Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Staphylococcus aureus”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 883 records · Page 49Linked to original sources
PubMed2006

Complete and SOS-mediated response of Staphylococcus aureus to the antibiotic ciprofloxacin.

Staphylococcus aureus infections can be difficult to treat due to both multidrug resistance and the organism's remarkable ability to persist in the host. Persistence and the evolution of resistance may be related to several complex regulatory networks, such as the SOS response, which modifies transcription in response to environmental stress. To understand how S. aureus persists during antibiotic therapy and eventually emerges resistant, we characterized its global transcriptional response to ciprofloxacin. We found that ciprofloxacin induces prophage mobilization as well as significant alterations in metabolism, most notably the up-regulation of the tricarboxylic acid cycle. In addition, we found that ciprofloxacin induces the SOS response, which we show, by comparison of a wild-type strain and a non-SOS-inducible lexA mutant strain, includes the derepression of 16 genes. While the SOS response of S. aureus is much more limited than those of Escherichia coli and Bacillus subtilis, it is similar to that of Pseudomonas aeruginosa and includes RecA, LexA, several hypothetical proteins, and a likely error-prone Y family polymerase whose homologs in other bacteria are required for induced mutation. We also examined induced mutation and found that either the inability to derepress the SOS response or the lack of the LexA-regulated polymerase renders S. aureus unable to evolve antibiotic resistance in vitro in response to UV damage. The data suggest that up-regulation of the tricarboxylic acid cycle and induced mutation facilitate S. aureus persistence and evolution of resistance during antibiotic therapy.

Anti-Bacterial Agents↗
PubMed1978

Human infections caused by thiamine- or menadione-requiring Staphylococcus aureus.

Stable dwarf forms of Staphylococcus aureus have been identified in clinical specimens as the sole or predominant isolate in eight cases. These organisms have been shown to be menadione or thiamine dependent, i.e., cultivation in the presence of one of these agents has permitted growth of colonies which appear typical of S. aureus. In vitro resistance to aminoglycosides was overcome by cultivation in the presence of menadione or thiamine. Menadione- or thiamine-requiring S. aureus can be considered as causative agents in severe human infections. Special care must be taken if they are to be identified in pathological specimens. Their antibiotic sensitivity testing should be done comparatively on supplemented and nonsupplemented media.

Aminoglycosides↗
PubMed1978

Phenotypic variations in gentamicin-resistant isolates of Staphylococcus aureus.

Eight clinical isolates of Staphylococcus aureus showing high level resistance to seven aminoglycosides are described. The resistance did not appear to be due to enzyme inactivation. Possible mechanisms of this resistance are discussed. Resistant strains showed phenotypic variations in the form of different colonial morphology and biochemical activity.

Drug Resistance, Microbial↗
PubMed2003

[Antimicrobial resistance of Staphylococcus aureus isolates from inpatients of departments of internal medicine, surgery, and pediatrics and intensive care unit].

OBJECTIVE: To investigate the antimicrobial resistance of Staphylococcus aureus isolates obtained from inpatients of departments of internal medicine, surgery, and pediatrics and intensive care unit (ICU), and study on the differences of resistant rates among the clinical isolates. METHODS: The strains of Staphylococcus aureus were cultured and their antimicrobial resistance was assayed by disc diffusion test (K-B method) and the data was analyzed by WHO NET 5 software. chi(2) test was made to identify the significance of difference. RESULTS: 2 625 strains of Staphylococcus aureus were obtained from the clinical departments of 60 hospitals all over China, among which 1 669 strains (63.3%) were obtained from the inpatients of departments of internal medicine, surgery, and pediatrics and ICU from 1 January to 31 December 2001. Most of the strains were isolated from sputum (34.3%, 572/1 669), secretion (13.2%, 221/1 669), pus (11.7%, 195/1 669), blood (10.2%, 171/1 669), and wound (5.6%, 94/1 669). The resistant rates of Staphylococcus aureus isolates from the inpatients in department pediatrics of to oxacillin, gentamicin, clindamycin, ciprofloxacin, levofloxacin, and chloramphenicol were 23.3%, 16.1%, 29.3%, 11.2%, 4.0% and 14.4% respectively, all significantly lower than those of the isolates from the inpatients of the departments of internal medicine and surgery, and ICU (all P < 0.001). The resistant rates of Staphylococcus aureus isolates from the inpatients of departments of internal medicine and surgery to oxacillin, gentamicin, clindamycin, ciprofloxacin, and levofloxacin were significantly lower than those of isolates from the patients of ICU (all P < 0.001). CONCLUSION: A high isolation rate of multi-drug resistant Staphylococcus aureus among the inpatients of departments of internal medicine, surgery, and pediatrics and ICU. It is important to select appropriate antimicrobial agents based on the origin of bacterial strains and avoid blindness before the results of drug sensitivity are obtained.

Anti-Bacterial Agents↗
PubMed2003

Short-term effects of topical fusidic acid or mupirocin on the prevalence of fusidic acid resistant (FusR) Staphylococcus aureus in atopic eczema.

BACKGROUND: Staphylococcus aureus has a role in the pathophysiology of atopic eczema. Topical fusidic acid is widely used in its treatment. There is concern that topical use of fusidic acid may be driving the selection and dissemination of fusidic acid-resistant (FusR) S. aureus. OBJECTIVES: To test the hypothesis that treatment of atopic eczema for 2 weeks with topical fusidic acid/steroid combination can increase carriage of FusRS. aureus. METHODS: Forty-six patients with atopic eczema were allocated randomly to one of two treatment groups. Group 1 (28 patients) were treated with topical 2% fusidic acid plus 0.1% betamethasone cream, and group 2 (18 patients) with topical 2% mupirocin and 0.1% betamethasone cream. The clinical response and nasal and skin colonization with S. aureus were recorded before treatment and after 1 and 2 weeks of therapy. RESULTS: Baseline samples from the site of worst eczema showed S. aureus (sensitive and resistant) in 76% of patients, and FusRS. aureus in 26%, with no significant difference between treatment groups. After 1 and 2 weeks, both groups showed similar significant clinical improvement. The overall median clinical improvement was paralleled by a reduction in prevalence and population density of S. aureus (sensitive and resistant) at the worst eczema site (P < 0.0001). However, for FusRS. aureus there was no significant change in the prevalence of carriage, or population density in either group compared to baseline. Over 50% of patients carried S. aureus in the nerves and over 20% carried FusRS. aureus. Neither regimen affected either the prevalence or population density of S. aureus or FusRS. aureus in the nerves. CONCLUSIONS: In this small study there is no evidence to support the hypothesis that short-term treatment of atopic eczema with fusidic acid/steroid combination increases fusidic acid resistant S. aureus during a 2-week period.

Administration, Topical↗
PubMed1986

Plasmids in multiresistant Staphylococcus aureus.

Contemporary clinical isolates of Staphylococcus aureus possess a formidable array of determinants for resistance to antimicrobial agents, a number of which are plasmid encoded. The plasmids detected in such multiresistant isolates from Australia, Europe and the USA are compared and some of the potential genetic rearrangements involved in their evolution discussed.

Biological Evolution↗
PubMed2006

Global transcriptome analysis of Staphylococcus aureus response to hydrogen peroxide.

Staphylococcus aureus responds with protective strategies against phagocyte-derived reactive oxidants to infect humans. Herein, we report the transcriptome analysis of the cellular response of S. aureus to hydrogen peroxide-induced oxidative stress. The data indicate that the oxidative response includes the induction of genes involved in virulence, DNA repair, and notably, anaerobic metabolism.

Gene Expression Profiling↗
PubMed1981

Purification, fine structure and characterization of temperate phages from drug-resistant Staphylococcus aureus.

Three kinds of temperate Staphylococcus aureus phages were differentiated by serological, sedimentation and electron microscopic studies. Phage S1 had a long hexagonal head and a long tail, a density in Cs2SO4 of 1.364 g/ml and belonged to serological group A; phage S2 had a short hexagonal head and a short tail, a density of 1.385 to 1.392 g/ml and belonged to serological group B; phage S3 had a shape similar to phage S2 except for some minor differences, but had a density of 1.416 g/ml and belonged to serological group F. S. aureus MS27 was found to be singly lysogenic for S2. However, S. aureus MS3878 was a doubly lysogenic strain carrying S1 and S2 and S. aureus E169 was a triply lysogenic strain carrying S1, S2 and S3. All these temperate phages showed similarity in shape to typing phages belonging to the same serological group. The temperate S. aureus phages revealed the presence of a hexagonal baseplate with spikes. The burst sizes of phages of S1, S2 and S3 were about 50, 110 and 120 respectively. The DNA from S1, S2 and S3 ranged from 29.4 to 30 megadaltons in size.

DNA, Viral↗
PubMed1977

In vivo effects of josamycin, erythromycin, and placebo therapy on nasal carriage of Staphylococcus aureus.

Healthy nasal carriers of Staphylococcus aureus were randomly assigned to one of three treatment regimens: josamycin (1.5 g/day), erythromycin stearate (1.0 g/day), or placebo, each administered orally for 7 days. Quantitative nasal cultures were obtained from each subject at intervals before, during, and after treatment. All 25 placebo-treated subjects had positive nasal cultures for S. aureus at all culture intervals. Both josamycin and erythromycin were equally effective in reducing the carrier rates and in decreasing the total numbers of S. aureus isolated from subjects with positive cultures during treatment. No increase in in vitro antibiotic resistance was detected in isolates obtained after therapy. Both antibiotics were well tolerated, and toxicity was not encountered with either drug.

Anti-Bacterial Agents↗
PubMed2005

Surveillance of Staphylococcus aureus in veterinary teaching hospitals.

Staphylococcus aureus isolates (n = 70) from 65 patients (36 canine, 18 equine, 7 bovine, 2 avian, and 2 feline) at seven veterinary teaching hospitals in the United States were studied. The majority of patients (83%) with an S. aureus infection were canine and equine, but this may have reflected a sample bias based on clinic case loads and diagnostic lab submissions at the participating institutions. Fourteen percent of patients with an S. aureus infection were infected with a methicillin-resistant S. aureus (MRSA) isolate. Six of seven institutions had at least one MRSA infection during the study. Pulsed-field gel electrophoresis on 63 of the 70 isolates yielded 58 unique strains of S. aureus. None of the strain types of the MRSA isolates matched each other or the type of any other S. aureus isolate. The proportions of patients infected with an MRSA isolate were not significantly different between institutions or animal species (P > or = 0.222). Methicillin-resistant S. aureus isolates in this study seemed to be community acquired rather than hospital acquired.

Animals↗
PubMed2002

The carboxyl terminus of peptidoglycan stem peptides is a determinant for methicillin resistance in Staphylococcus aureus.

A mecA-containing Staphylococcus aureus strain was grown in the presence of high concentrations of D-serine, D-threonine, and D-phenylalanine. These growth conditions resulted in the replacement of the carboxyl-terminal (fifth) D-alanine residue of peptidoglycan stem peptides with the D-amino acid present in the growth medium and a reduced ability to grow in the presence of methicillin. The most dramatic effect was seen with D-serine. With 32 mM D-serine, strains that had been able to grow in the presence of 800 micro g of methicillin per ml were only able to grow in the presence of less than 50 micro g/ml. The results also suggest that in S. aureus vancomycin resistance mediated through the incorporation of precursors not terminating in D-alanyl-D-alanine would be mutually exclusive with expression of mecA-mediated methicillin resistance.

Amino Acids↗
PubMed1997

Cloning and characterization of the fmt gene which affects the methicillin resistance level and autolysis in the presence of triton X-100 in methicillin-resistant Staphylococcus aureus.

In methicillin-resistant Staphylococcus aureus (MRSA) strains, Triton X-100 reduced the oxacillin resistance level, although the degree of reduction varied from strain to strain. To study the responses of MRSA strains to Triton X-100, we isolated a Tn551 insertion mutant of the COL strain that became more susceptible to oxacillin in the presence of 0.02% Triton X-100. The Tn551 insertion of the mutant was transduced back to the parent strain, other MRSA strains (strains KSA8 and NCTC 10443), and methicillin-susceptible strain RN450. All transductants of MRSA strains had reduced levels of resistance to oxacillin in the presence of 0.02% Triton X-100, while those of RN450 did not. Tn551 mutants of KSA8 and NCTC 10443 also had reduced levels of resistance in the absence of 0.02% Triton X-100. The autolysis rates of the transductants in the presence of 0.02% Triton X-100 were significantly increased. Amino acid analysis of peptidoglycan and testing of heat-inactivated cells for their susceptibilities to several bacteriolytic enzymes showed that there were no significant differences between the parents and the respective Tn551 mutants. The Tn551 insertion site mapped at a location different from the previously identified fem and llm sites. Cloning and sequencing showed that Tn551 had inserted at the C-terminal region of a novel gene designated fmt. The putative Fmt protein showed a hydropathy pattern similar to that of S. aureus penicillin-binding proteins and contained two of the three conserved motifs shared by penicillin-binding proteins and beta-lactamases, suggesting that fmt may be involved in cell wall synthesis.

Bacteriolysis↗
PubMed2003

The adhesive and immunomodulating properties of the multifunctional Staphylococcus aureus protein Eap.

Adherence of Staphylococcus aureus to the host tissue is an important step in the initiation of pathogenesis. At least 10 adhesins produced by S. aureus have been described and it is becoming clear that the expression of these adhesins and their interactions with eukaryotic cells involve complex processes. Some of these, such as the fibronectin-binding proteins (FnBPs) and Clumping Factor A, are well characterized. However, in the last 10 years a number of novel S. aureus adhesins have been described. Functional analyses of these proteins, one of which is Eap (extracellular adherence protein, also known as Map and p70), are revealing important information on the pathogenesis of staphylococcal disease. More than 10 years after the first report of Eap, we are beginning to understand that this protein, which has a broad spectrum of functions, may be a critical factor in the pathogenesis of S. aureus. This review will focus on the interactions of Eap with eukaryotic cells, plasma proteins and the extracellular matrix as well as on the recently recognized role of Eap as an important mediator in the immune response to staphylococcal infection.

Adhesins, Bacterial↗
PubMed1999

Determinants of chronic infection with Staphylococcus aureus in patients with bronchiectasis.

Staphylococcus aureus is an uncommon pathogen in bronchiectasis not caused by cystic fibrosis (CF). The object of this study was to identify characteristics that cause patients to be prone to infection with S. aureus. The study population consisted of patients with bronchiectasis attending the authors' unit, excluding those with a diagnosis of overt CF. All patients had a high resolution computer tomographic scan (HRCT) of the thorax which demonstrated bronchiectasis. Cases that were currently chronically infected with S. aureus (isolated consecutively on more than two occasions >3 months apart) were identified (n = 12) and compared with 74 control patients who had not been chronically infected with S. aureus. Patients were carefully evaluated to determine the aetiology of their disease. Odds ratios (OR) and 95% confidence intervals (CI) as measures of the association between disease characteristics and chronic infection with S. aureus were calculated. The results for patients chronically infected by S. aureus demonstrated significant associations with allergic bronchopulmonary aspergillosis (ABPA; OR = 8.8, 95% CI 1.8-41.9), atypical variants of CF (OR = 12.0, 95% CI 1.8-81.7) or equivocal sweat sodium values (OR = 4.0, 95% CI 1.0-15.3). The associations persisted when the analysis was based on cases (n = 28) in whom S. aureus had ever been isolated from sputum. In the latter analysis there was also a significant association with predominant upper zone disease on HRCT. These results suggest that patients with bronchiectasis in whom S. aureus is isolated from sputum should be carefully evaluated to exclude allergic bronchopulmonary aspergillosis or atypical cystic fibrosis.

Adult↗
PubMed1995

Variation in the size of the repeat region of the fibrinogen receptor (clumping factor) of Staphylococcus aureus strains.

The ability of Staphylococcus aureus to bind to fibrinogen and fibrin is believed to be an important factor in the initiation of foreign body and wound infections. Recently, the gene encoding the fibrinogen receptor (clumping factor, ClfA) of S. aureus strain Newman was cloned and sequenced. The ClfA protein possesses a highly unusual 308 residue dipeptide repeat region composed predominantly of Asp and Ser. Polymerase chain reaction analysis of seven different strains showed that the size of the clfA repeat coding region varies from 580 bp to 1320 bp. In contrast, the clfA region A is the same size in each strain. The size of the clfA repeat region did not correlate with the ability of these strains to form clumps in a solution of fibrinogen. Indeed, the strain with the smallest repeat size of 580 bp clumped almost as well as strain Newman. Each strain of S. aureus examined contained several high molecular mass proteins that reacted with anti-ClfA region A antibody. In some cases the molecular mass of the major protein varied in accordance with the length of the coding sequence for the repeat region R.

Bacterial Proteins↗
PubMed1992

Genetic evidence that bound coagulase of Staphylococcus aureus is not clumping factor.

Staphylococcus aureus Newman cells carry a surface receptor for fibrinogen called clumping factor. The bacteria also express coagulase, an extracellular protein that binds to prothrombin to form a complex with thrombinlike activity which coverts fibrinogen to fibrin. We have confirmed a recent report (M. K. Bodén and J.-I. Flock, Infect. Immun. 57:2358-2363, 1989) that coagulase can bind to fibrinogen as well as to prothrombin and also that a fraction of coagulase is firmly attached to the cell. A mutant with a deletion in the chromosomal coa gene was isolated by allelic replacement. Allelic replacement either was directly selected by electrotransformation of S. aureus R3N4220 with a nonreplicating suicide plasmid, pCOA18, carrying the delta coa::Tcr mutation or occurred after transduction of the integrated pCOA18 plasmid. The coa mutant was completely devoid of coagulase activity but interacted both with soluble fibrinogen and with solid-phase fibrinogen with the same avidity as the parental strain. This strongly suggests that the bound form of coagulase is not clumping factor and is not responsible for the adherence of S. aureus Newman to solid-phase fibrinogen. The fibrinogen binding determinant of coagulase was located in the C terminus of the protein, by analyzing truncated fusion proteins, in contrast to the prothrombin-binding region which was located in the N terminus.

Bacterial Adhesion↗
PubMed1998

Characterization of a chromosomal gene encoding type B beta-lactamase in phage group II isolates of Staphylococcus aureus.

In contrast to most Staphylococcus aureus isolates in which the gene for staphylococcal beta-lactamase (blaZ) is plasmid borne, isolates typeable by group II bacteriophages frequently carry blaZ on the chromosome. Furthermore, the chromosomal gene encodes the type B variant of staphylococcal beta-lactamase for which the nucleotide and deduced amino acid sequences have not yet been reported. To better understand beta-lactamase production among phage group II staphylococci and the nature of the type B beta-lactamase, we determined the type and amount of enzyme produced by 24 phage group II isolates. Of these isolates, 1 did not produce beta-lactamase, 8 produced the type B enzyme, and 15 produced the type C enzyme. In all eight type B beta-lactamase-producing isolates, blaZ was located on the chromosome. This was in contrast to the type C beta-lactamase-producing isolates, in which blaZ was located on a 21-kb plasmid. The nucleotide sequence corresponding to the leader peptide and the N-terminal 85% of the mature exoenzyme form of type B S. aureus was determined. The deduced amino acid sequence revealed 3 residues in the leader peptide and 12 residues in the exoenzyme portion of the beta-lactamase that differ from the prototypic type A beta-lactamase sequence. These include the serine-to-asparagine change at residue 216 found in the kinetically similar type C enzyme, a threonine-to-lysine change at residue 128 close to the SDN loop (residues 130 to 132), and several substitutions not found in any of the other staphylococcal beta-lactamases. In summary, modern isolates of S. aureus typeable by group II phages produce type B or type C staphylococcal beta-lactamase. The type B gene resides on the chromosome and has a sequence that, when compared to the sequences of the other staphylococcal beta-lactamases, corresponds well with its kinetic properties.

Bacteriophage Typing↗