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PubMed2006

Community-acquired methicillin-resistant Staphylococcus aureus: current perspectives.

Methicillin-resistant Staphylococcus aureus (MRSA) has become a worldwide problem, although its prevalence varies considerably among countries. The epidemiology of MRSA is now changing; infections are no longer confined to the hospital setting, but also appear in healthy community-dwelling individuals without established risk factors for the acquisition of MRSA. Reported prevalence rates of community-acquired MRSA (CA-MRSA) vary widely among studies-largely because of the different definitions employed and different settings in which the studies have been performed. At present, molecular epidemiological definitions, based on staphylococcal cassette chromosome mec (SCCmec) typing and phylogenetic analyses of the MRSA isolates, are considered the most reliable means by which to distinguish between hospital-acquired MRSA (HA-MRSA) and CA-MRSA. CA-MRSA has been isolated predominantly from skin and soft tissue infections, such as abscesses, cellulitis, folliculitis and impetigo. Although CA-MRSA infections are usually mild, they may also be severe, and can result in hospitalisation and even death. CA-MRSA strains differ from the major pandemic clones of MRSA that account for the majority of epidemic HA-MRSA strains. Differences are found in SCCmec types, bacterial growth rate, and the distribution of antibiotic resistance genes and toxin genes. Mathematical models have shown that CA-MRSA has a high potential to become endemic in the community, and this will impact significantly on the control of MRSA in the hospital setting. Well-designed, community-based studies with adequate risk factor analysis are required to further elucidate the epidemiology of CA-MRSA and to improve strategies to control MRSA in both the community and hospital settings.

Community-Acquired Infections↗
PubMed1996

The molecular architecture of the sar locus in Staphylococcus aureus.

The global regulator sar in Staphylococcus aureus controls the synthesis of a variety of cell wall and extracellular proteins, many of which are putative virulence factors. The sar locus in strain RN6390 contains a 339-bp open reading frame (sarA) and an 860-bp upstream region. Transcriptional analyses of this locus revealed three different transcripts of 0.58, 0.84, and 1.15 kb (designated sarA, sarC, and sarB, respectively). All three transcripts seemed to be under temporal, growth cycle-dependent regulation, with sarA and sarB being most abundant in early log phase and the sarC concentration being highest toward the late stationary phase. Mapping of the 5' ends of the sar transcripts by primer extension and modified S1 nuclease protection assays demonstrated that transcription is initiated from three separate, widely spaced promoters. The 3' ends of all three sar transcripts are identical, and transcriptional termination occurs upstream of a typical prokaryotic poly(T) termination signal. Northern (RNA) analysis of sar mutant clones containing plasmids that comprised various promoters and the termination signal revealed that individual transcripts can be generated from each of the three promoters, thus suggesting possible activation as independent promoters. The multipromoter system, from which transcription is initiated, bears conserved features for recognition by homologous sigma 70 transcription factors and also by those expressed in the general stress response. Downstream of the two distal promoters (P3 and P2) are two regions potentially encoding short peptides. It is conceivable that posttranslational cooperation between these short peptides and the sarA gene product occurs to modulate sar-related functions. Complementation studies of a sar mutant with a clone expressing all three sar transcripts showed that this clone was able to restore the sar wild-type phenotype to the sar mutant.

Amino Acid Sequence↗
PubMed1987

Production of low-affinity penicillin-binding protein by low- and high-resistance groups of methicillin-resistant Staphylococcus aureus.

Methicillin- and cephem-resistant Staphylococcus aureus (137 strains) for which the cefazolin MICs are at least 25 micrograms/ml could be classified into low-resistance (83% of strains) and high-resistance (the remaining 17%) groups by the MIC of flomoxef (6315-S), a 1-oxacephalosporin. The MICs were less than 6.3 micrograms/ml and more than 12.5 micrograms/ml in the low- and high-resistance groups, respectively. All strains produced penicillin-binding protein 2' (PBP 2'), which has been associated with methicillin resistance and which has very low affinity for beta-lactam antibiotics. Production of PBP 2' was regulated differently in low- and high-resistance strains. With penicillinase-producing strains of the low-resistance group, cefazolin, cefamandole, and cefmetazole induced PBP 2' production about 5-fold, while flomoxef induced production 2.4-fold or less. In contrast, penicillinase-negative variants of low-resistance strains produced PBP 2' constitutively in large amounts and induction did not occur. With high-resistance strains, flomoxef induced PBP 2' to an extent similar to that of cefazolin in both penicillinase-producing and -negative strains, except for one strain in which the induction did not occur. The amount of PBP 2' induced by beta-lactam antibiotics in penicillinase-producing strains of the low-resistance group correlated well with resistance to each antibiotic. Large amounts of PBP 2' in penicillinase-negative variants of the low-resistance group did not raise the MICs of beta-lactam compounds, although these strains were more resistant when challenged with flomoxef for 2 h. Different regulation of PBP 2' production was demonstrated in the high- and low-resistance groups, and factor(s) other than PBP 2' were suggested to be involved in the methicillin resistance of high-resistance strains.

Anti-Bacterial Agents↗
PubMed2003

Comparison of community- and health care-associated methicillin-resistant Staphylococcus aureus infection.

CONTEXT: Methicillin-resistant Staphylococcus aureus (MRSA) has traditionally been considered a health care-associated pathogen in patients with established risk factors. However, MRSA has emerged in patients without established risk factors (community-associated MRSA). OBJECTIVE: To characterize epidemiological and microbiological characteristics of community-associated MRSA cases compared with health care-associated MRSA cases. DESIGN, SETTING, AND PATIENTS: Prospective cohort study of patients with MRSA infection identified at 12 Minnesota laboratory facilities from January 1 through December 31, 2000, comparing community-associated (median age, 23 years) with health care-associated (median age, 68 years) MRSA cases. MAIN OUTCOME MEASURES: Clinical infections associated with either community-associated or health care-associated MRSA, microbiological characteristics of the MRSA isolates including susceptibility testing, pulsed-field gel electrophoresis, and staphylococcal exotoxin gene testing. RESULTS: Of 1100 MRSA infections, 131 (12%) were community-associated and 937 (85%) were health care-associated; 32 (3%) could not be classified due to lack of information. Skin and soft tissue infections were more common among community-associated cases (75%) than among health care-associated cases (37%) (odds ratio [OR], 4.25; 95% confidence interval [CI], 2.97-5.90). Although community-associated MRSA isolates were more likely to be susceptible to 4 antimicrobial classes (adjusted OR, 2.44; 95% CI, 1.35-3.86), most community-associated infections were initially treated with antimicrobials to which the isolate was nonsusceptible. Community-associated isolates were also more likely to belong to 1 of 2 pulsed-field gel electrophoresis clonal groups in both univariate and multivariate analysis. Community-associated isolates typically possessed different exotoxin gene profiles (eg, Panton Valentine leukocidin genes) compared with health care-associated isolates. CONCLUSIONS: Community-associated and health care-associated MRSA cases differ demographically and clinically, and their respective isolates are microbiologically distinct. This suggests that most community-associated MRSA strains did not originate in health care settings, and that their microbiological features may have contributed to their emergence in the community. Clinicians should be aware that therapy with beta-lactam antimicrobials can no longer be relied on as the sole empiric therapy for severely ill outpatients whose infections may be staphylococcal in origin.

Adult↗
PubMed2006

Risk factors for ICU-acquired methicillin-resistant Staphylococcus aureus infections.

BACKGROUND: Methicillin-resistant Staphylococcus aureus (MRSA) is a major nosocomial pathogen that causes severe morbidity and mortality in many hospitals worldwide, and MRSA infections are frequent in intensive care units (ICUs). OBJECTIVE: A prospective study was implemented to investigate the risk factors for ICU-acquired MRSA infections. METHODS: This study was conducted in surgical and neurologic ICUs from May to November 2003. The patients staying in ICUs more than 48 hours were included in the study. All of the patients were visited daily, and data were recorded on individual forms for each patient until discharge or death. Nasal swab cultures were done within 48 hours of ICU admission and repeated every week until the patients colonized with MRSA or were discharged from ICUs. ICU-acquired MRSA infection was diagnosed when MRSA was isolated from the infected site. RESULTS: Overall, 249 patients were followed during the study. MRSA infection was detected in 21 (8.4%) of these patients. The most frequent infection was primary bloodstream infection (10/21, 47%). It was followed by pneumonia (8/21, 38%) and surgical site infection (3/21, 14%). Nasal MRSA colonization was detected in 59 (23.7%) patients, and 12 of them (20.3%) developed MRSA infection. In univariate analysis, hospitalization period in an ICU, intraabdominal and orthopedic pathologies, mechanical ventilation, central venous catheter insertion, total parenteral nutrition, previous antibiotic use, surgical ICU stay, nasal MRSA colonization, and presence of more than 2 patients having nasal colonization in the same ICU at the same time were found significant for MRSA infections. In multivariate analysis; hospitalization period in an ICU (OR, 1.090; 95% CI: 1.038-1.144, P = .001), central venous catheter insertion (OR, 1.822; 95% CI: 1.095-3.033, P = .021), previous antibiotic use (OR, 2.337; 95% CI: 1.326-4.119, P = .003) and presence of more than 2 patients having nasal colonization in the same ICU at the same time (OR, 1.398; 95% CI: 1.020-1.917, P = .037) were independently associated with MRSA infections. CONCLUSION: According to the our results, hospitalization period in an ICU, presence of patients colonized with MRSA in the same ICU at the same time, previous antibiotic use, and central venous catheter insertion are independent risk factors for ICU-acquired MRSA infections. Detection of these factors helps to decrease the rate of MRSA infections in the ICUs.

Adult↗
PubMed1994

Molecular aspects of methicillin resistance in Staphylococcus aureus.

All clinical methicillin-resistant Staphylococcus aureus (MRSA) isolates examined so far contain the mecA gene, a 2130bp stretch of DNA of non-staphylococcal origin which, together with a larger block (up to 40-60 Kb) of 'foreign' DNA, is incorporated into the staphylococcal chromosome. mecA encodes for the 78 Kd penicillin-binding protein (PBP) 2A, which has very low affinity for beta-lactam antibiotics. The sequence of the mecA gene contains structural motifs characteristic of cell wall synthetic transpeptidases. It is generally assumed that the mecA gene product (PBP 2A) acts as a surrogate enzyme which takes over the task of cell wall synthesis from the normal complement of staphylococcal PBPs, since the latter are inhibited by relatively low (e.g. methicillin) concentrations of beta-lactam antibiotics. While direct biochemical evidence for a transpeptidase activity in PBP 2A is still missing, the essentiality of an intact mecA gene for the expression of high-level methicillin resistance has been clearly established by transposon inactivation experiments. On the other hand, it was already noted some time ago that an intact mecA and its gene product PBP 2A alone cannot be fully in control of the resistant phenotype, since all MRSA isolates, irrespective of their MIC values (from as low as 3 mg/L or as high as 1600 mg/L), were found to contain comparable amounts of PBP 2A. Such major disparities between cellular amounts of PBP 2A and the antibiotic MIC values suggested that a factor or factors of unknown nature ('factor X') other than the mecA gene product also played an essential role in the phenotypic expression of resistance. The same conclusion was reached in early genetic studies in which methicillin resistance could be reduced by insertional inactivation of a chromosomal site (omega 2003) within the so-called femA gene--(factor essential for the expression of methicillin resistance) outside the mecA determinant. More recently, several additional chromosomal sites were identified outside the mecA gene in which transposon inactivation reduced the level of beta-lactam resistance. The importance of these genes becomes clear if one realizes that it is the appropriate functioning of these determinants (in the genetic background of MRSA) rather than the quantity of PBP 2A in the cells that seems to determine the MIC value of an MRSA isolate. It is not clear at the present time how many such 'auxiliary genes' exist and exactly how these gene co-operate with the mecA gene in bringing about high-level beta-lactam resistance.(ABSTRACT TRUNCATED AT 400 WORDS)

Amino Acid Sequence↗
PubMed1997

Staphylococcus aureus in dairy products in the Bologna area.

A study was carried out to evaluate the extent of contamination by Staphylococcus spp. and in particular by Staphylococcus aureus in dairy products on sale in the Bologna area. Staphylococcus aureus was found in 16.30% of the 135 cheese samples examined: 8.3% in soft cheese, 17.60% in blue cheese, 18.9% in semi-soft cheese and 25.0% in mozzarella-type cheese. The mean concentration was 2699 CFU/g in the 22 positive samples. The most commonly found species were Staphylococcus epidermidis (14.8%), Staphylococcus hominis (19.5%), Staphylococcus xylosus 2 (19.2%) and Staphylococcus cohnii (16.3%). Staphylococcus aureus was found mostly during the hot months while the other common species were found mostly in the period October-March.

Animals↗
PubMed1992

Analysis of borderline-resistant strains of methicillin-resistant Staphylococcus aureus using polymerase chain reaction.

Identification of methicillin-resistant Staphylococcus aureus by drug-susceptibility tests alone poses a serious problem, because a considerable number of clinical S. aureus isolates are borderline resistant to methicillin. To circumvent this problem, we have developed a quick and sensitive method of PCR amplification for the detection of mecA gene, which, coding for PBP2', is the specific genetic element of methicillin-resistant Staphylococcus aureus. This method made it possible to identify MRSA strains in a short time using as few as 30 cells as a starting material for template DNA. Using this method, we found that the strains of borderline methicillin-resistance could be accurately identified. We also found one S. aureus clinical strain, T3, which lacked mecA gene in spite of its resistance to methicillin.

Base Sequence↗
PubMedDate not supplied

[Identification of Staphylococcus aureus within 2 hours in blood culture broths].

Staphylococcus aureus identification is one of the priorities of the microbiological diagnosis of the staphylococcal infections. Current identification methods are carried out after a first step of colony isolation on agar media. We describe a fluorogenic method for S. aureus identification, which is directly applied to blood culture broths. This method uses a gel tube which allows an optimized microculture of the bacteria. 129 clinical samples of blood cultures (HEC) containing gram positive cocci in grapelike clusters (35 Vital bottles, 94 Bactec bottles), and 77 inoculated blood culture (HE) with collection strains of S. aureus are included in the study. Bacteria are concentrated and separated from other components of sample in the gel tube. Staphylococci are revealed during a microculture in the gel phase, by using a colorimetric substrate of their dehydrogenases. Then, staphylococci are recovered in an adapted culture medium containing human prothrombin and a fluorogenic substrate, which is specific for the staphylocoagulase. After 1 to 2 h incubation at 37 degrees C, a blue fluorescence shows the presence of S. aureus. Among the 40 HEC containing S. aureus the test is positive for 37 samples. For 3 cases, the test is not interpretable, due to non lysis red blood cells in the gel phase of the tube. No false positive result is observed for the HEC containing coagulase-negative staphylococci. Moreover, our method is positive with the 77 HE. 94.7% of tested samples (HEC and HE) show a fluorescence after only one hour and half. Sensibility and specificity are both 100%. We propose a rapid method for S. aureus identification directly applied to blood culture broths. This method saves 24 h, avoiding the isolation step on agar. Therefore, the treatment of staphylococcal infections and possible isolation measures could earlier set up.

Agar↗
PubMed2005

Low-level vancomycin resistance in Staphylococcus aureus--an Australian perspective.

Low-level vancomycin resistance in Staphylococcus aureus has emerged as a clinical problem over the past 8 years. The clinical relevance of this resistance has been questioned, and laboratory detection remains difficult and time consuming. There is, however, increasing evidence linking low-level vancomycin resistance with glycopeptide treatment failure in serious Staphylococcus aureus infections. Diagnostic laboratories and clinicians need to be aware of this resistance phenotype, to have procedures in place to detect the resistance, and to have strategies for managing patients with infections caused by resistant strains.

Aged↗
PubMed1987

Staphylococcus aureus infection as a complication of isotretinoin therapy.

Eighteen patients developed Staphylococcus aureus infection during or shortly after a five-month course of therapy with isotretinoin. Staphylococcus aureus was recovered both from lesions and from the anterior nares. In a prospective study, 4% of control patients treated with isotretinoin alone developed S aureus infection, while none who applied topical antibiotic to the anterior nares developed infection. Control patients had a 64% prevalence of anterior nares colonization with S aureus, compared with 18% in the topical antibiotic group.

Administration, Topical↗
PubMed1984

Nasal carriage and antibiotic susceptibility of Staphylococcus aureus in general practice.

The incidence of nasal carriage of Staphylococcus aureus and the in vitro susceptibility of isolates to fusidic acid, penicillin, erythromycin, methicillin and tetracycline was determined in 204 patients who had been treated previously with a short course of a topical preparation of Fucidin for acute skin sepsis, and in an equal number of control subjects. Staphylococcus aureus was isolated from 36 per cent and 34 per cent of patients in the Fucidin and control groups respectively. Only one of the 144 isolates was resistant to fusidic acid. Short, single courses of topical therapy in general practice are unlikely to be epidemiologically hazardous in the long term. Evidence of possible cross-infection in general practice was obtained.

Administration, Topical↗
PubMed1974

Regulation of bacterial cell walls: turnover of cell wall in Staphylococcus aureus.

The cell wall of Staphylococcus aureus was shown to undergo turnover during exponential growth. The rate of turnover, about 15% per generation, was identical for both cell wall polymers, peptidoglycan and teichoic acid. Both the old and newly synthesized wall material appeared to undergo turnover at similar rates. The rate of turnover followed first-order kinetics until more than 90% of the original wall was lost. Cell wall turnover was completely blocked under conditions of unbalanced synthesis known to inhibit cellular autolysis, e.g., addition of chloramphenicol. Cell wall turnover was shown to occur in a number of different strains of S. aureus and appears to be widely distributed in this species.

Bacterial Proteins↗
PubMed1985

Effect of fibronectin on adherence of Staphylococcus aureus to fibrin thrombi in vitro.

Staphylococcus aureus binds to purified fibronectin in solution and may bind to fibronectin present in wound tissue. When incorporated into a solid fibrin thrombus, however, plasma fibronectin may fail to bind S. aureus, because the S. aureus-binding sites on fibronectin may be occupied by fibrin. Both S. aureus and fibrin bind to the same 27-kilodalton amino-terminal fragment of fibronectin. To determine whether fibronectin incorporated into fibrin still promotes the adherence of S. aureus, we clotted citrated normal plasma and fibronectin-depleted plasma onto petri dishes. We then measured bacterial adherence to these in vitro fibrin thrombi. We found that the adherence of five of seven S. aureus strains decreased significantly (by 26 to 58%) when fibronectin had been depleted from the fibrin thrombi. Adding fibronectin back reversed this decrease in adherence. The reversal was dose dependent; the increase was in proportion to the amount of fibronectin added back to the plasma. Bacteria known not to bind to fibronectin (Escherichia coli and Staphylococcus epidermidis) adhered 100-fold less than S. aureus, and their adherence was unaffected by the absence of fibronectin in the fibrin thrombus. We conclude that fibronectin incorporated into solid fibrin thrombi does mediate the adherence of most S. aureus strains to fibrin thrombi. Fibronectin may be an important molecule that mediates the adherence of S. aureus to fibrin in wounds.

Adhesiveness↗
PubMed1980

Aminoglycoside-modifying enzymes of Staphylococcus aureus; expression in Escherichia coli.

Staphylococcus aureus plasmids PSH2, RN1956 and pWA1 code for an aminoglycoside phosphotransferase; plasmid pWA1 also encodes an aminoglycoside-aminocyclitol adenylyltransferase. S. aureus plasmid pWA2 confers resistance to erythromycin and sulfonamide. Using plasmid ColE1-ApR (RSF2124) as a vehicle, we have transferred the genes determining aminoglycoside phosphotransferase and aminoglycoside-aminocyclitol adenylyltransferase activities from S. aureus to Escherichia coli. The new plasmids obtained confer aminoglycoside-aminocyclitol resistant phenotypes to E. coli, similar to, and by the same mechanisms as "naturally" occurring plasmids. By contrast, the results obtained after cloning of plasmid pWA2 indicate that certain S. aureus antibiotic resistance determinants (e.g. for erythromycin (Em) and sulfonamide (Su) cannot be phenotypically expressed in E. coli. The DNA of the constructed hybrid plasmids has been analysed by agarose gel electrophoresis following digestion with restriction endonucleases, by ultracentrifugation in cesium chloride, by hybridization, and by electron microscopy. Each hybrid is a cointegrate replicon, composed of an entire S. aureus plasmid covalently joined to ColE1-ApR.

Adenosine Triphosphate↗
PubMed1976

Epidemic infection by a gentamicin-resistant Staphylococcus aureus in three hospitals.

A Staphylococcus aureus strain, resistant to aminoglycosides, including gentamicin and tobramycin, and to penicillin, lincomycin, and other antibiotics, caused an outbreak of hospital infection in a surgical ward which spread to the intensive-therapy unit and to two other hospitals. 21 patients were colonised and 9 of these had overt clinical infection. Administration of antibiotics to which the staphylococcus was resistant was associated with colonisation. The use of gentamicin, tobramycin, and lincomycin in these hospitals has increased as has the occurrence of bacterial resistance to these agents. An antibiotic policy to control their use is essential to preserve their value in life-threatening infections by bacteria resistant to other agents.

Acetyltransferases↗
PubMed1962

Endogenous respiration of Staphylococcus aureus.

Ramsey, H. H. (Stanford University, Palo Alto, Calif.). Endogenous respiration of Staphylococcus aureus. J. Bacteriol. 83:507-514. 1962.-The endogenous respiration of Staphylococcus aureus is dependent upon the medium used to grow the cell suspension. Within wide ranges, the concentration of glucose in the medium has no effect upon subsequent endogenous respiration of the cells, but the concentration of amino acids in the medium, within certain limits, has a very marked effect. The total carbohydrate content of the cells does not decrease during endogenous respiration. As endogenous respiration proceeds, ammonia appears in the supernatant, and the concentration of glutamic acid in the free amino acid pool decreases. Organisms grown in the presence of labeled glutamic acid liberate labeled CO(2) when allowed to respire without added substrate. The principal source of this CO(2) is the free glutamate in the metabolic pool; its liberation is not suppressed by exogenous glucose or glutamate. With totally labeled cells, the free pool undergoes a rapid, but not total, depletion and remains at a low level for a long time. Activity of the protein fraction declines with time and shows the largest net decrease of all fractions. Exogenous glucose does not inhibit the release of labeled CO(2) by totally labeled cells. Other amino acids in the free pool which can serve as endogenous substrates are aspartic acid and, to much lesser extents, glycine and alanine. The results indicate that both free amino acids and cellular protein may serve as endogenous substrates of S. aureus.

Alanine↗
PubMed1992

Community-acquired methicillin-resistant Staphylococcus aureus infections in otolaryngology.

Soon after the introduction of methicillin, strains of Staphylococcus aureus resistant to methicillin were reported. Methicillin-resistant Staphylococcus aureus (MRSA) has become a common hospital pathogen, often resistant to multiple antibiotics, while causing significant morbidity and mortality. Community-acquired MRSA infections have been infrequently documented. Most reports have been associated with intravenous drug abuse. This report reviews 15 patients with community-acquired MRSA infections of the head and neck. None admitted to intravenous drug use. Additionally, no patient was known to be a healthcare worker. The MRSA strains showed antibiotic susceptibility and resistance profiles different from typical hospital-acquired MRSA isolates. All but one infection resolved with adequate surgical or appropriate antibiotic therapy. Clinicians should become aware of the possibility of community-acquired MRSA in the patient who has had continued infection despite antibiotic therapy.

Abscess↗