Opportunistic fungal pathogens that cause human disease pose a serious threat to public health. The rapid emergence of drug resistant pathogenic fungi such as Candida auris, along with the overuse of commercially available antifungal drugs and inadequacies in drug development, have meant that our therapeutic safety net for fungal infections has become limited 1, 2. Recently, the study of immunometabolism (how immune cells remodel their metabolism when challenged by fungal pathogens) during fungal infection, has offered significant insights into host-pathogen metabolic crosstalk as well as potential for innovation in antifungal treatments. We investigate the metabolic interactions of C. auris with macrophages during infection. We show that C. auris replicates robustly in macrophages and is able to escape macrophages without killing them. However, after escape, C. auris will outcompete macrophages for nutrients, ultimately resulting in macrophage death without inducing a strong immunological response. We also focus on how macrophages maintain glucose homeostasis to fight off fungal infections and demonstrate that glucose supplementation improves immune-cell outcomes. Utilising various mutants affecting glycolytic metabolism of C. auris, we demonstrate that the ability to utilise glucose plays a key role in the establishment and progression of infection. Our data suggests that C. auris escapes immune containment by mechanisms that differ from those used by other Candida pathogens and can leverage host metabolic shifts for survival and proliferation.