The gastrointestinal (GI) tract is a frequent source of hematogenous candidiasis in humans. Animal models of GI and hematogenous candidiasis have provided insights into the nature of candidal infection of host mucosal tissue, mechanisms of fungal dissemination to body organs, and features of host response to candidal infections. Biological systems such as these that simulate human candidiasis can be used for testing novel antifungal drugs. We have focused on two murine models of candidiasis with similarities to this fungal disease in humans. The first model simulates a commensal association of Candida albicans with the GI tract of immunocompetent hosts; it has permitted studies of innate and immune cell response to long-term ( > 60 days) infection of the esophageal, gastric, and intestinal mucosa. The second model simulates candidal infection in granulocytopenic patients with invasive candidiasis that originated from sites of colonization in the gut. Both models are well suited for investigating new approaches to prevention and treatment of hematogenous candidiasis. A review of the data on the role of GI candidiasis in hematogenous candidal infections is presented.