# Dissemination of Enterococcuscal Genetic Lineages: A One Health Perspective
## 2 Genetic Lineages  
_E. faecalis_ and _E. faecium_ exhibit conserved genomes, although they possess a significant accessory genome (up to 38% in _E. faecium_), which contributes to remarkable genomic plasticity [16]. The evolution of enterococci was predominantly influenced by recombination and proficiency in acquiring novel genes through HGT facilitated by MGEs, such as plasmids, transposons [16; 17], genomic islands (GI), and prognages [18]. The genome plasticity of clinical _E. faecium_ can be explained by the lack of genome defense mechanisms limiting HGT, such as CRISPR-Cas and restriction-modification systems [16]. Accordingly, an inverse correlation between the presence of the CRISPR-Cas locus and acquired antimicrobial resistance in _E. faecalis_ was first demonstrated in 2010 [19]. Recently, the lack of CRISPR-Cas genes was also associated with higher antimicrobial resistance rates and multidrug resistance in _E. faecalis_ and _E. faecium_ originating from hospital wastewater [20].  
The duality between commensals and infection-causing organisms, and the remarkable adaptability to various environmental sources, led to the division of _E. faecium_ into two distinct genomic clades: clade A, encompassing hospital-associated lineages (e.g., vancomycin-resistant isolates); and clade B, comprising community-associated enterococci [3; 21; 22]. However, the discovery of clinical isolates within the clade B lineage led some authors to challenge this classification [23]. [PERSON] et al. [17] pointed out two evolutionary theories to explain the emergence of the two clades. The first is that clade A and clade B may be endogenous to the gastrointestinal tracts of different hosts and now coexist among human microbiota, as a result of antibiotic elimination of competitors. The other is that clades A and B may be diverging from each other, due to antibiotic use and ecological isolation, although this is less likely [17]. clade A can be further classified into two distinct sub-clades: clade A1, consisting of human clinical epidemic strains, which account for the majority of human infections (mostly referred to as CC17, further explored in Section 4); and clade A2, typically associated with livestock/animal strains and some occasional human infection isolates [22]. Interestingly, some animal-origin enterococci found in clade A1 were isolated from pet dogs, suggesting an interconnection between hospital strains and household pets [22]. In fact, an additional study demonstrated that sub-clade A1 emerged from A2, and that hospital isolates identified as A2 represent a genetic continuum between A1 and community _E. ficeum_ placed in clade B [7]. Thus, the existence of this sub-clade division has been contested and remains uncertain [7; 23].  
In comparison to _E. ficeum_, _E. ficealis_ isolates do not exhibit a multiclade structure, instead displaying a significant reliance on the acquisition of mobile elements as a primary driver of genomic diversity [17]. Nevertheless, some major high-risk enterococcal clonal complexes (HiRECCs), namely CC2, CC9, and CC87 (further explored in Section 4), have been associated to hospital settings and healthcare-associated infections [1; 24].