The human fungal pathogen Candida albicans exists as commensal yeast cell but becomes invasive as hyphae. While several pattern recognition receptors recognize the carbohydrate rich cell wall of Candida, yeast and hyphae induce different cytokine and immune responses. This is largely because intracellular hyphae, but not yeast cells, are detected by the NLRP3 inflammasome leading to caspase-1 activation and Il-1β secretion. Here we show activation of the NLRP3 inflammasome by intracellular Candida also induces pyroptosis. In the absence of NLRP3, ASC or caspase-1, Candida is still able to form intracellular hyphae but fails to kill and escape from macrophages soon after phagocytosis. Conversely, we have generated Candida mutants that still form hyphae but display reduced levels of caspase-1 activation, pyroptosis and Il-1β secretion. These mutants show a breakdown of the cell wall architecture, in particular reduced expression of glucans, which are known targets of macrophage receptors. Importantly, despite forming hyphae in susceptible mice these Candida mutants are heavily attenuated in virulence, suggesting that pyroptosis is a critical escape mechanism of Candida. This is surprising, as we have recently shown that intracellular hyphae can also induce delayed macrophage death to escape, even in the absence of pyroptosis and other programmed cell death pathways. Thus, we provide the first report of a fungal pathogen to induce pyroptosis in macrophages and provide evidence that early macrophage escape by hijacking pyroptosis contributes to Candida virulence.