Wu Sheng-Wei, Bao Huai-En, Li Xiao-Yan, Ge Shuang
Zhongguo Ji Sheng Chong Xue Yu Ji Sheng Chong Bing Za Zhi. 2011 Oct;29(5):327-32.
To observe the symptoms and dynamic changes of histopathology in the organs from ICR mice infected by Toxoplasma gondii Prugniaud strain.
Thirty ICR mice were infected intraperitoneally with cysts, 10 cysts per mouse. 16 mice were injected with PBS. Incidence of the mice was observed. Three mice from the infected group and two mice from the control group were sacrificed, and the liver, spleen, lung, brain, kidney and heart were collected for pathology and immunohistochemistry examinations on the day 5, 10, 15, 20, 25, 30, 60 and 90 post-infection.
The infected mice began to fall ill at 6 d post-infection, symptoms including decreased appetite, pilomotor fur, sloth, shakes and diarrhea, with a mortality rate of 20%. From 5 d to 20 d post-infection, microscopic examination for HE stain-slides showed the destroyed liver structure, cellular edema, ballooning change, focal necrosis, sinus hepatic expansion and hyperemia, and inflammatory infiltration. Splenic corpuscles demolished and disappeared, red pulp widened and white pulp atrophied, splenic sinusoid extended with hyperemia. Lungs showed destruction of the structure and pathological changes of interstitial pneumonia. The pathological changes began to alleviate until recovery after 20 d post-infection. In the brain, neuronal degeneration and necrosis were found at 10 d post-infection. Some neuroglial cell tubercle, blood vessel sleeve cuffing, inflammatory cell infiltration on cavitas subarachnoidealis and cysts were observed from 15 d to 90 d. Granulation tissue was seen at 90 d post-infection. By immunohistochemistry test, internal organs showed toxoplasma antigen at 5 d post-infection, and the positive reaction was remarkable at 10 d post-infection, then began to taper until negative. Toxoplasma antigen was revealed in the brain from 10 d to 90 d post-infection.
Non-specific clinical manifestation and the degeneration, necrosis and inflammatory cell infiltration in poly-organs appear in earlier period of toxoplasma tachyzoite infection in the ICR mice, followed by the co-existing phenomenon of non-specific infection with cysts in the brain.
观察刚地弓形虫Prugniaud株感染ICR小鼠后脏器的症状及组织病理学动态变化。
30只ICR小鼠腹腔注射包囊，每只小鼠注射10个包囊。16只小鼠注射PBS。观察小鼠发病情况。感染组处死3只小鼠，对照组处死2只小鼠，于感染后第5、10、15、20、25、30、60和90天采集肝脏、脾脏、肺脏、脑、肾脏和心脏进行病理学及免疫组织化学检查。
感染小鼠于感染后6天开始发病，症状包括食欲减退、被毛竖立、懒动、震颤和腹泻，死亡率为20%。感染后第5天至20天，HE染色切片显微镜检查显示肝脏结构破坏、细胞水肿、气球样变、局灶性坏死、肝血窦扩张充血及炎症浸润。脾小体破坏消失，红髓增宽，白髓萎缩，脾血窦扩张充血。肺脏显示结构破坏及间质性肺炎病理改变。感染后20天病理改变开始减轻直至恢复。在脑内，感染后10天发现神经元变性坏死。感染后15天至90天观察到一些神经胶质细胞结节、血管袖套样改变、蛛网膜下腔炎症细胞浸润及包囊。感染后90天可见肉芽组织。免疫组织化学检测显示，感染后第5天各脏器出现弓形虫抗原，感染后第10天阳性反应明显，随后开始减弱直至阴性。感染后第10天至90天脑内均有弓形虫抗原显示。
ICR小鼠急性感染刚地弓形虫速殖子早期出现非特异性临床表现及多脏器变性、坏死和炎症细胞浸润，随后脑内出现包囊与非特异性感染并存现象。
