2. Enterococcus
• The genus Enterococcus includes the enterococcal members previously classified with the group D
streptococci.
• Can grow at 10°C and 45°C, growth in the presence of 6.5% NaCl, growth at pH 9.6, ability to
hydrolyze esculin in the presence of 40% bile, and production of pyrrolidonyl arylamidase (PYR).
• Most infections from E. faecalis or E. faecium; and are leading cause of nosocomial infections
• Enterococcus species commonly colonize the GI tract; however, they can be isolated from the
oropharynx, female genital tract, and skin.
• Clinical manifestations:-
1. urinary tract infections;
2. bacteremia;
3. endocarditis; and
4. intraabdominal, pelvic, wound, and soft tissue infections.
3. • Most enterococci are also intrinsically resistant to aminoglycosides and β-lactams. In addition, these
organisms are capable of acquiring and exchanging genes encoding resistance to antimicrobial agents. This
genus was the first clinically relevant group of gram-positive cocci to acquire and disseminate resistance to
vancomycin; hence the name vancomycin- resistant Enterococcus (VRE).
• Enterococci with acquired resistance to vancomycin (VRE, vancomycin-resistant enterococci) now account
for more than 30% of enterococcal infections, and greater than 90% of VRE isolates are E. faecium.
4. Mechanism of Action
The glycopeptides vancomycin and teicoplanin act by binding to the “D-alanyl-D-alanine” terminus of
cell wall peptidoglycan intermediates and inhibiting cell wall cross-linking. Acquired resistance to
glycopeptides results from the synthesis of different peptidoglycan precursors that become incorporated
into the cell wall and have decreased binding affinity for vancomycin, teicoplanin, or both.
Normally, vancomycin-susceptible strains have peptidoglycan side chains that terminate with the
depsipeptide “D-alanyl-D-alanine,” and the glycopeptide antibiotic binds to this depsipeptide. In
glycopeptide-resistant strains, the “D-alanyl-D-alanine” depsipeptide is replaced by “D-alanyl-D-lactate”
or by “D-alanyl-D-serine.”
5. Genes encoding the VanA and VanB phenotypes are the most
common and are carried on transposons that may be inserted into the chromosome or into plasmids. E.
faecium and E. faecalis isolates that have the vanA genotype and VanA phenotype display vancomycinand
teicoplanin-inducible, transposon-mediated, high-level resistance to both vancomycin (MIC, 64 to
1,000 μg/mL) and teicoplanin (MIC, 16 to 512 μg/mL).
7. Detection of Vancomycin-Resistant Enterococci
Enterococcus species grow well on most bacteriological media, including 5% sheep blood CNA, and
chocolate agars. On Blood Agar, most strains are nonhemolytic or α-hemolytic.
Most strains are able to grow at 35°C to 37°C in ambient air, although incubation in a CO2-enriched
environment stimulates growth of most isolates.
Isolates of E.faecium tend to be more resistant to penicillin and ampicillin than E. faecalis isolates, and the vast
majority of VRE are strains of E. faecium.
8. • Early detection of VRE in at-risk patients enables the timely institution of infection control practices that are
known to limit the spread of these opportunistic agents.
• The breakpoint for vancomycin resistance is ≥32 μg/mL, with intermediate susceptibility being 8 to 16
μg/mL. (CLSI) VREs from nosocomial outbreaks generally have vancomycin MIC’s ≥32 μg/mL.
Enterococcus faecium. This photograph shows a sheep blood agar plate
inoculated with E. faecium.
Colonies of this organism are smooth, gray, and nonhemolytic or α-
hemolytic. The swab, which was used to pick up some of the colony
growth from the plate, shows that the organism is nonpigmented.
This becomes important for the identification of certain other
enterococcal species.
9. Treatment
Recommended treatment includes a combination of a cellwall active agent, either a β-lactam or vancomycin,
and an aminoglycoside. Combination treatment is synergistic and, generally is sufficient even in the presence of
intrinsic resistance to one of the antibiotics.
Antimicrobials such as linezolid and daptomycin are commonly employed to treat patients with infections
caused by VRE
10. • REFERENCES
1. Koneman’s Color Atlas and Textbook of Diagnostic Microbiology, 7th ed.
2. Bailey & Scott’s DIAGNOSTIC MICROBIOLOGY, 15th ed
3. Cetinkaya Y, Falk P, Mayhall CG. Vancomycin-resistant enterococci. Clin Microbiol Rev. 2000
Oct;13(4):686-707. doi: 10.1128/CMR.13.4.686. PMID: 11023964; PMCID: PMC88957.
4. Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases
(NCEZID), Division of Healthcare Quality Promotion (DHQP)
