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Antibiotic-treated and untreated Syrian hamsters were inoculated intragastrically with Candida albicans to determine whether C. albicans could opportunistically colonize the gastrointestinal tract and disseminate to visceral organs. Antibiotic treatment decreased the total population levels of the indigenous bacterial flora and predisposed hamsters to gastrointestinal overgrowth and subsequent systemic dissemination by C. albicans in 86% of the animals. Both control hamsters not given antibiotics and antibiotic-treated animals reconventionalized with an indigenous microflora showed significantly lower gut populations of C. albicans, and C. albicans organisms were cultured from the visceral organs of 0 and 10% of the animals, respectively. Conversely, non-antibiotic-treated hamsters inoculated repeatedly with C. albicans had high numbers of C. albicans in the gut, and viable C. albicans was recovered from the visceral organs of 53% of the animals. Examination of the mucosal surfaces from test and control animals indicated further that animals which contained a complex indigenous microflora had significantly lower numbers of C. albicans associated with their gut walls than did antibiotic-treated animals. The ability of C. albicans to associate with intestinal mucosal surfaces also was tested by an in vitro adhesion assay. The results indicate that the indigenous microflora reduced the mucosal association of C. albicans by forming a dense layer of bacteria in the mucus gel, out-competing yeast cells for adhesion sites, and producing inhibitor substances (possibly volatile fatty acids, secondary bile acids, or both) that reduced C. albicans adhesion. It is suggested, therefore, that the indigenous intestinal microflora suppresses C. albicans colonization and dissemination from the gut by inhibiting Candida-mucosal association and reducing C. albicans population levels in the gut. Systemic Candida infections are important causes of morbidity and mortality among patients who are compromised immunologically or who are undergoing prolonged antibiotic therapy (41, 52, 69). The passage of viable Candida albicans through the gastrointestinal (GI) mucosa into the host bloodstream is believed to be an important mechanism leading to systemic candidosis (38, 61, 62), particularly in patients with acute leukemia (43). Patient and animal studies support this hypothesis and indicate that a number of opportunistic fungal pathogens can spread systemically from the intestinal lumen to invade visceral organs (28, 29, 67, 68). We recently reported, for instance, that C. albicans, Candida parapsilosis, Candida pseudotropicalis, Candida tropicalis, and Torulopsis glabrata could opportunistically colonize the gut and disseminate to visceral organs after intragastic challenge of antibiotic-treated mice (37). The feeding of C. albicans to animals not given antibiotics, in contrast, does not lead to Candida dissemination from the

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The fungal microflora of a dry valley in Southern Victoria Land near McMurdo Sound, Antarctica, was investigated. Samples were collected from introduced objects such as a mummified penguin and spent chewing tobacco in addition to the sparse soil found in rock fissures, isolated moss colonies, shoreline deposit materials, CaCO3 precipitates, and microbial mat debris obtained from the frozen surface of the lake in the basin of Taylor Valley. Using conventional media and techniques, all collection sites yielded populations of yeasts and filamentous fungi. Water samples and live microbial mats from beneath the lake ice yielded species of fungi along with an abundance of bacteria.