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At least 1,333 records · Page 74Linked to original sources
PubMed1995

Plasmid-mediated vanB glycopeptide resistance in enterococci.

Enterococcus faecium, which was highly resistant to vancomycin (MIC 256 mg/liter), but susceptible to teicoplanin (MIC 2 mg/liter), caused two distinct episodes of infection on a renal unit in the United Kingdom. Pulsed field gel electrophoresis (PFGE) indicated that a single strain caused the first episode, while the second episode, which occurred 1 year later, involved multiple strains, all of which were distinct from the original strain. Vancomycin resistance in all but one of these strains was mediated by transferable plasmids that carried the vanB glycopeptide resistance gene. Transfer either of resistance plasmids or the vanB resistance determinant itself to different strains occurred during the second episode. Plasmid-mediated vanB resistance has not been widely documented. A retrospective study of a reference collection revealed two other vanB-encoding plasmids from an E. faecalis and an E. faecium referred from two further UK centers. Although restriction analysis indicated no similarity between the plasmids from the three different centers, all contained a 2.1-kb EcoRV fragment that hybridized with a probe for the vanB gene. This suggests that there has been dissemination of a conserved glycopeptide resistance determinant, of which vanB is a part.

Anti-Bacterial Agents↗
PubMed1996

Penicillin resistance and autolysis in enterococci.

Comparison of several cell wall-related properties of the ATCC 9790 strain and the R40 strain, a penicillin-resistant, PBP5 overproducing strain, and Rev14, a penicillin-hypersensitive, PBP5-deficient strain, is consistent with a role of the genetic element, psr, in the global regulation of lysozyme sensitivity, autolytic capacity, and wall-rhamnose-containing polysaccharide content. These parameters appear to be independently regulated by a system that involves psr in a currently unknown manner.

Autolysis↗
PubMed1999

Interspecies recombination between enterococci: genetic and phenotypic diversity of vancomycin-resistant transconjugants.

Handwerger and colleagues demonstrated that a particular clinical isolate of Enterococcus faecium, designated GUC, and here redesignated as GUCR, can conjugatively transfer vancomycin resistance. The vancomycin resistance is encoded by a chromosomally born linked set of genes in the donor, designated the vanA cluster, to the chromosome of an E. faecalis recipient, JH2-2. Here it is reported that an earlier isolate of E. faecium from the same patient who later harbored the vancomycin-resistant E. faecium GUCR lacks the vanA gene cluster but is otherwise similar (by SmaI chromosomal fingerprint and metabolic fingerprinting) to the vancomycin-resistant GUCR. Therefore, "GUCS" is a strong suspect as the base strain for the clinical acquisition of the vanA cluster present in GUCR. Thirteen laboratory-generated vanA transconjugants derived from conjugation between GUCR and JH2-2 were subjected to further analysis, allowing a comparison between transfer in the laboratory and transfer that occurred in the clinical setting. Surprisingly, each JH2-2 transconjugant had a unique constellation of abilities to oxidize various members of a panel of potential carbon sources. This pattern was stable for each transconjugant, and it was not changed by growing the strains with or without vancomycin. Transconjugants had pulsed-field gel electrophoretic (PFGE) patterns largely consistent with that of JH2-2, the recipient in conjugation experiments. However, PFGE analysis showed that a large but variable amount of DNA, between 145 kb and 277 kb, was transferred into different transconjugants. The mechanism appears to be conjugative transposition in which new DNA is added to the pre-existing genome rather than substituting for a segment in the recipient. Mapping and hybridization studies of several transconjugants showed that each received similar, but not exactly the same, DNA fragment of at least 30 kb from the donor. Sequencing of 16S ribosomal genes was used to confirm that the recipient and donor strains used in transconjugation experiments were different species. Sequence analysis was also used to consider the possibility that rRNA operons might be mobilized in conjugation, but no evidence for the transfer of rDNA operons was found. An apparent insertion sequence in E. faecium almost identical to IS 1485 and 57% sequence identity to IS 199 of Streptococcus mutans was found in the region of DNA transferred. The results imply new consequences of conjugative transfer and interspecies recombination.

Anti-Bacterial Agents↗
PubMed2000

Quinupristin/dalfopristin-resistant enterococci of the satA (vatD) and satG (vatE) genotypes from different ecological origins in Germany.

The semisynthetic streptogramin combination quinupristin/dalfopristin (Synercid) is a promising alternative for treatment of infections due to multiply resistant gram-positive bacteria including vancomycin-resistant Enterococcus faecium. Resistance is mediated by acetyltransferases SatA (VatD) or SatG (VatE). Recent papers have indicated a possible link between the use of the streptogramin virginiamycin S/M as a feed additive in commercial animal husbandry and a selection of quinupristin/dalfopristin-resistant E. faecium (QDRE). We screened manure samples from two different turkey farms and from six different pig farms (using virginiamycin), samples from a sewage water treatment plant, 24 broiler carcasses, 10 pork samples, and 200 stool samples of nonhospitalized humans for QDRE. Our strain culture collection of hospital E. faecium isolates from the last 2 years was also reviewed for QDRE. All manure and sewage samples were positive for QDRE, as well as 11 from broiler carcasses (46%), 1 from pork (10%), and 28 from human stool specimens (14%). Thirty-six hospital isolates of E. faecium exhibited resistance to quinupristin/dalfopristin. In 141 QDRE of different origin satA (vatD) and satG (vatE) genes were detected (seven isolates from humans with an unknown resistance mechanism). Streptogramin resistance determinants were tansferable in filtermating experiments for 5 of 10 satA (vatD) and 9 of 22 satG (vatE) isolates. Different EcoRI patterns of satG (vatE) plasmids and corresponding hybridizations of the satG (vatE) gene indicated nonhomologous resistance plasmids in isolates of different origin. The results of this study indicate a common gene pool for streptogramin resistance in E. faecium of different ecological origin. A selection of QDRE using the streptogramin virginiamycin S/M as a feed additive and a spread of the resistance via the food chain to humans is probable.

Acetyltransferases↗
PubMed2006

Vancomycin-resistant Enterococci may obtain nutritional support by scavenging carbohydrate fragments generated during mucin degradation by the anaerobic microbiota of the colon.

Vancomycin-resistant Enterococcus (VRE) is an important nosocomial pathogen that colonizes the intestinal tract. The substrates that provide nutritional support for VRE in the colon are not known. We tested the hypothesis that enzymatic breakdown of complex polysaccharides and glycoconjugates by other members of the indigenous microbiota could provide a source of nutrients for VRE. Nine vancomycin-resistant E. faecium strains were unable to ferment complex plant polysaccharides or hog gastric or bovine submaxillary mucin; however, each of the strains was able to ferment monosaccharides that are components of mucins and plant polysaccharides. Preincubation of hog gastric mucin with partially purified enzyme mixtures obtained from supernatants of Ruminococcus torques or a human stool specimen resulted in release of monosaccharides that supported growth of VRE. These results suggest that enzymatic breakdown of complex polysaccharides such as mucin by members of the indigenous microbiota may provide a source of nutritional support for VRE.

Bacteroides↗
PubMed1983

High-level resistance to gentamicin in clinical isolates of enterococci.

Nine clinical isolates of Streptococcus faecalis from a university hospital were found to be resistant to high levels (minimal inhibitory concentration, greater than 2,000 micrograms/ml) of gentamicin, tobramycin, amikacin, streptomycin, and kanamycin. The high-level resistance to these aminoglycosides and resistance to penicillin-aminoglycoside synergism were transferable by conjugation to a susceptible recipient strain. In three strains tested, the aminoglycoside resistance was mediated by four aminoglycoside-modifying enzymes: a 3'-phosphotransferase transferred from two strains, a 2"-phosphotransferase and a 6'-acetyltransferase transferred from all three strains, and a streptomycin adenylyltransferase transferred from two strains. This is the first report of the occurrence of high-level gentamicin resistance in enterococcal isolates from the United States.

Aminoglycosides↗