Gastric colonization withCandida albicans

Abstract

We adapted a rat model of gastrointestinal candidiasis for studies of in vivo gastric colonization with Candida albicans. Whereas normal rats cleared a single intragastric inoculum of 5 x 10(6) C. albicans from the stomach within 4 hours, rats pretreated with chloramphenicol and gentamicin achieved stable gastric colonization for at least 5 days after administration of this inoculum. We next used this model to study host modifications hypothesized to alter gastric colonization. A first group received dilute HCl 4 hr before yeast inoculation, to induce acute superficial gastric erosions; another group was treated with glucocorticosteroid beginning 12 days before yeast inoculation; and another group received famotidine therapy beginning 3 days before yeast inoculation, to neutralize gastric acidity. Recovery of yeasts from stomachs was significantly different from the control group only in rats treated with steroids; greater colonization was found in the rats so treated. In a final group of experiments, we attempted to inhibit in vivo gastric colonization with yeasts by preincubation of yeasts in vitro with a polyclonal antiserum raised in rabbits against heat-killed C. albicans. We were not able to demonstrate inhibition of gastric colonization by preincubation with this antiserum in this model system.

Evaluation of the intranasal challenge route in mice as a mucosal model for Candida albicans infection

“…In rodents C. albicans has a limited ability to colonize the intestinal tract and to cause systemic disease after oral challenge. Significant colonization of the gastro-intestinal mucosa only occurs in adult immunocompetent mice if prolonged antibiotic treatment is given before and after C. albicans oral or intragastric challenge (Cenci et al, 1995 ;Greenfield & Joyce, 1993 ;Helstrom & Balish, 1979). Germ-free mice orally infected with C. albicans may develop localized mucosal infections in the -oro-intestinal tract (Jensen et al, 1996;Lacasse et al, 1993).…”

Influence of gastric colonization withCandida albicanson ulcer healing in rats: Effect of ranitidine, aspirin and probiotic therapy

“…an increase in the gastroduodenal pH, are believed to favor Candida overgrowth in the stomach [8,9], but the factors which initially permit colonization of the gut by Candida and promote its pathogenic action are not clear. Antibiotic treatment, for instance with clindamycin and gentamicin, has been shown to evoke highlevel and prolonged C. albicans colonization in rats and mice [4,10]. Among Candida species, C. albicans was shown to be present in the stomach irrespective of gastric acidity and was able to multiply in vitro up to pH 2.0 [11].…”

“…Colonization of the GI tract by C. albicans usually increases in individuals who show a reduction in local gastric defense mechanism(s) [2]. In patients with diabetes mellitus, malignant diseases or those with acquired immunodeficiency syndrome (AIDS), symptomatic oral or esophageal infections may develop from GI proliferation of Candida [3,4].…”