Silveira F T, Moraes M A, Lainson R, Shaw J J
Seção de Parasitologia, Instituto Evandro Chagas (Fundação SESP), Belém, Pará, Brasil.
Rev Inst Med Trop Sao Paulo. 1990 Nov-Dec;32(6):387-94. doi: 10.1590/s0036-46651990000600001.
We have studied the histopathological aspects related to the evolution of cutaneous lesions experimentally produced in the monkey Cebus apella (Primates: Cebidae) by Leishmania (V.) lainsoni, L. (V.) braziliensis and L. (L.) amazonensis. Microscopical examination of a series of biopsies obtained from these animals showed the kinetics of the cutaneous lesions regarding three species of Leishmania inoculated, as follows: 1) an initial non-specific chronic inflammatory infiltrate; 2) macrophagic nodules; 3) necrosis of parasitized phagocytic cells; 4) epitheliode granuloma; 5) absorption of the necrotic area (sometimes forming "foreign-body granuloma"); 6) a non-specific residual inflammatory infiltration; and 7) cicatrization. These pathological processes are, of course, responsible for both development and resolution of the leishmaniotic lesion. We also discuss some immunopathological mechanisms probably related with the sequential events, and that could be also responsible for the different clinical aspects found in man.
我们研究了与利什曼原虫（V.）lainsoni、利什曼原虫（V.）巴西利什曼原虫和利什曼原虫（L.）亚马逊利什曼原虫在僧帽猴（灵长目：卷尾猴科）身上实验性引发的皮肤病变演变相关的组织病理学方面。对从这些动物身上获取的一系列活检样本进行显微镜检查，显示了接种三种利什曼原虫后皮肤病变的动态变化，具体如下：1）初始非特异性慢性炎症浸润；2）巨噬细胞结节；3）被寄生吞噬细胞的坏死；4）上皮样肉芽肿；5）坏死区域的吸收（有时形成“异物肉芽肿”）；6）非特异性残余炎症浸润；7）瘢痕形成。当然，这些病理过程既导致了利什曼病病变的发展，也导致了其消退。我们还讨论了一些可能与这些相继发生的事件相关的免疫病理机制，这些机制也可能是人类所发现的不同临床症状的原因。
