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Epidemiology of Clostridium difficile in infants in Oxfordshire, UK: Risk factors for colonization and carriage, and genetic overlap with regional C. difficile infection strains.

TitleEpidemiology of Clostridium difficile in infants in Oxfordshire, UK: Risk factors for colonization and carriage, and genetic overlap with regional C. difficile infection strains.
Publication TypeJournal Article
Year of Publication2017
AuthorsStoesser, N., Eyre D. W., T Quan P., Godwin H., Pill G., Mbuvi E., Vaughan A., Griffiths D., Martin J., Fawley W., Dingle K. E., Oakley S., Wanelik K., Finney J. M., Kachrimanidou M., Moore C. E., Gorbach S., Riley T. V., Crook D. W., Peto T. E. A., Wilcox M. H., & A Walker S.
Corporate AuthorsModernising Medical Microbiology Informatics Group(MMMIG)
JournalPLoS One
Volume12
Issue8
Paginatione0182307
Date Published2017
ISSN1932-6203
KeywordsCarrier State, Clostridium difficile, Clostridium Infections, Cluster Analysis, Cross Infection, Diarrhea, DNA, Bacterial, Evolution, Molecular, Feces, Female, Genetic Variation, Humans, Infant, Infant, Newborn, Male, Prevalence, Risk Factors, Sequence Analysis, DNA, United Kingdom
Abstract

BACKGROUND: Approximately 30-40% of children <1 year of age are Clostridium difficile colonized, and may represent a reservoir for adult C. difficile infections (CDI). Risk factors for colonization with toxigenic versus non-toxigenic C. difficile strains and longitudinal acquisition dynamics in infants remain incompletely characterized.METHODS: Predominantly healthy infants (≤2 years) were recruited in Oxfordshire, UK, and provided ≥1 fecal samples. Independent risk factors for toxigenic/non-toxigenic C. difficile colonization and acquisition were identified using multivariable regression. Infant C. difficile isolates were whole-genome sequenced to assay genetic diversity and prevalence of toxin-associated genes, and compared with sequenced strains from Oxfordshire CDI cases.RESULTS: 338/365 enrolled infants provided 1332 fecal samples, representing 158 C. difficile colonization or carriage episodes (107[68%] toxigenic). Initial colonization was associated with age, and reduced with breastfeeding but increased with pet dogs. Acquisition was associated with older age, Caesarean delivery, and diarrhea. Breastfeeding and pre-existing C. difficile colonization reduced acquisition risk. Overall 13% of CDI C. difficile strains were genetically related to infant strains. 29(18%) infant C. difficile sequences were consistent with recent direct/indirect transmission to/from Oxfordshire CDI cases (≤2 single nucleotide variants [SNVs]); 79(50%) shared a common origin with an Oxfordshire CDI case within the last ~5 years (0-10 SNVs). The hypervirulent, epidemic ST1/ribotype 027 remained notably absent in infants in this large study, as did other lineages such as STs 10/44 (ribotype 015); the most common strain in infants was ST2 (ribotype 020/014)(22%).CONCLUSIONS: In predominantly healthy infants without significant healthcare exposure C. difficile colonization and acquisition reflect environmental exposures, with pet dogs identified as a novel risk factor. Genetic overlap between some infant strains and those isolated from CDI cases suggest common community reservoirs of these C. difficile lineages, contrasting with those lineages found only in CDI cases, and therefore more consistent with healthcare-associated spread.

DOI10.1371/journal.pone.0182307
Alternate JournalPLoS One
PubMed ID28813461
PubMed Central IDPMC5559064

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