Mucosal and disseminated candidiasis in gnotobiotic SCID mice.

The alimentary tracts of germ-free SCID (severe combined immunodeficient) mice were susceptible to colonization with Candida albicans. Large viable populations (10(6)-10(8) colony forming units g-1) of C. albicans, in pure culture, were present in all sections of the intestinal tract. Candida-colonized SCID mice, sacrificed at various time intervals over a 16 week study, manifested chronic superficial mucosal candidiasis of keratinized epithelial surfaces (tongue and stomach). Despite the continuous presence of large viable populations of C. albicans in their intestinal tract, only superficial mucosal candidiasis and no progressive disseminated candidiasis of endogenous origin was evident in these mice. Treatment with cyclophosphamide (100 mg kg-1, intraperitoneally) enhanced the susceptibility of SCID mice to mucosal (tongue and stomach) candidiasis. Gnotobiotic (C. albicans-colonized) SCID mice were also found to be as resistant as immunocompetent BALB/c mice to acute (intravenous challenge) renal candidiasis. Colonization of the alimentary tract with a bacterial flora appeared to enhance the resistance of SCID mice to disseminated candidiasis. This study demonstrates that innate immune mechanisms (phagocytic and/or NK cells), in the absence of functional T- and B-cells, play an important role in the resistance of SCID mice to mucosal and disseminated candidiasis of endogenous (intestinal tract) or acute (intravenous challenge) origin.