Shibayama-Salas M, Tsutsumi V, Campos-Rodríguez R, Martínez-Palomo A
Departamento de Patología Experimental, Centro de Investigación y de Estudios Avanzados del IPN, México DF, México.
Arch Med Res. 1992;23(2):203-7.
Gerbils are susceptible to amebic liver abscess (ALA) production under experimental conditions. However, little is known about the histopathological changes that occur during the evolution of the lesion. We analyzed microscopically the sequence of cellular events of ALA in gerbils inoculated intraportally or intrahepatically with E. histolytica. At early stages trophozoites were associated with different degrees of inflammatory reaction. Amebas were also observed in areas devoid of inflammatory cells. Damaged hepatocytes were either related or not to inflammatory reaction. At late stages, lysis of macrophages and epithelioid cells were seen in relation to necrotic tissue and trophozoites. We conclude that amebic liver necrosis in gerbils at early stages may result from lysis of inflammatory cells as shown previously by us in hamsters, but also by direct contact and lytic activity of amebas to hepatocytes. The late destruction and expansion of hepatic tissue necrosis is apparently associated with damage of macrophages and epithelioid cells.
在实验条件下,沙鼠易患阿米巴肝脓肿(ALA)。然而,对于病变发展过程中发生的组织病理学变化知之甚少。我们通过显微镜分析了经门静脉或肝内接种溶组织内阿米巴的沙鼠ALA的细胞事件序列。在早期,滋养体与不同程度的炎症反应相关。在没有炎症细胞的区域也观察到阿米巴。受损的肝细胞与炎症反应有关或无关。在晚期,可见巨噬细胞和上皮样细胞溶解与坏死组织和滋养体有关。我们得出结论,沙鼠早期的阿米巴肝坏死可能如我们之前在仓鼠中所表明的那样,是由炎症细胞溶解导致的,但也可能是由于阿米巴与肝细胞的直接接触和溶解活性。肝组织坏死的晚期破坏和扩大显然与巨噬细胞和上皮样细胞的损伤有关。