Etiology
Broad-spectrum antibiotics disrupt the normal bowel flora, the most common causative agents being ampicillin, cephalosporins, clindamycin, carbapenems, and fluoroquinolones.[21]Clostridioides difficile colonization occurs after this disruption to bowel flora by ingestion of heat-resistant spores, which convert to vegetative forms in the colon.[22] Risk factors for an increased risk of colonization among hospitalized patients include hospitalization in the previous 6 months, tube feeding, and the use of gastric acid suppression therapy or corticosteroids in the previous 8 weeks.[23]
Transmission in the healthcare setting is most likely to be the result of person-to-person spread through the fecal-oral route (e.g., via the hands of healthcare workers), high-risk fomites (e.g., inadequately cleaned bedpans or rectal thermometers), or direct exposure to a contaminated environment. Patients with colonization who are asymptomatic may also contribute to the spread.[2]
Transmission between family members has been reported. A case-control study of 224,000 cases found that 4.8% of infections occurred following a diagnosis in a separate family member. This highlights the importance of a shared environment in the transmission of infection.[24]
Pathophysiology
The incubation period is generally 2 to 3 days, but may be more than one week.[2] Clostridioides difficile are gram-positive, anaerobic, spore-forming rods that produce toxins A and B. These toxins cause an inflammatory response in the large intestine, leading to increased vascular permeability and pseudomembrane formation.[3] Colonic pseudomembranes have a distinct appearance of adherent raised yellow and white plaques against an inflamed mucosa, and are composed of neutrophils, fibrin, mucin, and cellular debris.[3]
Toxin A is thought to play a more critical role than toxin B in the pathogenesis as it has been found to induce greater tissue damage and fluid accumulation in experimental animal models. Toxin B is thought to play a role only after the colonic mucosa has already been damaged by toxin A.[3]
Depending on host immune responses and whether or not the strain of C difficile is toxigenic, either an asymptomatic carrier state develops or a C difficile-associated disease. Asymptomatic carriers are less likely to have evidence of toxin formation.
Clinical manifestations usually occur on days 4 through 9 of antibiotic therapy but may occur up to 8 weeks after discontinuation of antibiotics.[22]
Debilitated patients may be unable to mount an immunogammaglobulin immune response to toxin A.[22]
Classification
Case surveillance[2]
Healthcare facility-onset:
Laboratory-identified Clostridioides difficile infection that occurs more than 3 days after admission to the facility (i.e., on or after day 4). Healthcare facilities should track these cases in order to detect increases in the number of cases and outbreaks.
Community-onset-healthcare facility-associated:
C difficile infection occurring within 28 days after discharge from a healthcare facility.
Community-associated:
C difficile infection with no documented overnight stay in a healthcare facility in the prior 12 weeks.
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