Résistance aux quinolones de type qnr chez les entérobactéries productrices de bêta-lactamases à spectre élargi à Abidjan en Côte d’Ivoire

Guessennd, Nathalie; Brémont, Sylvie; Gbonon, V; Kacou-N'douba, A.; Ekaza, Euloge; Lambert, Thierry; Dosso, Mireille; Courvalin, Patrice

doi:10.1016/j.patbio.2008.07.025

Cited by 62 publications

(54 citation statements)

References 22 publications

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“…PMQR genes were ubiquitous among the analyzed Enterobacteriaceae (Table 1; for detailed information, see Table S2 in the supplemental material), consistent with previous reports of Entero bacteriaceae in West Africa (13)(14)(15)(16)(17)(18)(19). Observed in all species tested except E. coli and P. dispersa, various qnr genes and aac(6=)-Ib-cr were detected in 68% and 58% of the isolates, respectively.…”

supporting

confidence: 87%

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Prevalence of Quinolone Resistance in Enterobacteriaceae from Sierra Leone and the Detection of qnrB Pseudogenes and Modified LexA Binding Sites

Łęski

Stockelman

Bangura³

et al. 2016

Antimicrob Agents Chemother

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A collection of 74 Enterobacteriaceae isolates found in Bo, Sierra Leone, were tested for quinolone antibiotic susceptibility and resistance mechanisms. The majority of isolates (62%) were resistant to quinolones, and 61% harbored chromosomal gyrA and/or parC mutations. Plasmid-mediated quinolone resistance genes were ubiquitous, with qnrB and aac(6=)-Ib-cr being the most prevalent. Mutated LexA binding sites were found in all qnrB1 genes, and truncated qnrB pseudogenes were found in the majority of Citrobacter isolates.

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supporting

confidence: 87%

“…An increasing prevalence of quinolone resistance has been reported in West Africa (11)(12)(13), with several mechanistic surveys of quinolone nonsusceptibility within this region recently published (13)(14)(15)(16)(17)(18)(19). However, no such data are available for Sierra Leone (11).…”

mentioning

confidence: 99%

Prevalence of Quinolone Resistance in Enterobacteriaceae from Sierra Leone and the Detection of qnrB Pseudogenes and Modified LexA Binding Sites

Łęski

Stockelman

Bangura³

et al. 2016

Antimicrob Agents Chemother

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“…The nucleotide sequences and deduced protein sequences were analysed using the BLAST, ResFinder, and Clustal W programs. All ESBLE resistant to ciprofloxacin were screened by PCR amplification for the presence of the qnrA , qnrB , qnrS genes [28]. …”

Section: Methodsmentioning

confidence: 99%

Resistance to antimicrobial drugs in different surface waters and wastewaters of Guadeloupe

et al. 2017

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ObjectiveThe first aim of this study was to evaluate the antimicrobial resistance of Enterobacteriaceae in different water environments of Guadeloupe and especially those impacted by waste water treatment plants (WWTP) effluents.The second objective was to characterize the genetic basis for antibiotic resistance of extended-spectrum beta-lactamase (ESBL) and AmpC beta-lactamase producing Enterobacteriaceae isolates (ESBLE and AmpCE).MethodsWe have collected 70 surface waters (river and sea samples) impacted or not by WWTP and 18 waste waters from 2 WWTPs in 2012 and 2013. We i) determined the total and resistant bacterial counts and ii) tested isolated Enterobacteriaceae for their antimicrobial susceptibility. We also studied the genetic basis for antibiotic resistance of ESBLE and AmpCE, and the genetic background of Escherichia coli.ResultsIn rivers, contamination with Escherichia coli and antibiotic resistant coliforms (ARC) increased from the source to the mouth. Highest levels of river contamination with E. coli (9.26 x 105 MPN/100mL) and ARC (2.26 x 108 CFU/mL) were observed in surface water sampled near the discharge. A total of 246 Enterobacteriaceae strains resistant to antibiotics were isolated, mostly from waste waters and from river water collected near the discharge. Among these strains, 33 were Extended Spectrum Beta Lactamase (ESBLE) and 8 E. coli were AmpC beta-lactamase producers. All the ESBLE were isolated from waste waters or from river water collected near the discharge. The blaCTX-M gene was present in 29 of the 33 ESBLE strains, with 24 belonging to group 1. Numerous strains (68.7%) showed more than one acquired antibiotic resistance mechanism. E. coli strains belonged to different phylogenetic groups; among the B2 group, most strains belonged to the ST131 clone.ConclusionOur results demonstrated that many human activities can supply antibiotic-resistant bacteria in surface water. Nevertheless, WWTPs were the most important supplier of ESBLE in water environment of Guadeloupe.

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“…β-lactamase genes have been conspicuously common, including genes for AmpC β-lactamases (22, 96–101), CTX-M enzymes (96, 97, 99, 100, 102–114), IMP enzymes (74, 115), KPC enzymes (116–118), LAP-1 or LAP-2 (88, 89, 119–121), SHV-12 (96, 99, 104, 105, 107, 109, 115, 119, 121–127), VEB-1 (126, 128–130), and VIM-1 (111, 131). qnrB4 and bla DHA-1 have been found near each other on similar plasmids from around the world (96, 108, 127, 132–135).…”

Section: Qnr Plasmidsmentioning

confidence: 99%

Plasmid-Mediated Quinolone Resistance

2014

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Summary Three 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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Résistance aux quinolones de type qnr chez les entérobactéries productrices de bêta-lactamases à spectre élargi à Abidjan en Côte d’Ivoire

Cited by 62 publications

References 22 publications

Prevalence of Quinolone Resistance in Enterobacteriaceae from Sierra Leone and the Detection of qnrB Pseudogenes and Modified LexA Binding Sites

Prevalence of Quinolone Resistance in Enterobacteriaceae from Sierra Leone and the Detection of qnrB Pseudogenes and Modified LexA Binding Sites

Resistance to antimicrobial drugs in different surface waters and wastewaters of Guadeloupe

Plasmid-Mediated Quinolone Resistance

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