The ultrastructure of the amebocyte-producing organ in Biomphalaria glabrata.

The amebocyte-producing organ (APO) in normal and echinostome-sensitized Biomphalaria glabrata was studied at the ultrastructural level. The APO in unexposed snails consists of small clusters of primary ameboblasts resting on the epithelial cells lining the pericardium. The ameboblasts are held in a loose reticulum formed by extensions from smooth muscle and few fibroblastic cells. Secondary ameboblasts and amebocytes constitute further stages of this cell line. Amebocytes, resembling cells in the snail's circulation, appear in the blood sinus coursing through the interior of the APO. Exposure of snails to echinostome miracidia results in significant morphological changes in the organ. Large clusters of primary and and secondary ameboblasts appear, many of these cells undergoing mitosis. Fully activated APOs consist of masses of cells loosely arranged in zones of progressive maturation. Blood cells in activated APOs were significantly larger than those seen in normal APOs.

Identification and distribution of Echinostoma lindoense, E. audyi and E. revolutum (Trematoda; Echinostomatidae).

The closely related Echinostoma lindoense, E. audyi and E. revolutum can be differentiated by morphological characteristics of their adults and cercariae. We have found E. lindoense and E. audyi in Southeast and Southwest Asia and Central Europe and the former species also in South America. However, using the morphological characteristics described by Beaver (1937) for E. revolutum which is assumed to be cosmopolitan, we did not find this species in these regions.

Further characterization of acquired resistance in Biomphalaria glabrata.

The albino strain of Biomphalaria glabrata is capable of developing an acquired resistance to echinostomes that is relatively specific, i.e., strong against Echinostoma lindoense, challenged by the homologous species, moderate or weak against closely related E. paraensei and E. liei, and nonexistent against Paryphostomum segregatum and Schistosoma mansoni. The present results show that acquired resistance induced by E. paraensei is much stronger against the heterologous E. lindoense than against the homologous species. These observations indicate that although the response of snails with acquired resistance to a challenge exposure is relatively specific, the stimuli for inducing that resistance may be nonspecific.

Selective interference with granulocyte function induced by Echinostoma paraensei (Trematoda) larvae in Biomphalaria glabrata (Mollusca).

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.

Tissue reactions induced by Schistosoma mansoni in Biomphalaria glabrata.

In Biomphalaria glabrata with a strong natural resistance, Schistosoma mansoni sporocysts are rapidly encapsulated by granulocytes and killed, mainly by the strong phagocytic activity of the cells. Irradiated Echinostoma paraensei sporocysts seem able to suppress the function of the granulocytes. Tissue reactions in snails with self-cure demonstrate: involvement of two types of cells, granulocytes and hyalinocyte-like cells; formation of amoeba-fibrous capsules; limited tendency of granulocytes to become attracted to the parasites; a slow process of parasite destruction; and a possible involvement of humoral factors. It seems that there is partial suppression of the granulocyte function in smails with self-cure.

Failure of irradiated Echinostoma audyi and Hypoderaeum dingeri to sensitize Lymnaea rubiginosa snails.

Attempts to induce acquired resistance in Lymnaea rubiginosa snails against the echinostomes Echinostoma audyi and Hypoderaeum dingeri by means of irradiated miracidia were unsuccessful, although Lie and coworkers using similar methods had recently sensitized Biomphalaria glabrata against Echinostoma lindoense (1975a). In contrast to the B. glabrata-E. lindoense system, in Lymnaea rubiginosa the amebocytic response to irradiated parasites was slow: irradiated E. audyi sporocysts were encapsulated 15 to 28 days and H. dingeri sporocysts 20 to 27 days postexposure. No obvious enlargement of the amebocyte-producing organ was seen. No resistance was demonstrable to subsequent homologous challenge. Development of acquired resistance to a trematode infection in snails may be related to the speed with which the snails destroy the irradiated sporocysts.

Studies on resistance in snails. 7. Evidence of interference with the defense reaction in Biomphalaria glabrata by trematode larvae.

Echinostoma lindoense sporocysts that develop from irradiated miracidia normally are destroyed by amebocyte capsules in the ventricle of Biomphalaria glabrata within 10 days postexposure. The survival period of these ventricular sporocysts was considerably longer in snails that also harbored normal sporocysts of E. lindoense, Paryphostomum segregatum, or Schistosoma mansoni. Protection of irradiated E. lindoense sporocysts by the same of different trematode species is presumed to be the result of an active process by which normal sporocysts interfere with capsule formation and protect themselves and other trematode larvae from encapsulation. Homologous protection was stronger than heterologous.