[Phenotypes and mechanisms of resistance to macrolides and lincosamides in Streptococcus agalactiae isolates with clinical significance in an eight-year period (2002-2010)].

INTRODUCTION 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.