Silica treatment increases the susceptibility of the Cabo Frio strain of Biomphalaria tenagophila to Schistosoma mansoni infection but does not alter the natural resistance of the Taim strain.

The present work demonstrates that silica treatment represents a suitable in vivo method to evaluate the role of host phagocytic hemocytes in the mechanisms of resistance to parasitic infection. Silica inoculation into Biomphalaria tenagophila snail induced a significant reduction in the circulating hemolymph granulocytes in both strains tested (Taim and Cabo Frio). The granulocyte reduction was accompanied by a significant increase in the number of circulating dead cells. In B. tenagophila Cabo Frio, silica treatment enhanced snail susceptibility to Schistosoma mansoni, shortening the intramolluskan phase of the parasite and increasing the number of sporocysts and cercariae produced. In B. tenagophila Taim, the same treatment did not abrogate natural resistance to S. mansoni reported for this snail strain. These in vivo results demonstrate that macrophage-like granulocytes are involved in the mechanism of S. mansoni sporocyst destruction in Cabo Frio snails and suggest that another, different mechanism may be responsible to the natural resistance of B. tenagophila Taim.