Infection Control & Hospital Epidemiology (2019), 40,414–419 doi:10.1017/ice.2019.15
Original Article
A retrospective cohort study of antibiotic exposure and vancomycin-resistant Enterococcus recolonization Heather Y. Hughes MD MPH1,2
Abstract
Objective: In the National Institutes of Health (NIH) Clinical Center, patients colonized or infected with vancomycin-resistant Enterococcus (VRE) are placed in contact isolation until they are deemed “decolonized,” defined as having 3 consecutive perirectal swabs negative for VRE. Some decolonized patients later develop recurrent growth of VRE from surveillance or clinical cultures (ie, “recolonized”), although that finding may represent recrudescence or new acquisition of VRE. We describe the dynamics of VRE colonization and infection and their relationship to receipt of antibiotics.
Methods: In this retrospective cohort study of patients at the National Institutes of Health Clinical Center, baseline characteristics were col- lected via chart review. Antibiotic exposure and hospital days were calculated as proportions ofVREdecolonized days. Using survival analysis, we assessed the relationship between antibiotic exposure and time to VRE recolonization in a subcohort analysis of 72 decolonized patients.
Results: In total, 350 patients were either colonized or infected with VRE. Among polymerase chain reaction (PCR)-positive, culture (Cx)-
negative (PCRþ/Cx−) patients, PCR had a 39% positive predictive value for colonization. Colonization with VRE was significantly associated with VRE infection. Among 72 patients who met decolonization criteria, 21 (29%) subsequently became recolonized. VRE recolonization was 4.3 (P=.001) and 2.0 (P=.22) times higher in patients with proportions of antibiotic days and antianaerobic antibiotic days above the median, respectively.
Conclusion: Colonization is associated with clinicalVREinfection and increased mortality. Despite negative perirectal cultures, re-exposure to antibiotics increases the risk of VRE recolonization.
(Received 1 October 2018; accepted 13 January 2019)
Vancomycin-resistant Enterococcus faecium (VRE) are an impor- tant cause of healthcare-associated infections.1 Vancomycin resis- tance among E. faecium bloodstream isolates has increased in the United States from 57% in 2000 to >80% in 2010.2 The odds of death from enterococcal bloodstream infection are more than doubled if the isolate is vancomycin resistant.3 With increasing reports of resistance to additional antibiotics, infection control efforts must focus on preventing nosocomial spread of VRE.4,5 Factors contributing to colonization with VRE include pro-
longed hospital stay, immunosuppression, hematologic malig- nancy, residence in long-term care facilities, invasive procedures, proximity to colonized or infected patients, occupying a room vacated by a VRE-colonized patient, and use of third-generation cephalosporins, intravenous vancomycin, or antianaerobic antibi- otics.6–9 The likelihood of developing a bloodstream infection after
Author for correspondence: Tara N. Palmore, Email:
tpalmore@mail.nih.gov PREVIOUS PRESENTATION: Part of these data were presented as an abstract at ID
Week 2014 on October 9, 2014, in Philadelphia, Pennsylvania, and as a poster presentation at ID Week 2015 on October 9, 2015, in San Diego, California. Cite this article: Hughes HY, et al. (2019). A retrospective cohort study of antibiotic
exposure and vancomycin-resistant Enterococcus recolonization. Infection Control & Hospital Epidemiology, 40: 414–419,
https://doi.org/10.1017/ice.2019.15
VRE colonization is highest among immunosuppressed patients.10 Infection control measures to prevent the spread of VRE include active microbiological surveillance and contact precautions. Patients at the National Institutes of Health (NIH) Clinical
Center, a 200-bed hospital, are enrolled in research studies. Most patients are immunosuppressed from their underlying ill- nesses or from therapy, including chemotherapy, hematopoietic stem cell transplantation (HSCT), and immunotherapy. Patients who have VRE colonization or infection are placed in contact iso- lation, which is discontinued when the patient appears to be “decolonized,” that is, after 3 consecutive negative surveillance cul- tures at least 1 week apart.11,12 One challenge in the subsequent management of VRE is the patients’ dynamic state of colonization, which affects clinical care and isolation status. Recent literature on the natural history of VRE recolonization is sparse.13–15 Whether the same risk factors that promote initial colonization also encour- age recolonization with VRE is not well understood. Antibiotic exposure after decolonization could apply selective pressure in the setting of low-level persistent colonization, or it could alter the intestinal microbiome in a manner conducive to recoloniza- tion. Here, we present descriptive epidemiology and natural
© 2019 by The Society for Healthcare Epidemiology of America. All rights reserved. This work is classified, for copyright purposes, as a work of the U.S. Government and is not subject to copyright protection within the United States.
, Robin T. Odom MS3, Angela V. Michelin MPH3, Evan S. Snitkin PhD4, Ninet Sinaii PhD,
MPH3, Aaron M. Milstone MD MHS5, David K. Henderson MD3 and Tara N. Palmore MD3 1The Ralph H. Johnson VAMC, Charleston, South Carolina, 2The Medical University of South Carolina, Charleston, South Carolina, 3National Institutes of Health, Bethesda, Maryland, 4University of Michigan Medical School, Ann Arbor, Michigan and 5Johns Hopkins University School of Medicine, Baltimore, Maryland
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