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PubMed1999

glmM operon and methicillin-resistant glmM suppressor mutants in Staphylococcus aureus.

The Staphylococcus aureus phosphoglucosamine mutase gene glmM was shown to be the last gene of a three-cistron operon, orf1-orf2-glmM. One transcriptional start was identified upstream of orf1, and a second start producing a monocistronic transcript was identified upstream of glmM. Disruption of glmM abolished GlmM production, decreased methicillin resistance, and resulted in teicoplanin hypersusceptibility without affecting the production of the endogenous penicillin-binding proteins and PBP 2'. Complementation of the glmM mutation by the complete glmM operon restored both methicillin resistance and normal teicoplanin susceptibility. In contrast, a highly methicillin-resistant suppressor mutant obtained by selection for growth in the presence of methicillin remained GlmM deficient and teicoplanin hypersusceptible. The suppressor mutation was not linked to the glmM operon but was correlated with decreased autolysis and increased production of a 49-kDa protein, suggesting that there is an alternative pathway for glucosamine-1-phosphate synthesis in S. aureus.

Bacterial Proteins↗

PubMed2001

Prevalence of Rho-inactivating epidermal cell differentiation inhibitor toxins in clinical Staphylococcus aureus isolates.

Staphylococcus aureus produces exotoxins of the epidermal cell differentiation inhibitor (EDIN) family that ADP-ribosylate and inactivate Rho GTPases. The prevalence of genes encoding EDIN in clinical and nasal isolates of S. aureus was investigated. Of the 196 clinical S. aureus isolates tested, 15 (7.8%) were positive for 1 edin gene, whereas of 81 nasal isolates tested, only 3 (3.7%) were edin positive. Of the total 18 edin-positive isolates, 16 (90%) carried edin-B and 2 (10%) carried edin-C, but none was positive for edin-A. All edin-positive strains could produce the respective EDIN protein. Pulsed-field gel electrophoresis analysis suggested that the edin-B-positive S. aureus isolates are derived from one clone, and the edin-C-positive isolates are derived from another clone. Given that toxins acting on Rho GTPases are considered to be important for bacterial virulence, the EDIN toxins of S. aureus should receive more attention in future studies.

Adult↗

PubMed2005

The role of nasal carriage in Staphylococcus aureus infections.

Staphylococcus aureus is a frequent cause of infections in both the community and hospital. Worldwide, the increasing resistance of this pathogen to various antibiotics complicates treatment of S aureus infections. Effective measures to prevent S aureus infections are therefore urgently needed. It has been shown that nasal carriers of S aureus have an increased risk of acquiring an infection with this pathogen. The nose is the main ecological niche where S aureus resides in human beings, but the determinants of the carrier state are incompletely understood. Eradication of S aureus from nasal carriers prevents infection in specific patient categories-eg, haemodialysis and general surgery patients. However, recent randomised clinical trials in orthopaedic and non-surgical patients failed to show the efficacy of eliminating S aureus from the nose to prevent subsequent infection. Thus we must elucidate the mechanisms behind S aureus nasal carriage and infection to be able to develop new preventive strategies. We present an overview of the current knowledge of the determinants (both human and bacterial) and risks of S aureus nasal carriage. Studies on the population dynamics of S aureus are also summarised.

Adolescent↗

PubMed2006

Intranasal vaccination with a double mutant of staphylococcal enterotoxin C provides protection against Staphylococcus aureus infection.

Staphylococcus aureus expresses a repertoire of factors including staphylococcal exotoxins (SEs), exoenzymes, and numerous cell-associated components that contribute to the pathogenesis of disease. We constructed and expressed a nontoxic double mutant SEC (dmSEC), devoid of superantigenic activity, and investigated the ability of intranasal vaccination with dmSEC plus cholera toxin (CT) adjuvant to protect mice against S. aureus infection. Mice were vaccinated with dmSEC and inoculated with a viable S. aureus clinical isolate strain. The survival rate in the immunized mice was higher, and bacterial counts in the organs were significantly lower than those in the control group. Intranasal vaccination with dmSEC induced the production of SEC-specific antibodies such as IgG1, IgG2b and IgA. dmSEC-vaccinated mice elicited significantly higher titers of interleukin-4 (IL-4) and IL-10, and lower levels of interferon-gamma (IFN-gamma) after challenge with S. aureus compared with the control group. Furthermore, the sera from dmSEC-immunized mice significantly inhibited IFN-gamma and tumor necrosis factor-alpha production in vitro. These results indicate that intranasal vaccination with dmSEC devoid of superantigenic properties induces systemic immune responses and provides protection against S. aureus infection.

Administration, Intranasal↗

PubMed1992

Double-blind study comparing erythromycin and mupirocin for treatment of impetigo in children: implications of a high prevalence of erythromycin-resistant Staphylococcus aureus strains.

Staphylococcus aureus has been consistently isolated from a high proportion of impetiginous lesions, and in several recent studies, it was present in the majority of the cases. Since recently a large proportion of S. aureus strains in our community showed erythromycin resistance, we undertook a prospective double-blind controlled study comparing topical mupirocin with oral erythromycin to determine (i) the prevalence of erythromycin-resistant S. aureus strains in impetigo and (ii) whether an increased rate of failure of erythromycin treatment was associated with such resistance. A total of 102 patients 3 to 185 months old (median = 49 months) were enrolled. Culture was positive for 97 of 102 (95%) patients, and S. aureus was present in 93% of the patients for whom cultures were positive. S. aureus was the single pathogen in 64% of these patients. Erythromycin-resistant S. aureus strains were present in 27 of 91 (28%) patients for whom cultures were positive. In all cases but one, S. aureus was resistant to penicillin, and in all cases it was sensitive to mupirocin. A marked difference was observed in favor of mupirocin in the clinical courses of the disease. However, only patients with erythromycin-resistant S. aureus strains had unfavorable courses compared with those treated with mupirocin (failure rate, 47 versus 2%, respectively). Patients with erythromycin-susceptible S. aureus strains who received erythromycin had a failure rate of 8%. In four patients, S. aureus strains initially susceptible to erythromycin became resistant during treatment. We conclude that erythromycin-resistant S. aureus strains are commonly isolated from impetigo in our region.(ABSTRACT TRUNCATED AT 250 WORDS)

Bacteria↗

PubMed2004

Control of glucose- and NaCl-induced biofilm formation by rbf in Staphylococcus aureus.

Both Staphylococcus aureus and S. epidermidis are capable of forming biofilm on biomaterials. We used Tn917 mutagenesis to identify a gene, rbf, affecting biofilm formation in S. aureus NCTC8325-4. Sequencing revealed that Rbf contained a consensus region signature of the AraC/XylS family of regulators, suggesting that Rbf is a transcriptional regulator. Insertional duplication inactivation of the rbf gene confirmed that the gene was involved in biofilm formation on polystyrene and glass. Phenotypic analysis of the wild type and the mutant suggested that the rbf gene mediates the biofilm formation of S. aureus at the multicellular aggregation stage rather than at initial attachment. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis analysis demonstrated that the mutation resulted in the loss of an approximately 190-kDa protein. Biofilm production by the mutant could be restored by complementation with a 2.5-kb DNA fragment containing the rbf gene. The rbf-specific mutation affected the induction of biofilm formation by glucose and a high concentration of NaCl but not by ethanol. The mutation did not affect the transcription of the ica genes previously shown to be required for biofilm formation. Taken together, our results suggest that the rbf gene is involved in the regulation of the multicellular aggregation step of S. aureus biofilm formation in response to glucose and salt and that this regulation may be mediated through the 190-kDa protein.

Amino Acid Sequence↗

PubMed2004

Inhibition of complement activation by a secreted Staphylococcus aureus protein.

Staphylococcus aureus can cause a variety of acute and chronic diseases. The ability of S. aureus to cause persistent infections has been linked to its ability to evade or inactivate host immune responses. We have identified a secreted 19-kDa protein produced by S. aureus that binds to the complement protein C3. N-terminal sequencing of this protein identified it as the extracellular fibrinogen-binding protein (Efb). In this study, we demonstrate that Efb can bind to the alpha -chain of C3 and inhibit both the classical and alternative pathways of complement activation. In addition, we show that Efb can inhibit complement-mediated opsonophagocytosis in a dose-dependent manner and that Efb inhibits complement activity by blocking deposition of C3 or by preventing further complement activation beyond C3b. These data suggest that Efb is a virulence factor involved in facilitating persistent S. aureus infections by interfering with complement activity in vivo.

Bacterial Proteins↗

PubMed2003

Caenorhabditis elegans as a model host for Staphylococcus aureus pathogenesis.

Staphylococcus aureus, an important pathogen of humans and other warm-blooded animals, is also capable of killing the nematode Caenorhabditis elegans. Here, we show that C. elegans organisms that are fed S. aureus die over the course of several days in a process that is correlated with the accumulation of bacteria within the nematode digestive tract. Several S. aureus virulence determinants known or speculated to be important in mammalian pathogenesis, including the quorum-sensing global virulence regulatory system agr and the global virulence regulator sarA, the alternative sigma factor sigma(B), alpha-hemolysin, and V8 serine protease, are required for full pathogenicity in nematodes. In addition, several defined C. elegans mutants were examined for susceptibility to S. aureus infection. Enhanced susceptibility to S. aureus killing was observed with loss-of-function mutations in the C. elegans genes esp-2/sek-1 and esp-8/nsy-1, which encode components of a conserved p38 MAP kinase signaling pathway involved in nematode defense against multiple pathogens. These results suggest that key aspects of S. aureus pathogenesis have been conserved, irrespective of the host, and that specific C. elegans host factors can alter susceptibility to this gram-positive human pathogen.

Animals↗

PubMed1977

Formation of regular packets of Staphylococcus aureus cells.

Staphylococcus aureus, which usually forms grape-like clusters, has the ability to form regularly arranged cell packets. These regular cell packets are formed when the activity of its separation enzyme(s) is lost either by treatment with detergents, such as sodium dodecyl sulfate or Trition X-100, or by mutation of the cells. These cell packets consisted of 8 to 64 spherical cells that have a three-dimensional arrangement. Some irregularity in the arragement of cells in packets, however, can be observed by scanning electron microscopy. It is concluded that S. aureus fundametally divides along three definitely oriented planes that are located at right angles to each other. After cell division, the cells usually become translocated due to the action of a separation enzyme(s) to form grape-like clusters.

Cell Division↗

PubMed2001

Cell subpopulations and cytokine expression in cow milk in response to chronic Staphylococcus aureus infection.

Staphylococcus aureus is a major pathogen in bovine intramammary infections of subclinical and chronic nature. Persistent infection with S. aureus has been postulated to be associated with an impaired immune response. This study was designed to define changes in peripheral blood and milk cell subpopulations during chronic S. aureus infection. The expression of specific antigens on the surface of lymphocytes and neutrophils was studied by flow cytometry. Cytokines and cytokine transcripts elaborated by the milk-derived cells were also investigated, using ELISA and reverse transcription polymerase chain reaction, respectively. The results indicated that cell subpopulations in blood from infected cows were not modified. In contrast, changes occurred in infected milk: neutrophils were the main cell population, but they were not in a highly activated state; the CD8+ T-lymphocytes were mainly recruited compared with the CD4+ T-lymphocytes, suggesting that CD8+ T-lymphocytes play an important role in chronic S. aureus infection. Also, the proportion of the B-lymphocytes among the total lymphocyte population was increased, suggesting that a humoral response developed, and no change was observed in the gammadelta subset. No cytokine mRNA was found in milk cells from uninfected mammary glands. In contrast, interleukin (IL)-1alpha, IL-1beta, IL-6 and tumor necrosis factor alpha pro-inflammatory cytokine and IL-10 and IL-12 regulatory cytokine mRNA were synthesized in cells derived from infected mammary glands, whereas no IL-2 nor IL-4 mRNA were found. Therefore, cells present in milk during chronic S. aureus infection were activated, but did not reveal any polarization of the immune response.

Animals↗

PubMed1998

Localization of Staphylococcus aureus in infected airways of patients with cystic fibrosis and in a cell culture model of S. aureus adherence.

Staphylococcus aureus causes chronic respiratory tract infections in patients with cystic fibrosis (CF). Using immunofluorescence and scanning and transmission electron microscopy we located S. aureus in lung specimens of three infected CF patients, in a nasal polyp of one CF patient, and in a suspension cell culture system of primary nasal epithelial cells in vitro. Very little of S. aureus was attached to the lung epithelium, whereas abundant S. aureus was detectable in the mucus of obstructed airways. Similarly, S. aureus adhered to components of secreted mucus on primary nasal epithelial cells of CF patients and healthy control subjects, grown as cell balls in vitro (bacteria/cell +/- SD: CF: 21.9 +/- 1.5; controls: 22. 0 +/- 5.8). Mucus depletion of cell balls prior to incubation with S. aureus resulted in a significantly reduced binding (bacteria/cell +/- SD: CF: 4.2 +/- 0.3; P < 0.001; controls: 5.0 +/- 1.3; P < 0. 007). Binding of S. aureus to cell balls from CF patients or control subjects did not differ significantly. When cell balls were treated with human neutrophil elastase, hypersecretion caused removal of S. aureus from cell-associated mucus. The results suggest that S. aureus adheres primarily to mucus components of the respiratory epithelium and that significant differences do not exist in binding of S. aureus to CF or non-CF cells.

Adolescent↗

PubMed1992

Lantibiotic-mediated anti-lactobacillus activity of a vaginal Staphylococcus aureus isolate.

Staphylococcus aureus strain 26 inhibited the growth of 23 of 26 lactobacilli of endocervical origin, but only two of 17 staphylococci, in deferred antagonism tests. The inhibitory agent, a bacteriocin-like inhibitory substance (BLIS) named staphylococcin Au-26, was obtained from vigorously shaken liquid cultures containing a 0.1% (v/v) supplement of Tween 80 and was purified by chromatographic fractionation on XAD-2, carboxymethyl Sephadex and reversed phase HPLC. The molecular mass of staphylococcin Au-26 was estimated by SDS-PAGE to be approx. 2700. The detection of lanthionine residues in the molecule, the high stability to heating at acidic but not alkaline pH values and inactivation by proteinases indicate that staphylococcin Au-26 is a member of the lantibiotic class of peptide antibiotics--the first reported to be produced by a S. aureus strain. Primary sequence analysis showed that the N-terminus of the molecule is isoleucine, a characteristic also displayed by the lantibiotics nisin, epidermin and gallidermin.

Amino Acids↗

PubMed1989

Cloning and sequence determination of six Staphylococcus aureus beta-lactamases and their expression in Escherichia coli and Staphylococcus aureus.

The plasmid-encoded beta-lactamase genes of six strains of Staphylococcus aureus were cloned and shown to be expressed in Escherichia coli. The cloned genes were re-introduced into S. aureus via a shuttle vector, and expressed beta-lactamase. However, clones containing only the small amount of DNA found necessary for expression of ampicillin resistance in E. coli did not express beta-lactamase in S. aureus. Much larger pieces of DNA from the original plasmid were necessary to obtain expression in S. aureus. Some of the six strains of S. aureus synthesized beta-lactamase constitutively and some released only a small proportion of the enzyme into the medium. Both these characteristics were maintained in the clones so it is concluded that they are features either of the gene itself or of the surrounding DNA. The cloned genes were sequenced and the putative amino acid sequences of the beta-lactamases were compared. There are several differences between the sequences and in particular one change in the N-terminal region, at a position believed to be especially important for export of proteins from the cell, is thought to have a key effect on whether or not the enzyme is found in the medium.

Amino Acid Sequence↗

PubMed2004

Preoperative risk factors for nasal carriage of Staphylococcus aureus.

BACKGROUND: Staphylococcus aureus nasal carriage is a risk factor for surgical-site infections (SSIs) caused by S. aureus, and eradication of carriage reduces postoperative nosocomial infections caused by it. No study has compared large groups of preoperative carriers and non-carriers to identify factors that are linked to S. aureus nasal carriage. METHODS: While conducting a clinical trial evaluating whether mupirocin prevented S. aureus SSIs, we prospectively collected data on 70 patient characteristics that might be associated with S. aureus carriage. We performed stepwise logistic regression analysis. RESULTS: Of the 4,030 patients, 891 (22%) carried S. aureus. Independent risk factors for S. aureus nasal carriage were obesity (odds ratio [OR], 1.29; 95% confidence interval [CI95], 1.11-1.50), male gender (OR, 1.29; CI95, 1.11-1.51), and a history of a cerebrovascular accident (OR, 1.53; CI95, 1.03-2.25) for all patients. Factors associated with nasal carriage varied somewhat by surgical specialty. In all groups, preoperative use of antimicrobial agents was independently associated with a lower risk of carrying S. aureus in the nares. Previously identified risk factors were not significantly associated with S. aureus nasal carriage in this large group of surgical patients. CONCLUSION: Male gender, obesity, and a history of a cerebrovascular accident were identified as risk factors for S. aureus nasal carriage. It remains to be seen whether preoperative weight loss would reduce the rate of nasal carriage. In addition, the value of screening this patient population for S. aureus nasal carriage merits further investigation.

Adult↗

PubMed2006

Molecular characterization of the capsule locus from non-typeable Staphylococcus aureus.

Most Staphylococcus aureus express a serotype 5 or 8 capsular polysaccharide (CP). However, 20-25% of human isolates and up to 86% of bovine strains of S. aureus are non-typeable (NT), i.e. non-reactive with antibodies to CP types 1, 2, 5 or 8. A vaccine that targets the S. aureus CP would not protect against NT strains. The aim of this study was to characterize NT S. aureus isolates at the molecular level to explain their lack of type 5 or 8 capsule production. The cap5(8) locus was present in all 22 NT clinical isolates from humans, eight of 21 bovine isolates, and in all eight sequenced strains. NT strains positive for the cap5(8) transcript had mutations within essential capsule genes and could be complemented in trans. S. aureus strains with reduced cap5(8) transcript had mutations within the cap5A promoter, decreased RNAIII levels, or a truncated arlR gene product. More than one mutation was identified in several isolates. The cap5(8) locus was replaced by IS257 in 13 of 21 NT bovine isolates of S. aureus. Lack of capsule expression in NT S. aureus can be explained by multiple mechanisms, and the data argue against the existence of capsule serotypes other than 1, 2, 5 and 8.

Animals↗

PubMed1981

Protein A effect on alternative pathway complement activation and opsonization of Staphylococcus aureus.

Twelve Staphylococcus aureus strains with known amounts of protein A were compared with regard to alternative pathway complement activation and opsonization in human serum. "Protein A-poor" strains (less than or equal to 0.16 ng/10(6) bacteria) were, on the average, 3. 4-fold more efficient in alternative pathway complement activation than "protein A-rich" strains (greater than or equal to 0.625 ng/10(6) bacteria) (P less than 0.001). Protein A-poor strains were significantly better phagocytized by human polymorphonuclear leukocytes after opsonization in magnesium-ethylene glycol-bis (beta-amino-ethyl ether)-N, N-tetraacetic acid-chelated serum than were the protein A-rich strains (P less than 0.001). No significant differences between protein A-poor and -rich strains were found in complement activation and opsonization in normal serum. Cell wall-bound protein A appeared to hinder alternative pathway complement activation by S. aureus, which resulted in decreased opsonization of these bacteria in the absence of an intact classical pathway. These studies suggest that protein A may cover alternative pathway complement-activating sites within the peptidoglycan matrix of the staphylococcal cell wall.

Complement Activation↗

PubMedDate not supplied

Removal of cytokine inducing substances by polymyxin-B immobilized polystyrene-derivative fibers during in vitro hemoperfusion of 10% human plasma containing Staphylococcus aureus challenge.

Staphylococcus aureus (S. aureus) is frequently isolated from blood cultures in the hospital setting. The pathogenesis of S. aureus bacteremia probably replicates mechanisms implicated in gram negative bacterial infections. Cell wall components, such as peptidoglycans and lipoteichoic acids (LTA), can trigger cytokine production. Polymyxin-B (PMX-B) is a cationic peptide that binds endotoxin (ET) and inhibits its activity. Based on this principle, PMX-B was incorporated in polystyrene-derivative fibers, creating a hemoperfusion column (PMX-20R) that removes ET. The authors assessed whether S. aureus possesses PMX-B suppressible cytokine-inducing substances, and whether LTA, an anionic molecule, is one such substance. Heparinized blood was obtained from healthy volunteers, peripheral blood mononuclear cells (PBMC) were isolated by Ficoll-Hypaque separation, and 10% human plasma prepared. PBMC were incubated with 1, 5, or 10 microg/ml of S. aureus LTA, with and without 10 microg/ml of PMX-B. Also, using PMX-20R, in vitro hemoperfusion (IVH) was performed with 10% human plasma containing a 1:1,000 dilution of S. aureus challenge at 100 ml/min for 2 hours at 37 degrees C, and plasma obtained before and after IVH was incubated with PBMC. After a 24 hour incubation at 37 degrees C, PBMC were subjected to three freeze-thaw cycles, and total TNFalpha was measured by radioimmunoassay. TNFalpha production by PBMC incubated with LTA was 164+/-4 pg, 324+/-54 pg, 657+/-55 pg, and 1143+/-215 pg in control, and LTA 1, 5, and 10 microg/ml, respectively. The addition of PMX-B resulted in a 40+/-12% (p = 0.02), 61+/-6% (p = 0.002), and 62+/-14% (p = 0.02) decrease in TNFalpha production, respectively. Before IVH, TNFalpha production by PBMC incubated with 10% plasma containing S. aureus challenge was 1275+/-70 pg. After 2 hours of IVH, the decrease in TNFalpha production was 20+/-4% (p = 0.002). In conclusion, S. aureus LTA induces TNFalpha production that is significantly suppressed by PMX-B. Consequently, S. aureus cytokine-inducing substances are removed during IVH with PMX-20R, and this may be due to stoichiometric binding of LTA to PMX-B.

Anti-Bacterial Agents↗

PubMed1999

The effect of site-specific monoclonal antibodies directed to toxic shock syndrome toxin-1 in experimental Staphylococcus aureus arthritis.

Staphylococcus aureus produces a large number of potential virulence factors, among these the superantigen toxic shock syndrome toxin-1 (TSST-1). We have recently demonstrated that TSST-1 is involved in the pathogenesis of septic arthritis. Recent data show that the TSST-1 molecule is composed of two distinct domains, one proposed to interact with T cell receptor (TCR) and one with the MHC class II. The aim of this study was to assess if interaction between TSST-1-specific MoAbs directed to sites on the MHC and/or TCR Vbeta affects the development of experimental S. aureus-induced arthritis. For that purpose we used a panel of seven MoAbs, which were injected intraperitoneally before and after inoculation with a TSST-1-producing S. aureus strain. Administration of antibodies did not affect the development of arthritis, suggesting inefficacy of such a procedure in neutralization of exotoxin-mediated disease manifestations.

Animals↗