In the early 1970's clindamycin, an antibiotic used to help treat infection, was just on the market for a few months. It was noted by physicians that patients taking clindamycin were getting more and more recurrent episodes of diarrhea and colitis. Three gastroenterology fellows, decided to gather data on the subject. They found that no pathogenic organisms could be cultured on any of the 16 patients, all 16 subjects had severe colitis, and 7 of them had pseudomembranous colitis. Unfortunately, 4 of the 16 patients died. (Bartlett, 2008)
Several possibilities of etiology were considered including clindamycin related allergy or toxicity, bowel ischemia possibly induced by the antibiotic, an altered natural bacterial flora in the gut, or even the emergence of a new bacterial pathogen or virus. As the fellows did not have a definitive etiology for the disease, they treated the patients as they would for a patient with ulcerative colitis. A few years later Clostridium…show more content… C. difficile is a very common normal flora found in the gut and intestinal tract and does not usually cause any problems to the individual. However, in some cases, the C.difficile bacteria becomes too abundant and overcrowds the other naturally occurring bacteria. (New York State Deparment of Health, 2012) In this case, the C.difficile excretes 2 protein exotoxins, A and B, into the intestines that causes mucosal damage and inflammation. Toxin A is responsible for the colitis that allows Toxin B, a potent cytotoxin, to enter the cell. The binding of the 2 toxins produce the inflammation of the mucosa and secrete an exudate that contains neutrophils, monocytes, and sloughed enterocytes. Patients usually have symptoms including abdominal cramping, watery diarrhea, and intestinal damage. The clinical manifestations is greatly dependent on how quickly the serum antibody responds to the toxin. (Hamm,
