The relative pathogenicity of Candida krusei and C. albicans was investigated by assessing their colonisation and infectivity of the Sprague-Dawley rat oral mucosa. During an initial 21-week period with intermittent oral inoculation, both Candida spp. demonstrated variable surface colonisation of the oral mucosa. After 3 days of oral inoculation, both yeast species were recovered from all animals. During the 21-week period the mean oral load of C. albicans in the control group of rats varied between (26-274) x 10(1) cfu/ml whereas the two test groups of rats carrying C. krusei CK9 and CK13 had a mean load of (2-10) x 10(1) cfu/ml. Although oral colonisation by C. albicans was greater than that of C. krusei, neither species induced candidal infection during this period. Subsequent immunosuppression of the rats by intramuscular cyclophosphamide (40 mg/kg body weight) initiated C. albicans infection of the dorsal tongue (around the conical papillae area) after 4 weeks, in all of three animals while similar lesions due to C. krusei were seen--albeit after 5-7 weeks--in three of eight animals. Characteristic histological changes of mucosal candidosis were discernible on the lingual mucosa of rats infected with both Candida spp. including parakeratosis, absence of a stratum granulosum, thickened rete ridges, micro-abscess formation and polymorph infiltration of the lingual epithelium. Although both species produced fungal hyphae that penetrated the epithelium up to the prickle cell layer, C. albicans hyphae tended to be relatively more profuse. Taken together these results substantiate, for the first time in an animal model, the clinical evidence that C. krusei, once considered an innocuous commensal, is capable of transforming into an invasive pathogen under conditions of immunosuppression.