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为探索卡氏肺孢子虫肺炎的发病机制，将大鼠分为实验组和对照组。给予实验组大鼠肌注地塞米松以诱发肺孢子虫肺炎。每周剖杀，光镜及电镜下对其两组大鼠肺组织进行病原学和病理学观察。对照组大鼠健康，第８ｗｋ后体重增加４５％，肺组织未见病理改变，亦未观察到卡氏肺孢子虫。实验组大鼠慢性发病，第８ｗｋ后体重比原来减少约２６％。电镜下第４ｗｋ、光镜下第５ｗｋ开始查见卡氏肺孢子虫，第７～８ｗｋ达重度感染，阳性率为６６．７％。该虫在肺泡腔内多见，肺间质中少见，在中性粒细胞、肺泡巨噬细胞和Ⅱ型肺泡上皮细胞内也见到。肺组织在实验前４ｗｋ几乎没有什么改变，第５～６ｗｋ有少量虫体附着于肺泡壁，第７～８ｗｋ表现为卡氏肺孢子虫肺炎的典型组织病理学改变。大滋养体伸出丝状伪足与Ⅰ型上皮细胞粘连，该处上皮细胞发生变性改变，Ⅱ型上皮细胞发生凋亡。
To explore the pathogenesis of Pneumocystis carinii pneumonia, rats were divided into experimental group and control group. Rats in the experimental group were given intramuscular dexamethasone to induce pneumocystosis pneumonia. Pathological and pathological changes of the lungs of two groups of rats were observed under light microscope and electron microscope every week. The rats in the control group were healthy. After the 8th week, the body weight increased by 45%. No pathological changes were observed in the lung tissues and no Pneumocystis carinii was observed. The rats in the experimental group were chronically infected, and their body weight decreased about 26% after 8th week. Electron microscopy 4wk, light microscope 5wk began to see Pneumocystis carinii, the seventh ~ 8wk severe infection, the positive rate was 66.7%. The worm is more common in the alveolar space, interstitial lung is rare, in neutrophils, alveolar macrophages and type II alveolar epithelial cells are also seen. There was almost no change in lung tissue 4wk before the experiment. A small amount of worms adhered to the alveolar wall at the 5th to 6th week, and the typical histopathological changes of Pneumocystis carinii pneumonia at 7th to 8th week were observed. Large trophozoites extend filopodia and type Ⅰ epithelial cell adhesion, where degeneration of epithelial cells change, type Ⅱ epithelial cell apoptosis occurs.