portion of the colonic flora is made up of miscellaneous organisms and less than 5% of the
group D enterococcal colonic flora,95% isE. faecalis(VSE), and the remaining5% is
E. faecium(VRE) (1,2).
Epidemiology of VSE/VRE
All group D enterococci, i.e., VSE and VRE, are normal inhabitants of the human colon. The
carriage of VSE and VRE is intermittent but persistent of long duration. VRE colonization of
patients is determined by positive VRE rectal cultures. VRE does not normally inhabit the skin
but may transiently be present on the skin. VRE is an occasional contaminant of blood cultures
introduced during venipuncture from fecal contamination of the antecubital fossa. Fecal
colonization contamination of skin is not uncommon in hospitalized patients from the
mid-chest to the lower extremities. The recovery of VRE in blood cultures (1 out of 4)
unaccompanied by other signs of VRE infection represents colonization and should be
regarded as a contaminant of no clinical significance. Patients colonized with VRE remain on
VRE precautions for the duration of hospitalization because VRE in feces is intermittent and
discontinuation of precautions sets the stage for the spread of VRE when the fecal flora again
contains VRE (1,3–9).
Clinical Spectrum of VSE/VRE Infections
VSE/VRE intra-abdominal/pelvic infections.VSE and VRE differ only in their susceptibility to
antibiotics. The types of infection and spectrum of clinical severity is the same for VSE and
VRE. VSE and VRE are relatively avirulent pathogens with little inherent invasive ability. VRE
should be regarded as an innocent bystander or permissive pathogen in intra-abdominal/
pelvic infections. VSE or VRE are important single pathogens in gallbladder/biliary and UTIs.
In intra-abdominal infections, VSE or VRE are permissive pathogens and require other
organisms to initiate/maintain infection. Experimentally, VSE or VRE injected intra-
peritoneally will not cause infection unless other organisms, aerobic or anerobic, are present.
This is independent of inoculum size or location within the intra-abdominal cavity (1,2).
VSE/VRE CAB and UTIs.The second most common isolates in CAB are VSE and VRE that are
of no clinical consequence in normal hosts. In compromised hosts, i.e., diabetes mellitus,
systemic lupus erythematosus, myeloma, etc., CAB may be treated with oral or parenteral
antibiotics. VSE/VRE UTIs may present as cystitis or acute pyelonephritis in normal hosts.
Urosepsis due to VSE/VRE may occur in normal hosts with preexisting renal disease, partial/
total urinary tract obstructions, or in nonleukopenic hosts, i.e., diabetes mellitus, systemic
lupus erythematosus, or myeloma.
VSE/VRE Bacteremia/SBE.Group D enterococci also are the sole pathogens in infective
endocarditis. When causing infective endocarditis, VSE or VRE presents clinically as a
syndrome of intermediate severity between SBE and ABE (10). The clinical expression of an
“intermediate” and intensity of endocarditis with enterococcal group D streptococci also
pertains to non-enterococcal group D streptococci, i.e.,S. gallolyticus(S. bovis) (1).
Therefore, the major clinical manifestations of infections due to VRE are infective
endocarditis, wound infections, biliary, hepatic of lower intra-abdominal infections, UTIs, and
uncommonly CVC infections (10–13). Group D enterococci may also be pathogens in
ventriculoperitoneal (VP) shunt infections if the intra-abdominal catheter perforates an
abdominal viscus. Group D enterococci are ordinarily unimportant causes of acute bacterial
meningitis, CAP, nosocomial pneumonia, or bone/joint infections (Table 1) (1,13,14).
Antimicrobial Therapy of VSE/VRE
It is a common misconception that group D enterococci are becoming more resistant to
antibiotics. Rather, excessive use of some antibiotics, i.e., metronidazole forClostridium difficile
and vancomycin (IV, not PO) for empiric medical/surgical prophylaxis/therapy has resulted
in decrease in the concentration of VSE in the colonic flora and commensurate increase in
Antimicrobial Therapy of VRE and MRSA in Critical Care 499