SN5 SHORT NOTE 5M ★ High-yield

Describe the enterococci with their intrinsic resistance, infections and VRE.

Microbiology · 2nd Professional — Para-Clinical

Organism and Classification

Enterococci are gram-positive cocci in pairs or short chains, catalase negative, formerly classified as Lancefield group D streptococci and now a separate genus
Principal species — E. Faecalis (about 80 to 90% of human isolates) and E. Faecium (fewer but far more resistant)
Distinguishing features — they grow in 6.5% sodium chloride, in 40% bile, at 10°C and 45°C, and at pH 9.6, and they hydrolyse aesculin in the presence of bile. This remarkable hardiness lets them survive on surfaces and in the gut through antibiotic courses
Usually non-haemolytic (gamma), sometimes alpha; part of the normal gut flora

Intrinsic Resistance — WHY Enterococci Matter

Antibiotic class	Enterococcal response
Cephalosporins — all of them	Intrinsically resistant. This is why cephalosporin use selects for enterococci, and why "cephalosporin cover" leaves a gap that enterococci fill
Penicillins	Only inhibited, not killed — enterococci are tolerant, so penicillin alone is bacteriostatic against them
Aminoglycosides alone	Resistant, because the drug cannot cross the cell wall unaided
Penicillin plus an aminoglycoside	Synergistic and bactericidal — the penicillin damages the wall and lets the aminoglycoside in. This combination is essential in endocarditis, where killing rather than inhibition is required
Co-trimoxazole	Appears active in vitro but fails in vivo, because enterococci take up preformed folate from the environment
Clindamycin, macrolides	Intrinsically resistant or unreliable
Vancomycin	Active — unless the organism is VRE

CLINICAL PEARL

The enterococcus is not especially virulent; it is especially unkillable. Its clinical importance comes almost entirely from intrinsic resistance to whole classes of antibiotic, together with a talent for acquiring more. It is a weak pathogen that thrives precisely because everything used against other organisms leaves it untouched — which makes it a marker of heavy antibiotic exposure as much as a pathogen in its own right.

Vancomycin-resistant Enterococci (vre)

Mechanism — the vanA or vanB gene cluster replaces the terminal D-alanyl-D-alanine of the peptidoglycan precursor with D-alanyl-D-lactate, for which vancomycin has about a thousandfold lower affinity
Carried on transposons and plasmids, and therefore transferable — vanA has been transferred to Staphylococcus aureus, producing VRSA, which is why VRE is watched so closely
Commonest in E. Faecium, and associated with prolonged hospital stay, previous vancomycin or cephalosporin use, and intensive care
Treatment options — linezolid, daptomycin (not for pneumonia), tigecycline, and for urinary infection nitrofurantoin or fosfomycin

Clinical Infections and Applied Aspects

Urinary tract infection — the commonest, particularly in catheterised patients
Intra-abdominal and pelvic sepsis, usually as part of a polymicrobial infection following bowel surgery or perforation
Endocarditis — subacute, classically in older men after genitourinary instrumentation and in women after obstetric procedures; requires prolonged synergistic combination therapy
Bacteraemia and line infection; wound infection; neonatal sepsis
Distinguish colonisation from infection — enterococci grown from a wound swab, a catheter urine or a mixed abdominal culture are frequently passengers, and treating them selects resistance without benefit
Never treat enterococcal endocarditis with a single agent; synergistic combination therapy for several weeks is required, and inadequate treatment leads to relapse
Cephalosporin restriction reduces enterococcal and VRE pressure, which is a concrete stewardship target
VRE is emerging in Indian tertiary hospitals, and its containment depends on contact precautions, environmental cleaning and stewardship rather than on new drugs, of which there are few

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