Dataset Information

Vancomycin-Resistant Enterococcus Acquisition in a Tertiary Care Hospital: Testing the Roles of Antibiotic Use, Proton Pump Inhibitor Use, and Colonization Pressure.

ABSTRACT:

Background

Vancomycin-resistant Enterococcus (VRE) is a leading cause of healthcare-associated infections, and asymptomatic colonization precedes infection. VRE continues to spread despite widespread application of pathogen-specific control guidelines. A better understanding of the risk factors for transmission is needed.

Methods

A retrospective matched case-control study was performed from June 2013 through December 2016 in a single institution. Patients in 6 intensive care units, 1 hematology and oncology unit, and 1 bone marrow transplant unit were screened by means of rectal swab sampling on admission and weekly thereafter. Case patients had a negative swab sample followed by a positive sample >3 days after admission. Controls were closely matched to case patients based on time from admission to the second swab sample, unit in which the second sample was obtained, and date of admission. Comorbidity data, procedures, healthcare settings and exposures, culture data, and duration of antibiotic and proton pump inhibitor (PPI) therapy were abstracted from the electronic medical record. A multivariable risk factor model for conversion was generated using purposeful selection.

Results

A total of 551 case patients were matched with controls. The largest modifiable effects on VRE acquisition were ?1 day of vancomycin therapy (odd ratio, 1.98; P < .001), ?1 day of aerobic antibiotic therapy (1.90; P < .001), and a dose-dependent effect of PPI therapy (odds ratio per day of therapy, 1.09; P < .001). Colonization pressures from patients identified to be carriers and placed in contact precautions did not confer increased risk.

Conclusions

Decreasing PPI use and preventing the inappropriate initiation of antibiotic therapy are modifiable targets to decrease VRE transmission in the hospital.

SUBMITTER: Chanderraj R

PROVIDER: S-EPMC6475592 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Vancomycin-Resistant <i>Enterococcus</i> Acquisition in a Tertiary Care Hospital: Testing the Roles of Antibiotic Use, Proton Pump Inhibitor Use, and Colonization Pressure.

Chanderraj Rishi R Millar Jess A JA Patel Twisha S TS Read Andrew F AF Washer Laraine L Kaye Keith S KS Woods Robert J RJ

Open forum infectious diseases 20190315 4

<h4>Background</h4>Vancomycin-resistant <i>Enterococcus</i> (VRE) is a leading cause of healthcare-associated infections, and asymptomatic colonization precedes infection. VRE continues to spread despite widespread application of pathogen-specific control guidelines. A better understanding of the risk factors for transmission is needed.<h4>Methods</h4>A retrospective matched case-control study was performed from June 2013 through December 2016 in a single institution. Patients in 6 intensive car ...[more]

PMID: 31024976

Similar Datasets

Project description:Vancomycin-resistant Enterococcus (VRE) is a leading cause of hospital-acquired infections and continues to spread despite widespread implementation of pathogen-targeted control guidelines. Commensal gut microbiota provide colonization resistance to VRE, but the role of gut microbiota in VRE acquisition in at-risk patients is unknown. To address this gap in our understanding, we performed a case-control study of gut microbiota in hospitalized patients who did (cases) and did not (controls) acquire VRE. We matched case subjects to control subjects by known risk factors and "time at risk," defined as the time elapsed between admission until positive VRE screen. We characterized gut bacterial communities using 16S rRNA gene amplicon sequencing of rectal swab specimens. We analyzed 236 samples from 59 matched case-control pairs. At baseline, case and control subjects did not differ in gut microbiota when measured by community diversity (P = 0.33) or composition (P = 0.30). After hospitalization, gut communities of cases and controls differed only in the abundance of the Enterococcus-containing operational taxonomic unit (OTU), with the gut microbiota of case subjects having more of this OTU than time-matched control subjects (P = 0.01). Otherwise, case and control communities after the time at risk did not differ in diversity (P = 0.33) or community structure (P = 0.12). Among patients who became VRE colonized, those having the Blautia-containing OTU on admission had lower Enterococcus relative abundance once colonized (P = 0.004). Our results demonstrate that the 16S profile of the gut microbiome does not predict VRE acquisition in hospitalized patients, likely due to rapid and profound microbiota change. The gut microbiome does not predict VRE acquisition, but it may be associated with Enterococcus expansion, suggesting that these should be considered two distinct processes.IMPORTANCE The Centers for Disease Control and Prevention estimates that VRE causes an estimated 54,000 infections and 539 million dollars in attributable health care costs annually. Despite improvements in hand washing, environmental cleaning, and antibiotic use, VRE is still prevalent in many hospitals. There is a pressing need to better understand the processes by which patients acquire VRE. Multiple lines of evidence suggest that intestinal microbiota may help some patients resist VRE acquisition. In this large case-control study, we compared the 16S profile of intestinal microbiota on admission in patients that did and did not subsequently acquire VRE. The 16S profile did not predict subsequent VRE acquisition, in part due to rapid and dramatic change in the gut microbiome following hospitalization. However, Blautia spp. present on admission predicted decreased Enterococcus abundance after VRE acquisition, and Lactobacillus spp. present on admission predicted Enterococcus dominance after VRE acquisition. Thus, VRE acquisition and domination may be distinct processes.