热带海洋珍珠贝类立克次体病研究 Ⅴ.超微病理学及致病机理研究
Studies on the Rickettsia-like organism disease of tropical marine pearl oyster V. Ultrastructural pathology and pathogenesis of Rickettsia-like organism disease
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摘要: 对海水养殖大珠母贝和合浦珠母贝类立克次体(Rickettsia-like organism,RLO)病(简称RLO病)的超微病理学进行了研究.结果显示细胞及亚细胞结构经历由变性发展到坏死的病变过程,如胞核由核浓缩、核碎裂发展为核溶解;线粒体出现肿胀,嵴和基质改变及内质网脱颗粒、扩张和囊泡变等一系列混浊肿胀和水泡变性的基本特征;最终,细胞器完全溶解消失使胞质疏松,呈崩解或溶解状.结合先前组织细胞病理学和本文超微病理学研究的结果认为,RLO导致宿主细胞变性坏死的机制有:(1)直接损伤细胞的质膜;(2)直接干扰或破坏细胞的正常代谢;(3)对肝胰腺的广泛破坏可能通过破坏血管内皮系统间接造成肝胰腺上皮细胞的血供障碍,进而引起营养和呼吸代谢障碍或(和)与菌体释放的内毒素有关.Abstract: Detailed ultrastructural pathology of Rickettsia-like organism(RLO) disease which is extensively prevalent in maricutured pearl oyster, Pinctada maxima and P. fucata, was described. The RLO disease, at the ultrastructural level, presented a process from degeneration to necrosis of cellular organelles such as the nucleus underwent pyknosis, karyorrhexis and karyolysis; mitochondria and endoplasmic reticulums presented a series of clody swellings and vacuolar degenerations; at last, these cellular organelles were lysis and the cytoplasm become loose and disappeared. Combined with the results of previous histological pathology observed by light and present ultrastructural pathology observed by transmission electron microscope, there may be three mechanisms on the pathogenesis for the pearl oyster hosts causing by parasitizing RLO:(i) damaging cell membrane of host by large quantities of multiplications of RLO;(ii) interfering with normal metabolisms of host cell by growth and multiplication of RLO;(iii) causing nutrient and respiratory metabolic disorders as a result of compromising the small blood vessels by parasitizing RLO in endothelial cells or/and associating with releasing endotoxin of RLO for the extensive lesion of hepatopancreas.
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Key words:
- Pinctada maxima /
- P. fucata /
- Rickettsia-like organism /
- ultrastructural pathology /
- pathogenesis
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