Candida albicans is normally found as a commensal microbe, commonly colonising the gastrointestinal tract in humans. However, this fungus can also cause mucosal and systemic infections once immune function is compromised. Dectin-1 is an innate pattern recognition receptor essential for the control of fungal infections in both mice and humans, however its role in the control of C. albicans colonisation of the gastrointestinal tract has not been defined. Here, we demonstrate that in mice Dectin-1 is essential for the control of gastrointestinal invasion during systemic infection, with Dectin-1 deficiency associating with impaired fungal clearance and dysregulated cytokine production. Surprisingly, however, following oral infection Dectin-1 was not required for the control of mucosal colonisation of the gastrointestinal tract, either in terms of fungal burdens or cytokine response. Thus, in mice, Dectin-1 is essential for controlling systemic infection with C. albicans, but appears redundant for the control of gastrointestinal colonisation.