Diagnosis and Management of Clostridioides Difficile Infection in Patients With Inflammatory Bowel Disease

Rahul S. Dalal; Jessica R. Allegretti


Curr Opin Gastroenterol. 2021;37(4):336-343. 

In This Article

Clinical Features and Diagnosis of Clostridioides Difficile Infection in Inflammatory Bowel Disease

Recognizing CDI in the setting of active IBD presents a challenge, as the clinical presentations of these conditions are similar. A typical presentation of CDI in the general population includes watery diarrhea with associated abdominal cramping, nausea, and low-grade fever often in the setting of recent antibiotic therapy or healthcare exposure.[31] Common laboratory findings include an elevated white blood cell count to 15 000 cells/ml and the presence of fecal leukocytes.[32] Patients with IBD who develop CDI may have atypical clinical features including younger age, lack of recent antibiotic use, and community acquisition.[6,19,33]

When patients with IBD present with new or worsening diarrhea, stool testing for CDI is indicated regardless of recent antibiotic exposure.[23] A two-step approach for diagnosis is recommended.[34] An initial screen should be conducted with a highly sensitive test: either the enzyme immunoassays (EIAs) for clostridial glutamate dehydrogenase, which detects the presence of clostridia organisms, both toxigenic and nontoxigenic strains, or PCR for toxin genes. A positive screen is then followed by higher specificity testing using EIA for C. difficile toxins A and B. Patients who have a positive PCR for toxin genes but negative EIA for toxins A and B are colonized rather than infected. This two-step process ensures that patients with active CDI are treated and patients who are simply colonized with C. difficile undergo investigation for alternative causes for their symptoms. In a hospital-based study of universal screening for C. difficile, colonization via PCR testing was determined to be 4.2% of 47 048 patients screened over 3 years.[35] Asymptomatic carriage of C. difficile may be as high as 8% among patients with IBD.[6]

Sigmoidoscopy and biopsy plays a unique role in the assessment of IBD patients with concomitant CDI. The mucosal appearance in this setting may not allow for the differentiation of CDI from IBD, particularly as the hallmark pseudomembranes of CDI seen in the general population are rarely seen among patients with underlying IBD.[36] However, sigmoidoscopy can identify the extent and severity of inflammation and histologic examination of biopsies can potentially exclude other important causes of bloody diarrhea in this population, including cytomegalovirus infection, amoebiasis, and ischemic colitis.

Radiographic imaging does not provide characteristic features to differentiate CDI from IBD activation. However, patients who present with abdominal distention, fever, ileus, and/or hemodynamic instability require plain films or computed tomography of the abdomen and pelvis to exclude bowel perforation and toxic megacolon. Toxic megacolon is a potentially lethal complication of both severe CDI and IBD characterized by systemic toxicity and colonic dilatation to more than 6 cm.[37] Patients with toxic megacolon due to either CDI or IBD require supportive care, bowel rest, appropriate antimicrobial and/or immunosuppressive therapy, and surgical evaluation.