The primary host defense against candidiasis is intact barrier function. The most common portal of entry for infection is invasion from the mucosal surface of the GI tract due to disruption of normal barriers resulting from disease, trauma or cytotoxic therapy. Candida may also be acquired by direct contact with mucosal lesions in others. In infections related to vascular catheters, the skin at the puncture site is the likely source of entry. After invasion, neutrophils are the first line of defense, followed by monocytes, which kill blastoconidia by oxidative and nonoxidative mechanisms.
Humoral immunity is also important, as antibody can activate complement and is opsonic.
The clinical outcome depends largely on the host immune status. While defects in T cell function are mainly associated with mucocutaneous syndromes, neutropenia or defects in neutrophil and macrophage function are associated with systemic candidiasis. Other proposed virulence factors include germ tube formation and morphologic switching, as well as the production of proteases and phospholipases. The distinction between colonizer and pathogen can be problematic. Short-course azole therapy also used for vaginitis.