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Fluoroquinolone Prophylaxis Uncovers High Prevalence Rates of Fluoroquinolone-Resistant Enterobacterales Colonization
Chintan Patel1, Austin J Terlecky2, Melissa Baker1
1John Theurer Cancer Center, 92 Second Street, Hackensack, NJ 07601, USA.
Abstract:
Background: Fluoroquinolone prophylaxis during autologous stem cell transplantation (aSCT) reduces the risk of fever but raises the risk of bloodstream infection (BSI) with fluoroquinolone-resistant Enterobacterales (FRE). We performed a prospective cohort study to detect the presence and potential gain or loss of colonic FRE colonization using serial sampling before and after aSCT in a uniform population of patients with a diagnosis of multiple myeloma. Methods: Eligible subjects underwent aSCT after conditioning with dose-intense melphalan, 200 mg/m2. Peri-anal swabs were obtained before aSCT, upon hospital discharge, and 12-16 weeks after transplantation. Samples were cultured in tryptic soy broth supplemented with either ciprofloxacin or ceftriaxone with subsequent plating onto selective chromogenic agar designed to facilitate recovery and differentiation of Enterobacterales. Results: FRE colonization on pre-transplant sampling was detected for 23 of 117 subjects (19.7%) and 29 of 98 (29.6%) subjects at hospital discharge after a course of fluoroquinolone (116/117 subjects) prophylaxis (p < 0.001) and 28 of 92 (30.4%) subjects at 12-16 weeks. Including all three sampling time points, 48 of 117 subjects (41.0%) tested positive for FRE colonization. In total, 58 of the 90 FRE isolates (64.4%) from 48 subjects expressed extended-spectrum beta-lactamase (ESBL). Three FRE-colonized subjects developed FRE BSI. Bloodstream isolates for two subjects were identical to the organisms identified on pre-transplant sampling. Conclusions: We hypothesize that fluoroquinolone prophylaxis of subjects with undetected low levels of FRE colonization allows the expansion of the FRE population, placing subjects at risk of BSI with fluoroquinolone-resistant (and ESBL-expressing) Enterobacterales. Pre-transplant testing for FRE colonization permits patient-specific design of prophylactic and empiric antibiotic regimens.
Insights
Fluoroquinolone prophylaxis increases fluoroquinolone-resistant Enterobacterales colonization in multiple myeloma patients undergoing stem cell transplant. Pre-transplant screening can guide antibiotic strategies to prevent resistant bloodstream infections.
Area of Science:
- Infectious Diseases
- Hematology
- Microbiology
Background:
- Autologous stem cell transplantation (aSCT) patients receive fluoroquinolone prophylaxis to prevent fever.
- This prophylaxis increases the risk of bloodstream infections (BSI) caused by fluoroquinolone-resistant Enterobacterales (FRE).
- The study focuses on multiple myeloma patients undergoing aSCT.
Purpose of the Study:
- To prospectively detect the presence, gain, or loss of colonic FRE colonization.
- To assess the impact of fluoroquinolone prophylaxis on FRE colonization.
- To identify risk factors for FRE BSI in aSCT patients.
Main Methods:
- Prospective cohort study involving patients with multiple myeloma undergoing aSCT.
- Serial peri-anal swab sampling before aSCT, at discharge, and 12-16 weeks post-transplant.
- Culture on selective media to detect and differentiate Enterobacterales, including FRE.
Main Results:
- FRE colonization increased significantly from pre-transplant (19.7%) to discharge (29.6%) and remained elevated at 12-16 weeks (30.4%).
- Overall, 41.0% of subjects were colonized with FRE at any time point.
- 64.4% of FRE isolates expressed extended-spectrum beta-lactamase (ESBL). Three colonized subjects developed FRE BSI, with two isolates matching pre-transplant strains.
Conclusions:
- Fluoroquinolone prophylaxis may promote expansion of undetected low-level FRE colonization, increasing BSI risk.
- Pre-transplant FRE colonization screening is crucial for personalized antibiotic prophylaxis and empiric treatment.
- Targeted screening can help mitigate the risk of BSI with fluoroquinolone-resistant and ESBL-producing Enterobacterales.
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