Clostridium difficile infection (CDI) has been increasing in frequency and severity in patients with inflammatory bowel disease (IBD). Population based and single center studies have shown worse clinical outcomes in concomitant CDI and IBD, with several reporting longer length of hospital stay, higher colectomy rates and increased mortality. Clinically, CDI may be difficult to distinguish from an IBD flare and may range from an asymptomatic carrier state to severe life threatening colitis. The traditional risk factors for CDI have included hospitalization, antibiotic use, older age and severe co-morbid disease but IBD patients have several distinct characteristics including younger age, community acquisition, lack of antibiotic exposure, colonic IBD and steroid use. CDI can occur in the small bowel and specifically in ulcerative colitis patients who have had a colectomy and an ileal pouch anal anastomosis. PCR based assays and combination Elisa algorithms have improved the sensitivity and specificity of testing, though in IBD patients have raised clinical questions about how to best manage diarrhea in the setting of possible C. difficile colonization. Treatment modalities for CDI have not been examined in randomized clinical trials in the IBD population. Newer antibiotics, immunotherapy and fecal microbiota transplantation may alter current treatment strategies. This review will focus on the unique epidemiology of CDI in IBD patients, detail clinical disease states, and provide updated diagnostic strategies, prevention and treatment options.

Background In 10% to 15% of individuals, inflammatory bowel disease (IBD) is difficult to classify as ulcerative colitis (UC) or Crohn’s disease (CD). Previous work has demonstrated that probe-based elastic scattering spectroscopy (ESS) can produce spectra, informed by parameters like tissue ultrastructure and hemoglobin content, capable of differentiating pathologies. This study investigates whether ESS is an in vivo optical biomarker for the presence, activity, and type of IBD in the colon. Methods Pilot study, a retrospective data analysis. ESS spectra of endoscopically normal and inflamed colon were obtained from 48 patients with IBD and 46 non-IBD controls. Measurements from patients with IBD were categorized as CD or UC based on clinical diagnosis. Spectra were analyzed using high-dimensional methods. Leave-one-patient-out cross-validation was used to obtain diagnostic performance estimates. Results Patients with IBD were distinguishable from non-IBD controls with a sensitivity of 0.93 and specificity of 0.91 based on readings from endoscopically normal mucosa, and 0.94 and 0.93 from inflamed mucosa. In patients with IBD, histologically normal and inflamed colon were distinguishable with per-class accuracies of 0.83 and 0.89, respectively; histologically normal from inactive inflammation with accuracies of 0.73 and 0.89, respectively; and inactive from active colitis with accuracies of 0.87 and 0.84, respectively. The diagnosis of CD versus UC was made with per-class accuracies of 0.92 and 0.87 in normal and 0.87 and 0.85 in inflamed mucosa, respectively. Conclusions ESS, a simple, low-cost clinically friendly optical biopsy modality, has the potential to enhance the endoscopic assessment of IBD and its activity in real time and may help to distinguish CD from UC.

Background Clostridium difficile infection affects IBD patients. This study’s aim was to compare humoral response to C. difficile toxins in IBD and control outpatients. Methods We prospectively followed adult IBD and control subjects with serum and stool tested by PCR obtained at enrollment and during periods of CDI. Semi-quantitative serum levels of IgM, IgG and IgA to C. difficile toxins A and B were measured. Results 119 stool and 117 serum samples were obtained from 150 subjects. Different levels of IgA to toxin A (p=0.0016) and toxin B (p=0.0468) were noted between different IBD groups. Toxin A IgA levels were higher in the CD group (p=0.0321) and IPAA group (p=0.001) compared to the UC group and toxin B IgA levels were higher in the IPAA group compared to the UC group (p=0.0309). There were lower levels of toxin A IgA in IBD patients with compared with those in subjects without new CDI (P=0.0488) and higher levels in IBD patients with compared with those in subjects without CDI history before enrollment (P=0.016). There were nonsignificant lower toxin A IgG levels in IBD patients with compared to without prior CDI (p=0.095) and higher levels in controls with history of prior CDI compared to IBD patients with prior CDI (p=0.049). Conclusions UC patients have lower IgA levels to C. difficile toxins compared to Crohn’s and IPAA patients. IBD patients with prior CDI failed to demonstrate any increase in anti-toxin IgG. Our findings suggest that IBD patients may benefit from immunization strategies targeting C. difficile toxins.

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