Abstract
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.
Highlights
Vancomycin-resistant Enterococcus (VRE) is a leading cause of hospitalacquired infections and continues to spread despite widespread implementation of pathogen-targeted control guidelines
Though colonization resistance plays a crucial role in suppressing VRE expansion and preventing VRE infection [14, 15], to date, no study has evaluated whether variation in intestinal microbiota can explain variation in VRE acquisition among at-risk patients
We studied gut microbiome communities in 236 rectal swab samples from 59 matched pairs of case and control subjects (Table 1)
Summary
Vancomycin-resistant Enterococcus (VRE) is a leading cause of hospitalacquired infections and continues to spread despite widespread implementation of pathogen-targeted control guidelines. Though colonization resistance plays a crucial role in suppressing VRE expansion and preventing VRE infection [14, 15], to date, no study has evaluated whether variation in intestinal microbiota can explain variation in VRE acquisition among at-risk patients To address this gap in our understanding of VRE transmission, we investigated whether the gut microbiome of at-risk patients predicts VRE colonization in a hospitalized patient population. We hypothesized that if the gut microbiome can confer colonization resistance for VRE acquisition, variation in baseline microbiota would explain variation in patient susceptibility to VRE acquisition To test this hypothesis, we designed a case-control study using 16S rRNA gene amplicon sequencing of rectal swabs acquired from hospitalized patients
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