In the 1980s, Mc Farland et al reported that 7% of patients admitted to a hospital and 28% of patients who were hospitalized had positive cultures for the organism.By the 1990s, the incidence of Indeed, in contrast to the incidence rates of other nosocomial infections, which declined from 2000 to 2009, the number of hospitalized patients with any CDI as a discharge diagnosis more than doubled in the same period, from approximately 139,000 to 336,600.Toxin A is an enterotoxin, and toxin B is a cytotoxin; both are high–molecular weight proteins capable of binding to specific receptors on the intestinal mucosal cells.
In Canada's Estrie region of Quebec, the incidence quadrupled in 2003 to 92.2 cases per 100,000 population.Toxin A is an enterotoxin that is responsible for the major manifestations of colitis in humans.In a murine model deficient in the neurokinin-1 receptor, protection against inflammation from toxin A was demonstrated. Downstream effects from this protective effect included decreased intestinal levels of tumor necrosis factor (TNF)-alpha and leukocyte myeloperoxidase.infection (CDI) commonly manifests as mild to moderate diarrhea, occasionally with abdominal cramping.Pseudomembranes (adherent, yellowish white plaques on the intestinal mucosa) are occasionally observed (see the images below).Note that although intravenous immunoglobulin (IVIG) and tigecycline have been used in patients with severe refractory disease, delaying surgery may lead to worse outcomes.(See Treatment and Medication.) produce 2 distinct toxins.Many of the adverse event reports involved patients who were elderly, had chronic and/or concomitant underlying medical conditions, or were taking broad-spectrum antibiotics that could have predisposed them to developing CDAD.In a longitudinal study of 16,781 older adults (mean age, 67.9 y), 404 of whom had been diagnosed with CDI at least once, major depression was associated with a 36% increase in the odds of developing an infection with Two genome-wide association studies (GWAS) found an association between a common polymorphism in the upstream promoter of the interleukin (IL)-8 gene and an increased risk for both the initial occurrence and the recurrence of CDI.Agents occasionally reported to cause the disease include aminoglycosides, trimethoprim-sulfamethoxazole, metronidazole, chloramphenicol, tetracycline, imipenem, and meropenem.A multicenter retrospective (2010-2015) study of 100,615 pairs of patients who sequentially occupied a given hospital bed found that less than 1% (576 pairs; 0.57%) of subsequent patients developed CDI, regardless of whether they themselves received antibiotics or not.