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Disease-associated genotypes of the commensal skin bacterium Staphylococcus epidermidis

Identifieur interne : 000A01 ( Main/Exploration ); précédent : 000A00; suivant : 000A02

Disease-associated genotypes of the commensal skin bacterium Staphylococcus epidermidis

Auteurs : Guillaume Méric ; Leonardos Mageiros ; Johan Pensar [Finlande] ; Maisem Laabei [Suède] ; Koji Yahara [Japon] ; Ben Pascoe ; Nattinee Kittiwan [Thaïlande] ; Phacharaporn Tadee [Thaïlande] ; Virginia Post [Suisse] ; Sarah Lamble ; Rory Bowden ; James E. Bray ; Mario Morgenstern [Suisse] ; Keith A. Jolley ; Martin C. J. Maiden ; Edward J. Feil ; Xavier Didelot ; Maria Miragaia [Portugal] ; Herminia De Lencastre [Portugal, États-Unis] ; T. Fintan Moriarty [Suisse] ; Holger Rohde [Allemagne] ; Ruth Massey ; Dietrich Mack [Allemagne] ; Jukka Corander [Finlande, Norvège] ; Samuel K. Sheppard

Source :

RBID : PMC:6261936

Descripteurs français

English descriptors

Abstract

Some of the most common infectious diseases are caused by bacteria that naturally colonise humans asymptomatically. Combating these opportunistic pathogens requires an understanding of the traits that differentiate infecting strains from harmless relatives. Staphylococcus epidermidis is carried asymptomatically on the skin and mucous membranes of virtually all humans but is a major cause of nosocomial infection associated with invasive procedures. Here we address the underlying evolutionary mechanisms of opportunistic pathogenicity by combining pangenome-wide association studies and laboratory microbiology to compare S. epidermidis from bloodstream and wound infections and asymptomatic carriage. We identify 61 genes containing infection-associated genetic elements (k-mers) that correlate with in vitro variation in known pathogenicity traits (biofilm formation, cell toxicity, interleukin-8 production, methicillin resistance). Horizontal gene transfer spreads these elements, allowing divergent clones to cause infection. Finally, Random Forest model prediction of disease status (carriage vs. infection) identifies pathogenicity elements in 415 S. epidermidis isolates with 80% accuracy, demonstrating the potential for identifying risk genotypes pre-operatively.


Url:
DOI: 10.1038/s41467-018-07368-7
PubMed: 30487573
PubMed Central: 6261936


Affiliations:


Links toward previous steps (curation, corpus...)


Le document en format XML

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New York, 10065 USA</nlm:aff>
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<name sortKey="Rohde, Holger" sort="Rohde, Holger" uniqKey="Rohde H" first="Holger" last="Rohde">Holger Rohde</name>
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<institution>Universität Hamburg,</institution>
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Hamburg, 20246 Germany</nlm:aff>
<country xml:lang="fr">Allemagne</country>
<wicri:regionArea>Hamburg</wicri:regionArea>
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<name sortKey="Massey, Ruth" sort="Massey, Ruth" uniqKey="Massey R" first="Ruth" last="Massey">Ruth Massey</name>
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Bristol, BS8 1TD UK</nlm:aff>
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<name sortKey="Mack, Dietrich" sort="Mack, Dietrich" uniqKey="Mack D" first="Dietrich" last="Mack">Dietrich Mack</name>
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<wicri:noRegion>Ingelheim</wicri:noRegion>
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<name sortKey="Corander, Jukka" sort="Corander, Jukka" uniqKey="Corander J" first="Jukka" last="Corander">Jukka Corander</name>
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<institution>Department of Mathematics and Statistics,</institution>
<institution>University of Helsinki,</institution>
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Helsinki, 00100 Finland</nlm:aff>
<country xml:lang="fr">Finlande</country>
<wicri:regionArea>Helsinki</wicri:regionArea>
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<institution-id institution-id-type="GRID">grid.5510.1</institution-id>
<institution>Department of Biostatistics,</institution>
<institution>University of Oslo,</institution>
</institution-wrap>
Oslo, 0372 Norway</nlm:aff>
<country xml:lang="fr">Norvège</country>
<wicri:regionArea>Oslo</wicri:regionArea>
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<institution-wrap>
<institution-id institution-id-type="ISNI">0000 0004 0606 5382</institution-id>
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<institution>Pathogen Genomics,</institution>
<institution>Wellcome Trust Sanger Institute,</institution>
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Hinxton, CB10 1SA UK</nlm:aff>
<wicri:noCountry code="subfield">CB10 1SA UK</wicri:noCountry>
</affiliation>
</author>
<author>
<name sortKey="Sheppard, Samuel K" sort="Sheppard, Samuel K" uniqKey="Sheppard S" first="Samuel K." last="Sheppard">Samuel K. Sheppard</name>
<affiliation>
<nlm:aff id="Aff1">
<institution-wrap>
<institution-id institution-id-type="ISNI">0000 0001 2162 1699</institution-id>
<institution-id institution-id-type="GRID">grid.7340.0</institution-id>
<institution>The Milner Centre for Evolution,</institution>
<institution>University of Bath,</institution>
</institution-wrap>
Claverton Down Bath, BA2 7AY UK</nlm:aff>
<wicri:noCountry code="subfield">BA2 7AY UK</wicri:noCountry>
</affiliation>
<affiliation>
<nlm:aff id="Aff5">MRC Cloud-based Infrastructure for Microbial Bioinformatics (CLIMB) Consortium, Bath, BA2 7AY UK</nlm:aff>
<wicri:noCountry code="subfield">BA2 7AY UK</wicri:noCountry>
</affiliation>
<affiliation>
<nlm:aff id="Aff10">
<institution-wrap>
<institution-id institution-id-type="ISNI">0000 0004 1936 8948</institution-id>
<institution-id institution-id-type="GRID">grid.4991.5</institution-id>
<institution>Department of Zoology,</institution>
<institution>University of Oxford,</institution>
</institution-wrap>
Oxford, OX1 3SZ UK</nlm:aff>
<wicri:noCountry code="subfield">OX1 3SZ UK</wicri:noCountry>
</affiliation>
</author>
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<country xml:lang="fr">Suisse</country>
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<institution>University of Oxford,</institution>
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<wicri:noCountry code="subfield">OX1 3SZ UK</wicri:noCountry>
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<title level="j">Nature Communications</title>
<idno type="eISSN">2041-1723</idno>
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<date when="2018">2018</date>
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<term>Humans</term>
<term>Interleukin-8 (metabolism)</term>
<term>Skin Diseases (microbiology)</term>
<term>Staphylococcal Infections (microbiology)</term>
<term>Staphylococcus epidermidis (genetics)</term>
<term>Staphylococcus epidermidis (pathogenicity)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr">
<term>Génome bactérien (génétique)</term>
<term>Génotype</term>
<term>Humains</term>
<term>Infections à staphylocoques (microbiologie)</term>
<term>Interleukine-8 (métabolisme)</term>
<term>Maladies de la peau (microbiologie)</term>
<term>Staphylococcus epidermidis (génétique)</term>
<term>Staphylococcus epidermidis (pathogénicité)</term>
<term>Étude d'association pangénomique</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en">
<term>Interleukin-8</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en">
<term>Genome, Bacterial</term>
<term>Staphylococcus epidermidis</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr">
<term>Génome bactérien</term>
<term>Staphylococcus epidermidis</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr">
<term>Infections à staphylocoques</term>
<term>Maladies de la peau</term>
</keywords>
<keywords scheme="MESH" qualifier="microbiology" xml:lang="en">
<term>Skin Diseases</term>
<term>Staphylococcal Infections</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr">
<term>Interleukine-8</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en">
<term>Staphylococcus epidermidis</term>
</keywords>
<keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr">
<term>Staphylococcus epidermidis</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Genome-Wide Association Study</term>
<term>Genotype</term>
<term>Humans</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr">
<term>Génotype</term>
<term>Humains</term>
<term>Étude d'association pangénomique</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">
<p id="Par1">Some of the most common infectious diseases are caused by bacteria that naturally colonise humans asymptomatically. Combating these opportunistic pathogens requires an understanding of the traits that differentiate infecting strains from harmless relatives.
<italic>Staphylococcus epidermidis</italic>
is carried asymptomatically on the skin and mucous membranes of virtually all humans but is a major cause of nosocomial infection associated with invasive procedures. Here we address the underlying evolutionary mechanisms of opportunistic pathogenicity by combining pangenome-wide association studies and laboratory microbiology to compare
<italic>S. epidermidis</italic>
from bloodstream and wound infections and asymptomatic carriage. We identify 61 genes containing infection-associated genetic elements (k-mers) that correlate with in vitro variation in known pathogenicity traits (biofilm formation, cell toxicity, interleukin-8 production, methicillin resistance). Horizontal gene transfer spreads these elements, allowing divergent clones to cause infection. Finally, Random Forest model prediction of disease status (carriage vs. infection) identifies pathogenicity elements in 415 
<italic>S. epidermidis</italic>
isolates with 80% accuracy, demonstrating the potential for identifying risk genotypes pre-operatively.</p>
</div>
</front>
<back>
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<analytic>
<author>
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<name sortKey="Farris, Js" uniqKey="Farris J">JS Farris</name>
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<name sortKey="Schliep, Kp" uniqKey="Schliep K">KP Schliep</name>
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<name sortKey="Breiman, L" uniqKey="Breiman L">L Breiman</name>
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<li>Finlande</li>
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<li>Portugal</li>
<li>Suisse</li>
<li>Suède</li>
<li>Thaïlande</li>
<li>États-Unis</li>
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<name sortKey="De Lencastre, Herminia" sort="De Lencastre, Herminia" uniqKey="De Lencastre H" first="Herminia" last="De Lencastre">Herminia De Lencastre</name>
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<country name="Norvège">
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<name sortKey="Corander, Jukka" sort="Corander, Jukka" uniqKey="Corander J" first="Jukka" last="Corander">Jukka Corander</name>
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</record>

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