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Dissecting Colistin Resistance Mechanisms in Extensively Drug-Resistant Acinetobacter baumannii Clinical Isolates
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Zeitschriftentitel: | mBio |
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Personen und Körperschaften: | , , , , , , , , , , |
In: | mBio, 10, 2019, 4 |
Format: | E-Article |
Sprache: | Englisch |
veröffentlicht: |
American Society for Microbiology
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author_facet |
Trebosc, Vincent Gartenmann, Sarah Tötzl, Marcus Lucchini, Valentina Schellhorn, Birgit Pieren, Michel Lociuro, Sergio Gitzinger, Marc Tigges, Marcel Bumann, Dirk Kemmer, Christian Trebosc, Vincent Gartenmann, Sarah Tötzl, Marcus Lucchini, Valentina Schellhorn, Birgit Pieren, Michel Lociuro, Sergio Gitzinger, Marc Tigges, Marcel Bumann, Dirk Kemmer, Christian |
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author |
Trebosc, Vincent Gartenmann, Sarah Tötzl, Marcus Lucchini, Valentina Schellhorn, Birgit Pieren, Michel Lociuro, Sergio Gitzinger, Marc Tigges, Marcel Bumann, Dirk Kemmer, Christian |
spellingShingle |
Trebosc, Vincent Gartenmann, Sarah Tötzl, Marcus Lucchini, Valentina Schellhorn, Birgit Pieren, Michel Lociuro, Sergio Gitzinger, Marc Tigges, Marcel Bumann, Dirk Kemmer, Christian mBio Dissecting Colistin Resistance Mechanisms in Extensively Drug-Resistant Acinetobacter baumannii Clinical Isolates Virology Microbiology |
author_sort |
trebosc, vincent |
spelling |
Trebosc, Vincent Gartenmann, Sarah Tötzl, Marcus Lucchini, Valentina Schellhorn, Birgit Pieren, Michel Lociuro, Sergio Gitzinger, Marc Tigges, Marcel Bumann, Dirk Kemmer, Christian 2161-2129 2150-7511 American Society for Microbiology Virology Microbiology http://dx.doi.org/10.1128/mbio.01083-19 <jats:p> The discovery of antibiotics revolutionized modern medicine and enabled us to cure previously deadly bacterial infections. However, a progressive increase in antibiotic resistance rates is a major and global threat for our health care system. Colistin represents one of our last-resort antibiotics that is still active against most Gram-negative bacterial pathogens, but increasing resistance is reported worldwide, in particular due to the plasmid-encoded protein MCR-1 present in pathogens such as <jats:named-content content-type="genus-species">Escherichia coli</jats:named-content> and <jats:named-content content-type="genus-species">Klebsiella pneumoniae</jats:named-content> . Here, we showed that colistin resistance in <jats:named-content content-type="genus-species">A. baumannii</jats:named-content> , a top-priority pathogen causing deadly nosocomial infections, is mediated through different avenues that result in increased activity of homologous phosphoethanolamine (PetN) transferases. Considering that MCR-1 is also a PetN transferase, our findings indicate that PetN transferases might be the Achilles heel of superbugs and that direct targeting of them may have the potential to preserve the activity of polymyxin antibiotics. </jats:p> Dissecting Colistin Resistance Mechanisms in Extensively Drug-Resistant Acinetobacter baumannii Clinical Isolates mBio |
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10.1128/mbio.01083-19 |
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American Society for Microbiology, 2019 |
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American Society for Microbiology, 2019 |
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title |
Dissecting Colistin Resistance Mechanisms in Extensively Drug-Resistant Acinetobacter baumannii Clinical Isolates |
title_unstemmed |
Dissecting Colistin Resistance Mechanisms in Extensively Drug-Resistant Acinetobacter baumannii Clinical Isolates |
title_full |
Dissecting Colistin Resistance Mechanisms in Extensively Drug-Resistant Acinetobacter baumannii Clinical Isolates |
title_fullStr |
Dissecting Colistin Resistance Mechanisms in Extensively Drug-Resistant Acinetobacter baumannii Clinical Isolates |
title_full_unstemmed |
Dissecting Colistin Resistance Mechanisms in Extensively Drug-Resistant Acinetobacter baumannii Clinical Isolates |
title_short |
Dissecting Colistin Resistance Mechanisms in Extensively Drug-Resistant Acinetobacter baumannii Clinical Isolates |
title_sort |
dissecting colistin resistance mechanisms in extensively drug-resistant acinetobacter baumannii clinical isolates |
topic |
Virology Microbiology |
url |
http://dx.doi.org/10.1128/mbio.01083-19 |
publishDate |
2019 |
physical |
|
description |
<jats:p>
The discovery of antibiotics revolutionized modern medicine and enabled us to cure previously deadly bacterial infections. However, a progressive increase in antibiotic resistance rates is a major and global threat for our health care system. Colistin represents one of our last-resort antibiotics that is still active against most Gram-negative bacterial pathogens, but increasing resistance is reported worldwide, in particular due to the plasmid-encoded protein MCR-1 present in pathogens such as
<jats:named-content content-type="genus-species">Escherichia coli</jats:named-content>
and
<jats:named-content content-type="genus-species">Klebsiella pneumoniae</jats:named-content>
. Here, we showed that colistin resistance in
<jats:named-content content-type="genus-species">A. baumannii</jats:named-content>
, a top-priority pathogen causing deadly nosocomial infections, is mediated through different avenues that result in increased activity of homologous phosphoethanolamine (PetN) transferases. Considering that MCR-1 is also a PetN transferase, our findings indicate that PetN transferases might be the Achilles heel of superbugs and that direct targeting of them may have the potential to preserve the activity of polymyxin antibiotics.
</jats:p> |
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author | Trebosc, Vincent, Gartenmann, Sarah, Tötzl, Marcus, Lucchini, Valentina, Schellhorn, Birgit, Pieren, Michel, Lociuro, Sergio, Gitzinger, Marc, Tigges, Marcel, Bumann, Dirk, Kemmer, Christian |
author_facet | Trebosc, Vincent, Gartenmann, Sarah, Tötzl, Marcus, Lucchini, Valentina, Schellhorn, Birgit, Pieren, Michel, Lociuro, Sergio, Gitzinger, Marc, Tigges, Marcel, Bumann, Dirk, Kemmer, Christian, Trebosc, Vincent, Gartenmann, Sarah, Tötzl, Marcus, Lucchini, Valentina, Schellhorn, Birgit, Pieren, Michel, Lociuro, Sergio, Gitzinger, Marc, Tigges, Marcel, Bumann, Dirk, Kemmer, Christian |
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description | <jats:p> The discovery of antibiotics revolutionized modern medicine and enabled us to cure previously deadly bacterial infections. However, a progressive increase in antibiotic resistance rates is a major and global threat for our health care system. Colistin represents one of our last-resort antibiotics that is still active against most Gram-negative bacterial pathogens, but increasing resistance is reported worldwide, in particular due to the plasmid-encoded protein MCR-1 present in pathogens such as <jats:named-content content-type="genus-species">Escherichia coli</jats:named-content> and <jats:named-content content-type="genus-species">Klebsiella pneumoniae</jats:named-content> . Here, we showed that colistin resistance in <jats:named-content content-type="genus-species">A. baumannii</jats:named-content> , a top-priority pathogen causing deadly nosocomial infections, is mediated through different avenues that result in increased activity of homologous phosphoethanolamine (PetN) transferases. Considering that MCR-1 is also a PetN transferase, our findings indicate that PetN transferases might be the Achilles heel of superbugs and that direct targeting of them may have the potential to preserve the activity of polymyxin antibiotics. </jats:p> |
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spelling | Trebosc, Vincent Gartenmann, Sarah Tötzl, Marcus Lucchini, Valentina Schellhorn, Birgit Pieren, Michel Lociuro, Sergio Gitzinger, Marc Tigges, Marcel Bumann, Dirk Kemmer, Christian 2161-2129 2150-7511 American Society for Microbiology Virology Microbiology http://dx.doi.org/10.1128/mbio.01083-19 <jats:p> The discovery of antibiotics revolutionized modern medicine and enabled us to cure previously deadly bacterial infections. However, a progressive increase in antibiotic resistance rates is a major and global threat for our health care system. Colistin represents one of our last-resort antibiotics that is still active against most Gram-negative bacterial pathogens, but increasing resistance is reported worldwide, in particular due to the plasmid-encoded protein MCR-1 present in pathogens such as <jats:named-content content-type="genus-species">Escherichia coli</jats:named-content> and <jats:named-content content-type="genus-species">Klebsiella pneumoniae</jats:named-content> . Here, we showed that colistin resistance in <jats:named-content content-type="genus-species">A. baumannii</jats:named-content> , a top-priority pathogen causing deadly nosocomial infections, is mediated through different avenues that result in increased activity of homologous phosphoethanolamine (PetN) transferases. Considering that MCR-1 is also a PetN transferase, our findings indicate that PetN transferases might be the Achilles heel of superbugs and that direct targeting of them may have the potential to preserve the activity of polymyxin antibiotics. </jats:p> Dissecting Colistin Resistance Mechanisms in Extensively Drug-Resistant Acinetobacter baumannii Clinical Isolates mBio |
spellingShingle | Trebosc, Vincent, Gartenmann, Sarah, Tötzl, Marcus, Lucchini, Valentina, Schellhorn, Birgit, Pieren, Michel, Lociuro, Sergio, Gitzinger, Marc, Tigges, Marcel, Bumann, Dirk, Kemmer, Christian, mBio, Dissecting Colistin Resistance Mechanisms in Extensively Drug-Resistant Acinetobacter baumannii Clinical Isolates, Virology, Microbiology |
title | Dissecting Colistin Resistance Mechanisms in Extensively Drug-Resistant Acinetobacter baumannii Clinical Isolates |
title_full | Dissecting Colistin Resistance Mechanisms in Extensively Drug-Resistant Acinetobacter baumannii Clinical Isolates |
title_fullStr | Dissecting Colistin Resistance Mechanisms in Extensively Drug-Resistant Acinetobacter baumannii Clinical Isolates |
title_full_unstemmed | Dissecting Colistin Resistance Mechanisms in Extensively Drug-Resistant Acinetobacter baumannii Clinical Isolates |
title_short | Dissecting Colistin Resistance Mechanisms in Extensively Drug-Resistant Acinetobacter baumannii Clinical Isolates |
title_sort | dissecting colistin resistance mechanisms in extensively drug-resistant acinetobacter baumannii clinical isolates |
title_unstemmed | Dissecting Colistin Resistance Mechanisms in Extensively Drug-Resistant Acinetobacter baumannii Clinical Isolates |
topic | Virology, Microbiology |
url | http://dx.doi.org/10.1128/mbio.01083-19 |