Rickman W J, Cox H W
J Parasitol. 1980 Feb;66(1):28-33.
Rats infected with Trypanosoma brucei rhodesiense developed anemia, thrombocytopenia, and hypocomplementemia. Anemia, thrombocytopenia, and sharp reductions in parasitemia were associated with elevated titers of cold-active hemagglutinin, antibody to fibrinogen/fibrin-related products, and immunoconglutinin. Depletion of lytic complement, prolonged partial thromboplastin times, and presence of fibrin monomers in the blood occurred at the time anemia and significant elevations in precipitable immune complexes were observed. Terminally, consumption of immunologic factors coincided with accelerated partial thromboplastin times. At death, convulsions and hemoptysis with labored breathing suggested that the animals died of respiratory failure and that disseminated intravascular coagulation may have occurred. It is suggested that microthrombiosis might have resulted from the immunologic interaction of complex-coated blood cells with immunoconglutinin and contributed to the terminal disease signs.
感染罗德西亚布氏锥虫的大鼠出现贫血、血小板减少和补体减少。贫血、血小板减少和寄生虫血症的急剧下降与冷活性血凝素、纤维蛋白原/纤维蛋白相关产物抗体和免疫黏附素滴度升高有关。在观察到贫血和可沉淀免疫复合物显著升高时,血液中溶细胞补体耗竭、部分凝血活酶时间延长以及纤维蛋白单体的存在。末期,免疫因子的消耗与部分凝血活酶时间加速同时出现。死亡时,抽搐和咯血伴呼吸费力提示动物死于呼吸衰竭,可能发生了弥散性血管内凝血。有人认为,微血栓形成可能是由复合包被血细胞与免疫黏附素的免疫相互作用导致的,并促成了末期疾病症状。