Clinico-pathological study on the mechanism of anemia in piroplasmosis of domestic animals

为了建立家畜梨形虫病的有效治疗和预防方法，我们对吉氏巴贝斯虫引起家犬贫血的机制进行了研究。研究结果如下：1.吉氏巴贝斯虫在犬红细胞固定层中成功培养。2.在培养过程中，高铁血红蛋白和脂质过氧化终产物丙二醛的浓度显著升高。3.感染红细胞的葡萄糖消耗量、乳酸生成量和2，3-DPG浓度也有所增加。4.红细胞变形性降低。5.感染犬外周血巨噬细胞吞噬红细胞活性随寄生虫血症进行性增加而显著增强。6.给受感染的狗注射强的松龙后，这些狗的贫血得到了短暂的恢复。7.强的松龙对感染犬巨噬细胞的吞噬功能无抑制作用。这些结果表明，感染吉氏杆菌后的红细胞由于寄生虫的繁殖而遭受氧化损伤，感染犬的巨噬细胞对受损红细胞的吞噬活性可能被加速，从而导致犬贫血。

In order to establishethe effective therapy and prevention for piroplasmosis in domestic animals, we investigated the mechanism of anemia induced by Babesia gibsoni in dogs. The results were as follows. 1.Babesia gibsoni was successfully cultured in a settled layer of canine erythrocytes. 2. During the cultivation, the concentrations of methemoglobin and malondialdehyde, an end product of lipid peroxidation, in erythrocytes were significantly increased. 3. Glucose consumption and lactate production by infected erythrocytes, and 2,3-DPG concentration were also increased. 4. Erythrocyte deformability was decreased. 5. The erythrophagocytic activity of macrophages obtained from the peripheral blood of the infected dogs showed a marked increase in association with progressive parasitemia. 6. Administration of prednisolone to the infected dogs resuted in a transient recovery from anemia in these dogs. 7. The erythrophagocytic activity of macrophages was not suppressed by the administration of prednisolone in the infected dogs. These results indicate that erythrocytes infected with B.gibsoni were suffered from an oxidative damage by the multiplication of the parasites, and that the erythrophagocytic activity of macrophages against the damaged erythrocytes might be accelerated in infected dogs, resulting in anemia in these dogs.