Crl:CDI(ICR) BR adult mice were fed chow containing Candida albicans or regular chow. Both groups were subsequently given either antibiotics acting mainly against Gram-positive organisms or normal saline for 10 days. Stool cultures were performed before, at the end, and one week after discontinuation of treatment to determine the effects on the stool yeast concentration. Candida colonized mice treated with vancomycin, teicoplanin, linezolid, quinupristin-dalfopristin or telithromycin had higher colony counts of yeast in their stools than control Candida fed mice treated with saline. This increase was not statistically significant. Mice fed regular chow treated with the study drugs or saline did not have any yeasts in their stools. Dissemination of Candida was not observed in the visceral organs of any mouse.
Adult male Crl:CD1 (ICR) mice were fed chow containing Candida albicans to induce sustained gastrointestinal colonization by the yeast. Groups of mice were rendered neutropenic with cyclophosphamide and subsequently received ceftriaxone, while other groups received normal saline and served as controls. Stool cultures were obtained immediately before and at the end of treatment. The administration of cyclophosphamide substantially increased the C. albicans counts in the stools of mice. The addition of ceftriaxone to the cyclophosphamide regimen did not significantly increase the level of gastrointestinal colonization by C. albicans. There was no evidence of Candida dissemination to internal organs.
Crl:CD1(ICR) BR mice were fed chow containing Candida albicans or regular chow. Both groups were subsequently given either antibiotics or normal saline. Stool cultures were performed before, at the end of treatment and 1 week after treatment, to determine the effect on the stool yeast concentration. Candida-colonized mice treated with cefepime, cefixime or ceftibuten had higher (however not significantly) counts of the yeast in their stools than control Candida-fed mice treated with saline. A group of Candida-fed mice were treated with ceftriaxone, which is known to increase the yeast stool concentration significantly and served as positive control. Mice fed regular chow and treated with the study drugs or saline did not have any yeasts in their stools. Dissemination of Candida did not occur.
Adult male Crl:CD1 (ICR) BR mice were fed chow containing Candida albicans or regular chow. Both groups were subsequently given tigecycline or daptomycin or normal saline subcutaneously for 10 days. To determine the effect on the stool yeast concentration, stool cultures were performed immediately before, at the end, and 1 week after discontinuation of treatment. Candida-colonized mice treated with tigecycline or daptomycin had higher counts of the yeast in their stools than control C. albicans-colonized animals treated with saline. Tigecycline caused a significant increase of 2.1 log(10) CFU g(-1) of stools in C. albicans concentration, while daptomycin caused a minor increase of 0.4 log(10) CFU g(-1) of stools. Mice fed regular chow and treated with the study antibiotics or saline did not have any Candida in their stools. Dissemination of Candida was not detected in any animal. These data suggest that tigecycline induces a substantial increase in the intestinal concentration of C. albicans, while daptomycin causes only a minimal increase. However, these increases are not associated with dissemination of the yeast to internal organs. Clinical studies in humans are needed to validate our findings, especially in patients at risk of developing disseminated candidosis.
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