Disease relevance of Staphylococcus epidermidis

• Rifampin was added to existing antibiotic regimens in two patients with Staphylococcus epidermidis infections; one patient had prosthetic valve endocarditis and the other had an infection of a CSF shunt [1].
• Staphylococcus aureus, Staphylococcus epidermidis, and other coagulase-negative Staphylococci were sensitive to oxacillin in 89%, 60%, and 50% of cultures, respectively [2].
• Some wounds were seeded with Pseudomonas aeruginosa or Staphylococcus epidermidis, and some seeded wounds were treated with Sulfamylon or Silvadene [3].
• PGA is produced by the Gram-negative periodontopathogen Actinobacillus actinomycetemcomitans as well as by the Gram-positive device-associated pathogen Staphylococcus epidermidis [4].
• Cells were stimulated with peptidoglycan (PG) from Staphylococcus epidermidis or with Escherichia coli lipopolysaccharide (LPS), both in the presence of 10% human serum [5].

High impact information on Staphylococcus epidermidis

• At a bacteria/leukocyte ratio of 10:1, killing of gram-positive, BPI-resistant, Staphylococcus epidermidis is markedly impaired in the absence of oxygen (76.4 +/- 3.3% killing in room air, 29.2 +/- 8.2% killing in nitrogen) [6].
• Ciprofloxacin-resistant Staphylococcus epidermidis and hands [7].
• PGE(2) production was also increased by the addition of IL-18BP to PBMC stimulated with either IL-1beta or IL-12 and also in whole blood cultures stimulated with Staphylococcus epidermidis [8].
• The pathogenic role of Staphylococcus epidermidis capsular polysaccharide/adhesin in a low-inoculum rabbit model of prosthetic valve endocarditis [9].
• Incubation with different stimuli (lipopolysaccharide [LPS], phytohemagglutinin [PHA], Staphylococcus epidermidis, or IL-1 alpha) resulted in production of IL-6 [10].

Chemical compound and disease context of Staphylococcus epidermidis

• For example, Staphylococcus epidermidis elaborates a polysaccharide adhesin that also functions as a capsule and is a target for opsonic killing [11].
• We report here that TLR2 transduces the response to phenol-soluble modulin, a factor secreted by Staphylococcus epidermidis [12].
• Intrinsic methicillin-resistance in Staphylococcus epidermidis is often cryptic, requiring special tests for detection [13].
• Evidence for autolysin-mediated primary attachment of Staphylococcus epidermidis to a polystyrene surface [14].
• The presence of Staphylococcus epidermidis in every case was most striking as was the preponderance of methicillin sodium resistance [15].

Biological context of Staphylococcus epidermidis

• A novel mechanism of phase variation of virulence in Staphylococcus epidermidis: evidence for control of the polysaccharide intercellular adhesin synthesis by alternating insertion and excision of the insertion sequence element IS256 [16].
• The genetic nature of penicillin (Pc) and tetracycline (Tc) resistance plasmids in Staphylococcus epidermidis were studied and compared with those in S. aureus [17].
• DNA sequence analysis revealed that ciprofloxacin resistance in Staphylococcus epidermidis is associated with a novel Ser-84----Phe mutation in the DNA gyrase A protein, analogous to Ser-84----Leu changes observed in Staphylococcus aureus [18].
• mecA is not involved in the sigmaB-dependent switch of the expression phenotype of methicillin resistance in Staphylococcus epidermidis [19].
• Essential functional role of the polysaccharide intercellular adhesin of Staphylococcus epidermidis in hemagglutination [20].

Anatomical context of Staphylococcus epidermidis

• Ingestion of Staphylococcus epidermidis by normal neutrophils was shown to be partially inhibited by monoclonal antibodies to the alpha-chain of either CR3 or LFA-1, and monoclonal antibody to the common beta-chain inhibited ingestion by 75% [21].
• The migration-enhancing activity of Staphylococcus epidermidis cell walls was retained by a monomer as well as a polymer of disaccharide peptides which were prepared by digestion of the peptidoglycan with enzymes [22].
• Of importance is the observation that human monocytes infected with L. tropica for 6 hr and then challenged with a potent IL-1 inducer (Staphylococcus epidermidis) produced significantly less IL-1 than did uninfected monocytes that were similarly challenged (P less than .001) [23].
• Glycocalyx partially purified under endotoxin-free conditions from defined liquid medium cultures of Staphylococcus lugdunensis or Staphylococcus epidermidis was a strong stimulator of PGE2 and IL-1 production [24].
• We used transposon (Tn) mutagenesis to study the role of capsular polysaccharide/adhesin (PS/A) and slime in adherence of Staphylococcus epidermidis to catheters. pLTV1, containing Tn917-LTV1, was transformed into S. epidermidis M187 by protoplast fusion with S. aureus RN4220(pLTV1), creating M187(pLTV1) [25].

Gene context of Staphylococcus epidermidis

• PBMC obtained at entry, 6, 12, 18, and 24 months were stimulated to produce IL-1 beta with phytohemagglutinin (PHA), lipopolysaccharide (LPS), Staphylococcus epidermidis, recombinant IL-2, or mitochondrial antigen [26].
• The Staphylococcus epidermidis Fol62 isolate, harboring multiresistance plasmid pMS62, contained qacA/B and blaZ together with tetK [27].
• By contrast, preincubation (1 h) of cells, in amounts of tebufelone which decrease the formation of leukotriene (LT) B4, markedly enhanced (up to 500%) the synthesis of IL 1 beta and TNF-alpha following lipopolysaccharide (LPS), heat-killed Staphylococcus epidermidis or concanavalin A stimulation [28].
• We found that 30 or 33 isolates highly resistant to Tmp (MICs, > or = 512 micrograms/ml) contained dfrA sequences, whereas among the Tmpr (MICs, < or = 256 micrograms/ml) and Tmps isolates only the Staphylococcus epidermidis isolates (both Tmpr and Tmps) seemed to contain the dfrA gene [29].
• Results. In mice inoculated by Staphylococcus epidermidis or Escherichia coli, CD40 in PMC increased twofold at 24 hours and CD154 was induced and reached a peak at 48 hours [30].

Analytical, diagnostic and therapeutic context of Staphylococcus epidermidis

• To analyze and compare the adherence of Staphylococcus epidermidis to intraocular lenses (IOLs) made of five different biomaterials (native or heparinized polymethylmethacrylate, silicone, hydrophilic acrylic, or hydrogel) and to detail the different steps and mechanisms of bacterial adhesion to a polymer [31].
• SCCmec typing of a collection of 44 methicillin-resistant Staphylococcus epidermidis (MRSE) isolates recovered between 1973 and 1983 from the blood of patients with prosthetic valve endocarditis (PVE) was performed by PCR amplification of key genetic elements (mecA, mecI, IS1272, and ccrAB) [32].
• Antibiotic prophylaxis of experimental endocarditis due to methicillin-resistant Staphylococcus epidermidis [33].
• Lombazole, an antimicrobial agent of the imidazole class, induced profound ultrastructural changes in Staphylococcus epidermidis and Candida albicans, as observed by freeze fracture electron microscopy [34].
• Transmission electron microscopy of S. aureus and Staphylococcus epidermidis treated with CP29 (a 26-amino-acid alpha-helical peptide), CP11CN (a 13-amino-acid, proline- and tryptophan-rich peptide), and Bac2A-NH(2) (a linearized version of the 12-amino-acid loop peptide bactenecin) showed variability in effects on bacterial structure [35].

References