What is VRE (Vancomycin-Resistant Enterococcus) Enterococcus faecalis?

Vancomycin-Resistant Enterococcus faecalis: Clinical Significance and Management

Vancomycin-Resistant Enterococcus (VRE) faecalis is a serious healthcare-associated pathogen that has developed resistance to vancomycin, significantly limiting treatment options and requiring prompt isolation measures to prevent transmission. 1

Definition and Identification

• VRE faecalis is an enterococcal species that has acquired resistance to the glycopeptide antibiotic vancomycin, making infections difficult to treat 1
• Enterococci are identified in the laboratory using colonial morphology, Gram stain (gram-positive cocci), and pyrrolidonyl arylamidase (PYR) test 1
• Vancomycin resistance is confirmed when minimum inhibitory concentration (MIC) is ≥32 μg/mL or when growth occurs on brain heart infusion agar containing 6 μg/mL of vancomycin 1

Epidemiology and Clinical Significance

• While Enterococcus faecium is more commonly associated with vancomycin resistance, E. faecalis can also acquire this resistance mechanism 1
• VRE is predominantly found in nosocomial (hospital-acquired) infections, particularly in postoperative and tertiary peritonitis 1
• Risk factors for VRE acquisition include:
  • Previous antibiotic therapy (especially vancomycin and cephalosporins)
  • Prolonged hospitalization
  • ICU admission
  • Severe underlying illness
  • Invasive procedures
  • Gastrointestinal surgery
  • Organ transplantation
  • Proximity to other VRE-positive patients 1

Clinical Impact

• VRE infections are associated with increased mortality, particularly in immunocompromised patients and those in ICUs 2
• VRE faecalis can cause various infections including:
  • Bacteremia
  • Intra-abdominal infections
  • Urinary tract infections
  • Endocarditis
  • Wound infections 1, 3
• VRE infections are more difficult to treat than vancomycin-sensitive enterococci (VSE) due to limited antimicrobial options 1

Treatment Options

• For VRE faecalis infections, linezolid 600 mg IV or PO every 12 hours is the recommended first-line treatment, with duration based on the site of infection and clinical response 1
• For VRE bacteremia, high-dose daptomycin (8-12 mg/kg/day), either alone or in combination with β-lactams, is recommended 1, 3
• For intra-abdominal infections due to VRE, tigecycline (100 mg IV loading dose followed by 50 mg IV every 12 hours) is recommended 1
• For uncomplicated urinary tract infections caused by VRE, options include:
  • Single-dose fosfomycin 3 g PO
  • Nitrofurantoin 100 mg PO every 6 hours
  • High-dose ampicillin (if susceptible) 1

Infection Control Measures

• When VRE is isolated from a clinical specimen:
  • Confirm vancomycin resistance through appropriate susceptibility testing 1
  • Immediately notify the patient's primary caregiver, patient-care personnel, and infection-control staff 1
  • Implement appropriate isolation precautions promptly 1
• Screening procedures in hospitals where VRE has not been detected:
  • Perform periodic susceptibility testing on enterococcal isolates from high-risk patients 1
  • Consider culture surveys of stools or rectal swabs in high-risk units 1

Prevention Strategies

• Judicious use of vancomycin and other antibiotics to prevent selection pressure for resistant organisms 1
• Strict adherence to hand hygiene protocols 1
• Environmental cleaning and disinfection 1
• Education of healthcare personnel about VRE epidemiology and control measures 1
• Active surveillance in high-risk units 1

Clinical Pitfalls and Caveats

• Automated susceptibility testing methods may be unreliable for detecting vancomycin resistance in enterococci; manual methods are preferred 1
• Delay in identifying VRE can lead to unrecognized transmission and outbreaks 1
• Empiric coverage for VRE is not generally recommended for community-acquired infections but should be considered for healthcare-associated infections, particularly postoperative infections 1
• VRE faecalis may demonstrate "tolerance" to vancomycin (susceptible by MIC but resistant by minimum bactericidal concentration), leading to treatment failure despite in vitro susceptibility 3