Candida albicans and related species live as benign commensals in one or more body locations in a majority of healthy individuals. As opportunistic pathogens, they are poised to overgrow cavities and penetrate tissue in response to an alteration in host physiology that presumably compromises the immune functions that normally suppress their growth. There is little evidence of the emergence of successful drug-resistant or hypervirulent strains that predominate in either the commensal or disease states. It appears more likely that all strains possess similar capabilities for rapid adaptation to drug therapy, the immune response and changes in body location and in host physiology. It is suggested that the mechanisms for rapid adaptation lie in the developmental programs of the bud-hypha transition and high frequency phenotypic switching, and in the modulation of the expression of virulence genes in response to environmental cues.