The Vexed Relationship Between Clostridium Difficile and Inflammatory Bowel Disease: An Assessment of Carriage in an Outpatient Setting Among Patients in Remission

Clayton, Evelyn M.; Rea, Mary C.; Shanahan, Fergus; Quigley, Eamonn Martin; Kiely, Barry; Hill, Colin; Ross, R. Paul

doi:10.1038/ajg.2009.4

Cited by 177 publications

(141 citation statements)

References 35 publications

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“…Recent reports suggest a high prevalence of CDI in asymptomatic IBD patients. Clayton et al (34) in a retrospective study including 64 patients with UC and 58 with CD, all in clinical remission and without recent exposure to antibiotics, corticosteroids, immunomodulatory drugs or recent hospitalization, found that that the frequency of toxigenic C. difficile was higher in IBD patients than in healthy volunteers (8.2 vs. 1.0%; p=0.02), which is consistent with community-acquired infection.…”

Section: Introductionmentioning

confidence: 52%

“…Schneeweiss et al (36) found that corticosteroid initiation tripled the risk of CDI among the IBD patients (relative risk 3.4, 95% CI 1.9-6.1), while no such association with the initiation of immunomodulators or biologics (infliximab) was found. Biological agents (e.g., infliximab, adalimumab) are not associated with increased risk of CDI in IBD patients (36), nor is the use of aminosalicylates (34). PPI use in non-IBD patients has been suggested to increase the risk for CDI (6), but other studies did not find any association between PPI use and CDI in IBD patients (10).…”

Section: Risk Factorsmentioning

confidence: 89%

“…Asymptomatic carriage in IBD patients (remission/inactive disease) is more frequent than in general population. Screening for asymptomatic carriers in the general population is not recommended (34), but screening and treatment of asymptomatic IBD patients under immunosuppressant therapy may be important (8).…”

Section: Diagnosismentioning

confidence: 99%

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Clostridium difficile infection and inflammatory bowel disease

Cojocariu

Stanciu

Stoica³

et al. 2020

Turk J Gastroenterol

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Over the past 15 years, Clostridium difficile infection (CDI) in patients with inflammatory bowel disease (IBD) has increased both in incidence and severity. Traditional risk factors for CDI are similar in IBD and non-IBD populations, but there is a significant proportion of IBD patients which have distinctive characteristics. Patients with ulcerative colitis (UC) are more susceptible to CDI and have more severe outcomes than those with Crohn's disease (CD). CDI may be difficult to distinguish from an IBD flare due to similar clinical presentation, and therefore screening for CDI is recommended at every flare in such patients. Several studies showed worse clinical outcomes in IBD patients with CDI, including longer hospital stay, higher colectomy and mortality rates than in those without CDI. Vancomycin and metronidazole appear to have similar efficacy in patients with moderate disease, but vancomycin is preferred in severe disease. Measures must be taken to prevent the spread of infection. Clinicians should have a high index of suspicion for CDI when evaluating a patient with IBD flare, as rapid detection and prompt treatment of infection improve outcomes. This review summarizes the available literature on epidemiology, risk factors, clinical aspects, diagnostic methods, treatment, outcome, and prevention of CDI in IBD patients.

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Section: Introductionmentioning

confidence: 52%

Section: Risk Factorsmentioning

confidence: 89%

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Clostridium difficile infection and inflammatory bowel disease

Cojocariu

Stanciu

Stoica³

et al. 2020

Turk J Gastroenterol

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“…Several studies have linked acute bacterial enteritis with the onset or exacerbation of UC with causative agents including but not exclusively, Clostridium difficile, 11,105,106 Yersinia enterocolitica, 107,108 Campylobacter jejuni 109 and Salmonella spp. [109][110][111][112] It has been suggested that infection…”

Section: Ulcerative Colitis and Bacteriamentioning

confidence: 99%

“…Furthermore, reduced expression of human alpha-defensins in IBD patients may also play a role. 125 Since asymptomatic carriage of C. difficile exists in IBD patients 105 the main practical implication is that all patients with relapse of IBD should have a fecal sample checked for C. difficile, especially those receiving immunosuppressant therapy since this is known to be a risk factor for infection.…”

Section: Ulcerative Colitis and Bacteriamentioning

confidence: 99%

The Role of Bacteria in the Pathogenesis of Inflammatory Bowel Disease

Friswell¹,

Campbell²,

Rhodes³

2010

Gut Liver

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Crohn's disease (CD) and ulcerative colitis (UC) have features that suggest bacterial involvement, and all genetic models of inflammatory bowel disease (IBD) require the presence of commensal bacteria. CD is associated with innate immune response genes such as NOD2/CARD15 and the autophagy genes ATG16L1 and IRGM. However, IBD responds to immunosuppression, suggesting that any bacteria involved are not acting as conventional pathogens. Molecular techniques are rapidly advancing our knowledge of the gut microbiota. In CD there is reduced diversity, and notably a reduction in the probiotic Faecalibacterium prausnitzii, the presence of which in the terminal ileum is associated with a reduced risk of recurrence following surgery. There is also a consistent increase in mucosa-associated Escherichia coli with an "adherent and invasive" phenotype, which allows them to replicate inside macrophages and induce granulomas. Speculation that CD could be caused by the Mycobacterium avium subspecies paratuberculosis (MAP) continues. The response to antitumor necrosis factor treatments suggests that, if relevant at all, MAP is not acting as a conventional pathogen. However, there is increased colonization by MAP in CD, and there is evidence that it could have an indirect effect mediated by the suppression of macrophage function. UC relapse is frequently associated with infection by pathogens, but there is less evidence for involvement of a specific bacterial species. Poor barrier integrity followed by an inflammatory reaction to bacterial components, with chronicity maintained by an autoimmune process, seems a plausible pathogenic model. Bacterial theories of pathogenesis are now becoming testable by targeted therapeutic interventions.

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