Living Schistosoma mansoni of various developmental stages were studied with respect to their ability to activate the complement system in sera of humans, mice and rats. Immunofluorescence assays demonstrated that binding of human C3 occurred on fresh schistosomula as well as on schistosomula prepared from mouse lymph-nodes or lungs and on adult schistosomes. However, rodent C3 was deposited only on fresh schistosomula. Deposition of human C3 on the worms' surface required activation of the complement system. The alternative pathway was shown to be involved in deposition of human C3 on schistosomes of all ages, whereas activation of the classical pathway was demonstrable only with fresh schistosomula. Immunoelectrophoretic studies demonstrated a dose-dependent cleavage of human C3 and conversion of factor B by living adult schistosomes. The results demonstrate that the ability of living schistosomes to activate complement in vitro is dependent not only on their developmental stage but also on the species of the serum.

The influence of the late components of complement (C) on percutaneous primary infections with Schistosoma mansoni was studied in inbred mice genetically deficient or intact in C5. Worm recoveries were diminished in C5-deficient male mice as compared to C5-intact animals. Twenty-four-day-old parasites were also shorter following growth in C5-deficient animals. At 7 weeks after infection, female schistosomes, but not male parasites, were shorter and fewer eggs/schistosome pair were deposited in the livers of C5-deficient as compared to C5-intact male mice. In addition to the presence of C5, the mouse sex was found to influence the outcome of an infection. Schistosomes showed a reduced infection rate and were relatively stunted after 24 days of growth in female mice of the two strains as compared to male mice of the corresponding strains. The results suggest that C5 plays no role in defence against a primary infection in mice.