Various trematode larvae can interfere with the host snail's resistance to the same or unrelated trematode species, chiefly, it appears by interference with the function of the host's granulocytes. In Biomphalaria glabrata infected with the trematodes, Echinostoma paraensei, granulocytes lose their ability to encapsulate the larvae of trematodes to which the hosts were previously resistant. However, the granulocytes in these snails retain their ability to encapsulate injected latex spheres, or larvae of the metastrongyle nematode, Angiostrongylus malaysiensis, and to phagocytose epidermal plates cast off by miracidia of the trematode, Schistosoma mansoni. Cellular infiltration in injured preputial tissue of the snail also was not suppressed by the presence of E. paraensei larvae. Interference with the granulocyte function in B. glabrata induced by E. paraensei infection therefore appears to be a selective phenomenon.
Formation of an amebocyte aggregate in the ventricular cavity of Biomphalaria glabrata can be induced 30 hr or more after a single infection by irradiated or (less frequently) by normal Echinostoma lindoense miracidia. The resulting amebocyte mass frequently encapsulated and destroyed the developing E. lindoense sporocysts within the ventricle. The constituent amebocytes of the capsule correspond in vitro and by staining characteristics to circulating amebocytes of uninfected snails, but with additional inclusion bodies, increased mucopolysaccharide, acid phosphatases, and lipid-positive staining reactions. Mitotic activity, rapid growth, and later regression of the amebocyte-producing organ (located between the posterior mantle epithelium and anterior pericardial endothelium) follow the growth and regression sequence of the ventricular capsule. Though peripheral foci of secondary amebocyte production have been found and were previously known, the amebocyte-producing organ appears to be the primary amebocyte source responsible for the snails' rapid intraventricular sporocyst encapsulation.
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