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目的:探讨梨支原体(Mpi)和发酵支原体(Mf)致死性感染大鼠肺、肾超微结构改变。方法:38只免疫缺陷SD大鼠。实验组:Mf和Mpi致死性感染(n=12),免疫抑制NS和非免疫抑制Mf感染对照组(n=7)。观察死亡率,透射电镜下观察肺、肾超微结构改变。结果:实验组死亡率均为100%,高于对照组(P<0.01)。电镜下见Mf和Mpi感染致死大鼠肺泡Ⅰ型上皮细胞肿胀,胞核固缩,空泡变性;肾内皮细胞细胞质溶解,胞核固缩,细胞溶解、线粒体空泡形成等超微结构改变。结论:发酵支原体和梨支原体感染致死大鼠肺泡Ⅰ型上皮细胞和肾毛细血管内皮细胞超微结构异常。
Objective: To investigate the ultrastructural changes in the lung and kidney of fatal infected Mycoplasma pneumoniae (MpI) and Mycoplasma fermentum (Mf). Methods: 38 immunodeficient SD rats. Experimental groups: lethal infection with Mf and Mpi (n = 12), immunosuppressive NS and non-immunosuppressed Mf infected controls (n = 7). The mortality was observed. The ultrastructural changes of lung and kidney were observed under transmission electron microscope. Results: The mortality of the experimental group was 100%, higher than that of the control group (P <0.01). The ultrastructure changes of alveolar epithelial type I epithelial cells such as swollen, nucleus pyknosis and vacuolar degeneration in rats with lethal Mf and Mpi infection were observed under electron microscope. Cytoplasmic, nuclear pyknosis, cell lysis and mitochondrial vacuolization of renal endothelial cells were also observed. Conclusion: The ultrastructural changes of alveolar type I epithelial cells and renal capillary endothelial cells in the fatal rats were caused by Mycoplasma fermentor and Mycoplasma pear infection.