An Animal Model for Oropharyngeal, Esophageal and Gastric Candidosis

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Abstract
Conventional mice inoculated with Candida albicans by the oral-intragastric route as infants (6-day-old) have previously been shown to develop gastrointestinal (GI) candidosis which persists for at least 30–60 days post-challenge without the use of compromising procedures. Histological preparations of the stomachs of these animals reveal hyphae which have crossed the mucin barrier and are associated with the stratified squamous epithelium of the gastric mucosa primarily in the region of the cardial-atrium fold. Host inflammatory cells are frequently observed adjacent to these filaments and yeast cells. In this study, groups of neonates were challenged oral-intragastrically with either C. albicans strain CA30, or strain CA87. The two strains showed marked differences in the numbers of cells associated with tissue of the tongue, esophagus and stomach of non-immunocompromised mice at 20 days post-inoculation. After immunocompromising treatment by intraperitoneal administration of cyclosphosphamide and cortisone acetate, both groups of mice showed extensive colonization and tissue invasion of the tongue, proximal and distal portions of the esophagus, and cardial-atrium fold of the stomach. C. albicans-containing abscesses were occasionally observed on the tongue of these animals. Histological preparations of the cardiac antrum, located at the junction of esophagus and stomach, frequently revealed concentrations of hyphae and yeast cells associated with the stratified squamous epithelium. We suggest that these non-immunocompromised and immunocompromised mice with persistent C. albicans infections of oropharyngeal, esophageal and gastric tissue, initiated by oral-intragastric challenge at infancy, simulates conditions in different groups of chronically infected humans, and serves as a useful model for testing the efficacy of anti-Candida drugs in clearance of candidosis from the alimentary canal.