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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. Both control hamsters not given antibiotics and antibiotic-treated animals reconverted 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 further indicated that animals which contained a complex indigenous microflora had significantly lower numbers of C. albicans associated with their giit walls than did antibiotic-treated animals. The ability of C. albicans to associate with intestinal mucosal surfaces was also 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 inhibitory 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.

Teria are inhibitory to both in vitro growth and GI colonization by C. albicans (4, 32-34, 44, 47, 48). It is important to note, however, that these studies do not reflect interactions as they normally occur in the intestinal tract (17, 21). Most, if not all, in vitro studies have reported on C. albicans (17, 21). albicans suppression by a single bacterial species (45), which is hardly representative of the 400 to 500 different bacterial species that normally inhabit the intestinal tract (54). Likewise, studies in which a monoflora of Escherichia coli (or any other single bacterial species) antagonized C. albicans growth in the gut of gnotobiotic animals (4, 32, 33,44) cannot be expected to reflect interactions of a complex indigenous microflora (17, 21).

Bacteria under the former condition reach abnormally high numbers in the gut (31). E. coli itself is suppressed by the strict anaerobes which dominate the intestinal microflora (22, 63). Thus, it is still not known whether E. coli can exert an inhibitory mechanism(s) over C. coli. albicans under normal in vivo conditions, as has so often been suggested (4, 32-34, 44, 45). In fact, Clark (10) showed that C. albicans grew unchecked for several weeks in the GI tracts of gnotobiotic mice containing an intestinal flora of Bacteroids sp., Lactobacillus sp., Streptococcus faecalis, Streptococcus lactis, and E. coli. Recent studies also indicate that enteric bacilli (including E. coli) do not inhibit the growth of C. albicans in the GI tracts of conventional mice (2, 37a). The present studies were initiated to examine the mechanisms by which a complex indigenous microflora inhibits C. albicans colonization and dissemination from the GI tract.

Source:https://pubmed.ncbi.nlm.nih.gov/3897061//9619120/