In-vivo loss of carbapenem resistance by extensively drug-resistant Klebsiella pneumoniae during treatment via porin expression modification

Abstract Klebsiella pneumoniae, an Enterobacteriaceae that mostly causes hospital-acquired infections, belongs to the recently published WHO’s list of antibiotic-resistant pathogens that pose the greatest threat to human health. Indeed, K. pneumoniae is the enterobacterial species most concerned by...

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Autores principales:	Suzanne Bialek-Davenet, Noémie Mayer, Julia Vergalli, Marion Duprilot, Sylvain Brisse, Jean-Marie Pagès, Marie-Hélène Nicolas-Chanoine
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/f6ea51cee31945f1be1b64b1c5abb1dd
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spelling	oai:doaj.org-article:f6ea51cee31945f1be1b64b1c5abb1dd2021-12-02T15:05:31ZIn-vivo loss of carbapenem resistance by extensively drug-resistant Klebsiella pneumoniae during treatment via porin expression modification10.1038/s41598-017-06503-62045-2322https://doaj.org/article/f6ea51cee31945f1be1b64b1c5abb1dd2017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-06503-6https://doaj.org/toc/2045-2322Abstract Klebsiella pneumoniae, an Enterobacteriaceae that mostly causes hospital-acquired infections, belongs to the recently published WHO’s list of antibiotic-resistant pathogens that pose the greatest threat to human health. Indeed, K. pneumoniae is the enterobacterial species most concerned by both resistance to extended-spectrum cephalosporins, due to extended-spectrum β-lactamase (ESBL) production, and resistance to carbapenems, i.e. the β-lactams with the broadest activity. Carbapenem resistance is related not only to carbapenemase production, but also the production of ESBL or AmpC and the loss of general porins. Here, we characterized the mechanisms that deprived a urinary ESBL-producing, porin-deficient K. pneumoniae isolate, isolated 13 days after the end of a 40-day course of imipenem treatment, of its carbapenem resistance. These mechanisms were observed in two in-vivo derivatives of this isolate and consisted of mutations in genes encoding molecules that participate in the downregulation of the synthesis of PhoE, a porin specialized in phosphate transport. We obtained three new derivatives from one of the two original derivatives, following in-vitro antibiotic pressure, in which the carbapenem resistance was restored because of mutations in genes encoding molecules that participate in the upregulation of PhoE synthesis. Thus, we uncovered novel mechanisms of carbapenem resistance/susceptibility switching in K. pneumoniae.Suzanne Bialek-DavenetNoémie MayerJulia VergalliMarion DuprilotSylvain BrisseJean-Marie PagèsMarie-Hélène Nicolas-ChanoineNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-10 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Suzanne Bialek-Davenet Noémie Mayer Julia Vergalli Marion Duprilot Sylvain Brisse Jean-Marie Pagès Marie-Hélène Nicolas-Chanoine In-vivo loss of carbapenem resistance by extensively drug-resistant Klebsiella pneumoniae during treatment via porin expression modification
description	Abstract Klebsiella pneumoniae, an Enterobacteriaceae that mostly causes hospital-acquired infections, belongs to the recently published WHO’s list of antibiotic-resistant pathogens that pose the greatest threat to human health. Indeed, K. pneumoniae is the enterobacterial species most concerned by both resistance to extended-spectrum cephalosporins, due to extended-spectrum β-lactamase (ESBL) production, and resistance to carbapenems, i.e. the β-lactams with the broadest activity. Carbapenem resistance is related not only to carbapenemase production, but also the production of ESBL or AmpC and the loss of general porins. Here, we characterized the mechanisms that deprived a urinary ESBL-producing, porin-deficient K. pneumoniae isolate, isolated 13 days after the end of a 40-day course of imipenem treatment, of its carbapenem resistance. These mechanisms were observed in two in-vivo derivatives of this isolate and consisted of mutations in genes encoding molecules that participate in the downregulation of the synthesis of PhoE, a porin specialized in phosphate transport. We obtained three new derivatives from one of the two original derivatives, following in-vitro antibiotic pressure, in which the carbapenem resistance was restored because of mutations in genes encoding molecules that participate in the upregulation of PhoE synthesis. Thus, we uncovered novel mechanisms of carbapenem resistance/susceptibility switching in K. pneumoniae.
format	article
author	Suzanne Bialek-Davenet Noémie Mayer Julia Vergalli Marion Duprilot Sylvain Brisse Jean-Marie Pagès Marie-Hélène Nicolas-Chanoine
author_facet	Suzanne Bialek-Davenet Noémie Mayer Julia Vergalli Marion Duprilot Sylvain Brisse Jean-Marie Pagès Marie-Hélène Nicolas-Chanoine
author_sort	Suzanne Bialek-Davenet
title	In-vivo loss of carbapenem resistance by extensively drug-resistant Klebsiella pneumoniae during treatment via porin expression modification
title_short	In-vivo loss of carbapenem resistance by extensively drug-resistant Klebsiella pneumoniae during treatment via porin expression modification
title_full	In-vivo loss of carbapenem resistance by extensively drug-resistant Klebsiella pneumoniae during treatment via porin expression modification
title_fullStr	In-vivo loss of carbapenem resistance by extensively drug-resistant Klebsiella pneumoniae during treatment via porin expression modification
title_full_unstemmed	In-vivo loss of carbapenem resistance by extensively drug-resistant Klebsiella pneumoniae during treatment via porin expression modification
title_sort	in-vivo loss of carbapenem resistance by extensively drug-resistant klebsiella pneumoniae during treatment via porin expression modification
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/f6ea51cee31945f1be1b64b1c5abb1dd
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In-vivo loss of carbapenem resistance by extensively drug-resistant Klebsiella pneumoniae during treatment via porin expression modification

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