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dc.contributor.authorClayton, Evelyn M
dc.contributor.authorRea, Mary C
dc.contributor.authorShanahan, Fergus
dc.contributor.authorQuigley, Eamonn M M
dc.contributor.authorKiely, Barry
dc.contributor.authorHill, Colin
dc.contributor.authorRoss, R Paul
dc.date.accessioned2012-01-10T11:44:12Z
dc.date.available2012-01-10T11:44:12Z
dc.date.issued2009-05
dc.identifier.citationThe vexed relationship between Clostridium difficile and inflammatory bowel disease: an assessment of carriage in an outpatient setting among patients in remission. 2009, 104 (5):1162-9 Am. J. Gastroenterol.en
dc.identifier.issn1572-0241
dc.identifier.pmid19319128
dc.identifier.doi10.1038/ajg.2009.4
dc.identifier.urihttp://hdl.handle.net/10147/201210
dc.descriptionOBJECTIVES: Comorbidity with Clostridium difficile may cause diagnostic delay in newly presenting inflammatory bowel disease (IBD) patients, trigger relapse in established disease, confound therapies, and serve as an indicator of an underlying defect in innate immunity. Retrospective analyses have suggested community acquisition; to address this we conducted a prospective analysis of C. difficile carriage in IBD patients using molecular methods specifically in an outpatient setting. METHODS: Recruited participants had long-standing diagnoses of ulcerative colitis (n = 64) and Crohn's disease (n = 58), were in clinical remission, and had no recent exposure to antibiotics, corticosteroids, immunomodulatory drugs or recent hospitalization. Isolates were cultured from stools and confirmed by 16S sequencing. The antibiotic susceptibilities of the isolates were tested followed by further strain characterization by toxinotyping, ribotyping, and pulsed-field gel electrophoresis (PFGE). RESULTS: The frequency of toxigenic C. difficile was higher in IBD patients than in healthy volunteers at 8.2 and 1.0%, respectively (P = 0.02 Fisher's exact test). All strains belonged to toxinotype 0 with rare subtypes of this group noted in five isolates and represented by an altered repressor genotype. Patients harbored a diverse range of toxigenic ribotype groups, including those previously associated with C. difficile-associated disease (CDAD) (R015, R005, and R020) and the rarer types R062, R050, and R003. Interestingly, common nosocomial groups were not identified. The considerable nonclonal distribution of distinct strains was further demonstrated by PFGE genomic fingerprinting. None of the study subjects experienced a clinical episode of CDAD during a 6-month period of follow-up. CONCLUSIONS: Detection of C. difficile is increased in IBD outpatients in remission, and strain diversity is consistent with community acquisition from a multitude of sources.en
dc.description.abstractComorbidity with Clostridium difficile may cause diagnostic delay in newly presenting inflammatory bowel disease (IBD) patients, trigger relapse in established disease, confound therapies, and serve as an indicator of an underlying defect in innate immunity. Retrospective analyses have suggested community acquisition; to address this we conducted a prospective analysis of C. difficile carriage in IBD patients using molecular methods specifically in an outpatient setting.
dc.description.abstractRecruited participants had long-standing diagnoses of ulcerative colitis (n = 64) and Crohn's disease (n = 58), were in clinical remission, and had no recent exposure to antibiotics, corticosteroids, immunomodulatory drugs or recent hospitalization. Isolates were cultured from stools and confirmed by 16S sequencing. The antibiotic susceptibilities of the isolates were tested followed by further strain characterization by toxinotyping, ribotyping, and pulsed-field gel electrophoresis (PFGE).
dc.description.abstractThe frequency of toxigenic C. difficile was higher in IBD patients than in healthy volunteers at 8.2 and 1.0%, respectively (P = 0.02 Fisher's exact test). All strains belonged to toxinotype 0 with rare subtypes of this group noted in five isolates and represented by an altered repressor genotype. Patients harbored a diverse range of toxigenic ribotype groups, including those previously associated with C. difficile-associated disease (CDAD) (R015, R005, and R020) and the rarer types R062, R050, and R003. Interestingly, common nosocomial groups were not identified. The considerable nonclonal distribution of distinct strains was further demonstrated by PFGE genomic fingerprinting. None of the study subjects experienced a clinical episode of CDAD during a 6-month period of follow-up.
dc.description.abstractDetection of C. difficile is increased in IBD outpatients in remission, and strain diversity is consistent with community acquisition from a multitude of sources.
dc.language.isoenen
dc.subject.meshAdolescent
dc.subject.meshAdult
dc.subject.meshAge Distribution
dc.subject.meshAmbulatory Care
dc.subject.meshBacterial Toxins
dc.subject.meshCarrier State
dc.subject.meshCase-Control Studies
dc.subject.meshClostridium Infections
dc.subject.meshClostridium difficile
dc.subject.meshColitis, Ulcerative
dc.subject.meshComorbidity
dc.subject.meshCrohn Disease
dc.subject.meshFemale
dc.subject.meshFollow-Up Studies
dc.subject.meshHumans
dc.subject.meshIncidence
dc.subject.meshInflammatory Bowel Diseases
dc.subject.meshMale
dc.subject.meshMicrobial Sensitivity Tests
dc.subject.meshMiddle Aged
dc.subject.meshProbability
dc.subject.meshReference Values
dc.subject.meshRemission, Spontaneous
dc.subject.meshSeverity of Illness Index
dc.subject.meshSex Distribution
dc.subject.meshYoung Adult
dc.titleThe vexed relationship between Clostridium difficile and inflammatory bowel disease: an assessment of carriage in an outpatient setting among patients in remission.en
dc.typeArticleen
dc.contributor.departmentAlimentary Pharmabiotic Centre at Moorepark Food Research Centre, Teagasc, Fermoy Co., Cork, Ireland.en
dc.identifier.journalThe American journal of gastroenterologyen
dc.description.provinceMunster
html.description.abstractComorbidity with Clostridium difficile may cause diagnostic delay in newly presenting inflammatory bowel disease (IBD) patients, trigger relapse in established disease, confound therapies, and serve as an indicator of an underlying defect in innate immunity. Retrospective analyses have suggested community acquisition; to address this we conducted a prospective analysis of C. difficile carriage in IBD patients using molecular methods specifically in an outpatient setting.
html.description.abstractRecruited participants had long-standing diagnoses of ulcerative colitis (n = 64) and Crohn's disease (n = 58), were in clinical remission, and had no recent exposure to antibiotics, corticosteroids, immunomodulatory drugs or recent hospitalization. Isolates were cultured from stools and confirmed by 16S sequencing. The antibiotic susceptibilities of the isolates were tested followed by further strain characterization by toxinotyping, ribotyping, and pulsed-field gel electrophoresis (PFGE).
html.description.abstractThe frequency of toxigenic C. difficile was higher in IBD patients than in healthy volunteers at 8.2 and 1.0%, respectively (P = 0.02 Fisher's exact test). All strains belonged to toxinotype 0 with rare subtypes of this group noted in five isolates and represented by an altered repressor genotype. Patients harbored a diverse range of toxigenic ribotype groups, including those previously associated with C. difficile-associated disease (CDAD) (R015, R005, and R020) and the rarer types R062, R050, and R003. Interestingly, common nosocomial groups were not identified. The considerable nonclonal distribution of distinct strains was further demonstrated by PFGE genomic fingerprinting. None of the study subjects experienced a clinical episode of CDAD during a 6-month period of follow-up.
html.description.abstractDetection of C. difficile is increased in IBD outpatients in remission, and strain diversity is consistent with community acquisition from a multitude of sources.


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