胃肠道和播散性念珠菌病。免疫抑制大鼠的实验模型。

Gastrointestinal and disseminated candidiasis. An experimental model in the immunosuppressed rat.

作者信息

Myerowitz R L

出版信息

Arch Pathol Lab Med. 1981 Mar;105(3):138-43.

Abstract

An experimental model of invasive gastrointestinal (GI) candidiasis was studied in immunosuppressed rats. Normal rats were susceptible to disseminated candidiasis by intravascular inoculation (lethal dose for 50% survival [LD50], 1.6 x 10(6) blastospores). Cyclophosphamide-induced leukopenia decreased the LD50 to 1.2 x 10(4) blastospores. Feeding Candida albicans to rats resulted in low-grade GI colonization of normal rats. The intensity of colonization was increased by treatment with cyclophosphamide and broad-spectrum antibiotics. Only in animals fed Candida and treated with both antibiotics and cyclophosphamide did invasive GI lesions develop. However, hematogenous dissemination occurred in only about 10% of such rats. The addition of cortisone acetate to the treatment regimen increased the frequency of hematogenous dissemination to about 25%. Thus, disseminated candidiasis after invasive GI disease can be produced in the rat after exposure to the same predisposing factors as immunosuppressed human patients in whom the disease develops.

摘要

在免疫抑制大鼠中研究了侵袭性胃肠道念珠菌病的实验模型。正常大鼠通过血管内接种易患播散性念珠菌病（半数致死剂量[LD50]为1.6×10⁶芽生孢子）。环磷酰胺诱导的白细胞减少将LD50降至1.2×10⁴芽生孢子。给大鼠喂食白色念珠菌会导致正常大鼠出现低度胃肠道定植。用环磷酰胺和广谱抗生素治疗会增加定植强度。仅在喂食念珠菌且同时接受抗生素和环磷酰胺治疗的动物中才会出现侵袭性胃肠道病变。然而，此类大鼠中只有约10%发生血行播散。在治疗方案中添加醋酸可的松会使血行播散的频率增加至约25%。因此，在大鼠中，在接触与发生该疾病的免疫抑制人类患者相同的易感因素后，可引发侵袭性胃肠道疾病后的播散性念珠菌病。