The Enterococcus: a Model of Adaptability to Its Environment Original paper
Researched by:
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Divine Aleru
ID
Divine Aleru
Read MoreI am a biochemist with a deep curiosity for the human microbiome and how it shapes human health, and I enjoy making microbiome science more accessible through research and writing. With 2 years experience in microbiome research, I have curated microbiome studies, analyzed microbial signatures, and now focus on interventions as a Microbiome Signatures and Interventions Research Coordinator.
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Microbes
Microbes
Microbes are microscopic organisms living in and on the human body, shaping health through digestion, vitamin production, and immune protection. When microbial balance is disrupted, disease can occur. This guide explains key microbe types—bacteria, viruses, fungi, protozoa, and archaea—plus major pathogenic and beneficial examples.
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Divine Aleru
Read More
Researched by:
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Divine Aleru
ID
Divine Aleru
Read More
Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
Divine Aleru
What was reviewed?
This review examined how Enterococcus faecalis and Enterococcus faecium adapt to the gut microbiome, hospital environments, and host tissues through genetic plasticity, antimicrobial resistance, and virulence factor acquisition. The authors reviewed microbiological, genomic, and clinical evidence explaining how Enterococcus survives environmental stress, acquires resistance genes, and transitions from a gut microbiome commensal into a multidrug-resistant pathogen capable of causing systemic infection.
Who was reviewed?
The review evaluated microbiome-derived and clinical strains of Enterococcus faecalis and Enterococcus faecium isolated from the human gastrointestinal microbiome, bloodstream, urinary tract, wounds, and hospital environments. These strains included commensal microbiome populations and multidrug-resistant clinical isolates associated with hospital-acquired infections, antibiotic exposure, and microbiome disruption.
What were the most important findings?
Enterococcus adapted rapidly to microbiome disruption and antibiotic exposure through horizontal gene transfer, virulence factor acquisition, and antimicrobial resistance development. Major microbial associations included increased abundance of Enterococcus faecalis and Enterococcus faecium in the gut microbiome during antibiotic exposure and hospital-associated microbiome disruption. Enterococcus acquired resistance genes through conjugative plasmids, transposons, and mobile genetic elements, allowing resistance to vancomycin, aminoglycosides, and β-lactam antibiotics. Genome plasticity allowed up to 25–38% of the genome to consist of acquired foreign DNA, increasing virulence and survival. Virulence factors such as adhesins, pili, cytolysin, and aggregation substance promoted host tissue adherence, biofilm formation, immune evasion, and microbiome persistence. Clinical isolates contained larger genomes enriched with resistance and virulence genes compared to commensal strains. Enterococcus also survived harsh conditions including desiccation, disinfectants, and antibiotic exposure, allowing persistence in hospital environments and microbiome niches. These adaptations enabled microbiome dominance, resistance gene transfer, and systemic infection.
What are the greatest implications of this review?
This review showed that Enterococcus expansion represents a microbiome signature of antibiotic exposure, microbiome disruption, and infection risk. Genetic plasticity enables rapid adaptation, resistance development, and virulence activation. Enterococcus functions as a reservoir of resistance and virulence genes, promoting microbiome imbalance and infection progression.
Enterococcus faecalis
Enterococcus faecalis is a gut‑adapted, Gram‑positive, non‑spore‑forming facultative anaerobe that becomes an important opportunistic pathogen in healthcare when host barriers are breached or antibiotics select for enterococcal overgrowth. Its clinical impact is driven more by persistence, adhesion, and biofilm biology, quorum‑regulated secreted effectors (fsr‑controlled gelatinase GelE), and high genome plasticity than by a broad repertoire of classical tissue‑destroying toxins. Antimicrobial decision‑making must account for the intrinsic poor activity of cephalosporins, the potential for transferable glycopeptide resistance mediated by van gene clusters, and the need for regimen selection in endocarditis that respects synergy/tolerance and local high‑level aminoglycoside resistance patterns.