Antimicrobial Agents and Chemotherapy, October 1999, p. 2493-2496, Vol. 43, No. 10
0066-4804/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Department of Pathobiology, University of Washington, Seattle, Washington,1 and Division of Molecular Biology and Genetics, University of Utah, Salt Lake City, Utah2
Received 14 January 1999/Returned for modification 19 April 1999/Accepted 26 July 1999
The role of mutations in the genes for GyrA and ParC in quinolone
resistance in Mycoplasma 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 of Mycoplasma
hominis was ParC, whereas that for sparfloxacin was GyrA.
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