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Background <p>Vancomycin-resistant <i>Enterococcus</i> (VRE) infection poses a significant healthcare burden in intensive care units (ICUs), and is preceded by gut colonization. The gut microbiome may influence susceptibility to VRE, but its role in ICU patients remains incompletely defined.</p> Methods <p>We conducted a prospective study of patients admitted to a medical ICU from 2019 to 2021. Stool samples were collected for bacterial 16&#xa0;S rRNA gene sequencing, anal swabs were screened for VRE by culture, and bile acids were measured in initial stool samples.</p> Results <p>We enrolled 108 patients. Thirty-four patients were VRE + on initial screen and remained so (VRE+/+) while 74 were initially negative, of whom 23 acquired VRE (VRE-/+) and 51 remained negative (VRE-/-). There was no difference in alpha-diversity initially between VRE-/- and VRE-/+ groups, whereas VRE+/+ patients had significantly lower alpha-diversity (<i>P</i> &lt; 0.001). VRE-/+ patients had a significantly more rapid decrease in alpha-diversity than VRE-/- patients (<i>P</i> = 0.04). Beta-diversity of initial stool differed among groups (<i>P</i> = 0.001), driven mainly by VRE+/+ patients. A lower <i>Bacteroides/Enterococcus</i> ratio (<i>P</i> = 0.049) and low <i>Clostridium scindens</i> abundance (<i>P</i> = 0.031) were associated with VRE acquisition. Initial stool from VRE-/- patients had a higher combined concentration of deoxycholic acid and lithocholic acid than that of VRE-/+ patients (<i>P</i> = 0.034).</p> Conclusions <p>VRE acquisition in the ICU was associated with an initial gut microbiome characterized by lower <i>Bacteroides</i>/<i>Enterococcus</i> ratios, lower <i>C. scindens</i> abundance, and lower deoxycholic and lithocholic acid concentrations. Our findings are consistent with a possible role of these microbiome features in colonization resistance, as suggested by in vitro and animal models. However, given the single-center design, these associations should be considered hypothesis-generating and require validation before clinical application.</p>

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Gut microbiome features associated with vancomycin-resistant Enterococcus acquisition in intensive care unit patients

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月2日

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  • Yu-Chung Chuang,
  • Ronald G. Collman,
  • Sheng-Yuan Ruan,
  • Ying-Chun Chien,
  • Yu-Shan Huang,
  • Cheng-Chih Hsu,
  • Jann-Tay Wang,
  • Hsin-Bai Zou,
  • Shan-Chwen Chang

摘要

Background

Vancomycin-resistant Enterococcus (VRE) infection poses a significant healthcare burden in intensive care units (ICUs), and is preceded by gut colonization. The gut microbiome may influence susceptibility to VRE, but its role in ICU patients remains incompletely defined.

Methods

We conducted a prospective study of patients admitted to a medical ICU from 2019 to 2021. Stool samples were collected for bacterial 16 S rRNA gene sequencing, anal swabs were screened for VRE by culture, and bile acids were measured in initial stool samples.

Results

We enrolled 108 patients. Thirty-four patients were VRE + on initial screen and remained so (VRE+/+) while 74 were initially negative, of whom 23 acquired VRE (VRE-/+) and 51 remained negative (VRE-/-). There was no difference in alpha-diversity initially between VRE-/- and VRE-/+ groups, whereas VRE+/+ patients had significantly lower alpha-diversity (P < 0.001). VRE-/+ patients had a significantly more rapid decrease in alpha-diversity than VRE-/- patients (P = 0.04). Beta-diversity of initial stool differed among groups (P = 0.001), driven mainly by VRE+/+ patients. A lower Bacteroides/Enterococcus ratio (P = 0.049) and low Clostridium scindens abundance (P = 0.031) were associated with VRE acquisition. Initial stool from VRE-/- patients had a higher combined concentration of deoxycholic acid and lithocholic acid than that of VRE-/+ patients (P = 0.034).

Conclusions

VRE acquisition in the ICU was associated with an initial gut microbiome characterized by lower Bacteroides/Enterococcus ratios, lower C. scindens abundance, and lower deoxycholic and lithocholic acid concentrations. Our findings are consistent with a possible role of these microbiome features in colonization resistance, as suggested by in vitro and animal models. However, given the single-center design, these associations should be considered hypothesis-generating and require validation before clinical application.