probiotics to prevent c. difficile infection 769
of the same room. Their hypothesis is that antibiotics promote C. difficile proliferation and subsequent environmental con- tamination in colonized, but not necessarily symptomatic, patients. Our data were also limited by the fact that we did not have the resources to monitor antibiotic recipients after hos- pital discharge, a time during which patients remain at high risk to manifest CDI and when the full effect of probiotic receipt might be realized. Despite the largely proven safety of the probiotic mixture,
we and clinical staff were concerned about potential harms, particularly clinical infections by probiotic organisms. We believed that the 3 Lactobacillus spp were low risk given the frequency of patient exposure to probiotics and uncommon recovery from clinical specimens. During our intervention, only a single episode of Lactobacillus bacteremia was recorded for a probiotic recipient. When we performed blinded genetic analysis of the patient’s isolate to those recovered from the 3-strain probiotic capsules, we determined that the bacteremia was unrelated to probiotic receipt.26 Regarding safety, in prior studies, side effects were either reduced or unchanged in probiotic recipients compared with controls.27,28 A fundamental limitation of our project was low interven-
improvement intervention in a large hospital encountered substantial implementation challenges. It is critical that such real-world applications are evaluated and reported to guide future quality-improvement research efforts based on the lessons learned. Given the foundation of evidence supporting probiotics to prevent CDI, interventions that achieve better distribution of probiotic and focused environmental cleaning before interven- tion and control periods are needed to quantify the impact of probiotics on CDI.
acknowledgments
We acknowledge Chinyere Alu, Division Chief, Patient Safety and Quality, Illinois Department of Public Health, for identifying the project hospital and coordinating the early communications. Financial support: This study was supported by the Centers for Disease
tion fidelity among intended recipients, and a substantial number of at-risk patients were ineligible for the intervention (eg, pre-hospital or perioperative antibiotic receipt, clinical ineligibility, and no in-hospital antibiotic receipt). Through a chart review for the case-control study, we discovered that only 1 in 4 eligible antibiotic recipients received probiotic per pro- tocol. Among those not receiving the intervention per proto- col, the most common event was complete omission of probiotic, that is, not a single administered dose. Monitoring probiotic distribution during the intervention was performed, but the results were inconsistent with our retrospective chart review. Particularly influential factors impeding probiotic receipt were (1) frequent initiation of antibiotics before admission, either in the community or emergency room; (2) intention to administer only perioperative antibiotics; and (3) our system of probiotic distribution required manual evaluation of eligibility lists by pharmacists combined with the need for episodic pharmacy staffing with temporary personnel during the intervention. Anecdotally, patient refusal was rare and clinician refusal was uncommon. Future projects that pair probiotic with antibiotic administration would benefit (1) from an electronic, automated clinical decision support rule; (2) from the inclusion of emergency room patients; and (3) from possibly relaxing criteria for clinical eligibility (eg, a lower leukopenia threshold or requiring active pharmacologic immunosuppression for transplant recipients). In conclusion, we found a decreased rate of CDI during the
Bio-K+ . W.T. received compensation for travel to present findings to the advisory board. All authors report no conflicts of interest relevant to this article. Address correspondence to William E. Trick, MD, Collaborative Research
Control and Prevention, Prevention Epicenters Program (grant no. U54CK000161 to R.A.W.). The study hospital was supported by Bio-K+ through the provision of probiotic formulations at no cost and of monetary support for a research assistant to collect data. Potential conflicts of interest: S.J. is a member of the advisory board for
Unit, 1900WPolk Street, Ste 1600, Chicago, IL 60612 (wtrick@cookcountyhhs. org).
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2. Gerding DN, Muto CA, Owens RC. Measures to control and pre- vent Clostridium difficile infection. Clin Infect Dis 2008;46:S43–S49.
3. Trick WE, Temple RS, Chen D, Wright MO, Solomon SL, Peterson LR. Patient colonization and environmental con- tamination by vancomycin-resistant enterococci in a rehabilita- tion facility. Arch Phys Med Rehab 2002;83:899–902.
4. Sethi AK, Al-Nassir WN, Nerandzic MM, Donskey CJ. Skin and environmental contamination with vancomycin-resistant enter- ococci in patients receiving oral metronidazole or oral vanco- mycin treatment for Clostridium difficile–associated disease. Infect Control Hosp Epidemiol 2009;30:13–17.
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final 6 months of a 12-month before-and-after quality improvement intervention of a 3-strain probiotic mixture for primary prevention of CDI. The delayed effect is consistent with prior literature and may have been related to poor fidelity to the protocol for probiotic administration and a delayed gradual reduction in environmental contamination. Our quality
8. Johnson S, Clabots CR, Linn FV, Olson MM, Peterson LR, Gerding DN. Nosocomial Clostridium difficile colonisation and disease. Lancet 1990;336:97–100.
9. Goldenberg JZ, Ma SS, Saxton JD, et al. Probiotics for the pre- vention of Clostridium difficile–associated diarrhea in adults and children. Cochrane Libr 2013.
10. Lau CS, Chamberlain RS. Probiotics are effective at preventing Clostridium difficile–associated diarrhea: a systematic review and meta-analysis. Int J Gen Med 2016;9:27–37.
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