Both short-term (3 hr) exposure of Biomphalaria glabrata snails (M-line and 13-16-R1) to Schistosoma mansoni (PR1) miracidia and in vitro incubation of parasite sporocysts with host hemolymph components altered host phagocytic ability. Hemocytes obtained from susceptible (M-line) snails that had been exposed to parasite miracidia for 3 hr showed reduced levels of phagocytosis of yeast cells in vitro compared to hemocytes from unexposed individuals. Incubation of whole hemolymph with sporocysts in vitro also reduced yeast phagocytosis in this susceptible strain. In contrast, resistant (13-16-R1) hemocytes showed increased levels of yeast phagocytosis after in vitro incubation with the parasite, and the opsonic properties of 13-16-R1 plasma were greater after exposure of snails to miracidia. These strain-specific effects of S. mansoni on host hemocyte phagocytosis and plasma opsonization were seen only when both plasma and hemocytes were present at the time of exposure to the parasite.

Three species of bulinid snails were monitored to determine the effect of infection with 2 sympatric strains of Schistosoma haematobium on longevity, growth, and reproductive output, from the onset of cercarial production until death. Bulinus senegalensis was least affected by infection, with total fecundity reduced by less than 34%. Infected Bulinus truncatus showed an acceleration in growth accompanied by a 63% reduction in fecundity, although the majority of snails continued to oviposit at a low level. The longest-lived snails in this study, Bulinus globosus, showed decreased growth and survival when infected. In addition a significant proportion of infected individuals of this species failed to oviposit, and those that retained some reproductive capacity produced fewer embryos than controls. Total fecundity of B. globosus was reduced almost 90% by infection with S. haematobium, yet long-term monitoring of individuals showed that reproductive activity recovered when parasite productivity was low. Results from this and similar studies indicate that the time of infection by a trematode in relation to reproductive maturity of the molluscan host is important in determining the subsequent effects on host growth and fecundity.

Phagocytosis of yeast by haemocytes of Biomphalaria glabrata, intermediate host of Schistosoma mansoni, is influenced strongly by host plasma components, although it can occur without involvement of such factors. Plasma from two strains of B. glabrata which are resistant to S. mansoni differs in its opsonic properties from the plasma of a susceptible strain. This may reflect the principles which determine compatibility or incompatibility in this host-parasite system. Opsonization is a time-dependent process: short periods of incubation in plasma from all strains reduces subsequent phagocytosis in the absence of plasma factors, whereas longer incubation in resistant strain plasma is markedly opsonic. Haemocytes from all strains examined are equally competent in their recognition of either native or opsonized yeast.

The hemolymph of Biomphalaria glabrata, a molluscan host of Schistosoma mansoni, contains an alpha-macroglobulin proteinase inhibitor (alphaM). In this study we have demonstrated that this host molecule inhibits a cysteine proteinase produced by larval S. mansoni. Inhibition by alphaM involves conformational changes through proteolytic cleavage by the proteinase, thus the enzyme must be active for interactions to occur. A specific cysteine proteinase inhibitor (E64) was used to block the interaction between parasite cysteine proteinase and host alphaM during an in vitro parasite killing assay. Increased sporocyst mortality was not observed in hemolymph from susceptible strains of B. glabrata when E64 was included, nor was there decreased killing in similarly treated hemolymph from a resistant strain. This suggests that the inhibition of this parasite proteinase by host alphaM is not involved in processes determining either resistance or susceptibility to this trematode.

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