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Frequent topoisomerase IV mutations associated with fluoroquinolone resistance in Ureaplasma species

Jingjuan Song1, Yingli Qiao1, Yingying Kong2

  • 1Clinical Laboratory, Sir Run Run Shaw Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang 310016, PR China.

Journal of Medical Microbiology
|August 6, 2015
PubMed

Insights

Fluoroquinolone resistance in Ureaplasma spp. is primarily driven by mutations in topoisomerase IV, particularly Ser-83→Leu in ParC. Moxifloxacin demonstrates the best activity against resistant strains.

Area of Science:

  • Microbiology
  • Molecular Biology
  • Antimicrobial Resistance

Background:

  • Fluoroquinolones are crucial antibiotics for treating Ureaplasma spp. infections.
  • Understanding the genetic basis of fluoroquinolone resistance is essential for effective treatment strategies.
  • Quinolone resistance-determining regions (QRDRs) in DNA gyrase and topoisomerase IV are key targets for resistance mutations.

Purpose of the Study:

  • To investigate the role of QRDRs in DNA gyrase (gyrA, gyrB) and topoisomerase IV (parC, parE) in fluoroquinolone resistance in Ureaplasma spp.
  • To determine the species distribution and fluoroquinolone susceptibility of Ureaplasma strains from clinical samples.
  • To identify specific mutations within QRDRs associated with antimicrobial resistance.

Main Methods:

  • Analysis of 114 Ureaplasma spp. strains isolated from female patients with symptomatic infections.
  • Determination of species distribution and susceptibility testing against four fluoroquinolones (ciprofloxacin, ofloxacin, levofloxacin, moxifloxacin).
  • Sequencing of QRDRs of gyrA, gyrB, parC, and parE genes and comparison with reference strains.

Main Results:

  • Moxifloxacin exhibited the highest activity (MIC range: 0.125-32 μg/ml) against Ureaplasma spp.
  • High minimum inhibitory concentrations (MICs) were observed for ciprofloxacin and ofloxacin.
  • Seven amino acid substitutions were identified in GyrB, ParC, and ParE, with Ser-83→Leu in ParC (77.2%) and Arg-448→Lys in ParE (2.6%) being potentially responsible for resistance. Novel mutations in ParC and ParE were also found.

Conclusions:

  • Amino acid mutations in topoisomerase IV, particularly Ser-83→Leu in ParC, are the primary drivers of fluoroquinolone resistance in Ureaplasma spp.
  • Moxifloxacin remains the most effective fluoroquinolone against Ureaplasma strains, including those with the Ser-83→Leu mutation.
  • Genetic analysis of QRDRs is crucial for understanding and combating antimicrobial resistance in Ureaplasma.

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