The alimentary tracts of germ-free SCID (severe combined immunodeficie
nt) mice were susceptible to colonization with Candida albicans, Large
viable populations (10(6)-10(8) colony forming units g-1) of C. albic
ans, in pure culture, were present in all sections of the intestinal t
ract. Candida-colonized SCID mice, sacrificed at various time interval
s over a 16 week study, manifested chronic superficial mucosal candidi
asis 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 pr
ogressive disseminated candidiasis of endogenous origin was evident in
these mice. Treatment with cyclophosphamide (100 mg kg-1, intraperito
neally) enhanced the susceptibility of SCID mice to mucosal (tongue an
d stomach) candidiasis. Gnotobiotic (C. albicans-colonized) SCID mice
were also found to be as resistant as immunocompetent BALB/c mice to a
cute (intravenous challenge) renal candidiasis. Colonization of the al
imentary tract with a bacterial flora appeared to enhance the resistan
ce of SCID mice to disseminated candidiasis. This study demonstrates t
hat innate immune mechanisms (phagocytic and/or NK cells), in the abse
nce of functional T- and B-cells, play an important role in the resist
ance of SCID mice to mucosal and disseminated candidiasis of endogenou
s (intestinal tract) or acute (intravenous challenge) origin.