{'fraction_non_alphanumeric': 0.01717699775952203, 'fraction_numerical': 0.0, 'mean_word_length': 5.504854368932039, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Oral and esophageal Candida albicans infection in hyposalivatory rats

The opportunistic fungus Candida albicans is a major cause of oral and esophageal infections in immuno-compromised patients, individuals on drug therapy, and the chronically ill. Because it has been observed that persons suffering from hyposalivation have an increased prevalence of oral candididiasis, we developed an animal model of infection based on hyposalivation. The objectives of our studies were to understand the mechanisms by which C. albicans causes oral disease and to begin to elucidate the role played by saliva in controlling C. albicans in the oral cavity. Our results showed that (i) oral Candida infection was established by a small challenge inoculum, (ii) mucosal lesions developed in the oral cavities and esophagi of infected rats, and (iii) transmission of oral Candida infection from an inoculated rat to uninoculated cagemates occurred rapidly. In addition, we compared the abilities of a clinical isolate and a spontaneously derived morphological mutant from that isolate to infect hyposalivatory rats and to induce disease. Infection was induced by the morphological mutant in hyposalivatory rats; however, the morphological mutant took significantly longer to transmit oral infection to uninoculated cagemates than did the parental strain.