Mixed Bag: How C. Difficile Can Cause Pouchitis

Abstract

Clostridium difficile infection (CDI), a major cause of healthcare associated infections, has become a consistent frustration of hospital-based clinicians. Worldwide, the highest rates of hospital-associated CDI occur in North America, where an estimated 7.14 of 1000 hospital admissions are complicated by CDI [1]. Clostridium difficile is a fastidious spore-forming gram-positive anaerobic bacterium that causes infections ranging from mild diarrhea to fulminant colitis. One of the strongest risk factors for CDI is prior antibiotic exposure resulting presumably from the disruption of the intestinal microbiota, although a number of other risk factors have been identified. Infection with C. difficile occurs more commonly in patients with inflammatory bowel disease (IBD) compared to those without [2, 3]. The symptoms of active IBD and CDI can be clinically indistinguishable. Delayed recognition and treatment of CDI can result in serious morbidity as well as complicate treatment of the underlying IBD. Thus, early identification of CDI in IBD patients is of particular importance. Further, among hospitalized IBD patients, there have been repeated and consistent data associating CDI with increased mortality and longer, more costly hospital admissions [2, 3]. Patients with ulcerative colitis appear to be at higher risk of developing CDI than those with Crohn’s disease [2, 4]. Though the risk of CDI in IBD has been well characterized in the literature, there are limited data assessing the risk of CDI specifically in patients with ileal-pouch anal anastomosis (IPAA), as these patients are generally scarce and have been excluded from many clinical studies. Until recently, the description of CDI in IPAA patients has been limited to case reports and case series, which were reviewed in detail by Seril and Shen in 2014 [5]. A recent population-based study using administrative data identified 3470 IBD patients admitted to hospital with pouchitis, estimating that CDI occurs in 2.6% of these admissions [6]. Furthermore, there is a literature showing that CDI of the pouch may be manifest with more systemic symptoms (e.g., fever, night sweats, and weight loss) and is associated with higher rates of recurrent CDI and refractory infection [5]. In this issue of Digestive Diseases and Sciences, Gosai et al. further explore CDI among IPAA patients in a retrospective review of 160 IBD patients with pouchitis admitted to a tertiary care center over a three-year time period [7]. Of these patients, 72 underwent Clostridium difficile PCR testing over 96 hospital admissions with 16 (22%) diagnosed with CDI. In addition to patient and clinical factors that have previously been associated with CDI, the authors evaluated the association between body mass index (BMI) and CDI. Prior data from the same group had suggested that obesity and the obesity-related diseases, non-alcoholic fatty liver disease (NAFLD) and obstructive sleep apnea (OSA) were associated with increased risk of CDI among IBD patients with IPAA [6]. In contrast, the current study by Gosai et al. found that obesity was independently associated with a lower risk of CDI according to multivariable analysis. The prior association with obesity was identified in data available through a large national administrative database, whereas the current study reports the experience at a single expert center with detailed patient information. While administrative data can be very helpful at identifying signals within large groups of patients, the availability and reliability of patient-level data is often limited. Among patients with CDI, all were symptomatic with the majority (81%) reporting diarrhea, and half (50%) reporting abdominal pain. All of these patients had symptomatic relief with initiation of antibiotic treatment. Biochemical data typically associated with CDI severity (e.g., white blood count, albumin) were not assessed in this study. The typical risk factors that clinicians evaluate when considering CDI in non-IPAA patients were not replicated in this study. Specifically, the use of antibiotics, corticosteroids, biologic medications, and proton pump inhibitors, as * Michael J. Stewart [email protected]