Article

First report on IncN plasmid-mediated quinolone resistance gene qnrS1 in porcine Escherichia coli in Europe.

Veterinary Medical Research Institute of the Hungarian Academy of Sciences, Hungária krt. 21, Budapest, Hungary.
Microbial drug resistance (Larchmont, N.Y.) (impact factor: 1.99). 08/2011; 17(4):567-73. DOI:10.1089/mdr.2011.0068
Source: PubMed

ABSTRACT Plasmid-mediated quinolone resistance (PMQR) of enterobacteria encoded by qnr genes is an emerging concern in human and veterinary medicine. Here we aimed to study PMQR of porcine Escherichia coli in two large piggeries in Romania and Hungary. The studies identified PMQR E. coli strains in 34% of piglets in the Romanian farm. Clonality of six qnrS1 E. coli strains representing the Romanian pig farm was established by multilocus sequence typing (MLST), and the qnrS1 plasmids were characterized by plasmid transfer and PCR-based replicon typing. The six tested strains were assigned to three different MLST types. All proved to carry IncN plasmids, representing the first IncN-borne qnrS1 gene to be identified in E. coli from food-producing animals. DNA sequences flanking the qnrS1 gene showed ≥99% homology with the corresponding resistance region of the pINF5 plasmid from Salmonella Infantis isolated from chicken carcass and of IncN plasmids from human clinical E. coli strains. Thus, our data suggest that transfer of qnrS1 plasmids occurs between Salmonella and E. coli of animal and human origin, with pigs representing one of the potential reservoirs. Further, we report on identification and characterization of the qnrS1 gene in porcine E. coli for the first time in Europe.

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  • Article: Plasmid-Mediated Quinolone Resistance; Interactions between Human, Animal, and Environmental Ecologies.
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    ABSTRACT: Resistance to quinolones and fluoroquinolones is being increasingly reported among human but also veterinary isolates during the last two to three decades, very likely as a consequence of the large clinical usage of those antibiotics. Even if the principle mechanisms of resistance to quinolones are chromosome-encoded, due to modifications of molecular targets (DNA gyrase and topoisomerase IV), decreased outer-membrane permeability (porin defect), and overexpression of naturally occurring efflux, the emergence of plasmid-mediated quinolone resistance (PMQR) has been reported since 1998. Although these PMQR determinants confer low-level resistance to quinolones and/or fluoroquinolones, they are a favorable background for selection of additional chromosome-encoded quinolone resistance mechanisms. Different transferable mechanisms have been identified, corresponding to the production of Qnr proteins, of the aminoglycoside acetyltransferase AAC(6')-Ib-cr, or of the QepA-type or OqxAB-type efflux pumps. Qnr proteins protect target enzymes (DNA gyrase and type IV topoisomerase) from quinolone inhibition. The AAC(6')-Ib-cr determinant acetylates several fluoroquinolones, such as norfloxacin and ciprofloxacin. Finally, the QepA and OqxAB efflux pumps extrude fluoroquinolones from the bacterial cell. A series of studies have identified the environment to be a reservoir of PMQR genes, with farm animals and aquatic habitats being significantly involved. In addition, the origin of the qnr genes has been identified, corresponding to the waterborne species Shewanella sp. Altogether, the recent observations suggest that the aquatic environment might constitute the original source of PMQR genes, that would secondly spread among animal or human isolates.
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