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PubMed2005

Slime-producing Staphylococcus epidermidis and S. aureus in acute bacterial conjunctivitis in soft contact lens wearers.

In recent years, an increase in ocular pathologies related to soft contact lens has been observed. The most common infectious agents were Staphylococcus spp. Some strains produce an extracellular polysaccharidic slime that can cause severe infections. Polysaccharide synthesis is under genetic control and involves a specific intercellular adhesion (ica) locus, in particular, icaA and icaD genes. Conjunctival swabs from 97 patients with presumably bacterial bilateral conjunctivitis, wearers of soft contact lenses were examined. We determined the ability of staphylococci to produce slime, relating it to the presence of icaA and icaD genes. We also investigated the antibiotic susceptibility and Pulsed Field Gel Electrophoresis (PFGE) patterns of the clinical isolates. We found that 74.1% of the S. epidermidis strains and 61.1% of the S. aureus strains isolated were slime producers and showed icaA and icaD genes. Both S. epidermidis and S. aureus slime-producing strains exhibited more surface hydrophobicity than non-producing slime strains. The PFGE patterns overlapped in S. epidermidis strains with high hydrophobicity. The similar PFGE patterns were not related to biofilm production. We found scarce matching among the Staphylococcus spp. studied, slime production, surface hydrophobicity and antibiotic susceptibility.

Adolescent↗
PubMed1996

Genomic diversity of mec regulator genes in methicillin-resistant Staphylococcus aureus and Staphylococcus epidermidis.

Low-affinity penicillin-binding protein PBP-2a encoded by mecA is closely related to methicillin resistance in staphylococci, and expression of PBP-2a is controlled by regulator elements encoded by mecR1 and mecI which are located adjacent to mecA on the chromosome. Deletion or mutation which occurred in mec regulator gene is considered to be associated with constitutive production of PBP-2a. The distribution of the mec regulator genes in 176 strains of Staphylococcus aureus and 33 strains of S. epidermidis isolated from a single hospital was studied by polymerase chain reaction amplification. Most clinical isolates of methicillin-resistant S. aureus (MRSA) (94.3%) and S. epidermidis (MRSE) (83.9%) possessed both mecI and mecR1 genes (type I), whereas no mec regulator genes were detected in mecA-negative isolates. In contrast, 7 MRSA and 5 MRSE isolates were found to have incomplete regulator genes, and they were classified into three groups; strains which lacked only mecI gene (type II), strains which lacked mecI and 3'-end of mecR1 gene (type III), and strains which lacked both regulator genes (type IV). Analysis of mecI gene from all the strains having mecI by restriction fragment length polymorphism after Mse I digestion indicated that three MRSA strains possessed one of the known point mutations identified previously. These findings indicated the predominance of a single type of MRSA possessing both mecI and mecR1 in the study period and also suggested a high genomic diversity in mec regulator region of staphylococci.

Cross Infection↗
PubMed1981

Vancomycin and rifampin therapy for Staphylococcus epidermidis meningitis associated with CSF shunts: report of three cases.

Three patients with Staphylococcus epidermis meningitis associated with cerebrospinal fluid (CSF) shunt devices were treated with a combination of intravenous vancomycin and oral rifampin. Two of the isolates were methicillin-resistant. All patients had a favorable clinical response. Time-kill curves showed that the addition of rifampin to vancomycin resulted in enhanced bactericidal activity against all isolates when compared to either antibiotic alone. This finding suggests that the combination of oral rifampin and intravenous vancomycin may be useful in the treatment of methicillin-resistant and recalcitrant methicillin-sensitive S. epidermis meningitis associated with CSF shunts. In vitro susceptibility testing should be performed.

Aged↗
PubMed1995

Staphylococcus aureus but not Staphylococcus epidermidis can acquire iron from transferrin.

Staphylococci grow and cause infection under the iron-restricted conditions found in vivo. They therefore must possess mechanisms to obtain iron for metabolism from this environment. To determine if staphylococci can extract iron bound to human transferrin, we labelled transferrin with 55Fe and performed uptake assays on cells grown in iron-restricted and iron-plentiful conditions. Growing cultures of Staphylococcus aureus NCTC 8532 could take up radioactive iron during mid- to late-exponential phase of growth. This process was iron-regulated and did not require direct contact between the cell and the labelled transferrin. Siderophore production was detected during this phase, but reductase or protease activity was not. S. epidermidis ATCC 14990 could not access 55Fe bound to transferrin, nor did this isolate produce siderophore, reductase or protease. This difference in the ability to acquire iron bound to transferrin may contribute to the increased virulence of S. aureus when compared to S. epidermidis.

Biological Transport↗
PubMed1989

Characterization of a novel insertion of the macrolides-lincosamides-streptogramin B resistance transposon Tn554 in methicillin-resistant Staphylococcus aureus and Staphylococcus epidermidis.

Macrolides-lincosamides-streptogramin B resistance in staphylococci can result from a gene, ermA, that comprises part of transposon Tn554. Tn554 is unusual in (i) its high specificity for a primary chromosomal attachment site, att554, and (ii) the variability of its 3'-terminal six or seven nucleotides, which appear to copy the six or seven chromosomal nucleotides 5' to the parent transposon during transposition. We characterized a novel Tn554 insert in the chromosomes of methicillin-resistant Staphylococcus aureus strains involved in a current outbreak. This insert was found to resemble an insert recently discovered in S. epidermidis in its junctional fragment restriction pattern. Sequence analysis of the junctional regions showed that the attachment site, att155, exhibited 78% similarity to att554 (39 of the 50 nucleotides flanking the insertion sites) for both S. aureus and S. epidermidis inserts and that the 3' hexanucleotide of the S. epidermidis transposon (GACATC) resembled the reverse complement (TACATC) of its commonly occurring S. aureus counterpart (GATGTA). Epidemiologic and molecular data indicated that att155 is harbored by extra DNA characteristic of methicillin-resistant strains and absent from methicillin-susceptible ones. Further, Southern hybridization showed that, even in the absence of Tn554 inserts, some methicillin-resistant strains contain DNA related to att155 and Tn554.

Anti-Bacterial Agents↗
PubMed1989

Mobility of gentamicin resistance genes from staphylococci isolated in the United States: identification of Tn4031, a gentamicin resistance transposon from Staphylococcus epidermidis.

Homologous genes encoding resistance to gentamicin, tobramycin, and kanamycin through the bifunctional acetylating [AAC(6')] and phosphorylating [APH(2")] aminoglycoside-modifying enzyme were identified in staphylococci isolated from patients in the United States. The mobility of gentamicin resistance (Gmr) genes found on a prototype conjugative plasmid (pGO1) was compared with that of genes cloned from chromosomal sites. Plasmid-encoded Gmr genes and flanking sequences were introduced onto a temperature-sensitive plasmid (pRN3208) from pGO1 by homologous recombination between insertion sequence-like elements present on both replicons. Growth of Staphylococcus aureus strains containing the temperature-sensitive recombinant (pGO161) at the nonpermissive temperature for plasmid replication (42 degrees C) revealed no translocation of Gmr from its plasmid location. A transposon (Tn551) resident on the same replicon did translocate. Chromosomal Gmr determinants were cloned, together with the gene for trimethoprim resistance (dfrA), from three geographically distinct S. epidermidis isolates; two were subcloned onto temperature-sensitive Escherichia coli-S. aureus shuttle plasmids as 7.2-kilobase BglII fragments. Growth of both recombination-deficient and-proficient S. aureus strains containing the cloned genes at 42 degrees C allowed detection of transposition of Gmr sequences and identification of insertion into random chromosomal sites. We have designated this 5-kilobase transposon from S. epidermidis as Tn4031.

Cloning, Molecular↗
PubMed1989

Characterisation and molecular cloning of the novel macrolide-streptogramin B resistance determinant from Staphylococcus epidermidis.

A total of 110 staphylococcal isolates from human skin were found to express a novel type of erythromycin resistance. The bacteria were resistant to 14-membered ring macrolides (MIC 32-128 mg/l) but were sensitive to 16-membered ring macrolides and lincosamides. Resistance to type B streptogramins was inducible by erythromycin. A similar phenotype, designated MS resistance, was previously described in clinical isolates of coagulase-negative staphylococci from the USA. In the UK, MS resistance is widely distributed in coagulase-negative staphylococci but was not detected in 100 erythromycin resistant clinical isolates of Staphylococcus aureus. Tests for susceptibility to a further 16 antibiotics failed to reveal any other selectable marker associated with the MS phenotype. Plasmid pattern analysis of 48 MS isolates showed considerable variability between strains and no common locus for the resistance determinant. In one strain of S. epidermidis co-resistance to tetracycline, penicillin and erythromycin (MS) was associated with a 31.5 kb plasmid, pUL5050 which replicated and expressed all three resistances when transformed into S. aureus RN4220. The MS resistance determinant was localised to a 1.9 kb fragment which was cloned on to the high-copy-number vector, pSK265. A constitutive mutant of S. aureus RN4220 containing the 1.9 kb fragment remained sensitive to clindamycin. This observation, together with the concentration-dependent induction (optimum 5 mg/l of erythromycin) of virginiamycin S resistance suggests that the MS phenotype is not due to altered expression of MLS resistance determinants (erm genes) but probably occurs via a different mechanism.

Cloning, Molecular↗