Enterococcus faecalis
Enterococcus faecalis | |
---|---|
Scientific classification | |
Domain: | Bacteria |
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 D
Physiology
E. faecalis is a
Pathogenesis
E. faecalis is found in most healthy individuals, but can cause endocarditis and sepsis, urinary tract infections (UTIs), meningitis, and other infections in humans.[7][8] Several virulence factors are thought to contribute to E. faecalis infections. A plasmid-encoded hemolysin, called the cytolysin, is important for pathogenesis in animal models of infection, and the cytolysin in combination with high-level gentamicin resistance is associated with a five-fold increase in risk of death in human bacteremia patients.[9][10][11] A plasmid-encoded adhesin[12] called "aggregation substance" is also important for virulence in animal models of infection.[10][13]
E. faecalis contains a
Antibacterial resistance
Multi drug resistance
E. faecalis is usually resistant to many commonly used
Resistance to vancomycin in E. faecalis is becoming more common.[16][17] Treatment options for vancomycin-resistant E. faecalis include nitrofurantoin (in the case of uncomplicated UTIs),[18] linezolid, quinupristin, tigecycline[15] and daptomycin, although ampicillin is preferred if the bacteria are susceptible.[19] Quinupristin/dalfopristin can be used to treat Enterococcus faecium but not E. faecalis.[19]
In root-canal treatments,
Development of antibiotic resistance
This section needs expansion. You can help by adding to it. (January 2019) |
Combined drug therapies
According to one study combined drug therapy has shown some efficacy in cases of severe infections (e.g.
Daptomycin or linezolid may also show efficacy in case ampicillin and vancomycin resistance.[21]
A combination of penicillin and streptomycin therapy was used in the past.[21]
Tedizolid, telavancin, dalbavancin, and oritavancin antibiotics are FDA approved as treatments against EF.[15]
Survival and virulence factors
- Endures prolonged periods of nutritional deprivation
- Binds to dentin and proficiently spreads into dentinal tubules via chain propagation
- Alters host responses
- Suppresses the action of lymphocytes
- Possesses lytic enzymes, cytolysin, aggregation substance, pheromones, and lipoteichoic acid
- Utilizes serum as a nutritional source
- Produces extracellular superoxide under selected growth conditions that can generate chromosomal instability in mammalian cells[22][23]
- Resists intracanal medicaments (e.g. calcium hydroxide), although a study proposes elimination from root canals after using a mixture of a tetracycline isomer, an acid, and a detergent[24]
- Maintains pH homeostasis
- Properties of dentin lessen the effect of calcium hydroxide
- Competes with other cells
- Forms a biofilm[6]
- Activates the host protease plasminogen in a fashion that increases local tissue destruction[25]
DNA repair
In human blood, E. faecalis is subjected to conditions that damage its DNA, but this damage can be tolerated by the use of DNA repair processes.[26] This damage tolerance depends, in part, on the two protein complex RexAB, encoded by the E. faecalis genome, that is employed in the recombinational repair of DNA double-strand breaks.[26]
Historical
Prior to 1984, enterococci were members of the genus Streptococcus; thus, E. faecalis was known as Streptococcus faecalis.[27]
In 2013, a combination of cold denaturation and NMR spectroscopy was used to show detailed insights into the unfolding of the E. faecalis homodimeric repressor protein CylR2.[28]
Genome structure
The E. faecalis genome consists of 3.22 million base pairs with 3,113 protein-coding genes.[29]
Treatment research
Glutamate racemase, hydroxymethylglutaryl-CoA synthase, diphosphomevalonate decarboxylase, topoisomerase DNA 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.[15]
Bacillus haynesii CD223 and Advenella mimigardefordensis SM421 can inhibit the growth of Enterococcus faecalis.[30]
Small RNA
Bacterial small RNAs play important roles in many cellular processes; 11 small RNAs have been experimentally characterised in E. faecalis V583 and detected in various growth phases.[31] Five of them have been shown to be involved in stress response and virulence.[32]
A genome-wide sRNA study suggested that some sRNAs are linked to the antibiotic resistance and stress response in another Enteroccocus: E. faecium.[33]
Swimming pool contamination
Indicators of recreational water quality
Because E. 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 of E. faecalis to assess the quality of their water. The higher the concentration, the worse the quality of the water. The practice of using E. faecalis as a quality indicator is recommended by the World Health Organization (WHO) as well as many developed countries after multiple studies have reported that higher concentrations of E. faecalis correlate to greater percentages of swimmer illness. This correlation exists in both freshwater and marine environments, so measuring E. faecalis concentrations to determine water quality applies to all recreational waters. However, the correlation does not imply that E. faecalis is the ultimate cause of swimmer illnesses. One alternative explanation is that higher levels of E. faecalis correspond to higher levels of human viruses, which cause sickness in swimmers. Although this claim may sound plausible, there is currently little evidence that establishes the link between E. faecalis and human virus (or other pathogens) levels. Thus, despite the strong correlation between E. faecalis and water quality, more research is needed to determine the causal relationship of this correlation.[34]
Human shedding
For recreational waters near or at beaches, E. faecalis can come from multiple sources, such as the sand and human bodies. Determining the sources of E. faecalis is crucial for controlling water contamination, though often the sources are non-point (for example, human bathers). As such, one study looked at how much E. faecalis is shed from bathers at the beach. The first group of participants immersed themselves in a large pool with marine water for 4 cycles of 15 minutes, both with and without contacting sand beforehand. The result shows a decrease in E. faecalis levels for each cycle, suggesting that people shed the most bacteria 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 much E. faecalis in the pool came from the sand brought by the participants and how much came from the participants’ shedding. The result shows that E. 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 major non-point source of E. faecalis in recreational waters.[35]
See also
References
- PMID 30013618.
- ^ ISBN 0-8385-8529-9.
- ^ PMID 33771633.
- PMID 9823122.
- PMID 15107642.
- ^ PMID 16427453.
- PMID 2404568.
- S2CID 205988392.
- PMID 1929336.
- ^ PMID 8285637.
- PMID 6086531.
- PMID 1729187.
- PMID 11796604.
- PMID 31196984.
- ^ S2CID 195756723.
- PMID 17659211.
- PMID 16323116.
- PMID 11120989.
- ^ PMID 20569266.
- PMID 19082392.
- ^ PMID 29125098.
- S2CID 25075356.
- PMID 17258726.
- PMID 12877261.
- PMID 31604031.
- ^ PMID 33203752.
- .
- PMID 23396077.
- S2CID 45480495.
- PMID 36453920.
- PMID 21912655.
- PMID 24914223.
- PMID 28894187.
- PMID 24649503, retrieved 2023-05-08
- PMID 17113123.