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Abstract：
Lesions of adiaspiromycosis, a respiratory disease affecting wild animals, have been found mainly in dead mammals and free-living mammals captured for surveillance. No report has described an investigation of adiaspore formation progress in the lung. After establishing an experimental mouse model of intratracheal adiaspiromycosis infection with the causative agent Emmonsia crescens, we observed adiaspore development. The spores grew and reached a plateau of growth at 70 days post-infection. The median adiaspore diameter showed a plateau of around 40 μm. The characteristic three-layer cell-wall structure of adiaspores was observed in the lung at 70 days post-infection. We examined infection with a few spores, which revealed that adiaspores in the mouse lung progressed from intratracheal infection of at least 400 spores. Moreover, we developed adiaspores in vitro by culture in fetal bovine serum. Although most spores broke, some large spores were intact. They reached about 50 μm diameter. Thick cell walls and dense granules were found as common points between in vitro adiaspores and in vivo adiaspores. These models are expected to be useful for additional investigations of E. crescens adiaspores and adiaspiromycosis.
摘要：
脂肪肉芽肿病的病变，一种影响野生动物的呼吸道疾病，主要在被捕获用于监视的死亡哺乳动物和自由生活哺乳动物中发现。没有报告描述了肺中脂肪孢子形成进展的研究。在用病原体Emmonsiacrescens建立气管内脂肪肉芽肿感染的实验小鼠模型后，我们观察到了脂肪孢子的发育。孢子生长并在感染后70天达到生长平台。中值脂肪孢子直径显示约40μm的平台。感染后70天，在肺中观察到了特征性的脂肪孢子三层细胞壁结构。我们检查了一些孢子的感染，这表明小鼠肺中的脂肪孢子是由至少400个孢子的气管内感染引起的。此外，我们通过在胎牛血清中培养体外培养外生孢子。虽然大多数孢子破裂，一些大孢子完好无损。它们达到约50μm的直径。发现厚厚的细胞壁和致密的颗粒是体外绝热和体内绝热之间的共同点。这些模型预计可用于新月大肠杆菌的绝热孢子和无菌丝病的其他研究。
