We are using reverse genetics and various "omics" technologies to study the molecular interactions between phages and their enterococcal hosts. We demonstrated that the enterococcal polysaccharide antigen (epa) locus mediates phage infection of Enterococcus faecalis (Chatterjee, Johnson et al. 2019). Phage selective pressure promotes mutations in epa genes which subvert phage infection. As a consequence, E. faecalis epa mutants trade a fitness benefit for phage resistance. Mutation of epa genes renders E. faecalis more susceptible to cell wall targeting antibiotics. These strains fail to robustly colonize the intestinal tracts of mice and cannot expand their population upon antibiotic-mediated intestinal dysbiosis. We also discovered that phage driven mutations in polysaccharide biosynthesis are heavily selected in the absence of a conventional microbiota, suggesting that native intestinal bacteria direct the evolution of phage-bacteria interactions in vivo. Our work suggests that phage therapy could be used in combination with antibiotics to target enterococci within a dysbiotic microbiota. Enterococci that evade phage therapy by developing resistance may be less fit at colonizing the intestine and become sensitized to antibiotics preventing their overgrowth in the intestine.