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PubMed1997

Susceptibility of Streptococcus pyogenes from throat cultures to macrolide antibiotics and influence of collection criteria.

OBJECTIVE: To assess the incidence of resistance to erythromycin and to the three other macrolide antibiotics most extensively used in Italy (azithromycin, clarithromycin and roxithromycin) among clinical strains of Streptococcus pyogenes freshly isolated from throat cultures of pediatric patients in an area of Central Italy. METHODS: Two sets of isolates were examined. The strains of the first set (n=100) were collected according to a protocol admitting only throat swabs from untreated patients with symptoms of acute pharyngotonsillitis. The second set (n=180) consisted of strains isolated from throat cultures during the routine activity of diagnostic laboratories, no particular protocol being applied. RESULTS: A trimodal distribution of strains was observed in relation to their macrolide susceptibility levels: two clusters were constituted by highly susceptible and highly resistant strains, respectively; a third, middle cluster consisted of strains displaying low-level resistance (or even intermediate susceptibility, in a minority of isolates, to clarithromycin). The distribution of individual isolates in the three modal clusters was the same with all four drugs. Both MIC ranges and MIC50s almost overlapped in the isolates of the two sets, whereas MIC90s were far higher in the strains of the second set (4 micro g/mL for clarithromycin, 8 micro g/mL for erythromycin and azythromycin, and 16 micro g/mL for roxithromycin) than in those of the first (0.125 micro g/mL for all four drugs). Resistant strains were 5% among the isolates of the first set and three times as many among those of the second. CONCLUSIONS: The lower incidence of macrolide resistance recorded in the first set is probably more reliable: the threefold incidence observed in the second set may be overestimated due to the lower frequency of strains involved in drug-responsive infections and to the increased occurrence of strains from unsuccessfully treated patients.

Journal Article↗
PubMed1999

The effect of carbon dioxide on susceptibility testing of azithromycin, clarithromycin and roxithromycin against clinical isolates of Streptococcus pneumoniae and Streptococcus pyogenes by broth microdilution and the Etest: Artemis Project-first-phase study.

OBJECTIVE: To evaluate the effect of carbon dioxide on the susceptibility testing, using broth microdilution and the Etest (AB Biodisk, Solna, Sweden), of azithromycin, clarithromycin and roxithromycin against Streptococcus pneumoniae and Streptococcus pyogenes. METHODS: Fresh clinical isolates collected from 36 hospital laboratories in 12 countries were evaluated using the Etest in the presence of carbon dioxide. The isolates were retested under ambient conditions (absence of carbon dioxide) using broth microdilution and/or the Etest. RESULTS: Carbon dioxide falsely elevated azithromycin, clarithromycin and roxithromycin MIC90S for S. pneumoniae, determined by the Etest, approximately 12-fold. Also, the azithromycin MIC90 for S. pyogenes was increased fourfold; the effect was less marked for clarithromycin and roxithromycin. When isolates were retested in the absence of carbon dioxide, using the Etest or microdilution, susceptibilities to azithromycin were comparable to those to clarithromycin (S. pneumoniae, 93.4% versus 91.3%; S. pyogenes, 96.4% versus 95.8%). Both organisms were less susceptible to roxithromycin (S. pneumoniae, 71.3%; S. pyogenes, 85.7%). An internal standard control, consisting of 50 isolates each of S. pneumoniae, S. pyogenes and Haemophilus influenzae, confirmed that azithromycin susceptibility testing resulted in falsely elevated MICs. CONCLUSIONS: Carbon dioxide falsely elevated azithromycin MICs for S. pneumoniae and S. pyogenes, with an apparent reduction in susceptibility. When the in vitro activity of azithromycin and other macrolides against S. pneumoniae and S. pyogenes is being evaluated, awareness of the pH effect is essential.

Journal Article↗
PubMed1986

Mechanism of NK activation by OK-432 (Streptococcus pyogenes). I. Spontaneous release of NKCF and augmentation of NKCF production following stimulation with NK target cells.

The biological response modifier OK-432 (Picibanil) (manufactured in Japan) is produced by lyophilization of cultures of the low virulent Su strain of group A Streptococcus pyogenes of human origin. This preparation has been shown to have multiple effects on the immune system and has been used as an anti-cancer therapeutic agent in man. It has been shown that OK-432 augments the cytotoxic activity of human natural killer (NK) cells. We have proposed that natural killer cytotoxic factors (NKCF) derived from NK cells play a role in the mechanism of NK cell-mediated cytotoxicity (CMC). The present study investigates the underlying mechanism of the OK-432-mediated enhancement of NK activity by determining whether OK-432 has an effect on the induction and activity of NKCF produced by NK cells. Treatment of peripheral blood lymphocytes (PBL) with OK-432 for 20 hr and wash resulted in significant augmentation of NK CMC and this enhancement was dependent on the concentration of OK-432 used. Coculture of the OK-432-treated PBL with U937 resulted in a several-fold enhanced production of NKCF in the supernatant. The NKCF produced were similar to those produced by untreated effector cells in that they had the same NK target specificity for lysis. The time kinetics of stimulation of PBL with OK-432 for optimal production of NKCF was found to be 8-12 hr. It was also observed that culture of OK-432-treated PBL in the absence of stimulator cells spontaneously release significant amounts of NKCF into the supernatant. The supernatant containing NKCF was tested for interleukin 2 (IL-2) activity using an IL-2-dependent HT-2 line. It was found that there was no direct correlation between the levels of NKCF and IL-2 activity. The results of this study demonstrate that OK-432 stimulates NK cells to produce NKCF in the presence or absence of stimulator cells. The optimum concentration of OK-432-induced augmentation of NK CMC paralleled that seen for optimum NKCF production, suggesting that one mode of action of OK432 is to enhance NKCF production in a manner reminiscent of IFN and IL-2. The results also point out that OK-432 acts by a mechanism independent of the action of IL-2.

Biological Products↗
PubMed2006

Macrolide, lincosamide and tetracycline susceptibility and emm characterisation of invasive Streptococcus pyogenes isolates in Israel.

Group A beta-haemolytic streptococcus (GAS) causes a variety of infections, including life-threatening illnesses. Although the species is uniformly penicillin susceptible, resistance to other antibiotics is becoming more common. We studied the prevalence of resistance and associated factors in a nationwide, prospective, population-based study of invasive infections in Israel. Isolates were collected in collaboration with 24 hospitals in Israel during 1996-1999. Minimal inhibitory concentrations (MICs) of erythromycin (ERY), clindamycin (CLI) and tetracycline (TET) were determined as well as ERY and TET resistance phenotypes and genotypes. Five hundred isolates were examined: 136 (27.2%) were not susceptible to TET, 10 (2.0%) to ERY and 5 (1%) to CLI. ERY resistance was associated with emm types 12 and 83 (P<0.001 for both). MICs of TET had a bimodal distribution distinguishing sensitive and resistant populations. Non-susceptibility to TET was mainly due to the presence of tet(M) and was associated with T types 3, 3/13/B3624 and 9 and emm types 9, 33, 64, 73, 74, 76, 77 and 83. TET susceptibility was associated with T types 1, 2 and 11, emm types 1-4, 11, 12, 22, 26 and 75 and the presence of speA and speC. In Israel, resistance of invasive GAS isolates to ERY remains low and is associated with specific T and emm types, as is TET resistance. TET resistance is less frequent than previously reported in Israel and is associated with a lower prevalence of speA and speC.

Anti-Bacterial Agents↗
PubMed2025

Global spread of Streptococcus pyogenes A genomics-supported narrative review.

Group A Streptococcus (GAS) has recently reemerged as a leading cause of both mild and severe invasive infections worldwide, with recent upsurges in invasive disease among children and adults. Notwithstanding a partial synchronicity with the COVID-19 pandemic, this rapid global dissemination of more virulent GAS lineages has been promptly detected, as well as the molecular shifts underlying the observed changes in clinical patterns. Whole-genome sequencing (WGS)-based genomic epidemiology allowed us to gain relevant insights into this upsurge as it was happening. This review integrates the canonical research publication-based approach with genomic data and metadata and identifies a subset of genomic clusters playing a major role in invasive GAS (iGAS) infections worldwide, which were named as Global Pathogenic Lineages (GPLs). The four GPLs broadly coincide with five sequence types (STs): GPL1 with ST28, GPL2 with ST15 and ST315, GPL3 with ST52, and GPL4 with ST39. While non-GPLs clusters maintain a baseline reservoir of antimicrobial-resistance and virulence genes, GPLs show varying but noteworthy resistance profiles and are frequent causes of iGAS. The integration of WGS into routine diagnostics procedures is a forthcoming improvement, aimed not only at informing tailored therapy and implementing infection control strategies, but also to perform continuous surveillance. Ongoing WGS in clinical microbiology, as a matter of fact, will provide unparalleled insights into lineage emergence, transmission dynamics, and the geographic clustering of virulence and resistance determinants.

Streptococcus pyogenes↗
PubMed1992

[Toxic shock syndrome in infection due to Streptococcus pyogenes].

Acute infections with group A beta-hemolytic streptococcus normally take a favourable course under therapy with penicillin. Only in a few cases has a completely different manifestation been described with multisystem failure similar to toxic shock syndrome induced by Staphylococcus aureus. We report on 4 patients (1990/91) who showed this manifestation in spite of immediate antibiotic therapy. In 3 patients the suspected portal of entry was the skin, in 1 patient it was unknown. Group A streptococci were grown from blood cultures from all 4 patients. Without an underlying immune deficiency all 4 patients (age 22, 24, 38 and 51) went into septic shock with high fever, hepatic and renal impairment, diarrhea, DIC and cerebral confusion. 2 patients died within a few days after developing acute respiratory distress syndrome and cerebral edema. All strains isolated from the patients were penicillin-sensitive, group A streptococci. 3 of them were M-type 1, which are known to be more invasive. The bacteremia by itself is not sufficient to explain all complications and the high mortality rate. It is probable that streptococcal toxins, such as pyrogenic exotoxin A, streptolysin O, or a new unknown one, play a decisive role.

Adult↗
PubMed2004

Influence of thiamphenicol on the primary functions of human polymorphonuclear leucocytes against Streptococcus pyogenes.

Current antibiotic therapy encourages the use of antibiotics that may potentiate the host's immune defences. We therefore investigated the effect of thiamphenicol (TAP), the active principle of thiamphenicol glycinate acetylcysteinate (TGA), on human granulocyte functions, mainly phagocytosis and intracellular killing of Streptococcus pyogenes. Our findings support the use of thiamphenicol in the treatment of respiratory tract infections caused by S. pyogenes as it acts directly against the pathogen as well as in cooperation with PMNs by eliciting their intracellular killing.

Anti-Bacterial Agents↗
PubMed2004

Mutation at the position 2058 of the 23S rRNA as a cause of macrolide resistance in Streptococcus pyogenes.

BACKGROUND: In streptococci, three macrolide resistance determinants (erm(B), erm(TR) and mef(A)) have been found. In addition, certain mutations at the ribosomal 23S RNA can cause resistance to macrolides. Mutation at the position 2058 of the 23S rRNA of the Streptococcus pyogenes as a cause of macrolide resistance has not been described before. METHODS: Antibiotic resistance determinations for the clinical S. pyogenes strain ni4277 were done using the agar dilution technique. Macrolide resistance mechanisms were studied by PCR and sequencing. All six rRNA operons were amplified using operon-specific PCR. The PCR products were partially sequenced in order to resolve the sequences of different 23S rRNA genes. RESULTS: One clinical isolate of S. pyogenes carrying an adenine to guanine mutation at the position 2058 of the 23S rRNA in five of the six possible rRNA genes but having no other known macrolide resistance determinants is described. The strain was highly resistant to macrolides and azalides, having erythromycin and azithromycin MICs > 256 microgram/ml. It was resistant to lincosamides (clindamycin MIC 16 microgram/ml) and also MIC values for ketolides were clearly elevated. The MIC for telithromycin was 16 microgram/ml. CONCLUSION: In this clinical S. pyogenes strain, a mutation at the position 2058 was detected. No other macrolide resistance-causing determinants were detected. This mutation is known to cause macrolide resistance in other bacteria. We can conclude that this mutation was the most probable cause of macrolide, lincosamide and ketolide resistance in this strain.

Journal Article↗
PubMed1998

Control of endotoxin shock by the dried preparation of low virulent Streptococcus pyogenes OK-432.

Bacterial endotoxin, lipopolysaccharide (LPS), is a causative agent of Gram-negative septic shock. However, if preadministered at a low dose, LPS makes mice resistant to subsequent endotoxin challenge, the phenomenon known as LPS tolerance. Here we demonstrated that the pharmaceutical preparation of Gram-positive Streptococcus pyogenes, OK-432, also induced a state analogous to LPS tolerance if administered 6-48 h prior to LPS challenge. The preadministration of OK-432 increased the lethal dose of LPS threefold in BDF1 mice, and this was accompanied by reduced gene expression of IL-6, IFN-gamma, inducible nitric oxide synthase, and IL-10 in spleen and peritoneal cells. Serum concentrations of IL-6 and IFN-gamma were also suppressed by the preadministration of OK-432. In contrast to the LPS tolerance, the levels of TNF-alpha mRNA were not suppressed in OK-432-administered mice, and their peritoneal cells produced high levels of TNF-alpha and soluble TNF receptor p75 in response to LPS in vitro. Peritoneal cells from OK-432 but not LPS-administered mice were hyporesponsive to IFN-gamma in terms of nitric oxide synthesis, and this hyporesponsiveness to IFN-gamma was abrogated by anti-IL-10 antibodies. Likewise, peritoneal cells from both OK-432- and LPS-administered mice were hyporesponsive to LPS, serum, TNF-alpha, IFN-gamma, and PMA in terms of IL-6 production. Anti-IL-10 antibodies increased IL-6 production eightfold in cells from OK-432-administered mice, but marginally in cells from LPS-administered mice. Even in peritoneal cells from OK-432-administered mice, anti-IL-10 antibodies failed to fully restore IL-6 production. Thus, the hyporesponsive state of peritoneal cells was mediated by both IL-10-dependent and -independent mechanisms. These results demonstrated that OK-432 controlled endotoxin shock by blocking the cytokine cascade from TNF-alpha.

Animals↗
PubMed1987

Antitumor activity of a Streptococcus pyogenes preparation (OK-432). I. Sequential effector mechanisms following a single OK-432 injection in F344 rats leading to the rejection of syngeneic MADB106 tumor cells.

The effector mechanisms evoked in tumor-bearing rats following a single injection of the avirulent Su strain of type 3, group A Streptococcus pyogenes (OK-432) were sequentially examined. F344 rats challenged ip with a lethal dose of the syngeneic MADB106 mammary carcinoma could survive more than 100 days when given 50 mg OK-432/kg ip 1 day after tumor challenge. When the responsible effector mechanisms were examined in this therapeutic model, two distinct effector phases distinguished by the number of tumor cells were evident. Phase I, 1-6 days following OK-432 injection, resulted in a sharp decrease in tumor cell numbers and was related to the direct antitumor cytotoxicity of OK-432 and was coincident with an increase in the number of polymorphonuclear neutrophils. However, by day 6 a sharp increase in tumor cell numbers was again observed. Subsequently, a second phase of tumor cell destruction was observed 7-20 days following OK-432 injection and was reflected in a strong lymphocyte-mediated cytotoxicity response as well as the production of complement-dependent cytotoxic antibody against the MADB106 tumor cells. Further, the adoptive transfer of either peritoneal exudate cells or sera from the phase II animals revealed that both factors may be responsible for the antitumor activity observed in this therapeutic model. In conclusion, this study has demonstrated that the antitumor effects seen with OK-432 are due to a combination of sequential effector mechanisms leading to the eventual rejection of established tumor.

Animals↗
PubMed2006

[Necrotizing fasciitis due to Streptococcus pyogenes].

Necrotizing fasciitis is a severe infection, with systemic involvement and tissue necrosis. The clinical course is rapid and often fatal. Although this entity is uncommon, early recognition and treatment is essential to improve prognosis. Necrotizing fasciitis should be suspected when there are symptoms of toxicity and there is severe pain, frequently out of proportion to the clinical findings. In addition, in the last few years the incidence of invasive disease due to Streptococcus pyogenes in children has increased. Treatment is based on life support, aggressive debridement, and antimicrobial therapy. Intravenous immunoglobulin (IVIG) as adjunctive therapy seems useful and reduces mortality. The case of an infant with necrotizing fasciitis of four extremities is presented.

Fasciitis, Necrotizing↗
PubMed1996

Protein F2, a novel fibronectin-binding protein from Streptococcus pyogenes, possesses two binding domains.

Binding of the group A streptococcus (GAS) to respiratory epithelium is mediated by the fibronectin (Fn)-binding adhesin, protein F1. Previous studies have suggested that certain GAS strains express Fn-binding proteins that are different from protein F1. In this study, we have cloned, sequenced, and characterized a gene (prtF2) from GAS strain 100076 encoding a novel Fn-binding protein, termed protein F2. Insertional inactivation of prtF2 in strain 100076 abolishes its high-affinity Fn binding. prtF2-related genes exist in most GAS strains that lack prtF1 (encoding protein F1) but bind Fn with high affinity. These observations suggest that protein F2 is a major Fn-binding protein in GAS. Protein F2 is highly homologous to Fn-binding proteins from Streptococcus dysgalactiae and Streptococcus equisimilis, particularly in its carboxy-terminal portion. Two domains are responsible for Fn binding by protein F2. One domains (FBRD) consists of three consecutive repeats, whereas the other domain (UFBD) resides on a non-repeated stretch of approximately 100 amino acids and is located 100 amino acids aminoterminal of FBRD. Each of these domains is capable of binding Fn when expressed as a separate protein. In strain 100076, protein F2 activity is regulated in response to alterations in the concentration of atmospheric oxygen.

Adhesins, Bacterial↗
PubMed1998

Roles of integrins and fibronectin in the entry of Streptococcus pyogenes into cells via protein F1.

Entry of group A streptococcus (GAS) into cells has been suggested as an important trait in GAS pathogenicity. Protein F1, a fibronectin (Fn) binding protein, mediates GAS adherence to cells and the extracellular matrix, and efficient cell internalization. We demonstrate that the cellular receptors responsible for protein F1-mediated internalization of GAS are integrins capable of Fn binding. In HeLa cells, bacterial entry is blocked by anti-beta1 integrin monoclonal antibody. In the mouse cell line GD25, a beta1 null mutant, the alphavbeta3 integrin promotes GAS entry. Internalization of these cells by GAS is blocked by a peptide that specifically binds to alphavbeta3 integrin. In both cell lines, entry of GAS requires the occupancy of protein F1 by Fn. Neither the 29 kDa nor the 70 kDa N-terminal fragments or the 120 kDa cell-binding fragment of Fn promote bacterial entry. Fn-coated beads are taken up efficiently by HeLa cells. Both the entry of GAS via protein F1 and the uptake of Fn-coated beads are blocked by anti-beta1 antibody but are unaffected by a large excess of soluble Fn. Internalization of HeLa cells by bacteria bearing increasing amounts of prebound Fn to protein F1 reveals a sigmoidal ultrasensitive curve. These suggest that the ability of particles to interact via Fn with multiple integrin sites plays a central role in their ability to enter cells.

Adhesins, Bacterial↗