During the 2000s, the incidence of Clostridium difficile infection (CDI) increased dramatically, in large part due to the emergence of a hypervirulent strain, BI/NAP1/027, responsible for many hospital outbreaks in the United States. In 2011, C difficile accounted for 12% of all US health care–associated infections, surpassing Staphylococcus aureus as the most common cause of such infections.1 Hospitalized patients with CDI are a recognized source of health care–associated (HA) transmission, and a primary control measure is to limit the spread of the organism from symptomatic patients. However, increasing molecular evidence, based on genomic sequence–based methods, indicates that asymptomatic patients colonized with C difficile also contribute to transmission.2,3 A 2013 study3 found that incident CDI cases in a hospital were as frequently linked to transmission from asymptomatic carriers as to symptomatic patients. Despite the potential for patients with asymptomatic colonization to serve as a reservoir for CDI, no data currently exist to determine whether interventions targeting asymptomatically colonized patients could be effective in reducing HA-CDI.
Guh AY, McDonald LC. Active Surveillance and Isolation of Asymptomatic Carriers of Clostridium difficile at Hospital Admission: Containing What Lies Under the Waterline. JAMA Intern Med. 2016;176(6):805–806. doi:10.1001/jamainternmed.2016.1118
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