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Etiology of Community Acquired Clostridium
Difficile-Associated Disease

By: Shannan Sherman and Dr. Pamela Ark | Mentor: Dr. Pamela Ark



Simor, Yake, and Tsimidis (1993) found urinary and fecal incontinence to be a risk factor for CA-CDAD. The risk for infection may be due to an increase risk for fecal-oral transmission. Results from pulse-field gel electrophoresis showed diversity among the strains carried by each resident, suggesting the origin of infection is endogenous rather than exogenous. Exogenous bacteria are introduced internally to the gastrointestinal tract from the external world. Endogenous bacteria are part of our body's normal flora.

In their study, which was similar in form to others, Hirschhorn, Trnka, Onderdonk, Lee and Platt (1994) found underlying disease and gastrointestinal conditions such as inflammatory bowel disease to be a risk factor.

Both the number of comorbidities and the presence of lower intestinal conditions were significant risk factors for CDAD in a study conducted by McFarland, Clarridge, Beneda, and Raugi (2007). These conditions affect normal intestinal microflora similarly to antibiotics, thereby increasing the risk for CDAD. People who have inflammatory bowel disease have a disrupted colonic flora. Lower intestinal conditions such as polyps may alter the body's normal ability to resist overgrowth (McFarland, Clarridge, Beneda & Raugi, 2007).


Noren et al. (2004) found that CDAD is usually due to endogenous infection. Apart from type SE17 strain being mostly nosocomial, no C. difficile strain had superior transmission ability or ability to cause recurrent infection.


Karlström et al. (1998) reported an increase in the number of CDAD. A total of 5, 133 CDAD cases were recorded in 1995, compared to 86 in 1978. A possible explanation for the increase is an increase in the number of broad-spectrum cephalosporins prescribed in Sweden during the study timeframe. Most of the patients with CA-CDAD had taken antibiotics prior to diagnsis.

Dial, Delaney, Barkun, and Suissa (2005) performed a large population study and found gastric acid suppressive drugs were associated with an increased risk of CA-CDAD. There was a greater association with proton pump inhibitors and CA-CDAD than H2-receptor antagonists. These results may rise because the degree of acid suppression is greater in proton pump inhibitors than H2-receptor antagonists. Furthermore, a decrease in gastric acid is known to be a risk factor for acquiring other causes of diarrhea, such as cholera. In addition, when gastric acid is suppressed, there is an association of colonization of the upper gastrointestinal tract, which is normally sterile (Dial, Delaney, Barkin & Suissa, 2005).

Although antibiotic exposure is a major risk factor for the disease, there is a significant number of CA-CDAD with no history of antibiotic use 90 days prior to diagnosis. CA-CDAD with no history of antibiotics is a trend seen in most published studies. Therefore, reliance on antibiotic history could contribute to missed diagnoses. However, exposure to antibiotics, especially cephalosporins, are still a leading risk factor.

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