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Article: Genomic investigation of a sequence type 67 Clostridium difficile causing community-acquired fulminant colitis in Hong Kong

TitleGenomic investigation of a sequence type 67 Clostridium difficile causing community-acquired fulminant colitis in Hong Kong
Authors
KeywordsHypervirulent
Clostridioides difficile
Binary toxin
Pathogenicity locus
Trehalose repressor
Issue Date2019
PublisherUrban und Fischer Verlag. The Journal's web site is located at http://www.elsevier.com/locate/ijmm
Citation
International Journal of Medical Microbiology, 2019, v. 309 n. 5, p. 270-273 How to Cite?
AbstractIn 2017, we identified a Clostridium difficile strain HKCD4 that caused community-acquired fulminant colitis in a previously healthy child. Phylogenetically, it belonged to clade 2, sequence type 67 and was resistant to fluoroquinolone and tetracycline. The strain was pathogenicity locus and binary toxin positive. It has a mutation in the trehalose repressor treR leading to the L172I substitution that was previously reported in the epidemic ribotype 027 lineage. HKCD4 has a tcdB sequence that shared very high identities with 3 highly virulent reference strains. It has a CpG depleted genome that is characteristic of hypervirulent C. difficile. The emergence of ST67 lineage with molecular feature of hypervirulence in the community is concerning and emphasizes the need for full characterization of strains causing severe disease in patients without classical risk factors.
Persistent Identifierhttp://hdl.handle.net/10722/272000
ISSN
2017 Impact Factor: 3.298
2015 SCImago Journal Rankings: 1.604

 

DC FieldValueLanguage
dc.contributor.authorCao, H-
dc.contributor.authorWong, SCY-
dc.contributor.authorYam, WC-
dc.contributor.authorLiu, MCJ-
dc.contributor.authorChow, KH-
dc.contributor.authorWu, AKL-
dc.contributor.authorHo, PL-
dc.date.accessioned2019-07-20T10:33:44Z-
dc.date.available2019-07-20T10:33:44Z-
dc.date.issued2019-
dc.identifier.citationInternational Journal of Medical Microbiology, 2019, v. 309 n. 5, p. 270-273-
dc.identifier.issn1438-4221-
dc.identifier.urihttp://hdl.handle.net/10722/272000-
dc.description.abstractIn 2017, we identified a Clostridium difficile strain HKCD4 that caused community-acquired fulminant colitis in a previously healthy child. Phylogenetically, it belonged to clade 2, sequence type 67 and was resistant to fluoroquinolone and tetracycline. The strain was pathogenicity locus and binary toxin positive. It has a mutation in the trehalose repressor treR leading to the L172I substitution that was previously reported in the epidemic ribotype 027 lineage. HKCD4 has a tcdB sequence that shared very high identities with 3 highly virulent reference strains. It has a CpG depleted genome that is characteristic of hypervirulent C. difficile. The emergence of ST67 lineage with molecular feature of hypervirulence in the community is concerning and emphasizes the need for full characterization of strains causing severe disease in patients without classical risk factors.-
dc.languageeng-
dc.publisherUrban und Fischer Verlag. The Journal's web site is located at http://www.elsevier.com/locate/ijmm-
dc.relation.ispartofInternational Journal of Medical Microbiology-
dc.subjectHypervirulent-
dc.subjectClostridioides difficile-
dc.subjectBinary toxin-
dc.subjectPathogenicity locus-
dc.subjectTrehalose repressor-
dc.titleGenomic investigation of a sequence type 67 Clostridium difficile causing community-acquired fulminant colitis in Hong Kong-
dc.typeArticle-
dc.identifier.emailCao, H: hcao@hku.hk-
dc.identifier.emailWong, SCY: wcy288@HKUCC-COM.hku.hk-
dc.identifier.emailYam, WC: wcyam@hku.hk-
dc.identifier.emailChow, KH: khchowb@hku.hk-
dc.identifier.emailWu, AKL: alanklwu@hkucc.hku.hk-
dc.identifier.emailHo, PL: plho@hku.hk-
dc.identifier.authorityYam, WC=rp00313-
dc.identifier.authorityChow, KH=rp00370-
dc.identifier.authorityHo, PL=rp00406-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.ijmm.2019.05.003-
dc.identifier.pmid31113737-
dc.identifier.scopuseid_2-s2.0-85065777517-
dc.identifier.hkuros298359-
dc.identifier.volume309-
dc.identifier.issue5-
dc.identifier.spage270-
dc.identifier.epage273-
dc.publisher.placeGermany-

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