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Shigella sonnei genome sequencing and phylogenetic analysis indicate recent global dissemination from Europe

Identifieur interne : 001960 ( Main/Merge ); précédent : 001959; suivant : 001961

Shigella sonnei genome sequencing and phylogenetic analysis indicate recent global dissemination from Europe

Auteurs : Kathryn E. Holt [Australie] ; Stephen Baker [Viêt Nam] ; François-Xavier Weill [France] ; Edward C. Holmes [États-Unis] ; Andrew Kitchen [France] ; Jun Yu ; Vartul Sangal ; Derek J. Brown [Royaume-Uni] ; John E. Coia [Royaume-Uni] ; Dong-Wook Kim [Corée du Sud] ; Choi Seon Young [Corée du Sud] ; Su Hee Kim [Corée du Sud] ; Wanderley Dias Da Silveira [Brésil] ; Derek Pickard [Royaume-Uni] ; Jeremy J. Farrar [Viêt Nam] ; Julian Parkhill [Royaume-Uni] ; Gordon Dougan [Royaume-Uni] ; Nicholas R. Thomson [Royaume-Uni]

Source :

RBID : Hal:pasteur-01117702

Abstract

Shigella are human-adapted Escherichia coli that have gained the ability to invade the human gut mucosa and cause dysentery(1,2), spreading efficiently via low-dose fecal-oral transmission(3,4). Historically, S. sonnei has been predominantly responsible for dysentery in developed countries but is now emerging as a problem in the developing world, seeming to replace the more diverse Shigella flexneri in areas undergoing economic development and improvements in water quality(4-6). Classical approaches have shown that S. sonnei is genetically conserved and clonal(7). We report here whole-genome sequencing of 132 globally distributed isolates. Our phylogenetic analysis shows that the current S. sonnei population descends from a common ancestor that existed less than 500 years ago and that diversified into several distinct lineages with unique characteristics. Our analysis suggests that the majority of this diversification occurred in Europe and was followed by more recent establishment of local pathogen populations on other continents, predominantly due to the pandemic spread of a single, rapidly evolving, multidrug-resistant lineage.


Url:
DOI: 10.1038/ng.2369

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Hal:pasteur-01117702

Le document en format XML

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<orgName>Oxford University Clinical Research Unit [Ho Chi Minh City]</orgName>
<orgName type="acronym">OUCRU</orgName>
<desc>
<address>
<addrLine>190 Ben Ham Tu, District 5, Ho Chi Minh City</addrLine>
<country key="VN"></country>
</address>
<ref type="url">http://oucru.org/</ref>
</desc>
</hal:affiliation>
<country>Viêt Nam</country>
</affiliation>
</author>
<author>
<name sortKey="Parkhill, Julian" sort="Parkhill, Julian" uniqKey="Parkhill J" first="Julian" last="Parkhill">Julian Parkhill</name>
<affiliation wicri:level="1">
<hal:affiliation type="institution" xml:id="struct-232748" status="VALID">
<orgName>The Wellcome Trust Sanger Institute [Cambridge]</orgName>
<desc>
<address>
<addrLine>Hinxton, Cambridge CB10 1SA, UK</addrLine>
<country key="GB"></country>
</address>
<ref type="url">http://www.sanger.ac.uk/</ref>
</desc>
</hal:affiliation>
<country>Royaume-Uni</country>
</affiliation>
</author>
<author>
<name sortKey="Dougan, Gordon" sort="Dougan, Gordon" uniqKey="Dougan G" first="Gordon" last="Dougan">Gordon Dougan</name>
<affiliation wicri:level="1">
<hal:affiliation type="institution" xml:id="struct-232748" status="VALID">
<orgName>The Wellcome Trust Sanger Institute [Cambridge]</orgName>
<desc>
<address>
<addrLine>Hinxton, Cambridge CB10 1SA, UK</addrLine>
<country key="GB"></country>
</address>
<ref type="url">http://www.sanger.ac.uk/</ref>
</desc>
</hal:affiliation>
<country>Royaume-Uni</country>
</affiliation>
</author>
<author>
<name sortKey="Thomson, Nicholas R" sort="Thomson, Nicholas R" uniqKey="Thomson N" first="Nicholas R" last="Thomson">Nicholas R. Thomson</name>
<affiliation wicri:level="1">
<hal:affiliation type="institution" xml:id="struct-232748" status="VALID">
<orgName>The Wellcome Trust Sanger Institute [Cambridge]</orgName>
<desc>
<address>
<addrLine>Hinxton, Cambridge CB10 1SA, UK</addrLine>
<country key="GB"></country>
</address>
<ref type="url">http://www.sanger.ac.uk/</ref>
</desc>
</hal:affiliation>
<country>Royaume-Uni</country>
</affiliation>
</author>
</analytic>
<idno type="DOI">10.1038/ng.2369</idno>
<series>
<title level="j">Nature Genetics</title>
<idno type="ISSN">1061-4036</idno>
<imprint>
<date type="datePub">2012-08-05</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc>
<textClass></textClass>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">
<p>Shigella are human-adapted Escherichia coli that have gained the ability to invade the human gut mucosa and cause dysentery(1,2), spreading efficiently via low-dose fecal-oral transmission(3,4). Historically, S. sonnei has been predominantly responsible for dysentery in developed countries but is now emerging as a problem in the developing world, seeming to replace the more diverse Shigella flexneri in areas undergoing economic development and improvements in water quality(4-6). Classical approaches have shown that S. sonnei is genetically conserved and clonal(7). We report here whole-genome sequencing of 132 globally distributed isolates. Our phylogenetic analysis shows that the current S. sonnei population descends from a common ancestor that existed less than 500 years ago and that diversified into several distinct lineages with unique characteristics. Our analysis suggests that the majority of this diversification occurred in Europe and was followed by more recent establishment of local pathogen populations on other continents, predominantly due to the pandemic spread of a single, rapidly evolving, multidrug-resistant lineage.</p>
</div>
</front>
</TEI>
</record>

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