Prevalence of Plasmid-Mediated Quinolone Resistance Genes in Clinical Enterobacteria from Argentina.

LUCERO C; RAPOPORT M; RODRIGUEZ C; CORSO A; ALBORNOZ E; QUIROGA MP; ANDRES P; CENTRON D; ROMERO G; GUERRIERO L; GALAS M; PETRONI A

MICROBIAL DRUG RESISTANCE-MECHANISMS EPIDEMIOLOGY AND DISEASE

MARY ANN LIEBERT INC

Lugar: New York; Año: 2017 vol. 23 p. 177 - 187

1076-6294

This first nationwide study was conducted to analyze the prevalence of plasmid-mediated quinolone resistance(PMQR) genes in phenotypically unselected (consecutive) clinical enterobacteria. We studied 1,058 isolatesthat had been consecutively collected in 66 hospitals of the WHONET-Argentina Resistance SurveillanceNetwork. Overall, 26% of isolates were nonsusceptible to at least one of the three quinolones tested (nalidixicacid, ciprofloxacin, and levofloxacin). The overall prevalence of PMQR genes was 8.1% (4.6% for aac(6¢)-Ibcr;3.9% for qnr genes; and 0.4% for oqxA and oqxB, which were not previously reported in enterobacteria otherthan Klebsiella spp. from Argentina). The PMQR prevalence was highly variable among the enterobacterialspecies or when the different genes were considered. The prevalent PMQR genes were located in class 1integrons [qnrB2, qnrB10, and aac(6¢)-Ib-cr]; in the ColE1-type plasmid pPAB19-1 or Tn2012-like transposons(qnrB19); and in Tn6238 or bracketed by IS26 and blaOXA-1 [aac(6¢)-Ib-cr]. The mutations associated withquinolone resistance that were located in the quinolone resistance-determining region (QRDR mutations) ofgyrA, parC, and gyrB were also investigated. The occurrence of QRDR mutations was significantly associatedwith the presence of PMQR genes: At least one QRDR mutation was present in 82% of the PMQR-harboringisolates but in only 23% of those without PMQR genes ( p < 0.0001, Fisher?s Test). To the best of ourknowledge, this is the first report on the prevalence of PMQR genes in consecutive clinical enterobacteria whereall the genes currently known have been screened