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.
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机译：感染10（6）个白色念珠菌的静脉内攻击的小鼠在感染后1至16天死亡。在接近死亡时，超过98％的可回收真菌来自肾脏。从生理上讲，动物在死亡时将处于肾衰竭，这可通过血尿素氮（BUN）和血肌酐水平升高以及肌酐清除率约为正常值的一半来证明。肝糖原和血糖水平未发现异常。当小鼠接受4.5 X 10（6）存活的白色念珠菌攻击时，它们都在12小时内死亡。在接近死亡时，他们的BUN值正常且具有高血糖。在接受4.5 X 10（6）热杀死的白色念珠菌的小鼠中，没有死亡发生，肝糖原，血糖和BUN水平均保持在正常范围内，并且与细菌内毒素反应不同。累积地，结果证明了白色念珠菌感染的发病机理有两种不同的综合征。在较低剂量下，小鼠处于肾衰竭并伴有进行性肾脏感染。在较高剂量下，未观察到肾衰竭。如果毒素与后者剂量引起的死亡有关，则它与细菌内毒素不相似。
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