advertisement
On UrbanBaby: Are you glad you have siblings?
Find Articles in:
all
Business
Reference
Technology
News
Sports
Health
Autos
Arts
Home & Garden
advertisement

Content provided in partnership with
Thomson / Gale

Clostridium difficile—associated diarrhea

American Family Physician,  March 1, 2005  by Michael S. Schroeder

<< Page 1  Continued from page 2.  Previous | Next

C. difficile causes toxin-mediated colitis. Pathogenic strains of C. difficile produce two protein exotoxins: toxin A and toxin B. (1) Toxin A activates macrophages and mast cells. Activation of these cells causes the production of inflammatory mediators, which leads to fluid secretion and increased mucosal permeability. (1) Toxin B has little enterotoxic activity but is extremely cytotoxic in vitro. C. difficile toxins also cause leukocyte chemotaxis and the upregulation of cytokines and other inflammatory mediators. Consequently, there is a profound colonic inflammatory response, which is evidenced clinically by a high WBC count. (1) As colitis worsens, focal ulcerations occur, and the accumulation of purulent and necrotic debris forms the typical pseudomembrane. (9)

Most Popular Articles in Health
Fuel your workout: exercisers who eat before they work out have more energy ...
Soothe a dry, itchy scalp: 5 easy expert solutions
Cocktails and calories: Beer, wine and liquor calories can really add up. ...
The sour truth about apple cider vinegar - evaluation of therapeutic use
The, six best supplements you've never heard of: these secret weapons can ...
More »
advertisement

Diagnosis

The diagnosis of C. difficile-associated diarrhea requires a careful history, with particular emphasis on antibiotic use during the preceding three months (Figure 3). (18) The clinical presentation ranges from no symptoms to fulminant pseudomembranous colitis. A detailed description of the patient's diarrhea, including color, consistency, and frequency, is important in differentiating other causes of diarrhea from C. difficile-associated diarrhea. Other important factors include a history of fever, immunosuppression, a recent surgical procedure, previous infection with C. difficile, recent change in bowel habits, and the presence of abdominal symptoms (Table 1). (4,6) A selected differential diagnosis is provided in Table

[FIGURE 3 OMITTED]

The most common laboratory test for diagnosing C. difficile-mediated disease is an enzyme immunoassay that detects toxins A and B. This test provides results within two to six hours and has a specificity of 93 to 100 percent. The sensitivity is 63 to 99 percent, which means that false-negative results can occur. (13-16) However, the majority of combination enzyme immunoassays have a sensitivity of 85 to 95 percent. (8) The immunoassay should not be used as an indicator of response to therapy because results remain positive for extended periods in 25 percent of successfully treated patients. (8)

The gold standard for the diagnosis of C. difficile-mediated disease is a cytotoxin assay. Although this test is highly sensitive and specific, it is difficult to perform, and results are not available for 24 to 48 hours. C. difficile can be cultured. However, culture is not specific for pathogenic toxin-producing C. difficile strains and, therefore, is not clinically helpful except for strain typing in outbreaks of nosocomial infection. (9)

A combination immunoassay that is currently in development tests for C. difficile-specific glutamate dehydrogenase (sensitivity: 97 percent) and toxins A and B (specificity: 97 to 99 percent). The advantages of this test are same-day turnaround and a high negative predictive value.16

An important indicator of impending fulminant colitis is a sudden rise in the peripheral WBC count to between 30,000 and 50,000 per [mm.sup.3] (30 to 50 x [10.sup.9] per L), often accompanied by significant bandemia. (4,17) Because progression to shock can occur even in patients who have had relatively benign symptoms for weeks, early warning signs such as the leukemoid reaction are invaluable. (4)