title: Resistance patterns and occurrence of virulence determinants among GRE strains in southwestern Poland.
abstract: OBJECTIVE
  The aim of this study was to determine the antimicrobial resistance and the occurrence of virulence determinants among glycopeptide-resistant enterococci (GRE) isolated in 2007-2009 from patients hospitalized in southwestern Poland.
  
  
  METHODS
  The minimal inhibitory concentrations (MICs) of antibiotics were determined by agar dilution method or by E-test®. The presence of vanA - vanG resistance and virulence genes (agg, esp, gelE and cylA, cylB, cylM) was investigated using PCR. The ability to form biofilm and the activity of gelatinase, hemolysins, lipase and DNase were tested.
  
  
  RESULTS
  All the GRE strains were susceptible to linezolid, daptomycin, and tigecycline and resistant to norfloxacin. In the Enterococcus faecium group, 17 strains carried the vanA gene and 20 the vanB gene. In the Enterococcu faecalis group, 4 strains carried the vanA gene and 1 the vanB gene. There were differences in tetracycline susceptibility between the VanA (70%) and the VanB (55%) phenotypes. Only linezolid had high activity against both the VanA and the VanB phenotypes. The esp gene was present in most of the GRE strains, but only 3 E. faecalis strains produced biofilm. Lipase was produced by 10/42 examined strains, gelatinase by 4/42 and hemolysin by 3/42 isolates.
  
  
  CONCLUSIONS
  Linezolid seems to be the optimal option in empirical therapy of infections caused by GRE strains because of the relationship between its activity (MIC value) and susceptibility breakpoint. There was no correlation between the prevalence of different virulence genes and resistance to the antibiotics tested.
authors.affiliation: Departament of Microbiology, Wroclaw Medical University, Wroclaw, Poland.
authors.forename: B
authors.initials: B
authors.lastname: Kowalska-Krochmal
authors.forename: E
authors.initials: E
authors.lastname: Dworniczek
authors.forename: I
authors.initials: I
authors.lastname: Dolna
authors.forename: J
authors.initials: J
authors.lastname: Bania
authors.forename: E
authors.initials: E
authors.lastname: Wałecka
authors.forename: A
authors.initials: A
authors.lastname: Seniuk
authors.forename: G
authors.initials: G
authors.lastname: Gościniak
mesh_terms: D000081:Acetamides / Q000494:pharmacology; D000362:Agar / Q000737:chemistry; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D018441:Biofilms; D017576:Daptomycin / Q000494:pharmacology; D003851:Deoxyribonucleases / Q000378:metabolism; D004351:Drug Resistance; D024881:Drug Resistance, Bacterial; D016983:Enterococcus / Q000235:genetics / Q000378:metabolism*; D018093:Gelatinases / Q000378:metabolism; D006020:Glycopeptides / Q000737:chemistry; D006460:Hemolysin Proteins / Q000378:metabolism; D006760:Hospitalization; D006801:Humans; D000069349:Linezolid; D008049:Lipase / Q000378:metabolism; D008911:Minocycline / Q000031:analogs & derivatives / Q000494:pharmacology; D009643:Norfloxacin / Q000494:pharmacology; D023303:Oxazolidinones / Q000494:pharmacology; D010641:Phenotype; D011044:Poland; D000078304:Tigecycline; D014774:Virulence
chemical_list: D000081:Acetamides; D000900:Anti-Bacterial Agents; D006020:Glycopeptides; D006460:Hemolysin Proteins; D023303:Oxazolidinones; D000078304:Tigecycline; D000362:Agar; D003851:Deoxyribonucleases; D008049:Lipase; D018093:Gelatinases; D008911:Minocycline; D000069349:Linezolid; D009643:Norfloxacin; D017576:Daptomycin