Enterococcus faecalis and E. faecium
VRE (vancomycin resistant)
2 component regulatory system activated by extracellular glycopeptide antibiotics
Enhanced susceptibility to enterococcal infection is caused by
Antibiotic treatment GI barrier breakdown Abdominal surgery Indwelling devices Malignancy or other concurrent diseases
Treatment
B-lactam and aminoglycoside combination therapy Aminoglycosides target ribosomes (less effective against E. faecium) Linezolid, an antibiotic that inhibits protein synthesis, is often used with E. faecium Daptomycin is a peptide antibiotic that inserts itself into the membrane and alters cell architecture and division
Normal microbiota of the GI tract
In vitro growth in high salt, bile, temperatures between 10 and 40 C (and survive exposure for 60C for up to 30 minutes) and in high pH Common nosocomial infection (E. faecalis more common that E. faecium) Inherent resistance to B lactams and aminoglycosides Vancomycin-resistant strains (VRE) exist and are an infection control problem
VanB- type resistance
Resistant to vancomycin sensitive to teichoplanin
VanA-type resistance
Resistant to vancomycin glycopeptides and lipidated glycopeptides (eg. teicoplanin)
Enterococci change the last two amino acids of the glycopeptide target so vancomycin has less affinity for it
VRE strains produce peptidoglycan precursors that terminate with D-lactate
Opportunistic pathogen
causes endocarditis (especially E. faecalis) Bacteremia Wound and soft tissue infections Intra-abdominal and pelvic infections UTIsNeonatal infections
Diagnose
culture growth on bile esculin and in high salt concentrations
GPC usually diplococci
gram stain
can display any type of hemolysis
hemolysis
VanS
histidine protein kinase that miniters EC environment for glycopeptides
VanR
response regulator activated by VanS phosphorylation; turns on gene for expression of vancomycin resistance