Cellular immunity to Echinococcus granulosus cysts

A fundamental feature of Echinococcus granulosus infection is its chronicity. There are many reasons for this; including weak natural immunity and the ability of the larval stages to evade or resist elimination by the hosts' specific immune responses. To identify the types of hosts' cellular immune response; a series of ultrastructral studies of hydatid cysts surgically removed from Turkana patients was conducted based on transmission electron microscopy. Ultrastructurally; the ectocyst (adventitial layer) is organised into three layers; an inner layer containing mainly the infiltrating mononuclear leukocytes; a middle; loose connective tissue layer with inflammatory cells mainly plasma cells; fibroblasts; scant neutrophils; eosinophils and lymphocytes; and an outer loose connective tissue layer that blends with the surrounding host tissue. The mast cells and basophils were not observed. This study has showm that the adventitial layer of hydatid cysts infiltrated by leukocytes; principally by macrophages and plasma cells

Echinococcus granulosus: ultrastructural effect of albendazole therapy.

The effects of the anthelmintic Albendazole against Echinococcus granulosus hydatid cysts in Turkana patients given orally were studied by means of ultrasound as well as light microscopy, scanning and transmission electron microscopy. The treatment generally reduced the size of the cyst mass, making the patients feel well. The drug therapy caused collapse of the cyst wall and daughter cyst. The pathological changes on the germinal layer of Albendazole-treatment cysts differed widely from the untreated control hydatid tissue. The effects included morphological changes of the protoscolices, presence of lamellated bodies, necrosis with detachment of the germinal layer from the laminated layer. However, some parts of the Albendazole-treated hydatid tissue remained unaffected.