To fight off pathogens immune cells trigger a large reprogramming of metabolism, with activation of glycolysis and increased glucose consumption being a key feature. For macrophages, this sort of metabolic reprogramming has been linked to their ability to produce antimicrobial cytokines and reactive oxygen species, and drive inflammation. Microbes also reprogram their metabolism during infection. However, how metabolic reprogramming of host and pathogen interact during infection, and the impact of these metabolic interactions on disease outcomes, is poorly understood. We addressed these questions using the human fungal pathogen Candida albicans, and studying the interaction with macrophages and the importance of host glucose homeostasis in animal infection.