The ability of Candida albicans to rapidly and reversibly switch between yeast and filamentous morphologies is crucial to pathogenicity, and it is thought that the filamentous morphology provides some advantage during interaction with the mammalian immune system. Dectin‐1 is a receptor that binds β‐glucans and is important for macrophage phagocytosis of fungi. The receptor also collaborates with Toll‐like receptors for inflammatory activation of phagocytes by fungi. We show that yeast cell wall β‐glucan is largely shielded from Dectin‐1 by outer wall components. However, the normal mechanisms of yeast budding and cell separation create permanent scars which expose sufficient β‐glucan to trigger antimicrobial responses through Dectin‐1, including phagocytosis and activation of reactive oxygen production. During filamentous growth, no cell separation or subsequent β‐glucan exposure occurs, and the pathogen fails to activate Dectin‐1. The data demonstrate a mechanism by which C. albicans shape alone directly contributes to the method by which phagocytes recognize the fungus.