Zenner L, Foulet A, Caudrelier Y, Darcy F, Gosselin B, Capron A, Cesbron-Delauw M F
Mécanismes Moléculaires de la Pathogénèse des Sporozoaires, Institut Pasteur de Lille, France.
Pathol Res Pract. 1999;195(7):475-85. doi: 10.1016/S0344-0338(99)80051-X.
Since mice and rats are the most studied models of experimental toxoplasmosis, the aim of this work was to analyze the outcome of Toxoplasma infection in mice, rats and congenitally athymic nude rats; for this purpose, the parasitic load in different organs and the anatomic-pathological characteristics of infection were investigated in these animals. The data obtained after infection with two different strains and stages of Toxoplasma gondii (RH tachyzoites and Prugniaud cysts) concerned the following organs: brain, mesenteric lymph nodes, blood, spleen, heart, lungs, diaphragm and liver. In Fischer rats, the infection with either the Prugniaud or the RH strains displayed similar characteristics: after a peak in the parasite load, a complete disappearance of parasites was observed, except in the brain of Prugniaud strain-infected rats where toxoplasmas were evidenced throughout the experiment. In OF1 mice, where infection by the RH tachyzoites was lethal, infection with the Prugniaud strain led to survival; the parasitic burden peaked in the different organs and was then undetectable, except in the brain where toxoplasmas were still present during the chronic phase. Like mice, nude rats did not survive to the RH infection. Interestingly, for all the animals the observed histopathological changes in the infected organs, although more or less obvious in the acute phase, were not very severe in almost all cases. For instance, mice, although more susceptible to infection than rats, did not present more severe lesions. They consisted in a discrete inflammation with some focal areas of necrosis in some organs such as brain, liver and heart. Our results support the assumption that rats and nude rats constitute interesting experimental models relevant to either human acute toxoplasmosis, chronic toxoplasmosis, or disseminated toxoplasmosis in AIDS patients.
由于小鼠和大鼠是实验性弓形虫病研究最多的模型,本研究的目的是分析小鼠、大鼠和先天性无胸腺裸鼠感染弓形虫的结果;为此,对这些动物不同器官中的寄生虫负荷以及感染的解剖病理学特征进行了研究。用两种不同的弓形虫菌株和阶段(RH速殖子和Prugniaud包囊)感染后获得的数据涉及以下器官:脑、肠系膜淋巴结、血液、脾脏、心脏、肺、膈肌和肝脏。在Fischer大鼠中,感染Prugniaud或RH菌株表现出相似的特征:在寄生虫负荷达到峰值后,除了在感染Prugniaud菌株的大鼠脑中整个实验过程都能检测到弓形虫外,其他部位的寄生虫完全消失。在OF1小鼠中,感染RH速殖子是致命的,而感染Prugniaud菌株则能存活;不同器官中的寄生虫负荷达到峰值后便无法检测到,除了在慢性期脑中仍有弓形虫存在。与小鼠一样,裸鼠对RH感染也无法存活。有趣的是,对于所有动物来说,感染器官中观察到的组织病理学变化,虽然在急性期或多或少比较明显,但几乎在所有情况下都不太严重。例如,小鼠虽然比大鼠更容易感染,但并没有出现更严重的病变。病变表现为一些器官(如脑、肝和心脏)中出现离散性炎症和一些局灶性坏死区域。我们的结果支持这样的假设,即大鼠和裸鼠构成了与人类急性弓形虫病、慢性弓形虫病或艾滋病患者播散性弓形虫病相关的有趣实验模型。