9%) were positive for erm(A) subclass erm(TR), 18 (32.1%) mef(A) and five (8.9%) erm(B).

Anti-Bacterial Agents↗
PubMed1995

Invasion of cultured human cells by Streptococcus pyogenes.

The invasive capacity of streptococcal strains belonging to groups A and B was evaluated by infecting human epithelial and endothelial cells and monitoring the number of viable intracellular bacteria at different times postinfection. All strains tested entered eukaryotic cells (HeLa, HEp2 and HUVE), with Streptococcus pyogenes exhibiting a higher invasion efficiency than group B streptococci (GBS). No intracellular multiplication was observed, and GBS remained viable 24 h postinfection, whereas S. pyogenes were gradually killed. We found that cytochalasin D almost completely inhibited internalization of all bacterial strains, whereas colchicine had no effect, indicating that host microfilaments play a major role in bacterial internalization. Moreover, the use of the lysosomotropic agent ammonium chloride enabled us to demonstrate that a pH increase in the intracellular vesicles did not affect streptococcal entry. These results were documented by electron microscopic observations which revealed the different steps in the invasion pathway, including a fusion event between phagosomes containing S. pyogenes and lysosomes.

Ammonium Chloride↗
PubMed1976

Persistence, pathogenesis, and morphology of an L-form of Streptococcus pyogenes adapted to physiological isotonic conditions when in immunosuppressed mice.

Evidence obtained using nonimmunosuppressed and newborn mice suggests that the immune response of the host plays a role in the rapid removal of a physiologically isotonic L-form of Streptococcus pyogenes, since its inability to persist in vivo was not due to osmotic lysis. With mice immunosuppressed with methylprednisolone sodium succinate, viability and detection of this L-form by fluorescent antibody was prolonged for at least 2 weeks, the approximate duration of immunosuppression in these mice. However, heat-killed L-form cells only persisted for 3 days in such mice. Therefore, persistence of a viable L-form in these treated mice was not simply due to the lack of removal of L-forms by a compromised host. At no time was there any indication of illness in nonimmunosuppressed or immunosuppressed mice after L-form injection, and all internal organs, when examined macroscopically, remained normal. Thus, overt pathogenesis was not a characteristic of this L-form in a suitable host even when its immune response had been compromised. The microscopic morphology of the L-form after isolation from immunosuppressed mice changed drastically. It was typically micrococcal in appearance and exemplified the cellular variability achievable by this organism in vivo. Also, streptolysin S production was increased markedly by passage of the L-form in immunosuppressed mice. However, M protein, as a cellular component, was not detected serologically, nor was any reformation of a rigid cell wall apparent by electron microscopy after isolation of this streptococcal L-form from such mice.

Animals↗
PubMed2003

Interactions between M proteins of Streptococcus pyogenes and glycosaminoglycans promote bacterial adhesion to host cells.

Several microbial pathogens have been reported to interact with glycosaminoglycans (GAGs) on cell surfaces and in the extracellular matrix. Here we demonstrate that M protein, a major surface-expressed virulence factor of the human bacterial pathogen, Streptococcus pyogenes, mediates binding to various forms of GAGs. Hence, S. pyogenes strains expressing a large number of different types of M proteins bound to dermatan sulfate (DS), highly sulfated fractions of heparan sulfate (HS) and heparin, whereas strains deficient in M protein surface expression failed to interact with these GAGs. Soluble M protein bound DS directly and could also inhibit the interaction between DS and S. pyogenes. Experiments with M protein fragments and with streptococci expressing deletion constructs of M protein, showed that determinants located in the NH2-terminal part as well as in the C-repeat region of the streptococcal proteins are required for full binding to GAGs. Treatment with ABC-chondroitinase and HS lyase that specifically remove DS and HS chains from cell surfaces, resulted in significantly reduced adhesion of S. pyogenes bacteria to human epithelial cells and skin fibroblasts. Together with the finding that exogenous DS and HS could inhibit streptococcal adhesion, these data suggest that GAGs function as receptors in M protein-mediated adhesion of S. pyogenes.

Bacterial Adhesion↗
PubMed2006

Streptococcus pyogenes induces epithelial inflammatory responses through NF-kappaB/MAPK signaling pathways.

Innate immunity involves a cascade of inflammatory events, resulting in the secretion of chemokines and cytokines to recruit mediator cells in adaptive immunity. To study epithelial inflammatory responses initiated by Streptococcus pyogenes infection, we investigated chemotaxis ability in the supernatant of infected human respiratory epithelial HEp-2 cells. Our results showed that these supernatants showed significantly increased ability to attract monocytes, implying the release of inflammatory chemoattractants into the medium. Expression of interleukin (IL)-8 and IL-6 in HEp-2 cells was significantly increased at both the mRNA and protein levels after infection with S. pyogenes. Electrophoretic mobility shift and reporter-gene assays demonstrated that the transcription factors NF-kappaB and AP-1, regulated by mitogen-activated protein (MAP) kinase, were activated after streptococcal infection. The increases in mRNAs for IL-8 and IL-6 were abrogated by addition of NF-kappaB and MAP kinase inhibitors, suggesting that the upregulation of IL-8 and IL-6 is mediated through NF-kappaB and MAP kinase signaling pathways. Taken together, our results indicate that S. pyogenes infection of epithelial cells induces the secretion of pro-inflammatory chemokines/cytokines through activation of NF-kappaB and MAP kinase signaling pathways. These early innate responses initiated by S. pyogenes-infected respiratory epithelial cells may recruit immune cells to the airway and induce inflammation.

Apigenin↗
PubMed1976

Membrane studies of Streptococcus pyogenes and its L-form growing in hypertonic and physiologically isotonic media. An electron spin resonance spectroscopy approach.

Electron spin resonance spectroscopy (ESR) was used to compare the lipid organization, thermal stability and the physical state of the membrane of a human pathogen, Streptococcus pyogenes and its osmotically fragile L-form with this same L-form now adapted to grow under physiologically isotonic conditions (physiological L-form). Comparison of the hyperfine splittings of a derivative of 5-ketostearic acid spin label, I(12, 3), after incorporation into the membrane, revealed that the lipid chain rigidity of these membranes is in the order physiological L-form greater than osmotically fragile L-form greater than streptococcus. The signal intensity (of the center magnetic field line) versus temperature analysis showed two transitions for these membranes. The first with melting points of 45, 26 and 36 degrees C and second transition at 70, 63 and 60 degrees C for the physiological L-form, osmotically fragile L-form and streptococcal membranes, respectively. This same order of membrane lipid chain rigidity was seen from the cooperativities obtained for each of these systems from analysis based on the expression for an n-order reaction. The I(12, 3) and other probes with the paramagnetic group close to the methyl end of the molecule suggested that this difference in lipid chain rigidity between these organisms resides in the environment closer to the lipid head group region rather than in the hydrophobic lipid core. Another major finding was the binding of I(12, 3) at two or more different sites in each of the membranes examined. This change in lipid chain rigidity now provides an explanation to account for the survival of a previously osmotically fragile L-form in physiologically isotonic media by focusing on changes in the physical nature of its membrane. In so doing, it adds to and reinforces the speculation of the potential survival in vivo and involvement in pathogenesis of osmotically fragile aberrant forms of bacteria.

Cell Membrane↗