Inducible Clindamycin Resistance (3): Streptococci

Penicillin or ampicillin remains the drug of choice for intrapartum antibiotic prophylaxis for GBS colonization in pregnant women. Erythromycin and clindamycin are the drugs of choice for women with serious penicillin allergy who are colonized with GBS. Mechanisms of resistance to macrolides were first elucidated in group A streptococcus. Similar mechanisms were recognized in Streptococcus pneumoniae and staphylococci. An increase in resistance of GBS to erythromycin has been reported. Erythromycin resistance is mediated by two mechanisms: ribosomal methylation or an efflux pump. Methylation of 23S rRNA by erm (erythromycin ribosomal methylase) enzymes blocks binding of macrolides (including erythromycin), lincosamides (including clindamycin), and streptogramin B (MLS) to the 50S ribosomal subunit, leading to drug resistance. The methylase enzymes may be expressed constitutively (MLS-cr phenotype) or inducibly (MLS-ir phenotype) by erythromycin. In group A streptococcus, the MLS-cr phenotype is strongly associated with the ermB gene. We and others have shown that the MLS-cr phenotype in GBS is associated with either the ermA or ermB gene. This suggests that the ermA gene in some strains of GBS has mutated such that it is expressed constitutively.

AMH