ACQUIRED-RESISTANCE AND PERSISTENCE OF CANDIDA-ALBICANS FOLLOWING ORAL CANDIDIASIS IN THE MOUSE - A MODEL OF THE CARRIER STATE IN HUMANS

In our experimental model of oral candiasis in the CD1 mouse, the prim ary infection showed reproducible Candida overgrowth kinetics with a p eak level on day 5 of the infection. After day 7, the population stabi lized at about 300 colony-forming units per excised mucosal tissue. Th e primary infection triggered an inflammatory response that resolved i n under 8 days. At this point, the histological pattern of the mucosa reached a new equilibrium between recruited and resident mononuclear c ells. The primary infection also rapidly stimulated cellular immunity, as measured from day 4 by a delayed-type hypersensitivity footpad rea ction. Following a second topical challenge with Candida 30 days after the primary infection, the infection was barely detectable and a typi cal local delayed-type hypersensitivity reaction occurred between 24-7 2 h. It is proposed that acquired resistance, in conjunction with low- level persistence of Candida in our model, mimics the carrier state in sensitized humans.