Clostridium difficile is a spore-forming, gram-positive anaerobic bacillus that was first recognized as a major cause of antibiotic-associated diarrhea in 1977.1 Some strains of the bacterium (so called "toxigenic strains") produce two toxins, toxin A, an enterotoxin, and toxin B, a cytotoxin. Infection with toxin-producing C. difficile may result in a wide spectrum of clinical illness ranging in severity from diarrhea to inflammation of the colon and pseudomembranous colitis, to toxic megacolon, and death.2 Symptoms can occur within a few days of starting antibiotic therapy or a few months following a course of antibiotic therapy.
C. difficile is shed in feces as a highly contagious and easily spread spore.3 The organism thrives on any surface, device, or material (e.g., commodes, bathing tubs, and electronic rectal thermometers) that becomes contaminated with feces. These surfaces may serve as a reservoir for the C. difficile spores and spores can be spread from patient to patient, patient to health-care worker to patient, or patient to inanimate object to patient.4
Diagnosis of CDAD can be confirmed by a number of different tests including culture of C. difficile, a cytotoxicity assay or detection of one of the toxins.5 Diagnosis can also be made by endoscopy and biopsy.5
Toxigenic C. difficile is now recognized as a frequent cause of antibiotic-associated diarrhea and colitis. It is implicated in 20 to 30 percent of patients with antibiotic-associated diarrhea, in 50 to 75 percent of those with antibiotic-associated colitis, and in more than 90 percent of those with antibiotic-associated pseudomembranous colitis.6 Vancocin® HCl Capsules (vancomycin hydrochloride capsules, USP) can be used to treat antibiotic-associated pseudomembranous colitis caused by C. difficile.
CDAD occurs most commonly in hospitalized patients. Most patients have been exposed to an antimicrobial agent (the most commonly implicated agents include third-generation cephalosporins, ampicillin or amoxicillin, and clindamycin).7 Other non-antimicrobial agents (such as doxorubicin, cisplatin, cyclophosphamide, and proton-pump inhibitors) have also been implicated as potential triggers for C. difficile disease.8,9 The exposure to an antimicrobial agent alters the microecology of the gut,4 making patients more susceptible to C. difficile acquisition and overgrowth. This, in addition to other risk factors, is likely to determine whether or not a patient develops C. difficile infection and what severity of disease ultimately presents.
For more information on C. difficile infection, please visit the CDC website here.