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The streptokinase gene of the Streptococcus pyogenes strain CIP 56.57 was cloned and sequenced. This sequence coding for a 441 amino acid protein is well conserved among streptococcus species: there are two very conserved domains separated by a more variable region.
Occurrence and susceptibility to antimicrobial agents of Streptococcus pyogenes strains isolated from purulent infections of soft tissue were examined. The specimen was from hospital and ambulatory patients in 1996-1998. In general, 3665 samples were examined: 1841 wound swabs, 870 pus samples, 753 ulcer swabs and 101 from the decubitus ulcers. The ulcer of shank was the main diagnosis from which the Streptococcus pyogenes was isolated (38.8%). The susceptibility to antimicrobial agents according to the disc-diffusion method was analyzed among the 59 S. pyogenes strains. 10.2% strains with the MLSB resistance were detected. All S. pyogenes strains were susceptible to penicillin, new quinolons and glicopeptides.
Domingue, Gerald J. (Tulane University, New Orleans, La.), and William A. Pierce, Jr. Effect of partially purified streptococcal M protein on the in vitro phagocytosis of Streptococcus pyogenes. J. Bacteriol. 89:583-588. 1965.-M protein from Streptococcus pyogenes strain Bailey type 12 was adsorbed onto cells of a glossy mutant of this strain. Phagocytosis experiments were performed in vitro with rabbit peritoneal polymorphonuclear leukocytes. Direct microscopic counts suggested M protein-treated cells were more resistant to phagocytosis than were untreated cells. With the Cohn and Morse technique for evaluating quantitatively the fate of bacteria during phagocytosis, there was observed a more rapid drop in total and extracellular counts of treated, as compared with untreated, cells. Experiments with radioactively labeled streptococci showed that M-treated cells were more readily destroyed within leukocytes than were nontreated glossy streptococci, which suggested a reason for the scarcity of treated streptococci in direct microscopic counts.
Two patients with toxic shock-like syndrome are presented. Both patients had necrotizing cellulitis due to Streptococcus pyogenes, and both patients required extensive surgical debridement. The association of Streptococcus pyogenes infection and toxic shock-like syndrome is discussed.
An outbreak of Streptococcus pyogenes infection occurred in a colony of 800 Dunkin-Hartley guinea pigs resulting in 364 (46%) deaths involving breeders, sucklings, weaners, but mainly adults used as a source of blood meals for haematophagus flies (Glossina palpalis). Clinical signs included bleeding from the nose, mouth and vagina before death. Necropsy revealed pneumonia with consolidation of one or both lungs, haemopericardium and haemothorax. There were yellowish-grey deposits in the urinary bladder of more than 50% of both affected breeders and adults used for feeding haematophagus flies. Beta-haemolytic Streptococcus pyogenes was isolated in pure culture from many tissues including the urinary bladder. The survivors were treated with oxytetracycline (Terramycin-LA; Pfizer) using the intra-muscular route and the response was good.
Fifty-seven strains of Streptococcus pyogenes isolated from septic patients and 52 isolates from nonbacteremic patients in southern Israel were investigated for their susceptibility to new macrolides and other antimicrobial drugs. In addition, typing of the isolates by M protein and T antigen was performed. All organisms were susceptible to penicillin and chloramphenicol, 59% to tetracycline, and 7% to trimethoprim-sulfamethoxazole. All isolates but one (99%) were susceptible to clarithromycin, azithromycin, erythromycin, and clindamycin. The MIC90 of clarithromycin, erythromycin, and clindamycin was 0.064, 0.125, and 0.094 microgram/ml, respectively. Overall, 96% of the isolates could be typed by T antigen, but only 43% were M-protein typeable. No predominance of any particular M-protein type was observed. No significant differences between blood isolates and organisms derived from other sources were observed in the antibiotic susceptibility patterns or the distribution of serotypes. It is concluded that invasive Streptococcus pyogenes infections in southern Israel are caused by multiple unrelated strains. The organism remains susceptible to macrolides and clindamycin.
The human pathogen Streptococcus pyogenes possesses a chromosomal region, the mga regulon, that contains co-regulated genes important to the virulence of these bacteria. A novel gene located in the mga regulon of a S. pyogenes strain of serotype M1 was cloned and sequenced. It translates into a protein of 305 amino acid residues, including a signal sequence of 32 amino acids and a central region consisting of three tandem repeats. The sequence represents a novel structure with no significant homology to any previously published sequence. The protein was purified from the streptococcal culture media where it is present in substantial amounts. Affinity chromatography of human plasma on Sepharose coupled with the protein specifically absorbed two plasma proteins which were identified as clusterin and histidine-rich glycoprotein (HRG). The interactions between the streptococcal protein and the plasma proteins were further characterized using purified clusterin and HRG. Inhibition experiments indicated that they have affinity for overlapping or closely located sites in the streptococcal protein. Both clusterin and HRG are regulators of the membrane attack complex (C5b-C9) of complement. When the streptococcal protein was added to serum, complement-mediated lysis of sensitized sheep erythrocytes and guinea pig erythrocytes was inhibited. In addition, the streptococcal protein was incorporated into C5b-C9 in serum, indicating the location of its action. The name, protein SIC, streptococcal inhibitor of complement-mediated lysis, is therefore suggested for this novel protein. The occurrence of protein SIC and its gene was investigated in a collection of S. pyogenes strains comprising 55 different M serotypes. Only M1 and M57 strains were positive in this screening, indicating that protein SIC could be a virulence determinant. Thus, during recent years, the M1 serotype has been connected with a world-wide increase of severe and toxic S. pyogenes infections.
BACKGROUND: Streptococcus pyogenes is a bacteria which, at present, is seldom isolated in blood and articular fluid. An intravenous drug addict with human immunodeficiency virus infection, with bacteremia and arthritis by S. pyogenes, associated with tuberculosis is presented. METHODS: Blood and articular fluid cultures were collected in the usual and Löwenstein-Jensen media. RESULTS: The patient improved with penicillin and tuberculostatic drugs. Nine months after this episode, the patient reinitiated intravenous drug addiction, and developed another presentation of bacteremia and arthritis by S. pyogenes. CONCLUSIONS: Heroin addict patients constitute a risk group for bacteremias ans severe infections by S. pyogenes.
The surface-located M protein functions to protect Streptococcus pyogenes (the group A streptococcus) from phagocytosis by polymorphonuclear leukocytes. It has been suggested that this protection results from the ability of M protein to bind factor H, a serum protein that can inhibit the activation of complement. Among different serological variants of M protein, the C-repeat domain is highly conserved and is exposed on the bacterial surface. This domain has been implicated in binding to complement factor H and in M-protein-mediated adherence of streptococci to human keratinocytes in the cutaneous epithelium. In this study, we constructed an S. pyogenes mutant strain which expresses an M6 protein from which the entire C-repeat domain was deleted. As predicted, this mutant did not adhere well to human keratinocytes and was unable to bind to factor H. Unexpectedly, the mutant was able to survive and multiply in human blood. Therefore, while the binding of factor H and the facilitation of adherence to keratinocytes appear to involve recognition of the C-repeat domain, a region of the M-protein molecule distinct from the C-repeat domain confers upon S. pyogenes its ability to resist phagocytosis.
Changes in the structural components of the Streptococcus pyogenes membrane between exponential and early stationary phases of growth are reported. The overall protein composition ranged from 70 to 73% of the dry weight of the membranes, irrespective of the phase of growth from which they were isolated. Amino acid analyses of membranes isolated from streptococci in either the exponential or stationary phase of growth demonstrated that two amino acids, cysteine and tryptophan, were absent. Further analysis of the membrane proteins by sodium dodecyl sulfate-polyacrylamide gradient gel electrophoresis demonstrated that there were proteins unique to a particular phase of growth as well as differences in the amount of specific proteins from the various growth phases. In addition, membranes isolated from exponential-phase cultures contained a higher percentage of peripheral protein than did stationary-phase membranes. There also appeared to be an increase in the amount of outer surface proteins during this growth phase. The phosphorus content of the membranes increased during the stationary phase of growth, whereas the sugar composition remained constant. The only sugar found under various conditions of growth in any of the strains was glucose. Total fatty acid content and the mole percent composition of various fatty acids did not change in the different phases of growth. However, the mole percent composition of fatty acids in the membranes of various group A streptococci did differ between strains. Therefore, these results provide evidence that the composition of membranes of S. pyogenes does not remain constant throughout the growth phases of the culture.
Streptococcus pyogenes is an important Gram-positive pathogen that is strictly limited to infections in humans. Here we report that streptolysin O (SLO), a cytolytic exotoxin secreted by S. pyogenes, activates human polymorphonuclear neutrophils (PMNs) by perforating these cells. This appears to be followed by an influx of Ca(2+) and p38 MAPK activation. As a consequence, PMNs secrete heparin-binding protein, a potent inducer of vascular leakage, and neutrophil-borne proteins, including LL-37, alpha-defensins, and elastase. The results of the present work therefore suggest that the interaction between SLO and PMNs evokes an exaggerated host response which may contribute to the pathogenesis of local and generalized S. pyogenes infections.
The ability of Streptococcus pyogenes to enter a quiescent state, similar to the stationary phase of lab cultures, is believed to be an important factor in its ability to persist within the host and to subsequently cause disease. Using a model broth system, we determined that after entering the stationary phase, there was a 99.99% reduction in cell viability over a 4-day period, following which the cells appeared to enter a resistant starvation state where cell numbers remained constant over the subsequent 3-4 weeks. This starvation response was induced by carbon or phosphorous limitation, but not by nitrogen limitation in the form of amino acids where cells became non-culturable after 4 days. Amino acid utilization in the absence of a carbon source may be an essential factor for the long-term survival of this bacterium in the stationary phase. Early stationary phase cells showed a greater resistance to oxidative and pH stress compared to 24-h-starved cultures. There was evidence for the formation of a viable but non-culturable state as indicated by a comparison of the numbers of cells with a functional membrane potential (rhodamine 123) against culturable cells on either Todd Hewitt broth agar or sheep blood agar. Long-term survival of S. pyogenes was dependent on both cell wall and protein synthesis, suggesting that starving cultures are a dynamic cell population.
Streptococcus pyogenes infections often fail to respond to antibiotic therapy, leading to persistent throat carriage and recurrent infections. Such failures cannot always be explained by the occurrence of antibiotic resistance determinants, and it has been suggested that S. pyogenes may enter epithelial cells to escape antibiotic treatment. We investigated 289 S. pyogenes strains isolated from different clinical sources to evaluate their ability to form biofilm as an alternative method to escape antibiotic treatment and host defenses. Up to 90% of S. pyogenes isolates, from both invasive and noninvasive infections, were able to form biofilm. Specific emm types, such as emm6, appeared to be more likely to produce biofilm, although variations within strains belonging to the same type might suggest biofilm formation to be a trait of individual strains rather than a general attribute of a serotype. Interestingly, erythromycin-susceptible isolates formed a significantly thicker biofilm than resistant isolates (P < 0.05). Among resistant strains, those carrying the erm class determinants formed a less organized biofilm than the mef(A)-positive strains. Also, prtF1 appeared to be negatively associated with the ability to form biofilm (P < 0.01). Preliminary data on a selection of strains indicated that biofilm-forming isolates entered epithelial cells with significantly lower efficiency than biofilm-negative strains. We suggest that prtF1-negative macrolide-susceptible or mef(A)-carrying isolates, which are poorly equipped to enter cells, may use biofilm to escape antimicrobial treatments and survive within the host. In this view, biofilm formation by S. pyogenes could be responsible for unexplained treatment failures and recurrences due to susceptible microorganisms.
Streptococcus pyogenes is an important human pathogen. Betalactams are still the drug of choice for the treatment of infections caused by this microorganism. In recent years an increase in the use of macrolides for initial treatment in respiratory infections has been observed; consequently, the number of macrolide-resistant isolates has also increased. We investigated the susceptibility of S. pyogenes to penicillin, erythromycin, clarithromycin and clindamycin in Cordoba during 2000, 2001 and the first 6 months of 2002. We obtained 100 isolates of S. pyogenes from 1232 pharyngeal exudates, all of which were susceptible to penicillin and 39 of which were resistant to erythromycin and clarithromycin. Twenty-six of these 39 isolates were susceptible to clindamycin.
Twenty-eight emm12-type Streptococcus pyogenes isolates from patients with invasive and noninvasive infections or from asymptomatic carriers were genetically typed. Sequencing of drs (distantly related sic [streptococcal inhibitor of complement]) genes identified two novel alleles and revealed a polymorphism for drs similar to that of sic. No association was observed between the five different drs alleles and the five restriction patterns of the vir regulon for the isolates studied. These data suggest that drs sequencing may be useful for further differentiation of S. pyogenes isolates with emm12 and identical vir regulon restriction patterns.
BACKGROUND: Macrolide resistance among Streptococcus pyogenes strains is increasing in many European countries. Greece was not considered a country with high prevalence of macrolide-resistant S. pyogenes strains, and until now the genetic mechanism of resistance was unknown. METHODS: During the 25-month period from December, 1998, to December, 2000, pharyngeal cultures for S. pyogenes were performed on 743 Greek children with the clinical diagnosis of pharyngitis. The children were 1 to 16 years old (median age, 7 years) and were living in Central and Southern Greece. S. pyogenes isolates were tested for their susceptibility to erythromycin, clarithromycin, azithromycin, clindamycin, penicillin G, amoxicillin/clavulanate and cefprozil. The erythromycin-resistant isolates were further studied for their genetic mechanism of resistance by means of PCR. RESULTS: Of a total of 275 S. pyogenes isolates recovered, 105 (38%) were erythromycin-resistant (MIC > or = 1 microgram/ml) [corrected], with 54, 45 and 1% of them carrying mef(A), erm(A) [subclass erm(TR)] and erm(B) gene, respectively. The prevalence of erythromycin-resistant strains was 29 and 42% during the time periods December, 1998, to December, 1999, and January, 2000, to December, 2000, respectively. All erythromycin-resistant isolates were also resistant to clarithromycin and azithromycin. The isolates carrying the erm(A) gene were inducibly resistant to clindamycin. The 275 S. pyogenes isolates had ceprozil MICs < or = 0.032 microgram/ml. CONCLUSIONS: The current high (38%) prevalence of erythromycin-resistant S. pyogenes in Central and Southern Greece requires continuous surveillance and careful antibiotic policy.
A nutritionally variant Streptococcus pyogenes strain was isolated from a periorbital abscess. The organism was identified with the use of three rapid biochemical test kits, and the group A antigen was detected by conventional serology as well as direct antigen detection tests.
Most patients with acute cellulitis due to Streptococcus pyogenes have a striking onset of high fever and systemic toxicity. Even if hospitalization is deemed necessary for initial treatment, most patients respond promptly to appropriate antibiotic therapy and can be managed as outpatients for most of the treatment regimen. Described is a 48-year-old, previously healthy woman with acute cellulitis and lymphadenitis who did not initially respond to treatment despite proved in vitro activity against the patient's S. pyogenes isolate. The strain grew as a mucoid colony phenotype on blood agar plates. The mucoid characteristic of the strain may have accounted for the patient's lack of response to initial therapy, and previously published clinical and laboratory data support this impression.