Association of Transferable Quinolone Resistance Determinant qnrB19 with Extended-Spectrum β-Lactamases in Salmonella Give and Salmonella Heidelberg in Venezuela
Four nontyphoidal Salmonella strains with resistance to extended-spectrum cephalosporins and nonclassical quinolone resistance phenotype were studied. Two S. Give were isolated from pediatric patients with acute gastroenteritis, and two S. Heidelberg were recovered from raw chicken meat. Phenotypic characterization included antimicrobial susceptibility testing and detection of extended-spectrum β-lactamases (ESBLs) by the double-disc synergy method. The detection of quinolone resistance-determining regions (QRDR) of gyrA, gyrB, and gyrC genes, genes, and plasmid-mediated quinolone resistance (PMQR) determinants was carried out by molecular methods. Plasmid analysis included Southern blot and restriction patterns. Transferability of resistance genes was examined by transformation. genes were detected in S. Give SG9611 and in the other three strains: S. Give SG9811, S. Heidelberg SH7511, and SH7911. Regardless of origin and serovars, the qnrB19 gene was detected in the 4 strains studied. All determinants of resistance were localized in plasmids and successfully transferred by transformation. This study highlights the circulation of qnrB19 associated with , , and in S. Give and S. Heidelberg in Venezuela. The recognition of factors associated with increasing resistance and the study of the molecular mechanisms involved can lead to a more focused use of antimicrobial agents. 1. Introduction Nontyphoidal Salmonella (NTS) are one of the major causes of foodborne infections related to the ingestion of contaminated animal food products in humans [1]. In most cases, these infections are confined to the gastrointestinal tract and are self-limiting. However, for immunocompromised and/or elderly patients, as well as for invasive or prolonged infections, antibiotic treatment is recommended [2]. Fluoroquinolones and extended-spectrum β-lactams are the first-choice agents for these cases but the increase of the multidrug resistance (MDR) Salmonella strains reduces the available treatment options [1–5]. The emergence of Salmonella spp. isolates that display resistance to extended-spectrum β-lactams is mediated by plasmids and is an increasing public health concern [3–5]. The resistance to fluoroquinolones is typically mediated by alterations in the target enzymes DNA gyrase and topoisomerase IV or changes in drug entry and efflux. Also, three plasmid-mediated mechanisms conferring decreased susceptibility to ciprofloxacin have been recently described: QepA efflux, Aac(6′)-Ib-cr aminoglycoside acetyltransferase, and QNR proteins (qnrA, qnrB, qnrC, qnrD, and qnrS) [6,
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