Coprevalence of Plasmid-Mediated Quinolone Resistance Determinants QepA, Qnr, and AAC(6′)-Ib-cr among 16S rRNA Methylase RmtB-Producing
            <i>Escherichia coli</i>
            Isolates from Pigs

Liu, Jianhua; Deng, Yuting; Zeng, Zhenling; JunHua, Gao; Chen, Lin; Arakawa, Yoshichika; Zhang-liu, Chen

doi:10.1128/aac.01686-07

Cited by 99 publications

(82 citation statements)

References 14 publications

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“…Horizontallyacquired quinolone-resistance genes were identified using PCR. Primers from Cattoir et al (2007) were used to screen for qnrA, qnrB and qnrS and the primers reported by Liu et al (2008) were used for qepA. The quinolone-resistance determining regions of gyrA and parC genes were amplified using the primer pairs described in Wang et al (2001).…”

Section: Methodsmentioning

confidence: 99%

Screening of antimicrobial resistance and molecular detection of fluoroquinolone resistance mechanisms in chicken faeces-derived Escherichia coli

Lenart‐Boroń¹,

Augustyniak²,

Boroń³

2016

Vet. Med. - Czech

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This study was aimed at investigating the resistance to antimicrobial agents and to assess the predominant molecular mechanisms of fluoroquinolone resistance in faecal E. coli strains isolated from chickens farmed in central Poland. Bacterial strains were isolated from faecal samples of chickens reared on four conventional and one organic farm. The disk-diffusion method was applied to assess antimicrobial resistance and the prevalence of particular resistance mechanisms to fluoroquinolones was determined using specific polymerase chain reactions and sequencing of the gyrA and parC genes. Rep-PCR was used to determine the intra-specific variation of E. coli strains. The greatest resistance was observed for ß-lactams (e.g. from 25 to 100% of strains resistant to amoxicillin/clavulanate) and the smallest -for cephalotin (0 to 18.75% resistant strains). Three out of four conventional farms were characterised by very high resistance rates, particularly to enrofloxacin (from 87 to 93.3% of resistant isolates). The majority of multidrug-resistant strains were also isolated from these farms. The presence of plasmidmediated quinolone resistance genes (qnrB and qnrS) was detected very frequently, even in strains that exhibited phenotypic susceptibility to fluoroquinolones. With respect to point mutations in quinolone resistance determining regions, Ser-83 substitution was observed in numerous strains. Some of the fluoroquinolone-resistant strains appeared to possess both qnr genes coupled with point mutations, which indicates that a high level of resistance can be affected by multiple factors. Nevertheless, excessive use of antimicrobial agents in food-producing animals decreases the susceptibility of commensal strains, even those that never had contact with antibiotics.

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Section: Methodsmentioning

confidence: 99%

Screening of antimicrobial resistance and molecular detection of fluoroquinolone resistance mechanisms in chicken faeces-derived Escherichia coli

Lenart‐Boroń¹,

Augustyniak²,

Boroń³

2016

Vet. Med. - Czech

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“…A single E. coli isolate among 121 (0.8%) ESBL-positive Enterobacteriaceae strains isolated in 2007 was positive for a variant named qepA2 (28). In a study of pig farms in China, qepA was found in 28 of 48 (58.3%) rmtBpositive E. coli isolates (115). A follow-up study from the same region in China tested for qepA among ceftiofur-resistant isolates of Enterobacteriaceae.…”

Section: Epidemiology Of Qepamentioning

confidence: 99%

Plasmid-Mediated Quinolone Resistance: a Multifaceted Threat

et al. 2009

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SUMMARY Although plasmid-mediated quinolone resistance (PMQR) was thought not to exist before its discovery in 1998, the past decade has seen an explosion of research characterizing this phenomenon. The best-described form of PMQR is determined by the qnr group of genes. These genes, likely originating in aquatic organisms, code for pentapeptide repeat proteins. These proteins reduce susceptibility to quinolones by protecting the complex of DNA and DNA gyrase or topoisomerase IV enzymes from the inhibitory effect of quinolones. Two additional PMQR mechanisms were recently described. aac(6′)-Ib-cr encodes a variant aminoglycoside acetyltransferase with two amino acid alterations allowing it to inactivate ciprofloxacin through the acetylation of its piperazinyl substituent. oqxAB and qepA encode efflux pumps that extrude quinolones. All of these genes determine relatively small increases in the MICs of quinolones, but these changes are sufficient to facilitate the selection of mutants with higher levels of resistance. The contribution of these genes to the emergence of quinolone resistance is being actively investigated. Several factors suggest their importance in this process, including their increasing ubiquity, their association with other resistance elements, and their emergence simultaneous with the expansion of clinical quinolone resistance. Of concern, these genes are not yet being taken into account in resistance screening by clinical microbiology laboratories.

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“…qepA has often been found on plasmids also encoding aminoglycoside ribosomal methylase rmtB (12,167,198). Substantial differences in quinolone resistance produced by different qepA transconjugants suggest variability in the level of qepA expression, by mechanisms as yet to be defined (167). IS26 elements and ISCR3C have been implicated in mobilizing the qepA gene to plasmids (199).…”

Section: Qepa and Oqxabmentioning

confidence: 99%

Plasmid-Mediated Quinolone Resistance

Jacoby

2009

Antimicrobial Drug Resistance

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SummaryThree mechanisms for plasmid-mediated quinolone resistance (PMQR) have been discovered since 1998. Plasmid genes qnrA, qnrB, qnrC, qnrD, qnrS, and qnrVC code for proteins of the pentapeptide repeat family that protects DNA gyrase and topoisomerase IV from quinolone inhibition. The qnr genes appear to have been acquired from chromosomal genes in aquatic bacteria, are usually associated with mobilizing or transposable elements on plasmids, and are often incorporated into sul1-type integrons. The second plasmid-mediated mechanism involves acetylation of quinolones with an appropriate amino nitrogen target by a variant of the common aminoglycoside acetyltransferase AAC(6′)-Ib. The third mechanism is enhanced efflux produced by plasmid genes for pumps QepAB and OqxAB. PMQR has been found in clinical and environmental isolates around the world and appears to be spreading. The plasmid-mediated mechanisms provide only low-level resistance that by itself does not exceed the clinical breakpoint for susceptibility but nonetheless facilitates selection of higher-level resistance and makes infection by pathogens containing PMQR harder to treat.

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Coprevalence of Plasmid-Mediated Quinolone Resistance Determinants QepA, Qnr, and AAC(6′)-Ib-cr among 16S rRNA Methylase RmtB-Producing Escherichia coli Isolates from Pigs

Cited by 99 publications

References 14 publications

Screening of antimicrobial resistance and molecular detection of fluoroquinolone resistance mechanisms in chicken faeces-derived Escherichia coli

Screening of antimicrobial resistance and molecular detection of fluoroquinolone resistance mechanisms in chicken faeces-derived Escherichia coli

Plasmid-Mediated Quinolone Resistance: a Multifaceted Threat

Plasmid-Mediated Quinolone Resistance

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