Abstract

Fluoroquinolones are associated with an increased risk of Clostridioides difficile infection (CDI). Probiotic supplementation has been shown to reduce the risk of antibiotic-associated diarrhea with variable effects on CDI. The objective of this study was to evaluate receipt of probiotics on development of primary CDI among hospitalized patients receiving fluoroquinolones. A retrospective cohort was evaluated that consisted of two groups of 100 patients each, admitted August 2018 through August 2020 that received ≥3 days of definitive monotherapy with levofloxacin or ciprofloxacin within 72 h of admission. Primary outcome was incidence of CDI. Secondary outcomes included rates of C. difficile diagnostic stool testing, additional infectious diagnostic testing, and non-CDI related gastrointestinal side effects. Patients on fluoroquinolones who received probiotics had a non-statistically significantly lower incidence in overall cases of CDI compared to those who did not receive probiotics (0% vs. 3%, p = 0.246). Patients who received probiotics had statistically significantly fewer C. difficile diagnostic stool tests performed (4% vs. 16%, p = 0.005) and fewer additional infectious diagnostic testing performed (4% vs. 10%, p = 0.096), respectively. Further research is warranted to optimize and standardize probiotic prescribing in high-risk patients.

Highlights

  • Clostridioides difficile, previously Clostridium difficile, is a Gram-positive, anaerobic, spore-forming bacterium responsible for C. difficile infection (CDI), including the development of pseudomembranous colitis and toxic megacolon [1]

  • Ciprofloxacin and levofloxacin were evaluated from the fluoroquinolone class as they are the main two formulary agents used within the health system

  • There were 1104 patients who received IV or oral ciprofloxacin or levofloxacin who were screened for inclusion to obtain 100 eligible patients in each group

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Summary

Introduction

Clostridioides difficile, previously Clostridium difficile, is a Gram-positive, anaerobic, spore-forming bacterium responsible for C. difficile infection (CDI), including the development of pseudomembranous colitis and toxic megacolon [1]. In 2014, CDI became recognized as the leading cause of hospital-acquired infections in the United States [2]. Primary prevention of CDI is of interest due to the risk of recurrence (~20–25%) and associated health consequences, including increased morbidity and mortality, hospital length of stay, and healthcare costs [3]. The primary risk factor for development of CDI is antibiotic exposure. Risk varies based on antibiotic classes and patient risk factors; the highest associated risk has been identified with the use of clindamycin, fluoroquinolones, and ceftriaxone [1,4]. Fluoroquinolones are one of the most frequently and inappropriately prescribed antibiotic classes in the United States. Fluoroquinolone use has been associated with increased prevalence of the C. difficile ribotype 027 strain, which has significantly higher rates of morbidity and mortality [1]

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