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dc.contributor.authorDearlove, Bethany
dc.contributor.authorCody, Alison J
dc.contributor.authorPascoe, Ben
dc.contributor.authorMéric, Guillaume
dc.contributor.authorWilson, Daniel J
dc.contributor.authorSheppard, Samuel K
dc.date.accessioned2015-07-24T11:26:48Z
dc.date.available2015-07-24T11:26:48Z
dc.date.issued2016-03
dc.identifier.citationDearlove et al. The ISME Journal (2016), 10(3), pp. 721–729. doi: 10.1038/ismej.2015.149
dc.identifier.issn1751-7362
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/249058
dc.description.abstractCampylobacter jejuni and Campylobacter coli are the biggest causes of bacterial gastroenteritis in the developed world, with human infections typically arising from zoonotic transmission associated with infected meat. Because Campylobacter is not thought to survive well outside the gut, host-associated populations are genetically isolated to varying degrees. Therefore, the likely origin of most strains can be determined by host-associated variation in the genome. This is instructive for characterizing the source of human infection. However, some common strains, notably isolates belonging to the ST-21, ST-45 and ST-828 clonal complexes, appear to have broad host ranges, hindering source attribution. Here whole-genome sequencing has the potential to reveal fine-scale genetic structure associated with host specificity. We found that rates of zoonotic transmission among animal host species in these clonal complexes were so high that the signal of host association is all but obliterated, estimating one zoonotic transmission event every 1.6, 1.8 and 12 years in the ST-21, ST-45 and ST828 complexes, respectively. We attributed 89% of clinical cases to a chicken source, 10% to cattle and 1% to pig. Our results reveal that common strains of C. jejuni and C. coli infectious to humans are adapted to a generalist lifestyle, permitting rapid transmission between different hosts. Furthermore, they show that the weak signal of host association within these complexes presents a challenge for pinpointing the source of clinical infections, underlining the view that whole-genome sequencing, powerful though it is, cannot substitute for intensive sampling of suspected transmission reservoirs.
dc.description.sponsorshipThis study was supported by the Oxford NIHR Biomedical Research Centre and the UKCRC Modernising Medical Microbiology Consortium, the latter funded under the UKCRC Translational Infection Research Initiative supported by the Medical Research Council, the Biotechnology and Biological Sciences Research Council and the National Institute for Health Research on behalf of the UK Department of Health (Grant G0800778) and the Wellcome Trust (Grant 087646/Z/08/Z). BLD is supported by a Medical Research Council Methodology Research Programme grant (grant number MR/J013862/1). AJC was supported by the United Kingdom Department for Environment, Food, and Rural Affairs and Food Standards Agency (grant number OZ0624). DJW is a Sir Henry Dale Fellow, jointly funded by the Wellcome Trust and the Royal Society (Grant 101237/Z/13/Z). SKS is funded by the Biotechnology and Biological Sciences Research Council (BBSRC), the Medical Research Council (MR/L015080/1) and the Wellcome Trust. This publication made use of the Campylobacter Multi Locus Sequence Typing website (http://pubmlst.org/ campylobacter/) developed by Keith Jolley and sited at the University of Oxford (24). The development of this site has been funded by the Wellcome Trust.
dc.languageEnglish
dc.language.isoen
dc.publisherSpringer Science and Business Media LLC
dc.rightsAttribution 2.0 UK: England & Wales
dc.rights.urihttp://creativecommons.org/licenses/by/2.0/uk/
dc.subjectattribution
dc.subjectCampylobacter
dc.subjectmultilocus sequence typing
dc.subjecttransmission
dc.subjectzoonosis
dc.titleRapid host switching in generalist Campylobacter strains erodes the signal for tracing human infections.
dc.typeArticle
dc.description.versionThis is the final version of the article. It first appeared from Nature Publishing Group via http://dx.doi.org/10.1038/ismej.2015.149
prism.endingPage729
prism.publicationDate2015
prism.publicationNameISME J
prism.startingPage721
prism.volume10
dc.rioxxterms.funderNIHR
dc.rioxxterms.funderWellcome Trust
dc.rioxxterms.funderWellcome Trust
dc.rioxxterms.funderMRC
dc.rioxxterms.funderMRC
dc.rioxxterms.funderBBSRC
dc.rioxxterms.projectidG0800778
dc.rioxxterms.projectid087646/Z/08/Z
dc.rioxxterms.projectid101237/Z/13/Z
dc.rioxxterms.projectidMR/J013862/1
dc.rioxxterms.projectidMR/L015080/1
dcterms.dateAccepted2015-07-21
rioxxterms.versionofrecord10.1038/ismej.2015.149
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.licenseref.startdate2015-08-25
dc.contributor.orcidDearlove, Bethany [0000-0003-3653-4592]
dc.contributor.orcidPascoe, Ben [0000-0001-6376-5121]
dc.identifier.eissn1751-7370
rioxxterms.typeJournal Article/Review
pubs.funder-project-idMedical Research Council (MR/J013862/1)
pubs.funder-project-idMedical Research Council (G0800778)
cam.issuedOnline2015-08-25


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Except where otherwise noted, this item's licence is described as Attribution 2.0 UK: England & Wales