Search bioRxiv⌕ Search

bioRxiv · 10.64898/2026.01.09.698598

Population genetic structure of disease-causing vancomycin-resistant Enterococcus faecium in a hospital closely reflects the dynamics of colonizing populations in patients

Abstract

Vancomycin-resistant Enterococcus faecium (VREfm) is a common nosocomial pathogen that can lead to severe and difficult-to-treat infections. VREfm effectively exploits healthcare environments because transmission chains are difficult to prevent and eradicate. VREfm also readily acquires antimicrobial resistance (AMR), strongly reducing the likelihood of treatment success. Here we compare the genetic population structure and antimicrobial resistance load of VREfm strains that are typically associated with patient colonization, and those found to cause disease. We use two separate but contemporaneous collections of clinical bacterial isolates in a tertiary care medical center: one consisting of Enterococcus from blood samples, and a second originating from a hospital wide surveillance strategy screening for VREfm in perirectal swabs of incoming patients. Using whole-genome sequencing and analysis of 2061 VREfm clones, we found that the genetic structure of colonizing and disease-causing VREfm closely resemble each other, and that sequence type 117 (ST117) played an important role in shaping these populations. The population structures of strains acquired at the hospital and those present on arrival are also remarkably similar. We further observed a high likelihood that the colonizing clone genetically resembles the disease-causing strain in patients who are both colonized and infected. Finally, the AMR gene load and distribution did not vary significantly between the blood isolates and the gut-associated strains. Altogether, our results highlight the similarities between colonizing and infectious VREfm populations and further emphasize the need to focus infection prevention strategies to minimize gut colonization. Author SummaryVancomycin-resistant Enterococcus faecium (VREfm) often lives harmlessly in the human gut but can cause life-threatening infections when it enters the bloodstream. Hospitals struggle with is pathogen because it spreads easily and tends to resist many antibiotics. We compared bacteria collected from patients guts and from their blood to ask whether the strains that cause infection are different from those that only colonize. Studying more than 2,000 bacterial genomes, we found that the two groups look remarkably similar: the same genetic types dominate in both, patients are usually infected by the same strain already living in their gut, an both groups also carried similar sets of resistance genes. Overall, this is important because it suggests that preventing colonization--not just treating infection--may therefore be the most effective way to reduce VREfm disease in hospitals.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Barbosa Porras, C., Penkevich, A., Tracy, K., Losh, S. J., Read, A. F., Woods, R.. 2026-01-09. Population genetic structure of disease-causing vancomycin-resistant Enterococcus faecium in a hospital closely reflects the dynamics of colonizing populations in patients. https://doi.org/10.64898/2026.01.09.698598

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Characterization of Lactobacillus rhamnosus-Derived Extracellular Vesicles and Their Cellular Cytoprotective Effects Against Trimethylamine-Induced Oxidative Stress in Caco-2 Cells

Dietary trimethylamine (TMA) underwent gut microbiota-mediated catabolism and subsequent hepatic oxidation to generate trimethylamine N-oxide (TMAO), a key metabolic factor linked to vascular and colorectal diseases. While the systemic effects of circulating TMAO were heavily investigated, the direct localized cellular interactions of its precursor, TMA, at the intestinal epithelial level required further elucidation. This study characterized extracellular vesicles isolated from Lactobacillus rhamnosus (Lr-EVs) and evaluated their cytoprotective potential in an in vitro human intestinal Caco-2 cell model under TMA-induced stress. Exposure to a high concentration of TMA (20 mM) significantly reduced Caco-2 viability to 78.8%, triggered intracellular reactive oxygen species (ROS) accumulation, and compromised tight junction integrity as observed via the disruption of Zonula Occludens-1 (ZO-1) alignment. Co-treatment with Lr-EVs (100-300 g/mL) counteracted this cellular toxicity, enhancing cell survival up to 172%. Quantitative PCR analysis revealed that Lr-EVs suppressed the transcriptional upregulation of the pro-inflammatory gene IL-1{beta}, restored the expression of the metabolic regulator SIRT1, and stabilized transcript levels of key mitochondrial-encoded electron transport chain genes (ND6, CYTB, CO1, and ATP6). Additionally, Lr-EVs exhibited intrinsic radical scavenging activities in cell-free ABTS and DPPH assays. These preliminary in vitro findings demonstrated that Lr-EVs mitigated TMA-induced cellular injury, oxidative stress, and junctional disruption at the transcriptomic level, supporting further investigation of probiotic-derived EVs as prospective cell-free functional ingredients.

microbiology↗

Metagenomic Insights into the Fecal Microbiome, Resistome, and Mobilome of Beef Cattle in Cow-Calf Operations in Florida, United States

Food-producing animals are a focus of One Health approaches to antimicrobial resistance (AMR) as reservoirs of antimicrobial-resistant bacteria (ARB) and antimicrobial resistance genes (ARGs). We hypothesized that microbial composition, ARGs profiles, and mobile genetic element (MGE) profiles would differ by operation size and animal age group. Fecal samples from 162 cows and calves were combined into 54 composite samples, each comprising three animals of the same age group. Across operation sizes, Bacillota (51.4-64.9%), Bacteroidota (12.0-17.3%), Pseudomonadota (10.3-16.5%), and Actinomycetota (3.3-10.9%) were predominant phyla. Alpha diversity did not differ among operation sizes; however, cows exhibited greater observed richness, Shannon diversity, and Simpson diversity than calves (all P < 0.001). Microbial composition did not differ significantly among operation sizes (PERMANOVA, R{superscript 2} = 0.065, P = 0.609) but differed significantly between cows and calves (R{superscript 2} = 0.200, P < 0.001). Seventy-five ARGs representing 14 resistance classes were identified. Normalized ARG hit rates were higher in small operations (0.444) than in medium (0.278) and large operations (0.222; P = 0.088), whereas calves exhibited a higher estimated marginal mean normalized ARG hit rate than cows (0.383 vs. 0.247 hits/million reads; P < 0.001). Of 1,054 curated ARG hits, 23.9% occurred on predicted plasmid contigs, 0.9% on predicted viral contigs, and 7.1% on contigs containing insertion sequences. Overall findings demonstrate differences in fecal microbiome diversity and ARG abundance between cows and calves and indicate that predicted plasmids are associated with a notable proportion of ARG hits in Florida beef cow-calf operations.

microbiology↗

A global post-transcriptional regulator directs Acinetobacter baumannii carbon preference and gut colonization

Acinetobacter baumannii is a multidrug-resistant pathogen that colonizes the gut, increasing the risk of subsequent infection and transmission. Recent work showed that A. baumannii catabolizes ornithine, a non-preferred carbon source, to colonize the gut. However, the mechanisms of carbon preference were unknown in A. baumannii. Here, experimental evolution identified the conserved RNA-binding protein CsrA as a regulator of carbon preference in A. baumannii, a previously unreported CsrA function. RNA immunoprecipitation sequencing (RIP-Seq) revealed hundreds of CsrA-associated transcripts. A. baumannii CsrA directly bound and repressed expression of the ast arginine/ornithine catabolic operons. The Pseudomonas aeruginosa CsrA homolog RsmA repressed arginine/ornithine catabolic operon expression, suggesting this CsrA function extends to other bacterial taxa. Finally, CsrA was required for competitive fitness during A. baumannii gut colonization. These findings uncover a previously unrecognized role for a global regulator in A. baumannii carbon preference and persistence in the gut, a critical reservoir for multidrug-resistant pathogens.

microbiology↗