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Clostridium difficile is a spore-forming, obligate anaerobic, Gram-positive bacillus, which can spread via the fecal-oral route. The most common manifestation of Clostridium difficile–associated disease (CDAD) is mediated by toxins A and B.1,2

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Epidemiology and Pathophysicology

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A recent U.S. study showed a rate of C difficile infection or colonization in hospitalized patients of 13 per 1,000, being one of the most widespread and serious healthcare-associated infections acquired in a hospital or long-term care facility.

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Risk factors for developing CDAD include having gastrointestinal surgery, having prolonged stays in health care facilities, being immunocompromised, undergoing proton-pump inhibitor therapy, and having a history of cancer.1,2Breastfeeding may offer some protective benefits. Treatment with antibiotics and other chemotherapeutic agents (eg, fluorouracil, methotrexate) can alter the natural GI flora and favor the emergence of C difficile.

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CDAD results directly from toxin-mediated effects to the large intestine. The exact incubation period is unknown, but symptoms are known to develop up to 6 weeks after the discontinuation of antibiotics.1,2 Infants and children are more likely to carry C difficile asymptomatically in the GI tract than adults; it is estimated that 15% to 63% of neonates, 3% to 33% of infants and toddlers younger than two years of age, and up to 8.3% of children older than two years of age are asymptomatic carriers. Because the rates of symptomatic carriage (coexisting diarrhea) are not dissimilar to that for asymptomatic carriage, it is often difficult to establish a clear role for C difficile in causing mild GI disease in children. Over the past decade, more severe, sometimes fatal infection has been seen with outbreaks of C difficile infection caused by a virulent NAP-1/027 strain that appears to have an increased production of toxins A and B, fluoroquinolone resistance, and production of binary toxin. Infection is also more common in otherwise young, healthy individuals who have not been hospitalized or exposed to antibiotics.

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Clinical Manifestations

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The presentation of CDAD can range from asymptomatic colonization to life-threatening disease. Over the past decade, more severe, sometimes fatal infection has been seen with outbreaks of C difficile infection caused by a virulent NAP-1/027 strain that appears to have an increased production of toxins A and B, fluoroquinolone resistance, and production of binary toxin. Infection is also more common in otherwise young, healthy individuals who have not been hospitalized or exposed to antibiotics. CDAD illness can include watery diarrhea, pseudomembranous colitis, toxic megacolon, perforation, and bacteremia with distant metastatic infections.3,4 Therefore, a high index of suspicion is critical, as is awareness of the limitations of current diagnostic tests.3,4

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Diagnosis

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The diagnosis of C difficile colitis should only be made if a toxin is found in the stool. Culture of the bacteria is not sufficient evidence to support the ...

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