中文摘要：

为了比较不同种株利什曼原虫对实验动物的致病性，分别将5×10^7的杜氏利什曼原虫SC6株、热带利什曼原虫K27株、婴儿利什曼原虫LEM235株和婴儿利什曼原虫KXG-Liu株前鞭毛体与无鞭毛体感染Balb／c小鼠和金黄地鼠，观察各感染动物皮肤损害状况，3月后，有限稀释培养法分别检测肝和脾脏内的虫荷数。发现不同种株利什曼原虫引起的疾病存在极大的异质性，杜氏利什曼原虫四川SC6株致Balb／c小鼠轻微皮肤损害，肝和脾脏内重度虫荷数，金黄地鼠肝和脾脏内重度虫荷数；热带利什曼原虫K27株致Balb／c小鼠严重的皮肤损害，但肝和脾脏的虫荷数较低，金黄地鼠肝和脾脏中未查见原虫；婴儿利什曼原虫LEM235株致Balb／c小鼠严重的皮肤损害，肝和脾脏内重度虫荷数，金黄地鼠肝和脾脏内重度虫荷数；婴儿利什曼原虫KXG—Liu株可致Balb／c小鼠严重的皮肤损害，肝和脾脏中度虫荷数，金黄地鼠肝和脾脏内少量虫荷数。另外，还发现原虫的生活史状态和进入机体的途径及实验动物的类型对不同种株利什曼原虫感染致病产生影响。

英文摘要：

In order to compare the pathogenicity of different Leishmania spp. in experimental animal models, the Balb/c mice and golden hamsters were inoculated with 5 ×10^7 promastigotes and amastigotes of the L. donovani strain SC6, L. tropica strain K27, L. infantum strain LEM235, and L. infantum strain KXG-Liu, respectively. The infected mice and golden hamsters were regularly observed for changes in weight, mortality and skin lesion. 3 months after infection, the visceral parasitic loads of infected mice and golden hamsters were determined by quantitative limiting dilution culture of homogenized liver and spleen. It was found that the disease progression induced by different Leishmania spp. was largely heterogeneous. In the groups infected with L. donovani strain SC6, the slight skin lesions and heavy visceral parasitic loads developed in the Balb/c mice, and the heavy visceral parasitic loads developed in the golden hamsters. In the groups infected with L. tropica strain K27, the uncontrolled skin lesions and light visceral parasitic loads developed in the Balb/c mice, and no parasites in the liver and spleen of the golden hamsters. In groups infected with L. infantum strain LEM235, the progressively skin lesions and heavy visceral parasitic loads developed in the Balb/c mice, and the heavy visceral parasitic loads developed in the golden hamsters. And in groups infected with L. infantum strain KXG-Liu, the progressively skin lesions and moderate visceral parasitic loads developed in the Balb/c mice, and the light visceral parasitic loads developed in the golden hamsters. The disease progression is related to the life cycle stages of the infected protozoan, the inoculated pathway and the host type.