title: [Phenotypes and genetic mechanisms of resistance to macrolides and lincosamides in viridans group streptococci].
abstract: Viridans group streptococci (VGS) are part of the oropharyngeal, intestinal and genital flora, but they may cause endocarditis and bacteremia in susceptible patients. Penicillin- and macrolide-resistant strains are increasing every year. The aim of this study was to investigate genetic mechanisms of resistance to macrolides in clinically relevant isolates. We identified 85 isolates from January 2004 to June 2006. Susceptibility to penicillin, cefotaxime, erythromycin, clindamycin and gentamycin was determined. A resistance phenotype was assigned according to the disk approximation test (erythromycin-clindamycin). The mechanism of resistance was determined by PCR for the following genes: ermB, ermA, ermC, ermA (TR) and mefA/E. We identified 51 isolates belonging to Streptococcus anginosus species, most of which were obtained from abdominal abscesses, and 34 isolates belonging to other species, most of which were obtained from blood cultures. The macrolide resistance rate was 28.2% (24/85). The MLS(B) phenotype was observed in 66.7% of the isolates, primarily in the S. anginosus group. The M phenotype was predominant in S. mitis and S. oralis. Isolates that expressed the constitutive MLS(B) phenotype carried the ermB gene, and those that expressed the inducible MLSB phenotype carried the ermA gene. Isolates that expressed the M phenotype carried the mefA/E gene. There was coresistance with penicillin in 20.8% (5/24) of the isolates. Coresistance with penicillin was low. These results suggest that screening for macrolide resistance in VGS would be desirable because of the potential transmission of resistance genes to other pathogenic streptococci.
authors: Servicio de Microbiología, Hospital Universitario de Gran Canaria Dr. Negrín, Las Palmas de Gran Canaria.
authors: F
authors: F
authors: Artiles Campelo
authors: I
authors: I
authors: Horcajada Herrera
authors: I
authors: I
authors: Alamo Antúnez
authors: A
authors: A
authors: Cãnas Pedrosa
authors: B
authors: B
authors: Lafarga Capuz
mesh_terms: D000900:Anti-Bacterial Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001426:Bacterial Proteins / Q000235:genetics / Q000502:physiology; D004269:DNA, Bacterial / Q000235:genetics; D024901:Drug Resistance, Multiple, Bacterial / Q000235:genetics*; D005798:Genes, Bacterial / Q000235:genetics / Q000502:physiology; D006801:Humans; D055231:Lincosamides; D018942:Macrolides / Q000494:pharmacology* / Q000627:therapeutic use; D008565:Membrane Proteins / Q000235:genetics; D008780:Methyltransferases / Q000235:genetics / Q000502:physiology; D008826:Microbial Sensitivity Tests; D010641:Phenotype; D016133:Polymerase Chain Reaction; D013290:Streptococcal Infections / Q000188:drug therapy / Q000382:microbiology*; D034363:Viridans Streptococci / Q000187:drug effects* / Q000235:genetics / Q000302:isolation & purification
chemical_list: D000900:Anti-Bacterial Agents; D001426:Bacterial Proteins; D004269:DNA, Bacterial; D055231:Lincosamides; D018942:Macrolides; C117866:MefA protein, Streptococcus; D008565:Membrane Proteins; D008780:Methyltransferases; C431709:ErmA protein, Bacteria; C035181:rRNA (adenosine-O-2'-)methyltransferase