Abstract
Clostridium difficile remains the most common nosocomial cause of diarrhea and is becoming an increasingly important community-acquired infection.1,2 Antibiotic resistance, as well as the recently identified BI/NAP1/027 strain, is responsible for more cases of severe C difficile –associated diarrhea worldwide.3 The diagnosis of C difficile infection is usually based on a combination of history of antibiotic use, the presence of pseudomembranes on colonoscopy, appropriate histology on biopsy, and confirmatory laboratory stool tests for either the C difficile toxin or bacterial toxin genes. Most clinical laboratories employ a C difficile –associated toxin enzyme immunoassay (EIA). These assays are technically easy to perform and have a rapid turnaround time. Although they have specificities ranging from 65% to 100%, the sensitivities are limited, ranging from 31% to 99%.4 Recently, US Food and Drug Administration–approved, polymerase chain reaction (PCR)–based molecular assays performed on stool lysates have been increasingly recognized as the most sensitive and specific methods of diagnosing C difficile . These assays target C difficile toxin genes rather than the toxins themselves, with a sensitivity from 77% to 100% and a specificity from 93% to 99%.5–7 The tissue diagnosis of C difficile in a gastrointestinal mucosal biopsy specimen is generally straightforward, although some infections (eg, enterohemorrhagic Escherichia coli , Shigella , and toxin-producing Clostridium perfringens ) may produce similar features both macroscopically and morphologically. Ischemia is frequently in the histologic differential diagnosis as well, and the distinction between the two is extremely important because the treatments are different. In their article in this issue of the American Journal of Clinical Pathology , Wiland and colleagues8 examine the degree of interobserver agreement in the histologic diagnosis of C difficile colitis and correlate the histologic findings with clinical data. They also …
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