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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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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 ...