Fig. 1

a Enterococcal acquisition of niche specific genes and (b) dissemination routes for VanA genes. a A change of niche resulted in Enterococcus spp. acquiring a harder cell wall structure and increased mutatable phenotype. E. faecium acquired various substrate utilisation genes, namely glucose, mannose, galactose and fructose. Hospital acquired infection-related E. faecium lack CRISPR-Cas systems, rendering them susceptible to receiving ectopic DNA resulting in the acquisition of pathogenicity islands, plasmids and insertion sequences. Hospital-acquired, hypermutable clade E. faecium can also have single nucleotide polymorphism (SNP) mediated resistance to antibiotics, such as fosfomycin, an antibiotic used to treat acute non-complicated urinary tract infections (UTIs). A hypermu table phenotype due to mutations in the DNA-mismatch repair proteins MutS and MutL increases the mutation frequency of strains. Enterococci act as genomic reservoirs for antimicrobial resistance (AMR) genes which can then be passed to recipients like S. aureus and S. gordonii. b The possible dissemination of VRE AMR genes due to transposons, insertion sequences (IS) and plasmids. Nested mobile genetic elements (MGEs) resemble the Russian doll model similar to carbapenemase resistance genes in Enterobacteriaceae, resulting in numerous horizontal dissemination routes including movement of the plasmid, transposition of the transposon between plasmids and homologous recombination [23]. Vertical dissemination occurs through daughter progeny containing the plasmid; this is confirmed by detecting the same plasmids and MGEs amongst the same clonal background. These are often responsible for hospital outbreaks accounting for ~ 30% of dissemination [23]. Horizontal dissemination: (1) Mobilisation of a plasmid to previously susceptible strains via conjugation ~ 7%. (2) Transposon-mediated mobilisation of sequences to other plasmids containing target sequences. (3) Mobilisation of IS. Most cases are caused by separate events indicating the high frequency that strains become pathogenic post-antibiotic treatment [23]. The notation “⁺” indicates acquisition of DNA, “*” indicates a mutation in DNA, “⁻“ indicates missing DNA feature