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The β-lactamase inhibitor avibactam (NXL104) does not induce ampC β-lactamase in Enterobacter cloacae

Induction of ampC β-lactamase expression can often compromise antibiotic treatment and is triggered by several β-lactams (such as cefoxitin and imipenem) and by the β-lactamase inhibitor clavulanic acid. The novel β-lactamase inhibitor avibactam (NXL104) is a potent inhibitor of both class A and cla...

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Autores principales: Miossec, Christine, Claudon, Monique, Levasseur, Premavathy, Black, Michael T
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3857152/
https://www.ncbi.nlm.nih.gov/pubmed/24348054
http://dx.doi.org/10.2147/IDR.S53874
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author Miossec, Christine
Claudon, Monique
Levasseur, Premavathy
Black, Michael T
author_facet Miossec, Christine
Claudon, Monique
Levasseur, Premavathy
Black, Michael T
author_sort Miossec, Christine
collection PubMed
description Induction of ampC β-lactamase expression can often compromise antibiotic treatment and is triggered by several β-lactams (such as cefoxitin and imipenem) and by the β-lactamase inhibitor clavulanic acid. The novel β-lactamase inhibitor avibactam (NXL104) is a potent inhibitor of both class A and class C enzymes. The potential of avibactam for induction of ampC expression in Enterobacter cloacae was investigated by ampC messenger ribonucleic acid quantitation. Cefoxitin and clavulanic acid were confirmed as ampC inducers, whereas avibactam was found to exert no effect on ampC expression. Thus, avibactam is unlikely to diminish the activity of any partner β-lactam antibiotic against AmpC-producing organisms.
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spelling pubmed-38571522013-12-12 The β-lactamase inhibitor avibactam (NXL104) does not induce ampC β-lactamase in Enterobacter cloacae Miossec, Christine Claudon, Monique Levasseur, Premavathy Black, Michael T Infect Drug Resist Original Research Induction of ampC β-lactamase expression can often compromise antibiotic treatment and is triggered by several β-lactams (such as cefoxitin and imipenem) and by the β-lactamase inhibitor clavulanic acid. The novel β-lactamase inhibitor avibactam (NXL104) is a potent inhibitor of both class A and class C enzymes. The potential of avibactam for induction of ampC expression in Enterobacter cloacae was investigated by ampC messenger ribonucleic acid quantitation. Cefoxitin and clavulanic acid were confirmed as ampC inducers, whereas avibactam was found to exert no effect on ampC expression. Thus, avibactam is unlikely to diminish the activity of any partner β-lactam antibiotic against AmpC-producing organisms. Dove Medical Press 2013-12-03 /pmc/articles/PMC3857152/ /pubmed/24348054 http://dx.doi.org/10.2147/IDR.S53874 Text en © 2013 Miossec et al. This work is published by Dove Medical Press Limited, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
spellingShingle Original Research
Miossec, Christine
Claudon, Monique
Levasseur, Premavathy
Black, Michael T
The β-lactamase inhibitor avibactam (NXL104) does not induce ampC β-lactamase in Enterobacter cloacae
title The β-lactamase inhibitor avibactam (NXL104) does not induce ampC β-lactamase in Enterobacter cloacae
title_full The β-lactamase inhibitor avibactam (NXL104) does not induce ampC β-lactamase in Enterobacter cloacae
title_fullStr The β-lactamase inhibitor avibactam (NXL104) does not induce ampC β-lactamase in Enterobacter cloacae
title_full_unstemmed The β-lactamase inhibitor avibactam (NXL104) does not induce ampC β-lactamase in Enterobacter cloacae
title_short The β-lactamase inhibitor avibactam (NXL104) does not induce ampC β-lactamase in Enterobacter cloacae
title_sort β-lactamase inhibitor avibactam (nxl104) does not induce ampc β-lactamase in enterobacter cloacae
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3857152/
https://www.ncbi.nlm.nih.gov/pubmed/24348054
http://dx.doi.org/10.2147/IDR.S53874
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