Abstract
Enterococcus faecalis is an opportunistic pathogen and is one of the leading causes of nosocomial infections. E. faecalis harbors a number of antibiotic resistance genes, and most of these are present on mobile genetic elements (MGEs) that can be disseminated within the species, as well as to other members of the human microflora. In an article by Price and colleagues [V. J. Price et al., mSphere 1(3):e00064-16, 2016, http://dx.doi.org/10.1128/mSphere.00064-16], the authors demonstrated how E. faecalis uses a restriction-modification system along with a clustered regularly interspaced short palindromic repeat (CRISPR)-Cas to function as a bacterial innate and adaptive immune system to regulate the influx of MGEs. The absence of these systems in high-risk hospital-adapted lineages of E. faecalis, including the prototypical V583 strain, appears to allow the ready acquisition of new traits that aid in the adaptation to new environmental stresses, including the evolution of resistance to many of our best antibiotics.