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The role of mutations in the genes for GyrA and ParC in quinolone resistance inMycoplasma hominis was studied. Selection with sparfloxacin gave mutations at GyrA83 (Ser→Leu;Escherichia coli numbering) or GyrA87 (Glu→Lys), and mutants had increased levels of resistance to sparfloxacin (8- to 16-fold) but not to ofloxacin. Selection with ofloxacin gave changes at ParC80 (Ser→Ile) or ParC84 (Glu→Lys), and mutants were four- to eightfold more resistant to ofloxacin but not to sparfloxacin. Selection of second-step mutants from strains with ParC mutations with either quinolone yielded double mutants with additional mutations at GyrA83 (Ser→Trp or Ser→Leu) or GyrA87 (Glu→Lys). Second-step selection of GyrA mutants gave additional mutations at ParC80 (Ser→Ile) or ParC84 (Glu→Lys). Two-step mutants showed high levels of resistance to ofloxacin (MICs, 64 to 128 μg/ml) and moderate levels of resistance to sparfloxacin (MICs, 2 to 8 μg/ml). The primary target of ofloxacin in first-step mutants ofMycoplasma hominis was ParC, whereas that for sparfloxacin was GyrA.

Sparfloxacin Selects Gyrase Mutations in First-Step Mycoplasma hominis Mutants, whereas Ofloxacin Selects Topoisonmerase IV Mutations