Candida albicans is a pathogen of mucosal surfaces but can also cause systemic disease. Its evolution into a commensal and frequent pathogen of humans and animals progressed as the organism developed specific traits which allowed it to survive in a host. One can only speculate as to which traits promoted its survival; however, it would seem that recognition and colonization of host cells would afford a selective advantage over those organisms which could not adhere. Also, colonization could permit egress of the organism into tissues and, with that, escape from the competitive microbial ecology of mucosal surfaces. Recognition of host cells by C. albicans has been the focus of study by a number of investigators. Based upon a number of observations by several research groups, the recognition process appears complex and dependent upon the type of host cell studied. The C. albicans adhesins are cell surface macromolecules, one adhesin resembling the “integrin” receptors of mammalian cells. Based upon functional activity and the type of host cell molecule recognized by the organism, five adhesin systems have been described. Four of these adhesins are mannoprotein or mannan, while the fifth is thought to be chitin. The host cell ligand is either carbohydrate (fucosyl or glucosamine glycosides) or protein (arginine-glycine-aspartic acid, RGD peptide), depending upon the type of host cell, i. e., either epithelial or endothelial. The study of the Candida adhesins is now beginning to shift from its descriptive beginnings to molecular approaches with the ultimate intent of establishing the role of these molecules in virulence.