SEARCH · PubMed Health

Results for “Staphylococcus epidermidis”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 505 records · Page 28Linked to original sources

PubMed2004

Ultrasonically enhanced vancomycin activity against Staphylococcus epidermidis biofilms in vivo.

Infection of implanted medical devices by Gram-positive organisms such as Staphylococcus ssp. is a serious concern in the biomaterial community. In this research the application of low frequency ultrasound to enhance the activity of vancomycin against implanted Staphylococcus epidermidis biofilms was examined. Polyethylene disks covered with a biofilm of S. epidermidis were implanted subcutaneously in rabbits on both sides of their spine. The rabbits received systemic vancomycin for the duration of the experiment. Following 24 h of recovery, one disk was insonated for 24 or 48 h while the other was a control. Disks were removed and viable bacteria counted. At 24 h of insonation, there was no difference in viable counts between control and insonated biofilms, while at 48 h of insonation there were statistically fewer viable bacteria in the insonated biofilm. The S. epidermidis biofilms responded favorably to combinations of ultrasound and vancomycin, but longer treatment times are required for this Gram-positive organism than was observed previously for a Gram-negative species.

Animals↗

PubMed2006

Neither the presence of ica locus, nor in vitro-biofilm formation ability is a crucial parameter for some Staphylococcus epidermidis strains to maintain an infection in a guinea pig tissue cage model.

The pathogenesis of Staphylococcus epidermidis is thought to be based on its capacity to colonize medical devices by forming a biofilm. Biofilm formation is in part mediated by the polysaccharide intercellular adhesin (PIA), which is encoded by the icaADBC operon. We have previously investigated in vitro the correlation existing between biofilm formation (B+/-), presence of ica locus (I+/-) and PIA production (P+/-) in some clinical isolates of coagulase-negative staphylococci (CoNS). Here, we used a guinea pig model of subcutaneous implanted tissue cages to assess the implication of B, I and P parameters in the capacity of nine S. epidermidis and one S. carnosus strains to develop and maintain an infection in vivo. Using clinical isolates and a model strain of S. epidermidis, we showed that the "B+, I+, P+" type confers the ability to maintain an infection in vivo. Surprisingly, the opposite type "B-, I-, P-" tested with clinical and commensal isolates, presented infection rates ranging from 25% to 60%. Other clinical isolates having a "B+, I+, P-" type, were not able to cause an infection in the present model. These results showed that, depending on the strains the capacity to colonize the tissue cage might be independent of the ability to form biofilm.

Animals↗

PubMed1990

Development of a new set of phages as an epidemiological marker in Staphylococcus epidermidis causing nosocomial infections.

We describe the isolation of a new set of phages for typing Staphylococcus epidermidis. One hundred and eighty-two phages were obtained from S. epidermidis strains of human origin. Twelve phages were selected according to their potency and their lytic activity studied. Twenty phages of the Dean and Williams' set were also studied. Phage-typing was undertaken at 100 x RTD, 1000 x RTD and after heat treatment at 48 degrees C. When the two sets of phages were compared separately similar figures were obtained. When the two typing sets were combined, the percentage of typability for the 182 bacterial strains increased to 29.1% using 1000 x RTD and to 75.3% after heat treatment.

Bacteriophage Typing↗

PubMed1993

Platelet-mediated adhesion of Staphylococcus epidermidis to hydrophobic NHLBI reference polyethylene.

The effects of platelets and plasma proteins on the adhesion of Staphylococcus epidermidis strain RP62A to hydrophobic NHLBI reference polyethylene was quantitatively studied using a rotating disk system to generate well-defined shear conditions simulating the hemodynamics of human blood circulation. Bacterial adhesion was quantified by adhesive coefficient, the percentage of bacteria transported to the surface that becomes adherent. The results showed that surface modification by adsorption of plasma proteins reduced the adhesion of S epidermidis as compared to the bare polymer surface. This surface modification was not sufficient to eliminate completely bacterial adhesion, even at the highest physiologic shear stress level. S epidermidis did adhere strongly to polyethylene surface modified by platelets. This is readily evident as approximately 50% of the adherent S epidermidis were bound to contact-activated platelets which occupied only 4% of the surface area. Adhesive coefficients to platelets were significantly greater than to the protein-adsorbed polyethylene surface by at least one order of magnitude (P < or = .01) across the range of physiological shear conditions investigated. These studies show that it is biologic surface modification by contact-activated platelets, and not plasma proteins, which mediates S epidermidis adhesion to polyethylene.

Bacterial Adhesion↗

PubMed1971

Staphylococcus epidermidis BV: antibiotic resistance patterns, physiological characteristics, and bacteriophage susceptibility.

Staphylococcus epidermidis BV is a group of mannitol-fermenting coagulase-negative staphylococci characterized by multiple antibiotic resistance, very similar biochemical characteristics, and phage susceptibility. Clinical isolates belonging to this group are resistant to most antibiotics tested, including oxacillin, lincomycin, and novobiocin. The only antibiotic to which all tested strains are sensitive is vancomycin. Common biochemical traits of the tested S. epidermidis BV strains include fermentation of trehalose and ribose, phospho-beta-glucosidase activity, growth on synthetic medium with amino acids as carbon source, and lack of deoxyribonuclease, phosphatase, lipase, and gelatinase activity. Some of these characteristics appear more frequently in mannitol-positive control strains than in mannitol-negative strains. S. epidermidis BV strains carry lysogenic phages with a host range restricted to this group. These phages allow the differentiation of individual strains.

Agglutination Tests↗

PubMed2004

Polysaccharide intercellular adhesin (PIA) protects Staphylococcus epidermidis against major components of the human innate immune system.

The skin commensal and opportunistic pathogen Staphylococcus epidermidis is the leading cause of nosocomial and biofilm-associated infections. Little is known about the mechanisms by which S. epidermidis protects itself against the innate human immune system during colonization and infection. We used scanning electron microscopy to demonstrate that the exopolysaccharide intercellular adhesin (PIA) resides in fibrous strands on the bacterial cell surface, and that lack of PIA production results in complete loss of the extracellular matrix material that has been suggested to mediate immune evasion. Phagocytosis and killing by human polymorphonuclear leucocytes was significantly increased in a mutant strain lacking PIA production compared with the wild-type strain. The mutant strain was also significantly more susceptible to killing by major antibacterial peptides of human skin, cationic human beta-defensin 3 and LL-37, and anionic dermcidin. PIA represents the first defined factor of the staphylococcal biofilm matrix that protects against major components of human innate host defence.

Humans↗

PubMedDate not supplied

Comparison of cell wall teichoic acid fractions isolated from three different encapsulated strains of Staphylococcus epidermidis.

Teichoic acid preparations extracted from the cell wall of three serologically different encapsulated strains of Staphylococcus epidermidis, ATCC-31432 (capsular type I), SE-360 (capsular type II) and SE-10 (capsular type III) were purified by DEAE-cellulose and Sephadex G-50 column chromatography. The preparations showed immunological heterogeneity by an agar diffusion test. The chemical properties of the cell wall teichoic acid preparations of capsular types I and III were regarded as N-acetyl-glucosaminyl glycerol-phosphate polymers containing N-acetylglucosamine and phosphate at molar ratios of 0.22-1.0 and 0.33-1.0, respectively. The preparation of capsular type II was assumed to be an alpha-glucosyl glycerol-phosphate polymer containing glucose and phosphate at a molar ratio of 0.49-1.0, and it reacted strongly with concanavalin A. Moreover, alanine, glycine, serine and lysine were shown, among these preparations, to be a common amino acid composition. These results indicate that cell wall teichoic acids obtained from these strains were biochemically and immunologically different from each other.

Cell Wall↗

PubMed1988

Drug resistance and plasmid profiles in Staphylococcus epidermidis in 1964 and 1986.

An examination has been made of drug resistance and plasmid content of Staphylococcus epidermidis isolated from hospital patients in 1964 and 1986. Drug resistance was much more prevalent in isolates from 1986 than in isolates from 1964. Plasmids were demonstrated in 50 of 52 strains from 1964 and in 102 of 111 strains from 1986. The majority of both drug-sensitive and drug-resistant strains harboured more than one plasmid. Of five plasmids obtained from a multiply-drug-resistant S. epidermidis, four were shown to mediate drug resistance.

Anti-Bacterial Agents↗

PubMed1988

Effect of ciprofloxacin on subcutaneous abscesses induced with Staphylococcus epidermidis and a foreign body implant in the mouse.

Subcutaneous abscesses were induced in mice with Staphylococcus epidermidis strain G19-85 and a foreign body implant. The MIC of ciprofloxacin for this strain was 0.25 microgram/ml. The ciprofloxacin dosage, 120 mg/kg/day, was divided into three injections, administered to the mice subcutaneously at 8 h intervals. Serum concentration kinetics in normal mice (n = 50) were determined. The peak serum level of ciprofloxacin was 3.18 micrograms/ml at the 15 min sampling time; the trough level was 0.53 micrograms/ml at 8 h. Abscesses were found in 96% (n = 49) of the untreated, infected control mice. Three modes of treatment with ciprofloxacin were tested: (1) four prophylactic injections of ciprofloxacin prior to infection reduced abscess formation to 64% (p less than or equal to 0.0002, n = 50). (2) Eleven therapeutic injections, initiated 4 days after infection, reduced abscess formation to 86% (p less than or equal to 0.17, n = 49). (3) One prophylactic injection prior to surgery and five therapeutic injections after infection reduced abscess formation to 43% (p less than or equal to 0.0001, n = 49). Culture results correlated with the abscess formation rates.

Abscess↗

PubMed1977

Effect of warfarin on the induction and course of experimental Staphylococcus epidermidis endocarditis.

The effect of warfarin treatment on an experimental Staphylococcus epidermidis endocarditis was studied. Warfarin was found to affect both the induction and course of the infection of catheter-induced endocardial vegetations. In warfarin-treated rabbits, larger bacterial inocula were needed to induce an infection, and the degree of infection of the vegetations was also significantly lower, eventually resulting in the total elimination of the bacteria from the vegetations. Thus, warfarin treatment seems to have an inhibitory effect on the induction and development of an S. epidermidis infection of the endocardium. The results differ from previous findings in studies done with Streptococcus anguis, where warfarin was found to have no effect on the induction or course of the infection of endocardial vegetations, which suggests that different mechanisms are involved in the pathogenesis of endocarditis caused by these two species of bacteria.

Animals↗

PubMed1972

Polyfunctional penicillinase plasmid in Staphylococcus epidermidis: bacteriophage restriction and modification mutants.

Growth of multiply resistant Staphylococcus epidermidis BV strains at 45 C resulted in the independent elimination of tetracycline resistance, of kanamycin resistance coupled with oxacillin resistance, or of penicillinase activity. The pH optimum for the elimination of kanamycin and oxacillin resistance was 5.6, whereas that for elimination of penicillinase activity was 8.0. The genetic determinant for penicillinase activity was linked with the genetic determinants for the active uptake of mannitol and beta-glucosides, ribose fermentation, and phospho beta-glucosidase activity. The penicillinase linkage group also contained determinants for phage adsorption, restriction, and modification, and for growth factor requirements of still unknown nature. The same linkage group, which is apparently of extrachromosomal nature, was eliminated from several S. epidermidis BV strains. By selection for novobiocin resistance, deletion mutants affecting several loci of the penicillinase plasmid were isolated. The isolation of restriction-negative and modification-negative mutants which retained phage susceptibility allowed the investigation of restriction and modification phenomena. A preliminary deletion map of the polyfunctional penicillinase plasmid is proposed.

Carbon Isotopes↗

PubMed1979

[Bacterial endocarditis due to Staphylococcus epidermidis. Two cases (author's transl)].

Bacterial endocarditis due to Staphylococcus epermidis is rare and severe. In a first patient, a 58-year-old-man, it developed 40 days after the insertion of a double prosthesis (mitral and aortic). Cure was obtained by medical treatment using a combination of vancomycin and gentamicin, followed by pristinamycin and tobramycin. The second patient, a 50-year-old-woman, suffering from cirrhogenic hepatitis and treated with corticosteroids. Staphylococcus epidermidis endocarditis developed without any portal of entry being discovered. After the failure of various antibiotic combinations (even though bactericidal in vitro), a mitral Starr valve was inserted which resulted in cure. None of the patients showed any sign of valvular mutilations or disinsertion of prosthesis.

Adrenal Cortex Hormones↗

PubMed1985

Staphylococcus epidermidis arthritis following catheter-induced bacteremia in a neutropenic patient.

Sepsis due to methicillin-resistant Staphylococcus epidermidis occurred in a neutropenic man during management with a Hickman-Broviac catheter. Despite catheter removal and 10 days of i.v. cefazolin therapy, he developed septic arthritis 6 weeks later in a nonprosthetic hip joint. S. epidermidis was isolated from the joint and found to have plasmid and phage susceptibility patterns identical to the previous blood isolate. This case is the first to document a metastatic infection from catheter-associated S. epidermidis bacteremia. It suggests that cephalosporins may not be optimal in such infections despite in vitro sensitivity. Vancomycin appears to be the drug of choice for S. epidermidis bacteremia in the neutropenic population.

Adult↗

PubMed2001

Staphylococcus epidermidis with intermediate resistance to vancomycin: elusive phenotype or laboratory artifact?

The recent and troubling isolation of Staphylococcus aureus and coagulase-negative staphylococci that have increased resistance to glycopeptide antibiotics has prompted the use of aggressive surveillance measures in the clinical microbiology laboratory to aid in the recognition of these strains. Despite increasing awareness, the confirmation of glycopeptide resistance among staphylococci can be problematic; we present a case of catheter-associated peritonitis caused by Staphylococcus epidermidis to illustrate the dilemma.

Anti-Bacterial Agents↗

PubMed1979

Transduction of penicillinase production in Staphylococcus epidermidis and nature of the genetic determinant.

Four strains of Staphylococcus epidermidis from clinical sources were capable of serving as donors for the transduction of either penicillinase production, ethidium bromide resistance, or tetracycline resistance. Three typing phages served as transducing phages and, depending upon the combination of transducing phage, donor strain, and recipient strain, the rates of transduction ranged between 10(-5) and 10(-9). In one strain, cotransduction of penicillinase production and ethidium bromide resistance was observed. Although ultraviolet irradiation kinetics indicated that both the tetracycline resistance and the penicillin resistance determinants were located on plasmids, only resistance to tetracycline could be eliminated by growth in the presence of curing agents or at elevated temperature. However, evidence was obtained by agarose gel electrophoretic studies that both the tetracycline resistance and the penicillin resistance determinants are located on separate plasmids in this organism.

Drug Resistance, Microbial↗

PubMed2003

Antimicrobials as potential adjunctive agents in the treatment of biofilm infection with Staphylococcus epidermidis.

BACKGROUND: This study was performed to evaluate the interaction of erythromycin or rifampin with vancomycin against Staphylococcus epidermidis biofilms. METHODS: Biofilm-forming S. epidermidis strains (ATCC 35983, 35984) and polyurethane (PU) sheets were incubated for the formation of bacterial biofilms. Biofilms on PU sheets were treated with various antibiotic regimens. The number of viable bacteria on the sheets was counted. RESULTS: While erythromycin or vancomycin alone did not significantly reduce the biofilm bacterial concentration, the combination of vancomycin and erythromycin resulted in a clear reduction in bacterial concentration compared with the single agents. Rifampin was the most active single agent against biofilm-forming S. epidermidis, while the combination of rifampin and vancomycin showed further reduction in bacterial concentration. CONCLUSIONS: These data suggest that the combination of erythromycin or rifampin and vancomycin is more effective than vancomycin alone in the treatment of biofilm infections caused by biofilm-forming S. epidermidis.

Biofilms↗

PubMed1992

The use of nonsteroidal antiinflammatory drugs to prevent adherence of Staphylococcus epidermidis to medical polymers.

The effect of salicylates and other nonsteroidal antiinflammatory drugs on the production of Staphylococcus epidermidis extracellular slime was studied. A dose-related decrease in slime production was observed with increasing concentrations of salicylic acid. S. epidermidis grown in 5 mM salicylic acid were less likely to adhere to Silastic, polyvinyl chloride, polyurethane, and Teflon catheters (P less than .006); strains grown in 2 mM salicylic acid, ibuprofen, indomethacin, or phenylbutazone were less adherent to Silastic catheters (P less than .001). Similar results were obtained with polyurethane catheters. S. epidermidis strains were less likely to adhere (43%-82% inhibition) to polyurethane catheters treated with 500 mM salicylic acid diluted in ethanol (P less than .0001). Similar differences were not observed with acetaminophen, ibuprofen, or acetylsalicylic acid. Adherence of radiolabeled S. epidermidis to salicylic acid-treated Silastic catheters demonstrated a dose-related reduction. The use of salicylic acid to coat medical devices may decrease the incidence of device-related infection.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1994

The antibiotic susceptibility of Propionibacterium acnes and Staphylococcus epidermidis isolated from acne.

We studied the susceptibility of antimicrobial agents to Propionibacterium acnes (P. acnes) and Staphylococcus epidermidis (S. epidermidis) isolated from acne patients. We measured the minimum inhibitory concentrations (MICs) of the following five drugs: roxithromycin (RXM), erythromycin (EM), clindamycin (CLDM), minocycline (MINO) and ofloxacin (OFLX), which are frequently used to treat acne and skin infections. We found many resistant strains of S. epidermidis and some resistant strains of P. acnes. There was a correlation between the resistance of S. epidermidis and the former therapy for acne, but no distinct correlation between the resistance of P. acnes and the former therapy for acne.

Acne Vulgaris↗