Schistosoma mansoni: the ultrastructure of larval morphogenesis in Biomphalaria glabrata and of associated host-parasite interactions.

An electron microscopic study has been carried out to describe the transformation of the miracidium of S. mansoni into the mother sporocysts in the susceptible B. glabrata and the associated host-parasite interactions. The miracidium enters the snail host without morphological alterations. Within 3 hr after entering, all the ciliary epidermal plates of the miracidium are discarded. A new tegument is quickly formed by 5 hr postinfection by the expansion of epidermal ridges. The rapid formation of the new tegument reflects the participation of membrane-bound vesicles in the ridge cytons. The membranes of these vesicles become the new tegument membranes with the discharge of their electron-dense contents into the snail tissues. The vesicular contents discharged into the tissues apparently prevent snail amoebocytes (phagocytes) from attachment to the parasite tegument and thus prevent their interference with the further development of the postmiracidium. If a postmiracidium fails to mobilize membrane-bound vesicles in the formation of tegument, the parasite becomes surrounded by closely attached concentric layers of fibroblasts formed by amoebocytes and histiocytes within 24 hr. The membrane-bound vesicles are present in small numbers in the ridge cytons of the miracidium and become numerous in the postmiracidium stage and with many migrate to the ridges through connecting bridges within 24 hr. By 3 days postinfection when extensive microvilli have formed on the tegument the vesicles have disappeared and are replaced by mitochondria, ribosomes and complex carbohydrate particles. Many fibroblasts in the snail connective tissues have phagocytic capacities and are regarded as snail tissue histiocytes or fixed amoebocytes that eventually may become hypertrophic and detached.