title: [Phenotypes and mechanisms of resistance to macrolides and lincosamides in Streptococcus agalactiae isolates with clinical significance in an eight-year period (2002-2010)].
abstract: BACKGROUND
  Streptococcus agalactiae is the most prevalent agent of invasive disease in the newborn (sepsis, pneumonia, and meningitis), as well as an important cause of puerperal fever, urinary tract infection and surgical site infection. The aim of our study was to know the evolution of macrolide and lincosamide resistance in this microorganism.
  
  
  METHODS
  Resistance phenotypes were established according to the erythromycin-clindamycin induction test: M (efflux pump) or MLSB (methylase). Genetic mechanisms were detected by PCR for the following genes: ermB, ermA, ermTR, and mefA/E. Molecular typing was based on chromosomal DNA macrorestriction and detection of fragments using pulsed-field gel electrophoresis.
  
  
  RESULTS
  During 8 years, 300 isolates of S. agalactiae were recovered. Seventy-eight (26%) were resistant to macrolides, and seventy (23%) were resistant to lincosamides. Constitutive MLSB was observed in 21% of the isolates (all but one carrying the ermB gene), with a erythromycin MIC90 ≥ 256 mg/L. Inducible MLSB was observed in 2.3% of the isolates (all carrying the ermTR gene), with a MIC90 of 6 mg/L. M phenotype was observed in 2.7% of the isolates (all carrying the mefA/E gene), with a MIC90 of 6 mg/L. Molecular typing revealed the presence of two major clones (A and B) comprising 56.6% of the isolates. Most of the isolates (90.5%) belonging to clon A carried the ermB gene.
  
  
  CONCLUSIONS
  Macrolide resistance in our area is similar to that observed in the rest of Spain, but there has been no increase in the incidence rate along the study period.
authors.affiliation: Servicio de Microbiología. Hospital Universitario de Gran Canaria Dr. Negrín, Barranco de la Ballena, s/n. 35010 Las Palmas de Gran Canaria. fartcam@gobiernodecanarias.org
authors.forename: Fernando Artiles
authors.initials: FA
authors.lastname: Campelo
authors.forename: Ana Cañas
authors.initials: AC
authors.lastname: Pedrosa
authors.forename: Isabel Álamo
authors.initials: IÁ
authors.lastname: Antúnez
authors.forename: Bernardo Lafarga
authors.initials: BL
authors.lastname: Capuz
mesh_terms: D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D002981:Clindamycin / Q000494:pharmacology; D004269:DNA, Bacterial / Q000235:genetics; D024881:Drug Resistance, Bacterial; D016521:Electrophoresis, Gel, Pulsed-Field; D004917:Erythromycin / Q000494:pharmacology; D055231:Lincosamides / Q000494:pharmacology*; D018942:Macrolides / Q000494:pharmacology*; D008826:Microbial Sensitivity Tests; D010641:Phenotype; D016133:Polymerase Chain Reaction; D013290:Streptococcal Infections / Q000382:microbiology*; D013292:Streptococcus agalactiae / Q000187:drug effects*; D001618:beta-Lactamases / Q000235:genetics
chemical_list: D000900:Anti-Bacterial Agents; D004269:DNA, Bacterial; D055231:Lincosamides; D018942:Macrolides; D002981:Clindamycin; D004917:Erythromycin; D001618:beta-Lactamases