Emerging studies have highlighted the disproportionate role of Candida albicans in influencing both early community assembly of the bacterial microbiome and dysbiosis during allergic diseases and intestinal inflammation. Nonpathogenic colonization of the human gastrointestinal (GI) tract by C. albicans is common, and the role of this single fungal species in modulating bacterial community reassembly after broad-spectrum antibiotics can be readily recapitulated in mouse studies. One of the most notable features of C. albicans-associated dysbiotic states is a marked change in the levels of lactic acid bacteria (LAB). C. albicans and LAB share metabolic niches throughout the GI tract, and studies have identified various interactions between these microbes. The two predominant LAB affected are species and species. Lactobacilli can antagonize enterococci and C. albicans, while Enterococcus faecalis and C. albicans have been reported to exhibit a mutualistic relationship. E. faecalis and C. albicans are also causative agents of a variety of life-threatening infections, are frequently isolated together from mixed-species infections, and share certain similarities in clinical presentation-most notably their emergence as opportunistic pathogens following disruption of the microbiota. In this review, we discuss and model the mechanisms used by species, E. faecalis, and C. albicans to modulate each other's growth and virulence in the GI tract. With multidrug-resistant E. faecalis and C. albicans strains becoming increasingly common in hospital settings, examining the interplay between these three microbes may provide novel insights for enhancing the efficacy of existing antimicrobial therapies.