Resistance behaviour of inducible clindamycin-resistant staphylococci from clinical samples and aquatic environments

Abstract

In this study, the species diversity of staphylococci with inducible resistance to macrolides, lincosamides and streptogramin B (MLS B ) isolated from clinical samples, sewage and river water was investigated. Inducible clindamycin resistance was tested using a D-test and macrodilution assays. Inducible cross-resistance (iMLS B phenotype) was examined by PCR of erm gene classes A, B, C, F, G, Q, T and 43. Although ermC was the most frequently detected resistance gene in iMLS B phenotypes of environmental staphylococci (61.2 %), resistance genes encoding iMLS B were more diverse than in staphylococci from hospital samples. In 22.4 % of iMLS B staphylococci from aquatic environments, none of the eight tested erm genes was found. Those isolates and erm43-expressing Staphylococcus lentus displayed low erythromycin MICs (3-16 mg ml "1 ) compared with ermC-positive environmental staphylococci (¢256 mg ml "1 ). In contrast to clinical isolates with clearly defined resistance behaviour, resistance patterns against MLS B and MICs for clindamycin of environmental isolates were more diverse. Although the abundance of iMLS B staphylococci in the aquatic environment was lower than in staphylococci from hospital samples, the diversity of resistance genes encoding this phenotype seemed to be higher. Oleandomycin is the best marker to correlate iMLS B phenotype and the respective erm gene. The phenotypical behaviour of environmental isolates may differ from the resistance pattern of clinical iMLS B staphylococci expressing ermA or ermC, and this should be considered for successful treatment of infections.

The prevalence of genotypes that determine resistance to macrolides, lincosamides, and streptogramins B compared with spiramycin susceptibility among erythromycin-resistant Staphylococcus epidermidis

“…Among the S. epidermidis strains studied, the most frequently identified gene in strains exhibiting both cMLS B and iMLS B phenotypes was ermC , which is consistent with previous reports ( Reyes et al 2007 , Gherardi et al 2009 , Coutinho et al. 2010 , Bouchami et al 2011 , Brzychczy-Wloch et al 2013 , Heb & Gallert 2014 ). Only a few S. epidermidis exhibiting cMLS B phenotypes possessed ermA and/or ermB.…”

Phenotypic and genotypic characterization of macrolide, lincosamide and streptogramin B resistance among clinical isolates of staphylococci in southwest of Iran

“…In our findings, ermA gene was more prevalent in S. aureus compared to CoNS (P < 0.001). Previously, similar results have been cited by authors from Iran and other countries [ 9 , 23 , 33 ]. In contrast, we found msrA gene was more abundant in CoNS (P < 0.001).…”

“…Resistance to MLS antibiotics in S. aureus and coagulase negative staphylococci (CoNS), can resulted in the target site modification encoded by erm genes [ 7 , 8 ]. The methylation of the 23S rRNA conferred by erm genes prevents the binding of antibiotic to its ribosomal target [ 9 ]. Other mechanisms are efflux pumps encoded by msrA gene which mediated resistance to MS B , and the drug modification encoded by lnu gene [ 10 , 11 ].…”