Influence of Antibiotics or Certain Intestinal Bacteria on Orally Administered Candida albicans in Germ-Free and Conventional Mice

Abstract

Candida albicans, administered by gastric intubation, persisted in the gastrointestinal tract of gnotobiotic mice for long periods but was eliminated within a relatively short period of time in pathogen-free mice. Oxytetracycline administered by mouth had no reproducible effect on the persistence of C. albicans in the gastrointestinal tract of either germ-free or pathogen-free mice. Prolonged administration of streptomycin extended the time that C. albicans could be recovered from feces of pathogen-free mice when compared to mice not receiving the antibiotic or those receiving a single large dose. There was a brief interval of time during which C. albicans could not be recovered from the feces of gnotobiotic mice contaminated with certain intestinal bacteria, but eventually all mice began to shed the fungus again. C. albicans administered by mouth was not pathogenic for germ-free or pathogen-free mice. It can be concluded from these findings that mice do not possess an innate resistance to C. albicans but that pathogen-free mice do possess some ecological mechanism which prevents establishment of the fungus in their gastrointestinal tract. The reason for the difference in colonization of C. albicans in germ-free or gnotobiotic mice and pathogen-free mice was not determined.

Decontamination of gnotobiotic mice experimentally monoassociated with Candida albicans

“…The data reported herein confirm the findings of others (2,8) that C. albicans can be established readily in gnotobiotic mice by oral inoculation. Quantitative counts of approximately 108 C. albicans per g (wet weight) of stomach and cecum (wall plus luminal contents) indicated a well established Candida population in these mice, yet no pathology or evidence of illness was observed.…”

“…However, they did observe pathogenesis in one of three gnotobiotic mouse strains subjected to monoassociation with C. albicans. Clark (2), working with gnotobiotic and pathogen-free mice, concluded that, although mice do not have an innate resistance to colonization by Candida per se (based on the gnotobiotic mice), ecological mechanisms are operative in pathogen-free mice that affect colonization by Candida. Taking the work of Phillips and Balish (8) and of Clark (2) together, it appears that the strain of mouse, the diet fed, and the composition of the intestinal flora of the host may be factors that affect colonization.…”

Antibiotic-induced decreases in the levels of microbial-derived short-chain fatty acids promote gastrointestinal colonization ofCandida albicans

“…In this study, we also report that cecal SCFA concentrations in control mice are as follows: acetic acid (36.87 ± 7.11 μmol/g), butyric acid (7.52 ± 0.92 μmol/g), and propionic acid (8.18 ± 0.77 μmol/g), which are in agreement with the previous findings 63,65–67 . Since antibiotic-induced gut dysbiosis is an important factor for the GI colonization of C. albicans 7,16,68,69 , we examined if antibiotic-induced alterations in the levels of SCFAs play a role in the GI colonization of this fungal pathogen. In this study, we found that cefoperazone-treated mice susceptible to C. albicans infection had significantly decreased levels of SCFAs in the cecal contents.…”

Acute colonization study of polychlorinated biphenyl‐degrading pseudomonads in the mouse intestinal tract: Comparison of single and multiple exposures

“…E. coli strains that harbored plasmids were poorer colonizers than their plasmidless counterparts [lo, 1 1,261. The colonization by other microorganisms has also been studied. Germ-free animals were colonized by Candida albicans, but the organism failed to establish itself in the intestinal tract of conventional mice [27]. When the normal flora of conventional animals was altered by antibiotics, K. pneumoniae colonization, as monitored by organism enumeration in feces, was increased [24].…”

“…When the normal flora were altered by antibiotic treatment, P. aeruginosa [24], S. typhimurium [23], E. coli [10,12] and K. pneumoniae [24] showed increased survival in the mouse. Germ-free animals were colonized by E. coli [ 13,141 and C. albicans [27].…”