| Enterococcus faecalis | |
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Scientific classification | |
| Domain: | Bacteria |
| Kingdom: | Bacillati |
| Phylum: | Bacillota |
| Class: | Bacilli |
| Order: | Lactobacillales |
| Family: | Enterococcaceae |
| Genus: | Enterococcus |
| Species: | E. faecalis |
| Binomial name | |
| Enterococcus faecalis (Andrewes and Horder, 1906) Schleifer and Kilpper-Bälz, 1984 | |
Enterococcus faecalis – formerly classified as part of the group DStreptococcus, is aGram-positive,commensalbacterium naturally inhabiting thegastrointestinal tracts of humans.[1][2] Like other species in thegenusEnterococcus,E. faecalis is found in healthy humans and can be used as a probiotic. The probiotic strains such as Symbioflor1 and EF-2001 are characterized by the lack of specific genes related to drug resistance and pathogenesis.[3]
Despite its commensal role,E. faecalis is an opportunistic pathogen capable of causing severe infections, especially in thenosocomial (hospital) settings.[4]Enterococcus spp. is among the leading causes of healthcare-associated infections ranging from endocarditis to urinary tract infections (UTIs). Hospital-acquired UTIs are associated with catheterization because catheters provide an ideal surface for biofilm formation, allowingE. faecalis to adhere, persist, and evade both the immune response and antibiotic treatment.[4]
E. faecalis is able to grow in extreme environments due to its highly adaptive genome and lack of strong defense mechanisms.[4] Its ability to easily acquire and transfer genes across species contributes to rising antibiotic resistance.E. faecalis exhibits intrinsic resistance to multiple antibiotics, including oxazolidinones, quinolones, and most β -lactams, such as cephalosporins.[4][5]
E. faecalis has been frequently found in reinfected, root canal-treated teeth in prevalence values ranging from 30% to 90% of the cases.[6] Re-infected root canal-treated teeth are about nine times more likely to harborE. faecalis than cases of primary infections.[7]
E. faecalis is anonmotile microbe; itfermentsglucose without gas production, and does not produce acatalase reaction withhydrogen peroxide. It produces a reduction oflitmus milk, but does not liquefy gelatin. It shows consistent growth throughout nutrient broth which is consistent with being afacultative anaerobe. Itcatabolizes a variety of energy sources, includingglycerol,lactate,malate,citrate,arginine,agmatine, and manyketo acids. Enterococci survive very harsh environments, including extremely alkaline pH (9.6) and salt concentrations. They resistbile salts,detergents,heavy metals,ethanol,azide, anddesiccation. They can grow in the range of 10 to 45 °C and survive at temperatures of 60 °C for 30 min.[8]
In clinical settings,E. faecalis displays a relatively conserved metabolic profile compared to other enterococcal species. A recent large-scale study of urinary isolates from ICU patients showed thatE. faecalis consistently metabolizessorbitol,mannitol,amygdalin andsucrose but lacks the ability to utilizeL-arabinose,melibiose, orraffinose—substrates readily used byE. faecium andE. durans. This substrate profile provides a reliable metabolic signature that can help distinguishE. faecalis from related species in diagnostic and research contexts.[9]
E. faecalis is found in most healthy individuals, but can causeendocarditis andsepsis,urinary tract infections (UTIs),meningitis, and other infections in humans.[10][11] Several virulence factors are thought to contribute toE. faecalis infections. Aplasmid-encodedhemolysin, called thecytolysin, is important for pathogenesis in animal models of infection, and the cytolysin in combination with high-levelgentamicin resistance is associated with a five-fold increase in risk of death in human bacteremia patients.[12][13][14] Aplasmid-encodedadhesin[15] called "aggregation substance" is also important for virulence in animal models of infection.[13][16]
E. faecalis contains atyrosine decarboxylase enzyme capable of decarboxylatingL-DOPA, a crucial drug in the treatment ofParkinson's disease. If L-DOPA is decarboxylated in thegut microbiome, it cannot pass through theblood-brain barrier and be decarboxylated in the brain to becomedopamine.[17]
E. faecalis is usually resistant to many commonly usedantimicrobial agents (aminoglycosides,aztreonam andquinolones).[18] The resistance is mediated by the presence of multiple genes related to drug resistance in the chromosome or plasmid.[3]
Resistance tovancomycin inE. faecalis is becoming more common.[19][20] Treatment options for vancomycin-resistantE. faecalis includenitrofurantoin (in the case of uncomplicated UTIs),[21]linezolid,quinupristin,tigecycline[18] anddaptomycin, althoughampicillin is preferred if the bacteria are susceptible.[22]Quinupristin/dalfopristin can be used to treatEnterococcus faecium but notE. faecalis.[22]
In root-canal treatments,NaOCl andchlorhexidine (CHX) are used to fightE. faecalis before isolating the canal. However, recent studies determined that NaOCl or CHX showed low ability to eliminateE. faecalis.[23]
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According to one study combined drug therapy has shown some efficacy in cases of severe infections (e.g.heart valves infections) against susceptible strains ofE. faecalis.Ampicillin- andvancomycin-sensitiveE. faecalis (lacking high-level resistance toaminoglycosides) strains can be treated bygentamicin andampicillin antibiotics. A lessnephrotoxic combination of ampicillin andceftriaxone (even thoughE. faecalis is resistant to cephalosporins,ceftriaxone is working synergistically with ampicillin) may be used alternatively for ampicillin-susceptibleE. faecalis.[24]
Daptomycin orlinezolid may also show efficacy in case ampicillin and vancomycin resistance.[24]
A combination ofpenicillin andstreptomycin therapy was used in the past.[24]
Tedizolid,telavancin,dalbavancin, andoritavancin antibiotics are FDA approved as treatments against EF.[18]
UTIs are among the most common bacterial infections and their treatment is becoming increasingly challenging due to the rise of multidrug-resistantE. faecalis strains.[5][4]Current UTI treatments rely mainly on antibiotics. One promising alternative is the combination of bacteriophage therapy and β-lactam antibiotics.[5] This approach is known as phage-antibiotic synergy (PAS), it has been shown to enhance bacterial elimination, improve biofilm penetration, reduce the emergence of resistant mutants and increase bacterial susceptibility to antibiotics.
There have been many promising studies about phage-antibiotic synergy with different pathogens such asPseudomonas aeruginosa orStaphylococcus aureus.[5] WithE. faecalis there have been fewer studies, but promising results from a recent study by Moryl et al. (2024) demonstrated that the combination on phage therapy and β-lactam antibiotics enhanced treatment outcomes (more efficient bacteria elimination and increased bacterial sensitivity to antibiotics) and decreased resistance development.[5]
More research is still needed to identify optimal phage-antibiotic combinations and treatment protocols, but this could potentially be considered a possible alternative treatment for antibiotic-resistantE. faecalis infections in the future.
In human blood,E. faecalis is subjected to conditions thatdamage its DNA, but this damage can be tolerated by the use ofDNA repair processes.[29] This damage tolerance depends, in part, on the two protein complex RexAB, encoded by theE. faecalis genome, that is employed in therecombinational repair of DNA double-strand breaks.[29]
The ability ofE. faecalis to formbiofilms contributes to its capacity to survive in extreme environments, and facilitates its involvement in persistent bacterial infection, particularly in the case of multi-drug resistant strains.[30] Biofilm formation inE. faecalis is associated withDNA release, and such release has emerged as a fundamental aspect of biofilm formation.[30] Conjugativeplasmid DNA transfer inE. faecalis is enhanced by the release of peptidesex pheromones.[31]
Prior to 1984, enterococci were members of the genusStreptococcus; thus,E. faecalis was known asStreptococcus faecalis.[32]
In 2013, a combination of cold denaturation and NMR spectroscopy was used to show detailed insights into the unfolding of theE. faecalis homodimeric repressor protein CylR2.[33]
TheE. faecalis genome consists of 3.22 million base pairs with 3,113 protein-coding genes.[34]
Glutamate racemase,hydroxymethylglutaryl-CoA synthase,diphosphomevalonate decarboxylase, topoisomeraseDNA gyrase B,D-alanine—D-serine ligase,alanine racemase,phosphate acetyltransferase,NADH peroxidase, Phosphopantetheine adenylyltransferase (PPAT),acyl carrier protein,3‐Dehydroquinate dehydratase and Deoxynucleotide triphosphate triphosphohydrolase are all potential molecules that may be used for treating EF infections.[18]
Bacillus haynesii CD223 andAdvenella mimigardefordensis SM421 can inhibit the growth ofEnterococcus faecalis.[35]
Bacterial small RNAs play important roles in many cellular processes; 11 small RNAs have been experimentally characterised inE. faecalis V583 and detected in various growth phases.[36] Five of them have been shown to be involved in stress response and virulence.[37]
A genome-wide sRNA study suggested that some sRNAs are linked to the antibiotic resistance and stress response in anotherEnterococcus:E. faecium.[38]
BecauseE. faecalis is a common fecal bacterium in humans, recreational water facilities (such as swimming pools and beaches that allow visitors to swim in the ocean) often measure the concentrations ofE. faecalis to assess the quality of their water. The higher the concentration, the worse the quality of the water. The practice of usingE. faecalis as a quality indicator is recommended by theWorld Health Organization (WHO) as well as manydeveloped countries after multiple studies have reported that higher concentrations ofE. faecalis correlate to greater percentages of swimmer illness. Thiscorrelation exists in both freshwater and marine environments, so measuringE. faecalis concentrations to determine water quality applies to all recreational waters. However, the correlation does not imply thatE. faecalis is the ultimate cause of swimmer illnesses. One alternative explanation is that higher levels ofE. faecalis correspond to higher levels ofhuman viruses, which cause sickness in swimmers. Although this claim may sound plausible, there is currently little evidence that establishes the link betweenE. faecalis and human virus (or other pathogens) levels. Thus, despite the strong correlation betweenE. faecalis and water quality, more research is needed to determine thecausal relationship of this correlation.[39]
For recreational waters near or at beaches,E. faecalis can come from multiple sources, such as the sand andhuman bodies. Determining the sources ofE. faecalis is crucial for controllingwater contamination, though often the sources arenon-point (for example, human bathers). As such, one study looked at how muchE. faecalis is shed from bathers at the beach. The first group of participants immersed themselves in a large pool withmarine water for 4 cycles of 15 minutes, both with and without contacting sand beforehand. The result shows a decrease inE. faecalis levels for each cycle, suggesting that people shed the mostbacteria when they first get into a pool. The second group of participants entered small, individual pools after contact with beach sand, and researchers collected data on how muchE. faecalis in the pool came from the sand brought by the participants and how much came from the participants' shedding. The result shows thatE. faecalis from the sand is very small compared to that from human shedding. Although this result may not apply to all sand types, a tentative conclusion is that human shedding is a majornon-point source ofE. faecalis in recreational waters.[40]
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