Inquiry Basket
Loading ......
Enterococci are Gram-positive lactic acid-producing members of the gut microbiota in humans and animals. These facultative anaerobes are highly tolerant to diverse environmental conditions, including extreme pH, temperature and salt concentrations. This tolerance contributes to their colonization of diverse host niches, persistence in the environment and utility as an indicator for faecal contamination. Commensal gut enterococci are not typically pathogenic in healthy hosts, and both Enterococcus faecalis and Enterococcus faecium are the predominant species readily isolated from faeces of healthy babies. In susceptible hosts, however, they can cause infection and are a frequent cause of hospital-acquired infections. Infections with Enterococcus casseliflavus, Enterococcus gallinarum and Enterococcus raffinosus can also occur, although less frequently. The ability of enterococci to form biofilms increases their hardiness and contributes both to their persistence during infection and also their contamination of the environment and the food industry.
Biofilm development generally comprises four stages: initial attachment, microcolony formation, biofilm maturation (which is in part governed by quorum sensing) and dispersal. In contrast to model biofilm-forming organisms such as Pseudomonas aeruginosa and Bacillus subtilis, in which the spatiotemporal contribution of different factors to biofilm formation is better characterized, enterococcal biofilm development is less well understood. Various factors contribute to enterococcal biofilm formation in vitro and in vivo, but mediators of dispersion have yet to be identified.
Fig1. Stages of biofilm development in enterococci. (Nature Review Microbiology, 2018)
E. faecium, the second-most frequent Enterococcus species associated with disease, often harbours vancomycin resistance genes and is a priority pathogen for which new antibiotics are needed. Several E. faecium genes are involved in biofilm development, including atlA, ebpABC, esp, fsrB, luxS, spx, acm, scm, sgrA, pilA, pilB, ecbA and asrR. Only a few of these genes have been shown to affect biofilm-associated infection in vivo: atlA, ebpABC, esp, acm and asrR.
Low penetration of antibiotics through the biofilm matrix and the presence of persister cells contribute to antibiotic tolerance of biofilms, leading to persistent infections. Enterococci have higher rates of horizontal gene transfer of antibiotic resistance genes in biofilms than in plank-tonic cells, and transfer is facilitated by Ebp, Epa, pCF10 and PrgABC. Ebp promotes cell aggre-gation and biofilm formation, which facilitates con-jugation. Moreover, EpaI promotes efficient formation of mating pairs and thus can increase pCF10 conjuga-tion. Furthermore, pCF10 promotes its own transfer by encoding PrgB, which enables eDNA-dependent plasmid conjugation. Enterococcal biofilms can serve as gene reservoirs for antibiotic resistance transmission within and between species.
Most E. faecalis biofilm-associated infections are poly- microbial, with two or more species present at the infec- tion site. Next-generation sequencing can be used to identify species, and especially in CAUTI and wound infections, enterococci can constitute a substantial proportion of the population. Several uropathogens are frequently co-isolated with E. faecalis. For example, Proteus mirabilis is found in almost 40% of E. faecalis biofilms. E. coli and Klebsiella pneumoniae have been co-isolated on catheters, and P. aeruginosa and Candida albicans also co-occur in UTIs. By comparison, enterococci in diabetic ulcers, burns and surgical wounds are commonly co-isolated with Staphylococcus spp., P. aeruginosa, Corynebacterium spp. and E. coli.
Multiple properties of biofilms, including phenotypic antibiotic tolerance and synergistic protective attrib-utes of mixed-species communities, render biofilms recalcitrant to standard antibacterial therapies. As such, the prevention of biofilm formation, wherever possible, should be prioritized.
Surface coatings. Anti-adhesive or antibacterial surface coatings and materials can be used to prevent biofilm formation on the surface of catheters and implants.
Vaccination. Another approach to prevent biofilm for- mation is the use of EbpA as a vaccine against CAUTI.
Improving antibiotic effect. Because prevention is not always possible, the removal of pre-existing enterococcal biofilms remains a necessity.
Disinfection. Although disinfection is effective against planktonic cells, biofilms are resistant to disinfection and this is of particular relevance to recurring endodontic infection. Nanoparticles could be added to potentiate the effect of hypochlorite and other non-discriminating oxidizing agents.
Targeting dispersal. The release of planktonic bacteria during biofilm dispersal renders them susceptible to antibiotics and presents an opportunity for carefully considered adjuvant therapy.
Treating multispecies biofilms. Consideration of multispecies biofilms must begin at detection, and molecular methods should be used to detect fastidious organisms and organisms present at low levels that may influence infection outcomes.
| Target | Cat. No. | Product Name | Host | Isotype | Application | Inquiry |
| E. faecium | DPAB-DC4206 | Rabbit Anti-E. faecium Polyclonal antibody for IF | Rabbit | IgG | IF | Inquiry |
| Enterococcus | DPATB-H82377 | Rabbit Anti-Enterococcus Polyclonal antibody for IHC-P, ICC, IF | Rabbit | IgG | IHC-P, ICC, IF | Inquiry |
| Enterococcus | DPATB-H82299 | Rabbit Anti-Enterococcus Polyclonal antibody for ELISA, IF | Rabbit | IgG | ELISA, ICC, IF | Inquiry |
| Enterococcus | DPAB31496 | Rabbit Anti-Enterococcus Polyclonal antibody for ELISA, WB, IF | Rabbit | IgG | ELISA, WB, IF | Inquiry |
| Enterococcus | DPAB0143 | Rabbit Anti-Enterococcus Polyclonal antibody for sELISA | Rabbit | IgG | sELISA | Inquiry |
Loading ......
