Enterocins at the Catheter Interface: Harnessing Enterococcus faecalis Bacteriocins Against Multidrug-Resistant, Biofilm-Forming Klebsiella pneumoniae

Abstract

Background. Catheter-associated urinary tract infections (CAUTIs) caused by multidrug-resistant (MDR) Klebsiella pneumoniae are among the most refractory of healthcare-associated infections, largely because biofilm growth on indwelling devices shelters the pathogen from both host defences and conventional antibiotics. Bacteriocins produced by lactic acid bacteria, and enterocins from Enterococcus faecalis in particular, have re-emerged as candidate device-directed antimicrobials.

Objective. This review critically appraises the evidence that E. faecalis enterocins can act against MDR, biofilm-forming K. pneumoniae, situates a representative enterocin (here designated enterocin GLHM) within the broader bacteriocin landscape, and evaluates the strengths, contradictions, and translational gaps in the field.

Key findings. Across the literature, enterocins display proteinaceous, partially heat-stable, pH-tolerant profiles consistent with class II peptides, and several inhibit Gram-negative ESKAPE pathogens including K. pneumoniae despite the canonical view that bacteriocins act mainly on close relatives. A purified low-molecular-weight (~5.3 kDa) enterocin encoded by an ent1071-type structural gene retained activity across pH 5–7 and up to 90°C, lost activity after proteolytic digestion, and suppressed catheter biofilm more effectively than amikacin in vitro. Yet reported spectra, potency, and mechanisms remain heterogeneous, and Gram-negative activity is frequently confounded by co-purifying factors.

Conclusion. Enterocins are biologically credible adjuncts for preventing K. pneumoniae catheter colonisation, but their translation hinges on rigorous purification, mechanistic clarity against Gram-negative envelopes, and standardised antibiofilm testing rather than on additional descriptive screening.