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PubMed2005

Factors characterizing Staphylococcus epidermidis invasiveness determined by comparative genomics.

Virulence mechanisms of the leading nosocomial pathogen Staphylococcus epidermidis are poorly understood. We used microarray-based genome-wide comparison of clinical and commensal S. epidermidis strains to identify putative virulence determinants. Our study revealed high genetic variability of the S. epidermidis genome, new markers for invasiveness of S. epidermidis, and potential targets for drug development against S. epidermidis infections.

Bacterial Proteins↗
PubMed1998

Bacterial surface properties of clinically isolated Staphylococcus epidermidis strains determine adhesion on polyethylene.

The role of surface physiochemical properties of Staphylococcus epidermidis strains in adhesion to polyethylene (PE) was investigated under physiological flow conditions in phosphate buffered saline (PBS) and 1% platelet poor plasma (PPP). Four clinically isolated strains were divided into two groups: low and high relative hydrophobicity, and the F1198 and RP62A strains showing significantly greater hydrophobicity than the F21 and F1018 strains. In PBS, adhesion of all S. epidermidis strains was shear dependent from 0 to 15 dyn/cm2, after which adhesion becomes shear independent. Strains with higher surface hydrophobicity showed higher adhesion to PE, demonstrating the influence of bacterial surface hydrophobicity in nonspecific adhesion. Bacterial adhesion correlated well with bacterial surface hydrophobicity at low shear stresses (0-8 dyn/cm2). In 1% PPP, adhesion of all strains dramatically decreased and we found no correlation between bacterial surface hydrophobicity and adhesion. The presence of plasma proteins reduced nonspecific adhesion. S. epidermidis surface charge did not correlate with bacterial adhesion in either test media. The results suggested that S. epidermidis surface hydrophobicity may mediate nonspecific adhesion to PE at low shear stresses in protein-free media.

Bacterial Adhesion↗
PubMed1997

IgG subclasses specific to Staphylococcus epidermidis and Propionibacterium acnes in patients with acne vulgaris.

IgG subclasses specific to Staphylococcus epidermidis and Propionibacterium acnes were determined in sera from patients with mild, moderate or severe acne and from a control group. Titres specific to S. epidermidis were all within the same range and did not differ between groups. The titres of IgG subclasses to specific to P. acnes did vary between groups. IgG1 and IgG3 were significantly higher in severe acne patients compared with moderate acne patients, while IgG2 was significantly higher in moderate and severe patients compared with controls. Titres of IgG4 did not differ between groups. The pattern of titres observed suggests that, while the antibody response to S. epidermidis is relatively harmless, antibodies to P. acnes may be involved in the pathogenesis of acne vulgaris.

Acne Vulgaris↗
PubMed2002

Levels of specific antibodies towards the major antigenic determinant of slime-producing Staphylococcus epidermidis determined by an enzyme immunoassay and their protective effect in experimental keratitis.

Staphylococcus epidermidis is an important cause of bacterial keratitis. Certain S. epidermidis strains produce an extracellular slime layer rich in an acidic polysaccharide with a molecular size of 20 kDa (20-kDa PS). We have demonstrated that the level of 20-kDa PS-specific antibodies significantly rises after establishment of slime-producing S. epidermidis bacteraemia and, furthermore, that rabbit polyclonal antibodies to 20-kDa PS opsonize cells of slime-producing S. epidermidis to a great degree and promote their clearance by polymorphonuclear cells (Arch. Biochem. Biophys. 342 (1997) 389; J. Pharm. Biomed. Anal. 22 (2000) 1029). The purpose of this study was to examine the protective and therapeutic effects both of active immunization, using 20-kDa PS as antigen, and of passive administration of specific antibodies towards the 20-kDa PS in a rabbit keratitis model. For active immunization, 20 rabbits were subcutaneously immunized with 20-kDa PS, whereas for passive immunization specific polyclonal IgG antibodies against 20-kDa PS were administered to 20 rabbits 1 day before induction of infection. Clinical observations were made weekly for 1 month and levels of 20-kDa PS antibodies in serum and aqueous humor in both immunization groups were determined by an enzyme immunoassay. The levels of specific anti-20-kDa PS IgG in serum and aqueous humor following either active or passive immunization were significantly higher as compared with control groups (P<0.001). Although, actively immunized rabbits showed significantly less corneal damage than control animals, passively immunized ones were significantly better protected as compared with both control and those actively immunized. Obtained results suggest that 20-kDa PS plays crucial role in the pathogenesis of S. epidermidis keratitis and that both types of immunization significantly protect against corneal S. epidermidis pathology and damage.

Animals↗
PubMed2001

Staphylococcus epidermidis biofilms: importance and implications.

The coagulase-negative staphylococci and, in particular, Staphylococcus epidermidis, have emerged as major nosocomial pathogens associated with infections of implanted medical devices. These organisms, which are among the most prevalent bacteria of the human skin and mucous membrane microflora, present unique problems in the diagnosis and treatment of infections involving biofilm formation on implanted biomaterials. Epidemiological data that address whether invasive S. epidermidis strains can be traced to commensal organisms or an endemic occurrence of distinct strains with enhanced virulence have important implications for the implementation of appropriate infection control measures. An extracellular polysaccharide adhesin represents a key virulence determinant in S. epidermidis and is required for biofilm formation. Production of this adhesin, which is encoded by the ica operon, is subject to phase variable regulation (ON <---> OFF switching). Recent advances in understanding the molecular events controlling polysaccharide adhesin synthesis and the potential clinical implications of its phase variable regulation are outlined. Further research in this area may contribute to the development of novel strategies for therapeutic intervention. Finally, in addition to antibiotic prophylaxis, preventive strategies to control S. epidermidis medical device-related infections are focusing on the development of improved biomaterials and physical electrical barriers to impede bacterial colonisation.

Adhesins, Bacterial↗
PubMed1987

Recognition and importance of Staphylococcus epidermidis infections.

The bacteriology, epidemiology, pathogenesis, clinical features, antimicrobial susceptibility, and therapy of Staphylococcus epidermidis infections are reviewed. Staph. epidermidis is often regarded as a culture contaminant, but its importance as a pathogen has been recognized in recent years. Except for native-valve endocarditis, most Staph. epidermidis infections are hospital-acquired. Staph. epidermidis is a common cause of infections involving indwelling foreign devices, surgical wound infections, and bacteremia in immunocompromised patients. The occult nature of these infections and low virulence of the organism make diagnosis and treatment difficult. Staph. epidermidis isolates from nosocomial infections frequently are resistant to methicillin; however, resistant isolates often appear to be susceptible to methicillin unless reliable methods of susceptibility testing are used. Cross-resistance between methicillin and cephalosporins occurs in vitro. Virtually all Staph. epidermidis isolates are susceptible in vitro to vancomycin and rifampin. Penicillin G, semisynthetic penicillinase-resistant penicillins, and cephalosporins are effective for the treatment of methicillin-sensitive Staph. epidermidis infections. Vancomycin is the drug of choice for infections caused by methicillin-resistant organisms. Vancomycin, combined with rifampin or gentamicin, or both, is recommended for therapy of serious infections caused by methicillin-resistant strains. Staph. epidermidis is an important pathogen in immunocompromised patients and patients who develop nosocomial bacteremia; treatment usually consists of antimicrobial therapy and removal of indwelling catheters or devices.

Catheterization↗
PubMed1988

Phage typing set for differentiating Staphylococcus epidermidis.

A phage typing set composed of 13 phages is described for characterizing Staphylococcus epidermidis. Isolates (372) from cases of bovine mastitis were used in this study. Of these, 350 or 94% were successfully delineated, and 63 phage types were observed. Twenty two cultures were not typeable.

Animals↗
PubMed2006

Clonality of clinical methicillin-resistant Staphylococcus epidermidis isolates in a neonatal intensive care unit.

OBJECTIVE: Study of the clonality of methicillin-resistant Staphylococcus epidermidis responsible of epidemic infections in a neonatal intensive care unit. PATIENTS AND METHODS: All S. epidermidis isolates (mecA+) were collected during the epidemic period (December 2003-September 2004) from different pathological products of newborns. Isolates were characterized by genotyping in pulsed-field gel electrophoresis and by electrophoretic profiles obtained by PCR-based analysis of inter-IS256 spacer polymorphisms. RESULTS: Twenty methicillin-resistant S. epidermidis isolates were collected from newborns during the epidemic period and represented 41.6% of the total isolates of S. epidermidis, which is the first Staphylococcus species isolated from the unit. These isolates were collected from blood cultures (80%), vascular catheters (5%), pus (10%), and intra-tracheal tube (5%). Six genotypic profiles were individualized: type A, type B, type C, type D, type E, and type F, with clear dominance of type A. Five different PCR patterns were found with poor correlation to genotypes defined by PFGE. CONCLUSION: Neonatal nosocomial outbreak of methicillin-resistant S. epidermidis was caused by multiple clones of this species with predominance of one epidemic and multiresistant clone. This clone may be transmitted between babies and was able to persist in the unit. PCR IS 256 proved to be less discriminative than PFGE for typing MRSE.

Equipment Contamination↗
PubMed1995

Contribution of the host to test results in assays of Staphylococcus epidermidis.

From two human populations (one pediatric and one adult), clinically diagnosed with Staphylococcus epidermidis (S. epidermidis) sepsis of similar severity, bacteria were isolated from pre-antibiotic blood samples and evaluated for virulence. The LD50 of the bacteria in a mouse model was performed, with evaluation of animals dying acutely following intravenous S. epidermidis administration. More simple assays of virulence were also performed, including bacterial adherence to a fibrin clot and carbohydrate specific lectin binding. The eight pediatric-host S. epidermidis isolates required a significantly larger dose to produce lethality in dosed animals (LD50) when compared to the 20 adult-host S. epidermidis isolates. The fibrin clot assay, a test that has corroborated bacterial virulence in endocarditis models, did not differentiate the groups: all but one of the 28 isolates were well above the adherence seen with the ATCC control, suggesting endocarditis-producing potential. Glycocalyx (slime) from eight of the more virulent isolates showed reactivity with a glucose-specific biotinylated lectin which was lacking in other isolates. Necropsy of mice dying at 12 hr showed S. epidermidis strain differences in specific organ effects. Overall, this study demonstrates the utility of the LD50 to provide a highly sensitive quantification of bacterial virulence. Necropsy of test animals dying acutely has showed an apparent organ tropism of some of these isolates which are usually considered harmless commensals.

Adult↗
PubMed1989

Adherence of Staphylococcus epidermidis to intraocular lenses.

We have demonstrated, with an in vitro model, that Staphylococcus epidermidis is able to colonise intraocular lenses. Adherent organisms were quantitated by light microscopy, scanning electron microscopy, and viable counting. Bacterial adherence was associated with production of a polysaccharide glycocalyx. Organisms which were attached to the lenses were resistant to apparently bactericidal concentrations of antibiotics, as determined by conventional testing. We speculate on the role of colonisation in the pathogenesis of endophthalmitis.

Bacterial Adhesion↗
PubMed1992

Comparison of cell-wall teichoic acid with high-molecular-weight extracellular slime material from Staphylococcus epidermidis.

Extracellular high-mol.-wt material was separated from liquid cultures of Staphylococcus epidermidis. This material contained protein c. 20% w/w and polysaccharide c. 80% w/w. The polysaccharide was isolated by gel and ion-exchange chromatography and contained glycerol phosphate, glucose, N-acetylglucosamine, and D-alanine. Cell-wall teichoic acid was isolated from strain RP-62A and had a similar composition.

Acetylglucosamine↗
PubMed2005

Clonal analysis of Staphylococcus epidermidis isolates carrying or lacking biofilm-mediating genes by multilocus sequence typing.

Staphylococcus epidermidis is part of the normal microflora of the human skin but is also a leading cause of device-associated infections in critically ill patients. Commensal and clinical S. epidermidis isolates differ in their ability to form biofilms on medical devices; the synthesis of biofilms is mediated by the icaADBC operon. Currently, the epidemiological relatedness between ica-positive and -negative isolates is not known; neither is it known whether the ica genes can spread to biofilm-negative strains through horizontal gene transfer. In this study, multilocus sequence typing (MLST) was employed for the clonal analysis of 118 S. epidermidis ica-positive and -negative strains. MLST revealed that the majority of ica-positive and -negative strains were closely related and formed a single clonal complex. Within this complex one sequence type (ST27) was identified which contained exclusively ica-positive isolates and represented the majority of clinical strains tested. ST27 and related ica-positive clones carried different SCCmec cassettes (conferring methicillin resistance) and the insertion sequence IS256. The findings suggest that the S. epidermidis infections analyzed in this report are mainly caused by a single clone (ST27) which occurs preferentially in hospitals and differs from clones in the community. It is hypothesized that the successful establishment of ST27 within nosocomial environments has been facilitated by the presence of genes encoding biofilm and resistance traits.

Bacterial Adhesion↗
PubMed1994

The effects of extracellular slime from Staphylococcus epidermidis on phagocytic ingestion and killing.

Extracellular slime (Ecs) from three strains of Staphylococcus epidermidis was prepared and added to fresh suspensions of polymorphonuclear neutrophils. Phagocytic ingestion and killing of opsonised and unopsonised S. epidermidis strains was assessed over time using slide preparations stained by the Gram's method and microbiological culture. Both phagocytic ingestion and killing were inhibited. Investigation as to one possible mechanism of action of Ecs on phagocytes was performed using 1 mu polystyrene spheres which were incubated overnight with Ecs. It was found that the surface tension was altered with Ecs making the beads more hydrophilic, a factor which may interfere with the phagocytic response to infection.

Bacterial Proteins↗
PubMedDate not supplied

[New bacteriophages of Staphylococcus epidermidis: evaluation of their epidemiological value].

Coagulase-negative staphylococci, and in particular Staphylococcus epidermidis, are now being recognized as causing human infections with increasing frequency; the absence of an internationally accepted system of phage-typing for coagulase-negative staphylococci led us to isolate new phages. Fifty strains of S. epidermidis isolated from human infections were induced with mitomycin C: eight phages (41, 63, 118-II, 138, 245, 336, 392 and 550) were isolated. These phages were propagated on five different strains of S. epidermidis. Their phages were propagated on five different strains of S. epidermidis. Their lytic activity as studied on 561 strains. Phages 336, 392 and 550 had a different host-range and different propagative strains; they typed 93% of the strains susceptible to the 8 phages. The other phages had an activity similar to that of phage 336. Twenty-one per cent of non-epidemic strains were susceptible to at least one of the three phages. The reproducibility, specificity and discriminatory power of these phages suggest they may be a useful addition to previously recognized phages.

Bacteriophage Typing↗
PubMed1990

Staphylococcus epidermidis extracted slime inhibits the antimicrobial action of glycopeptide antibiotics.

Certain strains of Staphylococcus epidermidis produce a mucoid slime that appears to be an important virulence factor. After crude slime was isolated from selected strains of S. epidermidis, phenol and chloroform were used to remove proteins and lipids. The remaining extract contained a polysaccharide that was seen on SDS gels stained with Stains-all. This extract was an inhibitor of the antimicrobial action of vancomycin, raising the minimum inhibitory concentration (MIC) to vancomycin in all 18 isolates of S. epidermidis. A dose-response curve was seen between the amount of extract added and the degree of resistance, as measured by both MIC and growth curves. A similar effect was noted with MICs of organisms to teicoplanin. Addition of the extract did not change the MIC to LY146032, although a modest effect on growth rate was observed. The extract did not raise the MIC to clindamycin, rifampin, and cefazolin. The extract reversed the synergism seen between vancomycin and gentamicin in the 5 strains tested in time-kill studies. The interference by slime of the antimicrobial effect of vancomycin and teicoplanin may explain why these antibiotics are sometimes ineffective in eradicating foreign body infections due to slime-producing coagulase-negative staphylococci.

Microbial Sensitivity Tests↗
PubMed1992

Phenotypic variation of Staphylococcus epidermidis isolated from a patient with native valve endocarditis.

Two colonial variants of Staphylococcus epidermidis were isolated from the valvular tissue of a patient with native valve endocarditis. In addition to differing in colonial morphology, the two variants differed in hemolysis on blood-containing media, in adherence capacity, and in the expression of certain enzymes. Under suitable conditions, both variants were themselves capable of phenotypic variation, although they differed in the rate at which variants were generated. The variants yielded identical profiles on restriction endonuclease analysis of plasmid DNA and pulsed-field gel electrophoresis of whole-cell DNA. This report suggests a possible role for phenotypic variation in coagulase-negative staphylococcal virulence. Congo red agar would be an excellent medium for studying the contribution of variation to the virulence of these organisms.

Adult↗
PubMed1999

Necrotizing otitis externa caused by Staphylococcus epidermidis.

We present a case of malignant necrotizing otitis externa (MNOE) caused by Staphylococcus epidermidis, which is usually a non-pathogenic microorganism. The patient is an otherwise healthy, nondiabetic 58-year-old white man. Contributory history began in 1994 after surgery for bilateral exostoses of the external auditory canals. Between April 1994 and May 1998 persistent otalgia occurred, with progressive mixed hearing losses, purulent discharge from both ears, spontaneous perforations of the tympanic membranes and ulceration of canal wall skin. From the beginning, Staph. epidermidis was isolated in all but one culture, but was not recognized as the pathological agent because of the presence of other more frequently involved bacteria and fungi. After multiple intravenous and oral antibiotics and antifungal treatments failed, further management involved frequent debridement of both external auditory canals and tympanic membranes, right tympanoplasty, bilateral mastoidectomy, revision tympanomastoidectomies and left modified radical mastoidectomy. Antistaphylococcal therapy including ceftazidime, vancomycin, teicoplanin, clindamycin and rifampicin was tried. Following the modified radical radical mastoidectomy, normalization of the status of his ears took approximately 2 months and has since remained stable to date. His left ear is deaf because of vancomycin administration, while magnetic resonance imaging and gallium scintigraphy have shown persistent inflammation of the skull base.

Aminoglycosides↗