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Hospital strains of E. faecalis often exhibit multidrug resistance, even to last-resort antibiotics like vancomycin, making these infections difficult to treat
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.
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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.
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.
I 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.
Overview
Enterococcus faecalis is a Gram‑positive, non‑spore‑forming, facultative anaerobe that commonly resides in the human gastrointestinal tract and can transition from commensal to opportunist in the setting of barrier disruption, devices, or antibiotic selection pressure.[1] Enterococci are prominent gut‑associated cocci in humans, and E. faecalis (together with E. faecium) accounts for the great majority of enterococcal infections reported in clinical practice.[2] Clinically, E. faecalis contributes to urinary tract infection, bloodstream infection and sepsis, wound infection, and infective endocarditis, with outcomes shaped by biofilm formation and the ability to persist under host and environmental stresses.[3][4] A defining evolutionary feature is efficient horizontal gene transfer: pheromone‑responsive plasmids (exemplified by pCF10‑family systems) use peptide signalling to strongly induce conjugation, supporting rapid dissemination of resistance and fitness traits in dense communities such as the antibiotic‑perturbed gut.[5]
Antibiotic resistance
Antimicrobial resistance in E. faecalis reflects a blend of intrinsic features, acquired mobile determinants and clinically relevant tolerance, which together complicate eradication in deep‑seated infection.[6] Intrinsic non‑susceptibility to many cephalosporins is a recognised enterococcal trait linked to low‑affinity penicillin‑binding proteins, with Pbp5 frequently highlighted as a key determinant in β‑lactam binding/response and cephalosporin poor activity.[7][8] Glycopeptide resistance is mediated by van gene clusters that remodel the peptidoglycan precursor target (mechanistically reducing glycopeptide binding), and these determinants can be mobile and transferable.[9] Because phenotypic vancomycin testing can produce ambiguous patterns at low levels of resistance, the European Committee on Antimicrobial Susceptibility Testing advises confirmatory PCR for vanA and vanB when vancomycin resistance is suspected in E. faecalis or E. faecium.[10][11] At the population level, EU/EEA surveillance reports continue to track substantial and geographically heterogeneous vancomycin resistance in invasive enterococcal infections (particularly E. faecium), reinforcing the need for local epidemiology‑informed empiric therapy and prevention strategies.[12]
Pathogenicity
E. faecalis pathogenicity is best explained by persistence and adhesion biology (biofilm and extracellular‑matrix binding), regulated secreted functions, and niche adaptation to host constraints (including nutritional immunity), rather than by a single universal toxin.[13] In experimental urinary‑tract infection models, both the collagen adhesin Ace and the endocarditis‑ and biofilm‑associated pili (Ebp) contribute to binding host ligands and to in vivo infection phenotypes, supporting a mechanistic role for these determinants in colonisation of tissues and devices.[14] Virulence is also regulated by quorum sensing: the fsr system influences collagen adherence by controlling gelatinase GelE, and GelE can reduce Ace surface display by proteolytic cleavage, directly linking signalling state to adhesive phenotype.[15] Some strains produce cytolysin, a quorum‑linked pore‑forming toxin with activity against both bacteria and eukaryotic cells, which has been reviewed as a feature of highly virulent E. faecalis lineages.[16] Nutrient metals are a demonstrated in vivo constraint: manganese acquisition systems are essential for virulence in mammalian infection models, and multiple iron/heme uptake mechanisms collectively support virulence and dissemination, showing that metal homeostasis is integral to disease success.[17][18]
Morphology
Enterococcus faecalis is a Gram‑positive coccus, typically forming pairs or short chains, and is non‑spore‑forming and facultatively anaerobic, consistent with adaptation to the intestinal niche and survival across oxygen gradients.[19] In routine laboratory contexts, morphology and basic culture appearance are insufficient to predict virulence or resistance, because clinically important traits (e.g., cytolysin, van genes, and biofilm determinants) are variably present and often governed by mobile elements or regulation.[20][21] Practical infection‑control emphasis is therefore placed on colonisation status and environmental transmission routes rather than phenotypic appearance alone, as reflected in Centers for Disease Control and Prevention guidance for VRE prevention in healthcare settings.[22]
Virulence Factors
| Virulence factor | Description and role in pathogenicity |
|---|---|
| Cytolysin (cyl locus) | Quorum‑linked pore‑forming exotoxin produced by a subset of strains; lyses Gram‑positive bacteria and eukaryotic cells and is associated with higher virulence potential in clinical contexts.[23] |
| Ace (collagen adhesin) | Surface MSCRAMM that mediates binding to collagen/extracellular matrix; contributes to adherence phenotypes and infection burden in experimental urinary‑tract infection models.[24] |
| Ebp pili (ebpABC operon) | Endocarditis‑ and biofilm‑associated pili that promote adherence to host ligands and robust biofilm formation; deletion reduces adherence and attenuates urinary‑tract infection phenotypes in vivo.[25] |
| Gelatinase (GelE) | Secreted protease that modulates host interaction by altering surface protein display; GelE can cleave Ace from the surface, reducing collagen adherence and linking proteolysis to adhesive phenotype.[26] |
| fsr quorum‑sensing system | Signalling system that controls GelE expression and thereby remodels collagen adherence via Ace surface display; illustrates density‑dependent regulation of virulence‑relevant traits.[27] |
| Pheromone‑responsive conjugative plasmids (pCF10‑family; includes aggregation substance) | Peptide pheromone signalling induces conjugation at high efficiency, enabling dissemination of resistance and fitness determinants; plasmid‑encoded surface factors promote donor–recipient contact, indirectly shaping colonisation and persistence.[28] |
Metallomics
| Metal / Ion | Key features in E. faecalis |
|---|---|
| Manganese (Mn²⁺) | Multiple Mn uptake systems support growth under Mn limitation and are required for virulence in mammalian infection models, consistent with Mn restriction by host nutritional immunity (including calprotectin‑mediated sequestration).[29] |
| Iron (Fe²⁺/Fe³⁺) | The organism encodes multiple iron uptake mechanisms; combined disruption of iron transport systems perturbs iron homeostasis and reduces virulence, supporting iron acquisition as a collective virulence requirement.[30] |
| Heme‑iron (heme as an iron source) [12] | Heme can function as an iron source that restores growth/virulence in experimental contexts, indicating that heme utilisation contributes to fitness during dissemination and in iron‑restricted host environments.[31] |
Vulnerabilities
| Vulnerability of E. faecalis | Potential therapeuticpreventive opportunity |
|---|---|
| Intrinsic poor activity of cephalosporins (linked to low‑affinity PBPs such as Pbp5) | Avoid cephalosporin monotherapy for suspected/confirmed enterococcal infection; for endocarditis where enhanced killing is required, use guideline‑supported combination regimens rather than relying on cephalosporins as primary anti‑enterococcal agents.[32][33] |
| Dependence on Mn acquisition for virulence under host metal restriction | Target Mn uptake pathways (transporters/regulation) as anti‑virulence adjunct concepts, because Mn acquisition is essential for virulence in mammalian models and supports tolerance of host calprotectin‑mediated metal sequestration.[34] |
| Collective reliance on multiple iron/heme uptake systems | If therapeutically targeted, multi‑component interruption (rather than single‑transporter blockade) is more plausible given redundancy; experimental disruption of multiple iron transporters impairs virulence and heme can rescue iron‑limited fitness.[35] |
| Adhesion/biofilm dependence via Ace and Ebp pili | Develop anti‑adhesion approaches (e.g., antibodies or binding inhibitors) to reduce colonisation of damaged tissue and devices, supported by experimental reductions in adherence and UTI phenotypes after ace/ebp disruption.[36] |
| Density‑dependent regulation of surface display via fsr→GelE→Ace cleavage | Explore quorum‑sensing/protease pathway inhibition to remodel adhesion and biofilm behaviour, with mechanistic evidence that GelE modulates Ace surface display and collagen adherence.[37] |
| High horizontal transfer capacity via pheromone‑responsive plasmids | Reduce selection pressure and cross‑transmission opportunities in healthcare and high‑risk wards to limit plasmid‑mediated acquisition of resistance/fitness traits; conjugation‑interference remains conceptual but is mechanistically grounded in pheromone‑controlled transfer.[38][39] |
Interventions
| Intervention | Mechanism |
|---|---|
| Species‑level identification plus susceptibility testing for clinically significant isolates | Distinguishes likely β‑lactam options, flags intrinsic cephalosporin non‑susceptibility, and supports detection of resistance that changes management in invasive infection.[40] |
| Confirmatory vanA/vanB PCR when glycopeptide resistance is suspected | EUCAST recommends molecular confirmation/exclusion of vanA/vanB when vancomycin resistance is suspected, improving accuracy where phenotypes are borderline and enabling timely infection‑control actions.[41] |
| Ampicillin + ceftriaxone for E. faecalis infective endocarditis (when guideline‑appropriate) | Dual β‑lactam therapy exploits complementary PBP binding to enhance bactericidal activity and is recommended in contemporary ESC guidance for appropriate scenarios; cohort evidence supports comparable effectiveness to ampicillin + gentamicin with reduced aminoglycoside toxicity concerns.[42][43] |
| Regional surveillance‑informed risk assessment for vancomycin‑resistant enterococci | ECDC EU/EEA surveillance data on invasive isolates inform empiric therapy and prevention policies by quantifying and tracking vancomycin resistance trends (including substantial resistance in E. faecium with geographical variation).[44] |
Research Feed
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 the key types of microorganisms—bacteria, viruses, fungi, protozoa, and archaea—along with major examples of pathogenic and beneficial species.
Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.
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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 the key types of microorganisms—bacteria, viruses, fungi, protozoa, and archaea—along with major examples of pathogenic and beneficial species.
Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.
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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 the key types of microorganisms—bacteria, viruses, fungi, protozoa, and archaea—along with major examples of pathogenic and beneficial species.
Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.
Create a free account to unlock this study summary.
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 the key types of microorganisms—bacteria, viruses, fungi, protozoa, and archaea—along with major examples of pathogenic and beneficial species.
Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.
Create a free account to unlock this study summary.
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 the key types of microorganisms—bacteria, viruses, fungi, protozoa, and archaea—along with major examples of pathogenic and beneficial species.
Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.
Create a free account to unlock this study summary.
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 the key types of microorganisms—bacteria, viruses, fungi, protozoa, and archaea—along with major examples of pathogenic and beneficial species.
Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.
Create a free account to unlock this study summary.
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 the key types of microorganisms—bacteria, viruses, fungi, protozoa, and archaea—along with major examples of pathogenic and beneficial species.
Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.
Create a free account to unlock this study summary.
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 the key types of microorganisms—bacteria, viruses, fungi, protozoa, and archaea—along with major examples of pathogenic and beneficial species.
Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.
Create a free account to unlock this study summary.
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 the key types of microorganisms—bacteria, viruses, fungi, protozoa, and archaea—along with major examples of pathogenic and beneficial species.
Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.
Create a free account to unlock this study summary.
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 the key types of microorganisms—bacteria, viruses, fungi, protozoa, and archaea—along with major examples of pathogenic and beneficial species.
Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.
Create a free account to unlock this study summary.
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 the key types of microorganisms—bacteria, viruses, fungi, protozoa, and archaea—along with major examples of pathogenic and beneficial species.
Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.
Create a free account to unlock this study summary.
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 the key types of microorganisms—bacteria, viruses, fungi, protozoa, and archaea—along with major examples of pathogenic and beneficial species.
Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.
Create a free account to unlock this study summary.
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 the key types of microorganisms—bacteria, viruses, fungi, protozoa, and archaea—along with major examples of pathogenic and beneficial species.
Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.
Create a free account to unlock this study summary.
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 the key types of microorganisms—bacteria, viruses, fungi, protozoa, and archaea—along with major examples of pathogenic and beneficial species.
Alias iure reprehenderit aut accusantium. Molestiae dolore suscipit. Necessitatibus eum quaerat. Repudiandae suscipit quo necessitatibus. Voluptatibus ullam nulla temporibus nobis. Atque eaque sed totam est assumenda. Porro modi soluta consequuntur veritatis excepturi minus delectus reprehenderit est. Eveniet labore ut quas minima aliquid quibusdam. Vitae possimus fuga praesentium eveniet debitis exercitationem deleniti.
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Manganese plays a pivotal role in microbial pathogenesis. As a vital cofactor for enzymes involved in antioxidant defense and metabolism, manganese is essential for pathogens, enabling them to survive within the host. However, when not properly managed, manganese can become toxic to both the host and the pathogen. The host’s immune system, through mechanisms like the secretion of calprotectin, tries to limit microbial access to manganese, creating an ongoing battle between host defenses and microbial survival .
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
References
- From the Friend to the Foe—Enterococcus faecalis Diverse Impact on the Human Immune System.. Daca, A., & Jarzembowski, T. (2024).. (International Journal of Molecular Sciences, 25(4), 2422.)
- Structure, Function, and Biology of the Enterococcus faecalis Cytolysin.. Tyne, D. V., Martin, M. J., & Gilmore, M. S. (2013).. (Toxins, 5(5), 895.)
- Structure, Function, and Biology of the Enterococcus faecalis Cytolysin.. Tyne, D. V., Martin, M. J., & Gilmore, M. S. (2013).. (Toxins, 5(5), 895.)
- Model systems for the study of Enterococcal colonization and infection.. Goh, H. M. S., Yong, M. H. A., Chong, K. K. L., & Kline, K. A. (2017).. (Virulence, 8(8), 1525–1562.)
- The peptide pheromone-inducible conjugation system of Enterococcus faecalis plasmid pCF10: cell-cell signalling, gene transfer, complexity and evolution.. Dunny G. M. (2007).. (Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 362(1483), 1185–1193.)
- Mechanisms of antibiotic resistance in enterococci.. Miller, W. R., Munita, J. M., & Arias, C. A. (2014).. (Expert review of anti-infective therapy, 12(10), 1221–1236.)
- The Enterococcus: a Model of Adaptability to Its Environment.. García-Solache, M., & Rice, L. B. (2019).. (Clinical microbiology reviews, 32(2), e00058-18.)
- Mechanisms of antibiotic resistance in enterococci.. Miller, W. R., Munita, J. M., & Arias, C. A. (2014).. (Expert review of anti-infective therapy, 12(10), 1221–1236.)
- Regulation of VanA- and VanB-type glycopeptide resistance in enterococci.. Arthur, M., & Quintiliani, R., Jr (2001).. (Antimicrobial agents and chemotherapy, 45(2), 375–381.)
- Performance of the EUCAST disk diffusion method, the CLSI agar screen method, and the Vitek 2 automated antimicrobial susceptibility testing system for detection of clinical isolates of Enterococci with low- and medium-level VanB-type vancomycin resistance: a multicenter study.. Hegstad, K., Giske, C. G., Haldorsen, B., Matuschek, E., Schønning, K., Leegaard, T. M., Kahlmeter, G., Sundsfjord, A., & NordicAST VRE Detection Study Group (2014).. (Journal of clinical microbiology, 52(5), 1582–1589.)
- Regulation of VanA- and VanB-type glycopeptide resistance in enterococci.. Arthur, M., & Quintiliani, R., Jr (2001).. (Antimicrobial agents and chemotherapy, 45(2), 375–381.)
- Antimicrobial resistance in the EU/EEA (EARS-Net) - Annual Epidemiological Report for 2024.. European Centre for Disease Prevention and Control (ECDC).. (Stockholm: ECDC; 2025.)
- Enterococcus faecium: evolution, adaptation, pathogenesis and emerging therapeutics.. Wei, Y., Palacios Araya, D., & Palmer, K. L. (2024).. (Nature reviews. Microbiology, 22(11), 705–721.)
- Relative contributions of Ebp Pili and the collagen adhesin ace to host extracellular matrix protein adherence and experimental urinary tract infection by Enterococcus faecalis OG1RF.. Nallapareddy, S. R., Singh, K. V., Sillanpää, J., Zhao, M., & Murray, B. E. (2011).. (Infection and immunity, 79(7), 2901–2910.)
- The Fsr quorum-sensing system of Enterococcus faecalis modulates surface display of the collagen-binding MSCRAMM Ace through regulation of gelE.. Pinkston, K. L., Gao, P., Diaz-Garcia, D., Sillanpää, J., Nallapareddy, S. R., Murray, B. E., & Harvey, B. R. (2011).. (Journal of bacteriology, 193(17), 4317–4325.)
- Structure, Function, and Biology of the Enterococcus faecalis Cytolysin.. Tyne, D. V., Martin, M. J., & Gilmore, M. S. (2013).. (Toxins, 5(5), 895.)
- Manganese acquisition is essential for virulence of Enterococcus faecalis.. Colomer-Winter, C., Flores-Mireles, A. L., Baker, S. P., Frank, K. L., L Lynch, A. J., Hultgren, S. J., Kitten, T., & Lemos, J. A. (2018).. (PLoS Pathogens, 14(9), e1007102.)
- Identification of Multiple Iron Uptake Mechanisms in Enterococcus faecalis and Their Relationship to Virulence.. Brunson, D. N., Colomer-Winter, C., Lam, L. N., & Lemos, J. A. (2023).. (Infection and immunity, 91(4), e0049622.)
- Structure, Function, and Biology of the Enterococcus faecalis Cytolysin.. Tyne, D. V., Martin, M. J., & Gilmore, M. S. (2013).. (Toxins, 5(5), 895.)
- Structure, Function, and Biology of the Enterococcus faecalis Cytolysin.. Tyne, D. V., Martin, M. J., & Gilmore, M. S. (2013).. (Toxins, 5(5), 895.)
- Mechanisms of antibiotic resistance in enterococci.. Miller, W. R., Munita, J. M., & Arias, C. A. (2014).. (Expert review of anti-infective therapy, 12(10), 1221–1236.)
- Vancomycin-resistant Enterococcus faecium: A current perspective on resilience, adaptation, and the urgent need for novel strategies.. Almeida-Santos, A. C., Novais, C., Peixe, L., & Freitas, A. R. (2025).. (Journal of Global Antimicrobial Resistance, 41, 233-252.)
- Structure, Function, and Biology of the Enterococcus faecalis Cytolysin.. Tyne, D. V., Martin, M. J., & Gilmore, M. S. (2013).. (Toxins, 5(5), 895.)
- Relative contributions of Ebp Pili and the collagen adhesin ace to host extracellular matrix protein adherence and experimental urinary tract infection by Enterococcus faecalis OG1RF.. Nallapareddy, S. R., Singh, K. V., Sillanpää, J., Zhao, M., & Murray, B. E. (2011).. (Infection and immunity, 79(7), 2901–2910.)
- Relative contributions of Ebp Pili and the collagen adhesin ace to host extracellular matrix protein adherence and experimental urinary tract infection by Enterococcus faecalis OG1RF.. Nallapareddy, S. R., Singh, K. V., Sillanpää, J., Zhao, M., & Murray, B. E. (2011).. (Infection and immunity, 79(7), 2901–2910.)
- The Fsr quorum-sensing system of Enterococcus faecalis modulates surface display of the collagen-binding MSCRAMM Ace through regulation of gelE.. Pinkston, K. L., Gao, P., Diaz-Garcia, D., Sillanpää, J., Nallapareddy, S. R., Murray, B. E., & Harvey, B. R. (2011).. (Journal of bacteriology, 193(17), 4317–4325.)
- The Fsr quorum-sensing system of Enterococcus faecalis modulates surface display of the collagen-binding MSCRAMM Ace through regulation of gelE.. Pinkston, K. L., Gao, P., Diaz-Garcia, D., Sillanpää, J., Nallapareddy, S. R., Murray, B. E., & Harvey, B. R. (2011).. (Journal of bacteriology, 193(17), 4317–4325.)
- The peptide pheromone-inducible conjugation system of Enterococcus faecalis plasmid pCF10: cell-cell signalling, gene transfer, complexity and evolution.. Dunny G. M. (2007).. (Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 362(1483), 1185–1193.)
- Manganese acquisition is essential for virulence of Enterococcus faecalis.. Colomer-Winter, C., Flores-Mireles, A. L., Baker, S. P., Frank, K. L., L Lynch, A. J., Hultgren, S. J., Kitten, T., & Lemos, J. A. (2018).. (PLoS Pathogens, 14(9), e1007102.)
- Identification of Multiple Iron Uptake Mechanisms in Enterococcus faecalis and Their Relationship to Virulence.. Brunson, D. N., Colomer-Winter, C., Lam, L. N., & Lemos, J. A. (2023).. (Infection and immunity, 91(4), e0049622.)
- Identification of Multiple Iron Uptake Mechanisms in Enterococcus faecalis and Their Relationship to Virulence.. Brunson, D. N., Colomer-Winter, C., Lam, L. N., & Lemos, J. A. (2023).. (Infection and immunity, 91(4), e0049622.)
- Mechanisms of antibiotic resistance in enterococci.. Miller, W. R., Munita, J. M., & Arias, C. A. (2014).. (Expert review of anti-infective therapy, 12(10), 1221–1236.)
- 2023 ESC Guidelines for the management of endocarditis: Developed by the task force on the management of endocarditis of the European Society of Cardiology (ESC) Endorsed by the European Association for Cardio-Thoracic Surgery (EACTS) and the European Association of Nuclear Medicine (EANM),. Victoria Delgado, Nina Ajmone Marsan, Suzanne de Waha, Nikolaos Bonaros, Margarita Brida, Haran Burri, Stefano Caselli, Torsten Doenst, Stephane Ederhy, Paola Anna Erba, Dan Foldager, Emil L Fosbøl, Jan Kovac, Carlos A Mestres, Owen I Miller, Jose M Miro, Michal Pazdernik, Maria Nazarena Pizzi, Eduard Quintana, Trine Bernholdt Rasmussen, Arsen D Ristić, Josep Rodés-Cabau, Alessandro Sionis, Liesl Joanna Zühlke, Michael A Borger, ESC Scientific Document Group ,. (European Heart Journal, Volume 44, Issue 39, 14 October 2023, Pages 3948–4042,)
- Manganese acquisition is essential for virulence of Enterococcus faecalis.. Colomer-Winter, C., Flores-Mireles, A. L., Baker, S. P., Frank, K. L., L Lynch, A. J., Hultgren, S. J., Kitten, T., & Lemos, J. A. (2018).. (PLoS Pathogens, 14(9), e1007102.)
- Identification of Multiple Iron Uptake Mechanisms in Enterococcus faecalis and Their Relationship to Virulence.. Brunson, D. N., Colomer-Winter, C., Lam, L. N., & Lemos, J. A. (2023).. (Infection and immunity, 91(4), e0049622.)
- Relative contributions of Ebp Pili and the collagen adhesin ace to host extracellular matrix protein adherence and experimental urinary tract infection by Enterococcus faecalis OG1RF.. Nallapareddy, S. R., Singh, K. V., Sillanpää, J., Zhao, M., & Murray, B. E. (2011).. (Infection and immunity, 79(7), 2901–2910.)
- The Fsr quorum-sensing system of Enterococcus faecalis modulates surface display of the collagen-binding MSCRAMM Ace through regulation of gelE.. Pinkston, K. L., Gao, P., Diaz-Garcia, D., Sillanpää, J., Nallapareddy, S. R., Murray, B. E., & Harvey, B. R. (2011).. (Journal of bacteriology, 193(17), 4317–4325.)
- The peptide pheromone-inducible conjugation system of Enterococcus faecalis plasmid pCF10: cell-cell signalling, gene transfer, complexity and evolution.. Dunny G. M. (2007).. (Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 362(1483), 1185–1193.)
- Vancomycin-resistant Enterococcus faecium: A current perspective on resilience, adaptation, and the urgent need for novel strategies.. Almeida-Santos, A. C., Novais, C., Peixe, L., & Freitas, A. R. (2025).. (Journal of Global Antimicrobial Resistance, 41, 233-252.)
- Mechanisms of antibiotic resistance in enterococci.. Miller, W. R., Munita, J. M., & Arias, C. A. (2014).. (Expert review of anti-infective therapy, 12(10), 1221–1236.)
- Vancomycin-resistant Enterococcus faecium: A current perspective on resilience, adaptation, and the urgent need for novel strategies.. Almeida-Santos, A. C., Novais, C., Peixe, L., & Freitas, A. R. (2025).. (Journal of Global Antimicrobial Resistance, 41, 233-252.)
- Ampicillin Plus Ceftriaxone Is as Effective as Ampicillin Plus Gentamicin for Treating Enterococcus faecalis Infective Endocarditis,. Nuria Fernández-Hidalgo, Benito Almirante, Joan Gavaldà, Mercè Gurgui, Carmen Peña, Arístides de Alarcón, Josefa Ruiz, Isidre Vilacosta, Miguel Montejo, Nuria Vallejo, Francisco López-Medrano, Antonio Plata, Javier López, Carmen Hidalgo-Tenorio, Juan Gálvez, Carmen Sáez, José Manuel Lomas, Marco Falcone, Javier de la Torre, Xavier Martínez-Lacasa, Albert Pahissa,. (Clinical Infectious Diseases, Volume 56, Issue 9, 1 May 2013, Pages 1261–1268,)
- 2023 ESC Guidelines for the management of endocarditis: Developed by the task force on the management of endocarditis of the European Society of Cardiology (ESC) Endorsed by the European Association for Cardio-Thoracic Surgery (EACTS) and the European Association of Nuclear Medicine (EANM),. Victoria Delgado, Nina Ajmone Marsan, Suzanne de Waha, Nikolaos Bonaros, Margarita Brida, Haran Burri, Stefano Caselli, Torsten Doenst, Stephane Ederhy, Paola Anna Erba, Dan Foldager, Emil L Fosbøl, Jan Kovac, Carlos A Mestres, Owen I Miller, Jose M Miro, Michal Pazdernik, Maria Nazarena Pizzi, Eduard Quintana, Trine Bernholdt Rasmussen, Arsen D Ristić, Josep Rodés-Cabau, Alessandro Sionis, Liesl Joanna Zühlke, Michael A Borger, ESC Scientific Document Group ,. (European Heart Journal, Volume 44, Issue 39, 14 October 2023, Pages 3948–4042,)
- Antimicrobial resistance in the EU/EEA (EARS-Net) - Annual Epidemiological Report for 2024.. European Centre for Disease Prevention and Control (ECDC).. (Stockholm: ECDC; 2025.)
Daca, A., & Jarzembowski, T. (2024).
From the Friend to the Foe—Enterococcus faecalis Diverse Impact on the Human Immune System.International Journal of Molecular Sciences, 25(4), 2422.
Read ReviewTyne, D. V., Martin, M. J., & Gilmore, M. S. (2013).
Structure, Function, and Biology of the Enterococcus faecalis Cytolysin.Toxins, 5(5), 895.
Read ReviewTyne, D. V., Martin, M. J., & Gilmore, M. S. (2013).
Structure, Function, and Biology of the Enterococcus faecalis Cytolysin.Toxins, 5(5), 895.
Read ReviewGoh, H. M. S., Yong, M. H. A., Chong, K. K. L., & Kline, K. A. (2017).
Model systems for the study of Enterococcal colonization and infection.Virulence, 8(8), 1525–1562.
Read ReviewDunny G. M. (2007).
The peptide pheromone-inducible conjugation system of Enterococcus faecalis plasmid pCF10: cell-cell signalling, gene transfer, complexity and evolution.Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 362(1483), 1185–1193.
Read ReviewMiller, W. R., Munita, J. M., & Arias, C. A. (2014).
Mechanisms of antibiotic resistance in enterococci.Expert review of anti-infective therapy, 12(10), 1221–1236.
Read ReviewGarcía-Solache, M., & Rice, L. B. (2019).
The Enterococcus: a Model of Adaptability to Its Environment.Clinical microbiology reviews, 32(2), e00058-18.
Read ReviewMiller, W. R., Munita, J. M., & Arias, C. A. (2014).
Mechanisms of antibiotic resistance in enterococci.Expert review of anti-infective therapy, 12(10), 1221–1236.
Read ReviewArthur, M., & Quintiliani, R., Jr (2001).
Regulation of VanA- and VanB-type glycopeptide resistance in enterococci.Antimicrobial agents and chemotherapy, 45(2), 375–381.
Read ReviewHegstad, K., Giske, C. G., Haldorsen, B., Matuschek, E., Schønning, K., Leegaard, T. M., Kahlmeter, G., Sundsfjord, A., & NordicAST VRE Detection Study Group (2014).
Performance of the EUCAST disk diffusion method, the CLSI agar screen method, and the Vitek 2 automated antimicrobial susceptibility testing system for detection of clinical isolates of Enterococci with low- and medium-level VanB-type vancomycin resistance: a multicenter study.Journal of clinical microbiology, 52(5), 1582–1589.
Read ReviewArthur, M., & Quintiliani, R., Jr (2001).
Regulation of VanA- and VanB-type glycopeptide resistance in enterococci.Antimicrobial agents and chemotherapy, 45(2), 375–381.
Read ReviewEuropean Centre for Disease Prevention and Control (ECDC).
Antimicrobial resistance in the EU/EEA (EARS-Net) - Annual Epidemiological Report for 2024.Stockholm: ECDC; 2025.
Wei, Y., Palacios Araya, D., & Palmer, K. L. (2024).
Enterococcus faecium: evolution, adaptation, pathogenesis and emerging therapeutics.Nature reviews. Microbiology, 22(11), 705–721.
Read ReviewNallapareddy, S. R., Singh, K. V., Sillanpää, J., Zhao, M., & Murray, B. E. (2011).
Relative contributions of Ebp Pili and the collagen adhesin ace to host extracellular matrix protein adherence and experimental urinary tract infection by Enterococcus faecalis OG1RF.Infection and immunity, 79(7), 2901–2910.
Read ReviewPinkston, K. L., Gao, P., Diaz-Garcia, D., Sillanpää, J., Nallapareddy, S. R., Murray, B. E., & Harvey, B. R. (2011).
The Fsr quorum-sensing system of Enterococcus faecalis modulates surface display of the collagen-binding MSCRAMM Ace through regulation of gelE.Journal of bacteriology, 193(17), 4317–4325.
Read ReviewTyne, D. V., Martin, M. J., & Gilmore, M. S. (2013).
Structure, Function, and Biology of the Enterococcus faecalis Cytolysin.Toxins, 5(5), 895.
Read ReviewColomer-Winter, C., Flores-Mireles, A. L., Baker, S. P., Frank, K. L., L Lynch, A. J., Hultgren, S. J., Kitten, T., & Lemos, J. A. (2018).
Manganese acquisition is essential for virulence of Enterococcus faecalis.PLoS Pathogens, 14(9), e1007102.
Read ReviewBrunson, D. N., Colomer-Winter, C., Lam, L. N., & Lemos, J. A. (2023).
Identification of Multiple Iron Uptake Mechanisms in Enterococcus faecalis and Their Relationship to Virulence.Infection and immunity, 91(4), e0049622.
Read ReviewTyne, D. V., Martin, M. J., & Gilmore, M. S. (2013).
Structure, Function, and Biology of the Enterococcus faecalis Cytolysin.Toxins, 5(5), 895.
Read ReviewTyne, D. V., Martin, M. J., & Gilmore, M. S. (2013).
Structure, Function, and Biology of the Enterococcus faecalis Cytolysin.Toxins, 5(5), 895.
Read ReviewMiller, W. R., Munita, J. M., & Arias, C. A. (2014).
Mechanisms of antibiotic resistance in enterococci.Expert review of anti-infective therapy, 12(10), 1221–1236.
Read ReviewAlmeida-Santos, A. C., Novais, C., Peixe, L., & Freitas, A. R. (2025).
Vancomycin-resistant Enterococcus faecium: A current perspective on resilience, adaptation, and the urgent need for novel strategies.Journal of Global Antimicrobial Resistance, 41, 233-252.
Read ReviewTyne, D. V., Martin, M. J., & Gilmore, M. S. (2013).
Structure, Function, and Biology of the Enterococcus faecalis Cytolysin.Toxins, 5(5), 895.
Read ReviewNallapareddy, S. R., Singh, K. V., Sillanpää, J., Zhao, M., & Murray, B. E. (2011).
Relative contributions of Ebp Pili and the collagen adhesin ace to host extracellular matrix protein adherence and experimental urinary tract infection by Enterococcus faecalis OG1RF.Infection and immunity, 79(7), 2901–2910.
Read ReviewNallapareddy, S. R., Singh, K. V., Sillanpää, J., Zhao, M., & Murray, B. E. (2011).
Relative contributions of Ebp Pili and the collagen adhesin ace to host extracellular matrix protein adherence and experimental urinary tract infection by Enterococcus faecalis OG1RF.Infection and immunity, 79(7), 2901–2910.
Read ReviewPinkston, K. L., Gao, P., Diaz-Garcia, D., Sillanpää, J., Nallapareddy, S. R., Murray, B. E., & Harvey, B. R. (2011).
The Fsr quorum-sensing system of Enterococcus faecalis modulates surface display of the collagen-binding MSCRAMM Ace through regulation of gelE.Journal of bacteriology, 193(17), 4317–4325.
Read ReviewPinkston, K. L., Gao, P., Diaz-Garcia, D., Sillanpää, J., Nallapareddy, S. R., Murray, B. E., & Harvey, B. R. (2011).
The Fsr quorum-sensing system of Enterococcus faecalis modulates surface display of the collagen-binding MSCRAMM Ace through regulation of gelE.Journal of bacteriology, 193(17), 4317–4325.
Read ReviewDunny G. M. (2007).
The peptide pheromone-inducible conjugation system of Enterococcus faecalis plasmid pCF10: cell-cell signalling, gene transfer, complexity and evolution.Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 362(1483), 1185–1193.
Read ReviewColomer-Winter, C., Flores-Mireles, A. L., Baker, S. P., Frank, K. L., L Lynch, A. J., Hultgren, S. J., Kitten, T., & Lemos, J. A. (2018).
Manganese acquisition is essential for virulence of Enterococcus faecalis.PLoS Pathogens, 14(9), e1007102.
Read ReviewBrunson, D. N., Colomer-Winter, C., Lam, L. N., & Lemos, J. A. (2023).
Identification of Multiple Iron Uptake Mechanisms in Enterococcus faecalis and Their Relationship to Virulence.Infection and immunity, 91(4), e0049622.
Read ReviewBrunson, D. N., Colomer-Winter, C., Lam, L. N., & Lemos, J. A. (2023).
Identification of Multiple Iron Uptake Mechanisms in Enterococcus faecalis and Their Relationship to Virulence.Infection and immunity, 91(4), e0049622.
Read ReviewMiller, W. R., Munita, J. M., & Arias, C. A. (2014).
Mechanisms of antibiotic resistance in enterococci.Expert review of anti-infective therapy, 12(10), 1221–1236.
Read ReviewVictoria Delgado, Nina Ajmone Marsan, Suzanne de Waha, Nikolaos Bonaros, Margarita Brida, Haran Burri, Stefano Caselli, Torsten Doenst, Stephane Ederhy, Paola Anna Erba, Dan Foldager, Emil L Fosbøl, Jan Kovac, Carlos A Mestres, Owen I Miller, Jose M Miro, Michal Pazdernik, Maria Nazarena Pizzi, Eduard Quintana, Trine Bernholdt Rasmussen, Arsen D Ristić, Josep Rodés-Cabau, Alessandro Sionis, Liesl Joanna Zühlke, Michael A Borger, ESC Scientific Document Group ,
2023 ESC Guidelines for the management of endocarditis: Developed by the task force on the management of endocarditis of the European Society of Cardiology (ESC) Endorsed by the European Association for Cardio-Thoracic Surgery (EACTS) and the European Association of Nuclear Medicine (EANM),European Heart Journal, Volume 44, Issue 39, 14 October 2023, Pages 3948–4042,
Colomer-Winter, C., Flores-Mireles, A. L., Baker, S. P., Frank, K. L., L Lynch, A. J., Hultgren, S. J., Kitten, T., & Lemos, J. A. (2018).
Manganese acquisition is essential for virulence of Enterococcus faecalis.PLoS Pathogens, 14(9), e1007102.
Read ReviewBrunson, D. N., Colomer-Winter, C., Lam, L. N., & Lemos, J. A. (2023).
Identification of Multiple Iron Uptake Mechanisms in Enterococcus faecalis and Their Relationship to Virulence.Infection and immunity, 91(4), e0049622.
Read ReviewNallapareddy, S. R., Singh, K. V., Sillanpää, J., Zhao, M., & Murray, B. E. (2011).
Relative contributions of Ebp Pili and the collagen adhesin ace to host extracellular matrix protein adherence and experimental urinary tract infection by Enterococcus faecalis OG1RF.Infection and immunity, 79(7), 2901–2910.
Read ReviewPinkston, K. L., Gao, P., Diaz-Garcia, D., Sillanpää, J., Nallapareddy, S. R., Murray, B. E., & Harvey, B. R. (2011).
The Fsr quorum-sensing system of Enterococcus faecalis modulates surface display of the collagen-binding MSCRAMM Ace through regulation of gelE.Journal of bacteriology, 193(17), 4317–4325.
Read ReviewDunny G. M. (2007).
The peptide pheromone-inducible conjugation system of Enterococcus faecalis plasmid pCF10: cell-cell signalling, gene transfer, complexity and evolution.Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 362(1483), 1185–1193.
Read ReviewAlmeida-Santos, A. C., Novais, C., Peixe, L., & Freitas, A. R. (2025).
Vancomycin-resistant Enterococcus faecium: A current perspective on resilience, adaptation, and the urgent need for novel strategies.Journal of Global Antimicrobial Resistance, 41, 233-252.
Read ReviewMiller, W. R., Munita, J. M., & Arias, C. A. (2014).
Mechanisms of antibiotic resistance in enterococci.Expert review of anti-infective therapy, 12(10), 1221–1236.
Read ReviewAlmeida-Santos, A. C., Novais, C., Peixe, L., & Freitas, A. R. (2025).
Vancomycin-resistant Enterococcus faecium: A current perspective on resilience, adaptation, and the urgent need for novel strategies.Journal of Global Antimicrobial Resistance, 41, 233-252.
Read ReviewNuria Fernández-Hidalgo, Benito Almirante, Joan Gavaldà, Mercè Gurgui, Carmen Peña, Arístides de Alarcón, Josefa Ruiz, Isidre Vilacosta, Miguel Montejo, Nuria Vallejo, Francisco López-Medrano, Antonio Plata, Javier López, Carmen Hidalgo-Tenorio, Juan Gálvez, Carmen Sáez, José Manuel Lomas, Marco Falcone, Javier de la Torre, Xavier Martínez-Lacasa, Albert Pahissa,
Ampicillin Plus Ceftriaxone Is as Effective as Ampicillin Plus Gentamicin for Treating Enterococcus faecalis Infective Endocarditis,Clinical Infectious Diseases, Volume 56, Issue 9, 1 May 2013, Pages 1261–1268,
Victoria Delgado, Nina Ajmone Marsan, Suzanne de Waha, Nikolaos Bonaros, Margarita Brida, Haran Burri, Stefano Caselli, Torsten Doenst, Stephane Ederhy, Paola Anna Erba, Dan Foldager, Emil L Fosbøl, Jan Kovac, Carlos A Mestres, Owen I Miller, Jose M Miro, Michal Pazdernik, Maria Nazarena Pizzi, Eduard Quintana, Trine Bernholdt Rasmussen, Arsen D Ristić, Josep Rodés-Cabau, Alessandro Sionis, Liesl Joanna Zühlke, Michael A Borger, ESC Scientific Document Group ,
2023 ESC Guidelines for the management of endocarditis: Developed by the task force on the management of endocarditis of the European Society of Cardiology (ESC) Endorsed by the European Association for Cardio-Thoracic Surgery (EACTS) and the European Association of Nuclear Medicine (EANM),European Heart Journal, Volume 44, Issue 39, 14 October 2023, Pages 3948–4042,
European Centre for Disease Prevention and Control (ECDC).
Antimicrobial resistance in the EU/EEA (EARS-Net) - Annual Epidemiological Report for 2024.Stockholm: ECDC; 2025.
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