In vivo reversion to the wild-type β-lactam resistance phenotype mediated by a plasmid carrying ampR and qnrA1 in Enterobacter cloacae

J. J. González-López; M. Sabaté; S. Lavilla; M. N. Larrosa; R. M. Bartolomé; G. Prats

doi:https://doi.org/10.1128/AAC.00273-06

In vivo reversion to the wild-type β-lactam resistance phenotype mediated by a plasmid carrying ampR and qnrA1 in Enterobacter cloacae

J. J. González-López, M. Sabaté, S. Lavilla, M. N. Larrosa, R. M. Bartolomé, G. Prats

Department of Genetics and Microbiology

Research output: Contribution to journal › Article › Research › peer-review

Abstract

Resistance to β-lactams and quinolones in two isogenic Enterobacter cloacae isolates was studied. One was susceptible to cefoxitin and amoxicillin-clavulanate. The other one showed its natural β-lactam resistance pattern. Both isolates had a nonfunctional AmpR regulator. However, within the second one, the presence of a plasmid carrying ampR and qnrA1 allowed reversion to the wild-type β-lactam resistance phenotype and decreased susceptibility to fluoroauinolones. Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Original language	English
Pages (from-to)	3175-3178
Journal	Antimicrobial Agents and Chemotherapy
Volume	50
DOIs	https://doi.org/10.1128/AAC.00273-06
Publication status	Published - 1 Sep 2006

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@article{f3d68d717639487b9c9cb45d4d4044e9,

title = "In vivo reversion to the wild-type β-lactam resistance phenotype mediated by a plasmid carrying ampR and qnrA1 in Enterobacter cloacae",

abstract = "Resistance to β-lactams and quinolones in two isogenic Enterobacter cloacae isolates was studied. One was susceptible to cefoxitin and amoxicillin-clavulanate. The other one showed its natural β-lactam resistance pattern. Both isolates had a nonfunctional AmpR regulator. However, within the second one, the presence of a plasmid carrying ampR and qnrA1 allowed reversion to the wild-type β-lactam resistance phenotype and decreased susceptibility to fluoroauinolones. Copyright {\textcopyright} 2006, American Society for Microbiology. All Rights Reserved.",

author = "Gonz{\'a}lez-L{\'o}pez, {J. J.} and M. Sabat{\'e} and S. Lavilla and Larrosa, {M. N.} and Bartolom{\'e}, {R. M.} and G. Prats",

year = "2006",

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doi = "https://doi.org/10.1128/AAC.00273-06",

language = "English",

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In vivo reversion to the wild-type β-lactam resistance phenotype mediated by a plasmid carrying ampR and qnrA1 in Enterobacter cloacae. / González-López, J. J.; Sabaté, M.; Lavilla, S.; Larrosa, M. N.; Bartolomé, R. M.; Prats, G.

In: Antimicrobial Agents and Chemotherapy, Vol. 50, 01.09.2006, p. 3175-3178.

Research output: Contribution to journal › Article › Research › peer-review

TY - JOUR

T1 - In vivo reversion to the wild-type β-lactam resistance phenotype mediated by a plasmid carrying ampR and qnrA1 in Enterobacter cloacae

AU - González-López, J. J.

AU - Sabaté, M.

AU - Lavilla, S.

AU - Larrosa, M. N.

AU - Bartolomé, R. M.

AU - Prats, G.

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N2 - Resistance to β-lactams and quinolones in two isogenic Enterobacter cloacae isolates was studied. One was susceptible to cefoxitin and amoxicillin-clavulanate. The other one showed its natural β-lactam resistance pattern. Both isolates had a nonfunctional AmpR regulator. However, within the second one, the presence of a plasmid carrying ampR and qnrA1 allowed reversion to the wild-type β-lactam resistance phenotype and decreased susceptibility to fluoroauinolones. Copyright © 2006, American Society for Microbiology. All Rights Reserved.

AB - Resistance to β-lactams and quinolones in two isogenic Enterobacter cloacae isolates was studied. One was susceptible to cefoxitin and amoxicillin-clavulanate. The other one showed its natural β-lactam resistance pattern. Both isolates had a nonfunctional AmpR regulator. However, within the second one, the presence of a plasmid carrying ampR and qnrA1 allowed reversion to the wild-type β-lactam resistance phenotype and decreased susceptibility to fluoroauinolones. Copyright © 2006, American Society for Microbiology. All Rights Reserved.

U2 - https://doi.org/10.1128/AAC.00273-06

DO - https://doi.org/10.1128/AAC.00273-06

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