Gut Microbiota Predict <italic toggle="yes">Enterococcus</italic> Expansion but Not Vancomycin-Resistant <italic toggle="yes">Enterococcus</italic> Acquisition

ABSTRACT 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 VR...

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Autores principales:	Rishi Chanderraj, Christopher A. Brown, Kevin Hinkle, Nicole Falkowski, Piyush Ranjan, Robert P. Dickson, Robert J. Woods
Formato:	article
Lenguaje:	EN
Publicado:	American Society for Microbiology 2020
Materias:	microbiome vancomycin-resistant Enterococcus colonization resistance hospital-acquired infection Microbiology QR1-502
Acceso en línea:	https://doaj.org/article/7aa111b144d441559d5636e14361a989
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spelling	oai:doaj.org-article:7aa111b144d441559d5636e14361a9892021-11-15T15:31:13ZGut Microbiota Predict <italic toggle="yes">Enterococcus</italic> Expansion but Not Vancomycin-Resistant <italic toggle="yes">Enterococcus</italic> Acquisition10.1128/mSphere.00537-202379-5042https://doaj.org/article/7aa111b144d441559d5636e14361a9892020-12-01T00:00:00Zhttps://journals.asm.org/doi/10.1128/mSphere.00537-20https://doaj.org/toc/2379-5042ABSTRACT 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.Rishi ChanderrajChristopher A. BrownKevin HinkleNicole FalkowskiPiyush RanjanRobert P. DicksonRobert J. WoodsAmerican Society for Microbiologyarticlemicrobiomevancomycin-resistant Enterococcuscolonization resistancehospital-acquired infectionMicrobiologyQR1-502ENmSphere, Vol 5, Iss 6 (2020)
institution	DOAJ
collection	DOAJ
language	EN
topic	microbiome vancomycin-resistant Enterococcus colonization resistance hospital-acquired infection Microbiology QR1-502
spellingShingle	microbiome vancomycin-resistant Enterococcus colonization resistance hospital-acquired infection Microbiology QR1-502 Rishi Chanderraj Christopher A. Brown Kevin Hinkle Nicole Falkowski Piyush Ranjan Robert P. Dickson Robert J. Woods Gut Microbiota Predict <italic toggle="yes">Enterococcus</italic> Expansion but Not Vancomycin-Resistant <italic toggle="yes">Enterococcus</italic> Acquisition
description	ABSTRACT 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.
format	article
author	Rishi Chanderraj Christopher A. Brown Kevin Hinkle Nicole Falkowski Piyush Ranjan Robert P. Dickson Robert J. Woods
author_facet	Rishi Chanderraj Christopher A. Brown Kevin Hinkle Nicole Falkowski Piyush Ranjan Robert P. Dickson Robert J. Woods
author_sort	Rishi Chanderraj
title	Gut Microbiota Predict <italic toggle="yes">Enterococcus</italic> Expansion but Not Vancomycin-Resistant <italic toggle="yes">Enterococcus</italic> Acquisition
title_short	Gut Microbiota Predict <italic toggle="yes">Enterococcus</italic> Expansion but Not Vancomycin-Resistant <italic toggle="yes">Enterococcus</italic> Acquisition
title_full	Gut Microbiota Predict <italic toggle="yes">Enterococcus</italic> Expansion but Not Vancomycin-Resistant <italic toggle="yes">Enterococcus</italic> Acquisition
title_fullStr	Gut Microbiota Predict <italic toggle="yes">Enterococcus</italic> Expansion but Not Vancomycin-Resistant <italic toggle="yes">Enterococcus</italic> Acquisition
title_full_unstemmed	Gut Microbiota Predict <italic toggle="yes">Enterococcus</italic> Expansion but Not Vancomycin-Resistant <italic toggle="yes">Enterococcus</italic> Acquisition
title_sort	gut microbiota predict <italic toggle="yes">enterococcus</italic> expansion but not vancomycin-resistant <italic toggle="yes">enterococcus</italic> acquisition
publisher	American Society for Microbiology
publishDate	2020
url	https://doaj.org/article/7aa111b144d441559d5636e14361a989
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Gut Microbiota Predict <italic toggle="yes">Enterococcus</italic> Expansion but Not Vancomycin-Resistant <italic toggle="yes">Enterococcus</italic> Acquisition

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