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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

吴信忠 潘金培

吴信忠, 潘金培. 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[J]. 海洋学报, 1999, 21(3): 113-118.
引用本文: 吴信忠, 潘金培. 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[J]. 海洋学报, 1999, 21(3): 113-118.
Wu Xinzhong, Pan Jinpei. Studies on the Rickettsia-like organism disease of tropical marine pearl oyster V. Ultrastructural pathology and pathogenesis of Rickettsia-like organism disease[J]. Haiyang Xuebao, 1999, 21(3): 113-118.
Citation: Wu Xinzhong, Pan Jinpei. Studies on the Rickettsia-like organism disease of tropical marine pearl oyster V. Ultrastructural pathology and pathogenesis of Rickettsia-like organism disease[J]. Haiyang Xuebao, 1999, 21(3): 113-118.

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

基金项目: 中国科学院重点基金资助项目(编号:KS85-121);广东省自然科学基金资助项目(编号:970269)

Studies on the Rickettsia-like organism disease of tropical marine pearl oyster V. Ultrastructural pathology and pathogenesis of Rickettsia-like organism disease

  • 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.
  • Elston R, Wilkinson M T.Pathology,management and diagnosis of oyster velar virus disease(OVVD).Aquaculture,1985,48,189-210
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    吴信忠,播金培.热带海洋珍珠贝类立克次体病研究Ⅳ.组织细胞病理学研究.海洋学报,1999,21(2):93-98
    昊信忠,潘金培.热带海洋珍珠贝类立克次体病研究Ⅲ.合浦珠母贝寄生类立克次体形态学研究.热带海洋研究,1997,(5):110-117
    吴信忠,潘金培.热带海洋珍珠贝类立克次体病研究—大珠母贝病原RLO包涵体的组织学及超微结构研究.海洋与湖沼,1999.30(1):73-80
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出版历程
  • 收稿日期:  1997-12-29
  • 修回日期:  1998-04-06

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