The causative agent of Legionnaires disease, Legionella pneumophila, resides within alveolar macrophages by exporting 295 bacterial virulence proteins (effectors) to modulate host cell processes. This leads to the formation of a unique vacuolar niche and the suppression of macrophage cell death pathways, which, in turn, promote bacterial survival and allow sufficient time for replication. However, once nutrients within the vacuole are depleted, Legionella must act to induce host cell death in order to facilitate bacterial egress and reinfect new cells. Intracellular Legionella also evade detection by the host cell s innate immune system, which seeks to destroy invading pathogens by activating inflammasome complexes, thereby promoting proinflammatory cytokine activation and pyroptotic cell death. Understanding how different forms of programmed cell death contribute to Legionella infectivity and are manipulated by Legionella effector proteins will be important for identifying novel antibacterial therapeutic targets.