Mutations Associated with Decreased Susceptibility to Seven Antimicrobial Families in Field and Laboratory-Derived Mycoplasma bovis Strains [PublishAheadOfPrint]

The molecular mechanisms of resistance to fluoroquinolones, tetracyclines, an aminocyclitol, macrolides, a lincosamide, a phenicol and pleuromutilins were investigated in Mycoplasma bovis. For the identification of mutations responsible for the high minimal inhibitory concentrations (MICs) to certain antibiotics, whole genome sequencing of 35 M. bovis field isolates and 36 laboratory-derived antibiotic resistant mutants was performed. In vitro resistant mutants were selected by serial passages of M. bovis in broth medium containing subinhibitory concentrations of the antibiotics. Mutations associated with high MICs to fluoroquinolones were found at positions 244-260 and 232-250 (according to E. coli numbering) of quinolone resistance determining regions of gyrA and parC genes, respectively. Alterations related to elevated MICs to tetracyclines were described at positions 962-967, 1058, 1195, 1196 and 1199 of genes encoding the 16S rRNA and forming the primary tetracycline binding site. Single transversion at position 1192 of rrs1 gene resulted in 256 μg/ml MIC to spectinomycin. Mutations responsible for high MICs to macrolide, lincomycin, florfenicol and pleuromutilin antibiotics were identified in genes encoding the 23S rRNA.

Understanding antibiotic resistance mechanisms is an important tool for future developments of genetic-based diagnostic assays for the rapid detection of resistant M. bovis strains.

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