New genetic environments of aac(6′)-Ib-cr gene in a multiresistant Klebsiella oxytoca strain causing an outbreak in a pediatric intensive care unit

Ruiz, Elena; Rezusta, Antonio; Sáenz, Yolanda; Rocha-Gracia, Rosa del Carmen; Vinué, Laura; Vindel, Ana; Villuendas, Cruz; Azañedo, María Luisa; Monforte, María Luisa; Revillo, María José; Torres, Carmén

doi:10.1016/j.diagmicrobio.2010.09.004

Cited by 19 publications

(12 citation statements)

References 14 publications

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“…Association with ESBL CTX-M-15 is particularly common (110, 184–190). A mobile genetic element, especially IS 26, is often associated (191). aac(6′)-Ib-cr may also be chromosomal (192, 193).…”

Section: Aac(6′)-ib-crmentioning

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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Section: Aac(6′)-ib-crmentioning

confidence: 99%

Plasmid-Mediated Quinolone Resistance

2014

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“…Association with ESBL CTX-M-15 is particularly common (110,(184)(185)(186)(187)(188)(189)(190). A mobile genetic element, especially IS26, is often associated (191). aac(6′)-Ib-cr may also be chromosomal (192,193).…”

Section: Aac(6′)-ib-crmentioning

confidence: 99%

Plasmid-Mediated Quinolone Resistance

2015

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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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Section: Aac(6′)-ib-crmentioning

confidence: 99%

Plasmid-Mediated Quinolone Resistance

Jacoby¹

2017

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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New genetic environments of aac(6′)-Ib-cr gene in a multiresistant Klebsiella oxytoca strain causing an outbreak in a pediatric intensive care unit

Cited by 19 publications

References 14 publications

Plasmid-Mediated Quinolone Resistance

Plasmid-Mediated Quinolone Resistance

Plasmid-Mediated Quinolone Resistance

Plasmid-Mediated Quinolone Resistance

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