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Antimicrobial Agents and Chemotherapy, October 1999, p. 2493-2496, Vol. 43, No. 10
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
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Copyright © 1999, American Society for Microbiology. All rights reserved.
Sparfloxacin Selects Gyrase Mutations in First-Step
Mycoplasma hominis Mutants, whereas Ofloxacin Selects Topoisonmerase IV
Mutations
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.
*
Corresponding author. Mailing address: Department of
Pathobiology, Box 357238, University of Washington, Seattle, WA 98195. Phone: (206) 543-1036. Fax: (206) 543-3873. E-mail:
kennyg{at}u.washington.edu.
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