It has recently become clear that metabolic shifts underpin immune response to infection, giving birth to the field of “immunometabolism”. To date, the focus has largely been on host metabolic pathways. However, microbes also adjust their metabolism, to survive and thrive during infection. We are studying the nexus of host and pathogen metabolism, to understand how it impacts on host responses and immune evasion by pathogens to ultimately control infections. Our experimental system is Candida albicans, a yeast that can cause systemic infections with high mortality. Candida mounts a counter-attack against innate immune phagocytes through sophisticated pathways that involve a developmental switch from yeast to hyphal morphology, and metabolic competition for an essential nutrient. Our recent work has illuminated how the interaction of host and pathogen glucose metabolism controls macrophage viability and immune responses to C. albicans. We have further shown that mdivi-1, a putative inhibitor of mitochondrial division, represses hyphal development of C. albicans through a novel mechanism. Treatment with mdivi-1 delays macrophage cell death in response to C. albicans challenge, and reduces inflammatory responses.