De Brito T, Böhm G M, Yasuda P H
J Pathol. 1979 Aug;128(4):177-82. doi: 10.1002/path.1711280403.
The pathogenesis of the haemorrhagic diathesis in experimental leptospirosis of the guinea-pig was investigated in the lung, diaphragm and kidney. The vascular damage was found to be focal and mainly capillary. Swollen endothelium with dilated endoplasmic reticulum, enlarged mitochondriae and open junctions seemed to be the initial lesions and endothelial necrosis the final picture in all tissues. The lung capillaries showed endothelial and epithelial blebs and desquamation with many myelin figures. Capillary thrombosis was observed in the pulmonary microcirculation, probably acting as an aggravating factor and being partly responsible for the particularly impressive lung haemorrhages. The peritubular renal capillaries as well as open junctions and gaps due to necrosis also had enlarged fenestrae which were permeable to colloidal carbon particles. The paucity of micro-organisms in the vicinity of the lesions is in accordance with the toxic genesis postulated for the vascular damage in leptospirosis. It is suggested that the vascular lesions induced by leptospirosis begin with increased permeability prior to endothelial necrosis.
在豚鼠实验性钩端螺旋体病中,对肺、膈肌和肾脏出血素质的发病机制进行了研究。发现血管损伤是局灶性的,主要累及毛细血管。内皮细胞肿胀,内质网扩张,线粒体增大,连接开放,这些似乎是初始病变,而内皮细胞坏死则是所有组织中的最终表现。肺毛细血管出现内皮和上皮小泡以及脱屑,并伴有许多髓鞘样结构。在肺微循环中观察到毛细血管血栓形成,这可能是一个加重因素,部分导致了特别明显的肺出血。肾周毛细血管以及由于坏死导致的开放连接和间隙也有扩大的窗孔,这些窗孔对胶体碳颗粒具有通透性。病变附近微生物数量稀少,这与钩端螺旋体病血管损伤的毒素成因假说相符。有人提出,钩端螺旋体病引起的血管病变在内皮细胞坏死之前始于通透性增加。