Clostridium difficile colitis



Clostridium difficile colitis

Overview of Clostridium difficile colitis

C. difficile was first identified in 1935. At that time, C. difficile was found to be a part of the normal bacterial colonic flora in newborns and was subsequently shown to produce a toxin that was lethal in mice, although it was not linked to clinical disease in humans. In addition, clinicians had observed pseudo membranous changes in the intestinal tract, which are characterized as inflammation of the colon and white or yellow plaques consisting of white blood cells and inflammatory debris. Subsequently called pseudo membranous colitis (PMC), these findings were generally considered to be a complication of colonic, pelvic, or gastric surgeries. Following the introduction of antimicrobials in the 1950s, most felt that pseudo membrane formation and antibiotic use were associated, although most deemed Staphylococcus aureus or Candida albicans as the causative organisms. Forty years later, in 1974, Tedesco et al. published a report of high rates of PMC among patients at Barnes Hospital who were receiving clindamycin. Stool cultures of these patients were negative for S. aureus, suggesting that this 'clindamycin-associated colitis' might be related to other pathogens. Further investigation revealed that C. difficile toxin was present within the Barnes Hospital population and in other available stool specimens from patients with diarrheal disease of unknown etiology. A few years later, Bartlett et al. proved that colitis induced by clindamycin in hamsters was indeed caused by C. difficile, while Larson et al. showed that C. difficile cytotoxin was present in the stools of patients with histologically-confirmed pseudo membranous colitis. Since the late 1970s, C. difficile has become the most common cause of hospital-acquired infectious diarrhea and has been recognized as a significant cause of morbidity and mortality (Dotan, 2009, 63).

Clinical Presentation of Clostridium difficile Infection

The clinical presentation of CDI ranges from asymptomatic colonization to pseudo membranous colitis with severe diarrhea. Mild C. difficile disease typically presents as acute watery diarrhea, occurring up to but most often less than 10 bowel movements per day. These patients usually do not have systemic symptoms, although colonic inflammation can typically be identified by endoscopy or computed tomography (CT) scan. Patients with severe cases of CDI can present with watery diarrhea, occurring up to 15-20 times per day. Severe disease is typically accompanied with lower abdominal pain and cramping, fevers, and marked increases in white blood cell counts. Fulminant C. difficile colitis (i.e., sudden and severe colitis) occurs in approximately 3-8% of cases. Patients with fulminant disease may experience systemic complications such as nausea, vomiting, dehydration, lethargy, or tachycardia. Hospitalized patients at increased risk for fulminant colitis include those with leukocytosis, recent prior surgical therapy, a history of inflammatory bowel disease (IBD), immunosuppressant, or history of successfully treated CDI. The most severe cases of CDI may progress to toxic mega colon or paralytic ileus. These conditions may prevent passage of stool; therefore, if clinicians are highly suspicious of CDI, they must recognize that patients with severe disease may present without ...