A preliminary in vitro study on inducible and constitutive clindamycin resistance in Staphylococcus aureus from a South Indian tertiary care hospital.

摘要

Macrolide resistance in Staphylococcus aureus involves two mechanisms. The first mechanism is known as the MLS_B phenotype and is encoded by the erm gene (A, B, C) which results in target site modification through methylation of the adenine residue of bacterial 23S ribosomal RNA, conferring resistance not only to macrolides (erythromycin), but also to lincosamides (clindamycin) and streptogramin-B(MLS) antibiotics. This phenotype can be expressed either constitutively, which means the isolate is resistant to all MLS antibiotics, or it can be inducible which can be detected by the D test. The second mechanism is through the efflux pump encoded by the msr A gene which confers resistance to the macrolides and type B streptogramins only. In vitro, the staphylococci carrying the erythromycin-inducible resistanceare resistant to macrolides (erythromycin) but are susceptible to dindamycin. However, following exposure to dindamycin in vivo, they can mutate to constitutive resistance thus becoming resistant to MLS antibiotics. To document this resistance pattern among S. aureus in vitro, a preliminary study was undertaken in the Department of Microbiology, PES Institute of Medical Sciences and Research, a 530-bed tertiary care center.