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ICU patients admitted with C. difficile colonization at risk for subsequent infections
Patients admitted to an ICU for Clostridium difficile infection were at risk for developing subsequent C. difficile infections, according to recent research.
Trish M. Perl, MD, MSc, of the Johns Hopkins University School of Medicine, and colleagues prospectively screened 542 patients for C. difficile admitted to the ICU at Johns Hopkins Hospital between April and July 2013. Rectal swabs were used to screen for C. difficile at admission and weekly until ICU discharge. Patients also were monitored by medical chart review for 1 month after discharge.
The researchers found that 3.1% of patients admitted had toxigenic C. difficile colonization on admission, and three patients of 35 had a subsequent C. difficile infection during weekly follow-up. Colonization with toxigenic C. difficile before admission was associated with developing infection (RR = 10.29; 95% CI, 2.24–47.4), as was colonization during hospital stay (RR = 15.66; 95% CI, 4.01–61.08). After adjusting for confounders, the investigators found colonization before admission (RR = 8.62; 95% CI, 1.48–50.25) and during hospital stay (RR = 10.93; 95% CI, 1.49–80.2) were independent risk factors for infection.
Trish M. Perl
Perl and colleagues noted that age, use of proton pump inhibitors or antibiotics or prior health care visits up to 12 weeks were not associated with C. difficile infection. During their hospital stays, 1.5% of patients developed C. difficile infection; four patients were diagnosed within 1 month of discharge.
“Importantly in this study, colonization with toxigenic C. difficile on admission was identified as a strong and independent predictor for development of subsequent [C. difficile infection,]” the researchers wrote. “This finding suggests that traditional infection control measures may not suffice to avoid further increase in disease burden. For patients colonized with toxigenic C. difficile, the challenge for disease prevention is not to prevent exposure but to reduce the risk of C. difficile toxin expression by restricting use of antibiotics, acid-suppressive agents and narcotics.” – by Jeff Craven
Disclosure: Tschudin-Sutter reports funding from the Swiss National Science Foundation, the Medical Division of the Lichtenstein Foundation of the University of Basel and the Scientific Society Basel. All other authors report no relevant financial disclosures.
Perspective
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With nearly a half million cases of Clostridium difficile infections a year in the United States and a majority of cases associated with health care exposures, reducing health care-associated C. difficile is increasingly important. Traditional approaches to reduce hospital-onset C. difficile infection have focused on preventing the spread of the disease from one patient to another. However, in their report in Infection Control and Hospital Epidemiology, Tschudin-Sutter and colleagues show that the patients who are at increased risk for developing C. difficile infection are patients who are already colonized with C. difficile upon admission (adjusted RR = 8.62, 95% CI, 1.48-50.25).
This finding — that colonization increases risk — may seem intuitive, but studies 10 to 20 years ago suggested that colonized patients may be at a lower risk for developing C. difficile infection, possibly due to the ability to form antibodies to toxigenic C. difficile. This current study did not discuss how many of their colonized patients had previous symptomatic infection, a clear risk for subsequent infections. But this variability between studies shows that colonized patients are likely to be a heterogeneous group, and further understanding of colonized patients (such as risk factors for colonization, antibody response, degree of dysbiosis and duration of colonization) may help us better estimate who is at risk for infection.
Universal screening is unlikely to be effective as only 3% of these C. difficile infection admissions were colonized (previous studies showed colonization rates of 7% to 15%). But improving infection prevention strategies are still a priority; 9% of the patients who had subsequent screening acquired C. difficile colonization, which suggests ongoing transmission. In addition to preventing transmissions, reducing the risk for infection in colonized patients will need to focus on limiting the disruption of the microbiome with stewardship of antimicrobials and other dysbiosis-producing agents such as proton pump inhibitors. This study provides further evidence that the combination of preventing new transmission events and improving stewardship activities are needed to reduce hospital-associated C. difficile infections.