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Enterococcus faecalis (VRE)
Structure and Physiology
Enterococcus faecalis is a Gram-positive, nonmotile, facultative anaerobic microbe. Vancomycin Resistant Enterococcus (VRE) are strains that are resistant to the antibiotic vancomycin. There are six different types of vancomycin resistance shown by Enterococcus: Van-A, Van-B, Van-C, Van-D, Van-D, Van-E, Van-F. Van-A, Van-B, Van-C have been tested in clinical trials and have shown to be resistant to vancomycin and teicoplanin. The current treatment in the U.S for VRE is linezolid. Under normal conditions, vancomycin binds to D-alanyl-D-alanine, which is a key structure in the biosynthesis of the cell wall. The source of Entercoccus’ resistances comes from an alteration to the terminal amino acid residues of the N-acetylglucosamine (NAG) and N-acetlymuramic acid (NAM)-peptide subunits. NAM/NAG-peptide subunits are associated with the bacteria’s cell wall. The alterations to NAG/NAM cause D-alanyl-D-lactate to lose one of its five hydrogen bonds. This hydrogen loss results in a 1000-fold decrease in affinity between vancomycin and D-alanyl-D-alanine.
Transmission and Disease
E. faecalis can cause urinary tract infections, endocarditis, bacteremia, and meningitis and has been frequently found in root canal-treated teeth.
Due to this bacterium’s robust survival factors and resistance to commonly used antimicrobial agents, it proves very challenging to disinfect.
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