Macrolide and tetracycline resistance in clinical strains of Streptococcus agalactiae isolated in Tunisia.

Between 2007 and 2009, 226 clinical strains of Streptococcus agalactiae, recovered from female genital specimens and from gastric fluid or ear specimens from infected newborns, were isolated at the Laboratory of Microbiology of Charles Nicolle Hospital of Tunis. They were investigated to determine the prevalence of antibiotic resistance and to characterize the mechanisms of resistance to macrolide and tetracycline. All strains were susceptible to penicillin, ampicillin and quinupristin-dalfopristin. They were resistant to chloramphenicol (3.1%), rifampicin (19.1%), erythromycin (40%) and tetracycline (97.3%); 3.1% were highly resistant to streptomycin and 1.3% to gentamicin. Among the erythromycin-resistant isolates, 78.7% showed a constitutive macrolide-lincosamide-streptogramin B (MLS(B)) phenotype with high-level resistance to macrolides and clindamycin (MIC(50) >256 µg ml(-1)), 10% showed an inducible MLS(B) phenotype with high MICs of macrolides (MIC(50) >256 µg ml(-1)) and low MICs of clindamycin (MIC(50)=8 µg ml(-1)) and 2.2% showed an M phenotype with a low erythromycin-resistance level (MIC range=12-32 µg ml(-1)) and low MICs of clindamycin (MIC range: 0.75-1 µg ml(-1)). All strains were susceptible to quinupristin-dalfopristin and linezolid (MIC(90): 0.75 µg ml(-1) for each). MLS(B) phenotypes were genotypically confirmed by the presence of the erm(B) gene and the M phenotype by the mef(A) gene. Resistance to tetracycline was mainly due to the tet(M) gene (93.1%) encoding a ribosome protection mechanism. This determinant is commonly associated with the conjugative transposon Tn916 (P≤0.0002). tet(O) and tet(T) existed in a minority (2.2% and 0.4%, respectively). The efflux mechanism presented by tet(L) was less frequently present (4.5%). No significant association was found between erm(B) and tet(M) genes.