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Vancomycin-resistant Enterococcus domination of intestinal microbiota is enabled by antibiotic treatment in mice and precedes bloodstream invasion in humans
Carles Ubeda, … , Mini Kamboj, Eric G. Pamer
Carles Ubeda, … , Mini Kamboj, Eric G. Pamer
Published November 22, 2010
Citation Information: J Clin Invest. 2010;120(12):4332-4341. https://doi.org/10.1172/JCI43918.
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Research Article

Vancomycin-resistant Enterococcus domination of intestinal microbiota is enabled by antibiotic treatment in mice and precedes bloodstream invasion in humans

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Abstract

Bloodstream infection by highly antibiotic-resistant bacteria, such as vancomycin-resistant Enterococcus (VRE), is a growing clinical problem that increasingly defies medical intervention. Identifying patients at high risk for bacterial sepsis remains an important clinical challenge. Recent studies have shown that antibiotics can alter microbial diversity in the intestine. Here, we characterized these effects using 16s rDNA pyrosequencing and demonstrated that antibiotic treatment of mice enabled exogenously administered VRE to efficiently and nearly completely displace the normal microbiota of the small and large intestine. In the clinical setting, we found that intestinal domination by VRE preceded bloodstream infection in patients undergoing allogeneic hematopoietic stem cell transplantation. Our results demonstrate that antibiotics perturb the normal commensal microbiota and set the stage for intestinal domination by bacteria associated with hospital-acquired infections. Thus, high-throughput DNA sequencing of the intestinal microbiota could identify patients at high risk of developing bacterial sepsis.

Authors

Carles Ubeda, Ying Taur, Robert R. Jenq, Michele J. Equinda, Tammy Son, Miriam Samstein, Agnes Viale, Nicholas D. Socci, Marcel R.M. van den Brink, Mini Kamboj, Eric G. Pamer

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Figure 7

Incomplete recovery of the intestinal microbiota allows VRE intestinal colonization.

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Incomplete recovery of the intestinal microbiota allows VRE intestinal c...
The number of VRE CFUs was determined 8 days after infection in the small intestine or cecum of untreated mice, mice treated with ampicillin for 1 week before infection and switched back to antibiotic-free water 1 day after infection (i.e., no recovery time), and mice treated with ampicillin for 1 week and allowed to recover for 2 or 4 weeks from ampicillin treatment before infection. If VRE was not detected (ND), the limit of detection was considered to be the number of CFUs in the sample. n = 9 per group, except 2-week recovery (n = 10). ***P < 0.001 versus untreated, 1-way ANOVA with Bonferroni correction on the log-transformed CFU values.

Copyright © 2023 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

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