Candida is a dimorphic fungal pathogen that colonizes the mucosal surfaces of approximately 30% of healthy individuals at any given moment [1]. In immunocompetent hosts, colonization by Candida spp. does not cause disease, but during a breach of the anatomical barriers or in immunocompromised hosts important clinical consequences may ensue. The spectrum of clinical diseases caused by Candida spp.comprises syndromes as diverse as mucocutaneous infections of the oral and vaginal mucosa, candidemia, and deep-seated infections that are often associated with sepsis [2–4]. Clinical observations have taught us that mucocutaneous candidiasis develops in the setting of defective T-cell immunity (as probably best exemplified in the case of HIV infection), whereas invasive infections tend to occur when there is phagocytic dysfunction (such as in neutropenia and neutrophil disorders). In recent years, insight into host defense against candidiasis has greatly increased and this gain in knowledge has begun to be applied to clinical medicine.