candida

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Ecology of Candida albicans gut colonization: inhibition of Candida

adhesion, colonization, and dissemination from the gastrointestinal

tract by bacterial antagonism.

M J Kennedy and P A Volz

ABSTRACT

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.