Physiological and metabolic alterations accompanying systemic candidiasis in mice.
Mice challenged intravenously with 10(6) viable Candida albicans died between 1 and 16 days after infection. Near the time of death, over 98% of the recoverable fungi came from the kidneys. Physiologically, animals were in renal failure near the time of death as evidenced by elevated blood urea nitrogen (BUN) and blood creatinine levels and a creatinine clearance rate which was about one-half normal. No abnormalities in liver glucogen and blood glucose levels were detectable. When mice were challenged with 4.5 X 10(6) viable C. albicans, they all died within 12 h. Near the time of death they had normal BUN values and were hyperglycemic. In mice receiving 4.5 X 10(6) heat-killed C. albicans, no deaths occurred and liver glycogen, blood glucose, and BUN levels all remained within a normal range and were different from responses to bacterial endotoxin. Cumulatively, the results demonstrate two distinct syndromes for the pathogenesis of experimental C. albicans infections. At the lower dose, mice were in renal failure associated with progressive renal infection. At the higher dose, renal failure was not observed. If a toxin was associated with death from the latter dose, it was not similar to bacterial endotoxin.
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001806:Blood Urea Nitrogen; D002177:Candidiasis / Q000097:blood / Q000378:metabolism* / Q000503:physiopathology; D003404:Creatinine / Q000097:blood; D004731:Endotoxins / Q000494:pharmacology; D005260:Female; D006358:Hot Temperature; D007668:Kidney / Q000503:physiopathology; D008112:Liver Glycogen / Q000378:metabolism; D051379:Mice; D009392:Nephrectomy; D012486:Salmonella typhimurium; D012965:Sodium Chloride
D001786:Blood Glucose; D004731:Endotoxins; D008112:Liver Glycogen; D012965:Sodium Chloride; D003404:Creatinine