Cooperating Commensals Restore Colonization Resistance to Vancomycin-Resistant Enterococcus faecium.

TitleCooperating Commensals Restore Colonization Resistance to Vancomycin-Resistant Enterococcus faecium.
Publication TypeJournal Article
Year of Publication2017
AuthorsCaballero S, Kim S, Carter RA, Leiner IM, Sušac B, Miller L, Kim GJ, Ling L, Pamer EG
JournalCell Host Microbe
Volume21
Issue5
Pagination592-602.e4
Date Published2017 May 10
ISSN1934-6069
KeywordsAmpicillin, Animals, Anti-Bacterial Agents, Bacteria, Bacterial Physiological Phenomena, Clostridium, Colony Count, Microbial, DNA, Bacterial, Drug Resistance, Bacterial, Enterococcus faecium, Feces, Female, Gram-Positive Bacterial Infections, Intestines, Mice, Mice, Inbred C57BL, Microbiota, RNA, Ribosomal, 16S, Symbiosis, Vancomycin, Vancomycin-Resistant Enterococci
Abstract

Antibiotic-mediated microbiota destruction and the consequent loss of colonization resistance can result in intestinal domination with vancomycin-resistant Enterococcus (VRE), leading to bloodstream infection in hospitalized patients. Clearance of VRE remains a challenging goal that, if achieved, would reduce systemic VRE infections and patient-to-patient transmission. Although obligate anaerobic commensal bacteria have been associated with colonization resistance to VRE, the specific bacterial species involved remain undefined. Herein, we demonstrate that a precisely defined consortium of commensal bacteria containing the Clostridium cluster XIVa species Blautia producta and Clostridium bolteae restores colonization resistance against VRE and clears VRE from the intestines of mice. While C. bolteae did not directly mediate VRE clearance, it enabled intestinal colonization with B. producta, which directly inhibited VRE growth. These findings suggest that therapeutic or prophylactic administration of defined bacterial consortia to individuals with compromised microbiota composition may reduce inter-patient transmission and intra-patient dissemination of highly antibiotic-resistant pathogens.

DOI10.1016/j.chom.2017.04.002
Alternate JournalCell Host Microbe
PubMed ID28494240
PubMed Central IDPMC5494988
Grant ListU01 AI124275 / AI / NIAID NIH HHS / United States
P30 CA008748 / CA / NCI NIH HHS / United States
R01 AI095706 / AI / NIAID NIH HHS / United States
R37 AI039031 / AI / NIAID NIH HHS / United States
R01 AI042135 / AI / NIAID NIH HHS / United States

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