Gut microbiota predict Enterococcus expansion but not Vancomycin-resistant Enterococcus acquisition

ABSTRACT BACKGROUND 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. METHODS 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. RESULTS 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=.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). CONCLUSIONS 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 may be associated with Enterococcus expansion , suggesting that these should be considered as two distinct processes. Summary 16S profile of the gut microbiome does not predict VRE acquisition in hospitalized patients, likely due to the rapid and profound microbiota change in this) opulation. VRE expansion and VRE acquisition may be two distinct processes.