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目的 :研究伯氏疟原虫 (Plasmodium berghei)的抗药性与致病力的关系。 方法 :比较伯氏疟原虫氯喹敏感株 (N)和抗性株 (RC)感染 ICR鼠的肝、脾、脑、心、肺、肾等重要脏器病理组织学的动态变化。结果 :N株感染后 ,小鼠肝、脾有较多的疟色素沉着 ,肺脏呈郁血性水肿 ;脑微血管充血和阻塞 ;各脏器呈急性炎症的病理变化特点。 RC株感染后 ,小鼠肝、脾脏的病理组织学改变与原虫血症的变化有关。肺脏呈间质性肺炎 ,各脏器呈慢性增生性炎症的病理变化特点。结论 :N株致病力较强 ,感染后引起宿主死亡的主要原因是感染疟原虫的红细胞对脑微血管内皮细胞的粘附 ,造成微血管阻塞 ;RC株致病力较弱 ,宿主的应答反应在感染早期可能是 CD4+ Th1相关的迟发型超敏炎症反应 ,而感染后期是 CD4+ Th2辅助作用下的抗体依赖性的免疫应答 ,并在疟原虫的最后清除上起着关键性的作用
Objective: To study the relationship between drug resistance and pathogenicity of Plasmodium berghei. Methods: The histopathological changes of liver, spleen, brain, heart, lung, kidney and other important organs in ICR mice infected with chloroquine sensitive (N) and resistant (RC) strains of Plasmodium berghei were compared. Results: After infected with N strains, the liver and spleen of mice had more malaria and pulmonary edema; congestion and obstruction of cerebral microvessels; pathological changes of acute inflammation in various organs. RC strain infection, the mouse liver and spleen histopathological changes and parasitemia changes. Pulmonary interstitial pneumonia, the various organs showed chronic proliferative inflammation pathological changes. CONCLUSIONS: The virulence of N strain is strong, and the main cause of host death after infection is the adhesion of erythrocytes infected with Plasmodium to cerebral microvascular endothelial cells, resulting in microvascular obstruction. The pathogenicity of RC strain is weak and the host response Early infection may be a delayed type hypersensitivity response associated with CD4 + Th1, and late phase infection is an antibody-dependent immune response that is aided by CD4 + Th2 and plays a key role in the eventual clearance of Plasmodium