Fig. 6

Aetiology of VRE invasive infection. a Enterococci typically represent ~ 0.1% of the human gut microbiota. Invasive infections can occur at various body sites, but one of the main routes in infection other than the GIT is through UTIs. Environmental Enterococcus spp. can migrate and form robust biofilms on urinary catheters incorporating fibrinogen into a matrix where persistence can result in invasive infection and urethral migration to infect the kidney. b Invasive infection can occur through a weakened GIT lining, where translocation can lead to systemic disease of the blood or lymph systems. The presence of commensals prevents VRE colonisation through multiple modes (1) production of REglllY by enterocytes stimulated by commensal gram-negative bacteria in the GIT [144]. (2) Direct inhibition by the production of bactericidal peptides, eg. lanthipeptide production by Blautia producta and pheromone production by commensal enterococci [44, 145]. (3) Preoccupation of shared niche. (4) Cooperating commensals allow a microbiota-wide reduced sensitivity to ampicillin, allowing peptide producing strains to confer colonisation resistance to VRE [146]. c The administration of cephalosporin antibiotics significantly reduce the microbiota and alter the host physiology decreasing the thickness of the colon wall, reducing the mucus layer and MUC2 (Mucin-2) and damaging the integrity of tight junctions via elevated Ca²⁺ [147]. Host factors such as E-cadherin, sIgA and pIgR also cause agglutination of E. faecium after an antibiotic induced “bloom” to protect the host and shed clustered VRE into the lumen [147]