Anand B S, Vinayak V K, Bushnurmath S R, Bhagwat A G, Jain S K
Trans R Soc Trop Med Hyg. 1985;79(5):626-30. doi: 10.1016/0035-9203(85)90172-5.
The histological abnormalities of amoebic colitis have been well described but their evolution over a period of time has not been clearly examined. To study this, three- to four-week-old guinea-pigs were inoculated intracaecally with 80,000 to 100,000 Entamoeba histolytica trophozoites, left untreated and killed at 3, 5, 8, 11, 14 and 21 days, when the caecum was removed and the tissue sectioned and stained with H & E and PAS. Although there was considerable variation in the type of histological abnormality seen on different days of the experiment, there was a definite pattern of evolution. Initially there was diffuse infiltration of the lamina propria by lymphomononuclear cells in the presence of an intact surface epithelial lining. This was followed firstly by superficial and then by deep ulceration of the mucosa. Mucosal invasion by the trophozoites was seen only at this stage and was accompanied by tissue necrosis; the most severe abnormalities occurred on day 11. The final development was regenerative activity which was first noted on day 11, and became more prominent subsequently. The presence of cellular infiltrate in the lamina propria in the absence of trophozoites and damage to the surface epithelium, suggests that these abnormalities are not the direct effect of amoebae. It is suggested that the initial damage is caused by an enterotoxin; the trophozoites enter the mucosa only when there is a break in the surface epithelium. Once within the tissues, trophozoites aggravate the damage by their ability to phagocytose and to release cytotoxic enzymes.
阿米巴结肠炎的组织学异常已有详尽描述,但对其随时间的演变情况尚未进行明确研究。为对此展开研究,将3至4周龄的豚鼠盲肠内接种80,000至100,000个溶组织内阿米巴滋养体,不予治疗,并分别在第3、5、8、11、14和21天处死,届时取出盲肠,将组织切片并用苏木精和伊红以及过碘酸雪夫染色法染色。尽管在实验的不同天数观察到的组织学异常类型存在相当大的差异,但仍有明确的演变模式。最初,在表面上皮衬里完整的情况下,固有层出现淋巴细胞单核细胞的弥漫性浸润。随后先是黏膜浅层溃疡,接着是深层溃疡。仅在这个阶段可见滋养体对黏膜的侵袭,并伴有组织坏死;最严重的异常出现在第11天。最后的发展是再生活动,在第11天首次出现,随后变得更加明显。在没有滋养体且表面上皮未受损的情况下固有层中存在细胞浸润,这表明这些异常并非阿米巴的直接作用。据推测,最初的损伤是由一种肠毒素引起的;只有当表面上皮出现破损时,滋养体才会进入黏膜。一旦进入组织,滋养体通过其吞噬和释放细胞毒性酶的能力加剧损伤。