Mutations ingyrAandparCQRDRs Are Not Relevant for Quinolone Resistance in Epidemiological UnrelatedStenotrophomonas maltophiliaClinical Isolates

Abstract

Clinical strains of Stenotrophomonas maltophilia are often highly resistant to multiple antibiotics and this resistance is steadily rising. Quinolones are included in the group of antimicrobial agents to which this microorganism is developing resistance. Therefore, the aim of this study was to analyze the epidemiological relationship among 22 clinical isolates of S. maltophilia as well as the molecular mechanisms responsible for the acquisition of quinolone-resistance in these strains. The results of the pulsed-field gel electrophoresis (PFGE) showed an heterogenicity of 82% among the strains used in the study. On the other hand, no amino acid changes were found in the quinolone resistance-determining region (QRDR) of either gyrA and parC genes among quinolone-susceptible and -resistant S. maltophilia strains. Besides, the amino acid of the GyrA found in the position equivalent to Ser-83 of E. coli was Gln instead of a Ser or Thr, the amino acids usually encountered in this position among Gram-negative bacteria. The results suggest that there is not a relationship between the presence of this Gln and the resistance to quinolones in S. maltophilia. We can conclude that, contrary to what has been described in other microorganisms, in these S. maltophilia isolates, the development of resistance to quinolones was not related to mutations in the QRDR of gyrA and parC genes. Thus, to our knowledge, this is the first report describing this phenomenon.

Effects of a Mutation in the gyrA Gene on the Virulence of Uropathogenic Escherichia coli

“…Susceptibility to several antimicrobial agents was determined in the presence and absence of 20 mg/liter of the efflux pump inhibitor Phe-Arg-␤-naphthylamide using the agar dilution method according to the CLSI (17) guidelines as described elsewhere (18).…”

Antibacterial evaluation of a collection of norfloxacin and ciprofloxacin derivatives against multiresistant bacteria

“…Although the interplay between low permeability and constitutive expression of some efflux pumps [10] can produce a low level of intrinsic resistance in A. baumannii, the main mechanisms of resistance to quinolones are mutations in topoisomerase genes (gyrA and/or parC) [17,18]. Meanwhile, in S. maltophilia, quinolone-susceptible and -resistant strains presented identical amino acid sequences in GyrA and ParC [19,20], suggesting that in this microorganism low permeability, overexpression of efflux pumps or the interplay between both effects may play an important role in the acquisition of quinolone resistance [21]. However, the amino acid of GyrA found in the position equivalent to Ser-83 of E. coli was Gln instead of Ser or Thr.…”

SmQnr Contributes to Intrinsic Resistance to Quinolones in Stenotrophomonas maltophilia

“…In contrast to what has been described for other bacteria, quinolone-resistant S. maltophilia mutants do not present mutations in bacterial topoisomerases (10,13). One of the causes of this situation might be that the efflux pump SmeDEF confers high-level quinolone resistance upon its overexpression (1-3).…”