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