Microbiome
How did some Enterococcus faecium become hospital pathogens?
Open access · cc by · source: Europe PMC
Comparative pangenomes split E. faecium into a mixed-source subclade I and a human-only subclade II with larger genomes packed with resistance, virulence, bacteriocin, and mobile genes likely gained by HGT.
How this study connects
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Study at a glance
- Design
- Computational / modelling — Comparative pangenome analysis of dereplicated E. faecium and E. lactis genomes
- N
- All available dereplicated genomes of the two species (counts in full text tables)
- Population
- Enterococcus faecium and Enterococcus lactis genomes from diverse isolation sources
- Outcome
- Subclade structure and enrichment of resistance/virulence/mobile genes
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Inspect source passages
How did some Enterococcus faecium become hospital pathogens?
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Two E. faecium subclades; II exclusively human-derived.
E. faecium was divided into two subclades: subclade I, comprising strains derived from humans, animals, and food, and the more recent phylogenetic subclade II, consisting exclusively of human-derived strains.
Subclade II had significantly larger genomes and higher gene counts.
Notably, E. faecium subclade II strains exhibited significantly larger genome sizes and higher gene counts compared to both E. faecium subclade I and E. lactis strains.
Key findings
Subclade II was exclusively human-derived, larger, and richer in resistance/virulence/mobile elements; phylogenetic patterns support horizontal acquisition tied to antibiotic pressure. E. lactis did not cluster by isolation source.
Methodology
They analyzed all available dereplicated genomes of E. faecium and closely related E. lactis, comparing phylogeny, genome size/gene content, and resistance/virulence gene histories.
Limitations
Genome catalogs do not measure in-host virulence experimentally or prove causality for every gene’s clinical effect.
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