Model systems for the study of Enterococcal colonization and infection Original paper
Researched by:
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Divine Aleru
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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 experimental model systems used to study how Enterococcus faecalis and Enterococcus faecium colonize the microbiome and cause infection. These bacteria normally live in the human gut microbiome but become pathogenic when microbiome balance is disrupted. The review explained how Enterococcus adheres to host tissues, forms biofilms, activates virulence genes, and spreads from the gut into systemic sites. It emphasized how microbiome disruption, antibiotic exposure, and immune compromise enable Enterococcus to expand and transition from commensal colonizer to invasive pathogen.
Who was reviewed?
The review evaluated microbiome-derived and clinical Enterococcus strains studied in humans and experimental models including mice, rats, rabbits, and invertebrates. These models examined Enterococcus colonization of the gut microbiome, bloodstream, urinary tract, and heart valves. The review also examined polymicrobial infections involving Enterococcus and other microbiome organisms such as Escherichia coli, Staphylococcus aureus, Klebsiella, and Pseudomonas aeruginosa, which commonly coexist and interact during infection.
What were the most important findings?
Enterococcus expanded rapidly when microbiome diversity decreased, especially after antibiotic treatment. This expansion allowed Enterococcus to dominate the microbiome and increase infection risk. Major microbial associations included increased Enterococcus abundance during microbiome disruption and frequent coexistence with pathogens such as E. coli, Staphylococcus aureus, and Klebsiella. Enterococcus promoted polymicrobial biofilm formation, increased antibiotic resistance, and enhanced microbial survival. Virulence factors such as cytolysin, adhesins, pili, and polysaccharides allowed Enterococcus to attach to host tissues, evade immune clearance, and persist in the microbiome. Enterococcus also uses quorum-sensing and stress response systems to survive immune defenses and hostile host environments. Mobile genetic elements allowed Enterococcus to acquire virulence and resistance genes, further strengthening microbiome dominance and pathogenic potential.
What are the greatest implications of this review?
This review showed that Enterococcus acts as a microbiome pathobiont whose expansion signals microbiome imbalance and increased infection risk. Microbiome disruption enables Enterococcus to dominate microbial communities, persist in host tissues, and spread systemically. Enterococcus expansion represents an important microbiome signature associated with infection development, severity, and poor clinical outcomes.
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.
Staphylococcus aureus (S. Aureus)
Staphylococcus aureus is a versatile skin and mucosal commensal that can transition into a highly virulent pathobiont. Known for its immune-evasive strategies, toxin production, and antibiotic resistance, it plays a significant role in chronic infections and microbiome imbalance.