Whole Genome Analysis Reveals New Insights into Macrolide Resistance in Mycoplasma pneumoniae.
- Author:
Shao Li LI
1
;
Hong Mei SUN
1
;
Bao Li ZHU
2
;
Fei LIU
2
;
Han Qing ZHAO
1
Author Information
- Publication Type:Journal Article
- Keywords: Drug resistance; Efflux pump inhibitors; Macrolide-specific efflux pump; Mycoplasma pneumoniae; Whole-genome sequencing
- MeSH: Anti-Bacterial Agents; pharmacology; Drug Resistance, Bacterial; genetics; Genome-Wide Association Study; Macrolides; pharmacology; Microbial Sensitivity Tests; Mutation; Mycoplasma pneumoniae; drug effects; genetics
- From: Biomedical and Environmental Sciences 2017;30(5):343-350
- CountryChina
- Language:English
-
Abstract:
OBJECTIVEMutations in 23S rRNA gene are known to be associated with macrolide resistance in Mycoplasma pneumoniae (M. pneumoniae). However, these mutations alone do not fully explain the high resistance rates in Asia. The aim of this study was to investigate other possible mutations involved in macrolide resistance in M. pneumoniae.
METHODSThe whole genomes of 10 clinical isolates of M. pneumoniae with macrolide resistance were sequenced by Illumina HiSeq2000 platform. The role of the macrolide-specific efflux transporter was assessed by efflux-pump inhibition assays with reserpine and carbonyl cyanide m-chlorophenyl-hydrazone (CCCP).
RESULTSA total of 56 single nucleotide polymorphisms (SNPs) were identified in 10 clinical isolates in comparison to the reference strains M129 and FH. Strikingly, 4 of 30 SNPs causing non-synonymous mutations were clustered in macrolide-specific efflux system gene macB encoding macrolide-specific efflux pump protein of the ATP-binding cassette transporter family. In assays of the minimal inhibitory concentrations (MIC) of macrolide antibiotics in the presence of the efflux pump inhibitors caused a significant decrease of MICs, even under detectable levels in some strains.
CONCLUSIONOur study suggests that macrolide efflux pump may contribute to macrolide resistance in M. pneumoniae in addition to the common point mutations in 23S rRNA gene.
