Abstract
BackgroundThis study determined macrolide resistance genotypes in clinical isolates of Streptococcus pneumoniae from multiple medical centers in Lebanon and assessed the serotype distribution in relation to these mechanism(s) of resistance and the source of isolate recovery.MethodsForty four macrolide resistant and 21 macrolide susceptible S. pneumoniae clinical isolates were tested for antimicrobial susceptibility according to CLSI guidelines (2008) and underwent molecular characterization. Serotyping of these isolates was performed by Multiplex PCR-based serotype deduction using CDC protocols. PCR amplification of macrolide resistant erm (encoding methylase) and mef (encoding macrolide efflux pump protein) genes was carried out.ResultsAmong 44 isolates resistant to erythromycin, 35 were resistant to penicillin and 18 to ceftriaxone. Examination of 44 macrolide resistant isolates by PCR showed that 16 isolates harbored the erm(B) gene, 8 isolates harbored the mef gene, and 14 isolates harbored both the erm(B) and mef genes. There was no amplification by PCR of the erm(B) or mef genes in 6 isolates. Seven different capsular serotypes 2, 9V/9A,12F, 14,19A, 19F, and 23, were detected by multiplex PCR serotype deduction in 35 of 44 macrolide resistant isolates, with 19F being the most prevalent serotype. With the exception of serotype 2, all serotypes were invasive. Isolates belonging to the invasive serotypes 14 and 19F harbored both erm(B) and mef genes. Nine of the 44 macrolide resistant isolates were non-serotypable by our protocols.ConclusionMacrolide resistance in S. pneumoniae in Lebanon is mainly through target site modification but is also mediated through efflux pumps, with serotype 19F having dual resistance and being the most prevalent and invasive.
Highlights
This study determined macrolide resistance genotypes in clinical isolates of Streptococcus pneumoniae from multiple medical centers in Lebanon and assessed the serotype distribution in relation to these mechanism(s) of resistance and the source of isolate recovery
Target site modification is encoded by the erm(B) gene which leads to reduction in the binding affinity of all macrolides to the 23S rRNA
While isolates harboring the erm gene are resistant to all macrolides, isolates expressing an efflux pump encoded by the mef gene are resistant to only 14 and 15membered macrolides
Summary
This study determined macrolide resistance genotypes in clinical isolates of Streptococcus pneumoniae from multiple medical centers in Lebanon and assessed the serotype distribution in relation to these mechanism(s) of resistance and the source of isolate recovery. Treatment of Macrolide resistance in S. pneumoniae is primarily due to two mechanisms; target site modification and efflux pump expulsion. Target site modification is encoded by the erm(B) gene which leads to reduction in the binding affinity of all macrolides to the 23S rRNA (domain V). This mechanism relies on methylation of specific adenine residues (A2058) in 23S rRNA by the methylase-product of the erm gene leading to cross resistance to macrolides, lincosamides, and streptogramins. While isolates harboring the erm gene are resistant to all macrolides, isolates expressing an efflux pump encoded by the mef gene are resistant to only 14 and 15membered macrolides. Isolates harboring the mef gene have the M (resistance to macrolides) phenotype [9,10]
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