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dc.contributor.authorE. Wickham, Mark
dc.contributor.authorLupp, Claudia
dc.contributor.authorMascarenhas, Mariola
dc.contributor.authorVazquez, Alejandra
dc.contributor.authorK. Coombes, Brian
dc.contributor.authorF. Brown, Nat
dc.contributor.authorA. Coburn, Bryan
dc.contributor.authorDeng, Wanyin
dc.contributor.authorL. Puente, Jose
dc.contributor.authorA. Karmali, Mohamed
dc.contributor.authorBrett Finlay, B.
dc.date.accessioned2017-05-03T12:25:15Z
dc.date.available2017-05-03T12:25:15Z
dc.date.issued2006
dc.date.modified2009-08-13T06:44:59Z
dc.identifier.issn00221899
dc.identifier.doi10.1086/506620
dc.identifier.urihttp://hdl.handle.net/10072/20473
dc.description.abstractAlthough O157:H7 Shiga toxin-producing Escherichia coli (STEC) are the predominant cause of hemolytic-uremic syndrome (HUS) in the world, non-O157:H7 serotypes are a medically important cause of HUS that are underdetected by current diagnostic approaches. Because Shiga toxin is necessary but not sufficient to cause HUS, identifying the virulence determinants that predict severe disease after non-O157 STEC infection is of paramount importance. Disease caused by O157:H7 STEC has been associated with a 26-gene pathogenicity island known as O island (OI) 122. To assess the public-health significance of this pathogenicity island, we examined the association between OI122 genes and outbreaks and HUS after non-O157 STEC infection. We found that a subset of OI122 genes is independently associated with outbreaks and HUS after infection with non-O157 STEC. The presence of multiple virulence genes in non-O157 serotypes strengthened this association, which suggests that the additive effects of a variable repertoire of virulence genes contribute to disease severity. In vivo, Citrobacter rodentium mutants lacking outbreak- and HUS-associated genes were deficient for virulence in mice; in particular, nleB mutant bacteria were unable to cause mortality in mice. The present study shows that virulence genes associated epidemiologically with outbreaks and HUS after non-O157 STEC infection are pivotal to the initiation, progression, and outcome of in vivo disease.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.format.extent1044388 bytes
dc.format.mimetypeapplication/pdf
dc.languageEnglish
dc.language.isoeng
dc.publisherChicago University Press
dc.publisher.placeChicago
dc.publisher.urihttps://academic.oup.com/jid/article/194/6/819/865488
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrom819
dc.relation.ispartofpageto827
dc.relation.ispartofissue6
dc.relation.ispartofjournalThe Journal of Infectious Diseases
dc.relation.ispartofvolume194
dc.rights.retentionN
dc.subject.fieldofresearchBiological Sciences
dc.subject.fieldofresearchMedical and Health Sciences
dc.subject.fieldofresearchcode06
dc.subject.fieldofresearchcode11
dc.titleBacterial genetic determinants of non-O157 STEC outbreaks and hemolytic-uremic syndrome after infection
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.rights.copyright© 2006 by University of Chicago Press. The attached file is reproduced here in accordance with the copyright policy of the publisher. First published in The Journal of Infectious Diseases with publishing partner the Infectious Diseases Society of America. Use hypertext link to access the journal's webpage.
gro.date.issued2006
gro.hasfulltextFull Text
gro.griffith.authorBrown, Nathaniel F.


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