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Young schistosomes collected after penetration through isolated mouse skin (3 h schistosomula) were cultured in medium containing immune rhesus monkey serum with a high titre of antibody known to kill schistosomula in the presence of complement. Morphological signs of damage in electron micrographs were confined to the surface tegument of the schistosomula. Antibodies in immune rhesus serum were shown to bind to the surface membrane of 3 h schistosomula using an antibody-enzyme bridge technique involving labelling with horseradish peroxidase and histochemical localization of the enzyme at the ultrastructural level. Schistosomula recovered from the lungs of mice 4 days after infection did not bind monkey antibodies at the surface and these 4-day schistosomula are not susceptible to damage by immune serum in vitro. Mouse erythrocyte antigens were detected on the surface of 4-day schistosomula using an appropriate antibody-enzyme bridge but these host antigens could not be found on 3 h schistosomula. This correlation between the presence of mouse host antigens on the surface of schistosomula and the inability of immune monkey antibodies to bind to the surface membrane is consistent with the hypothesis that host antigens are acquired by young schistosomes and serve to protect the surface membrane against antibody-mediated damage.

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Acquired immunity toSchistosoma mansoniin the rat can be assayed by the recovery of a proportion of the schistosomula of a challenge infection from the lungs 5 days after the challenge has been given. The recoveries from immune rats, which are significantly less than those from control animals, demonstrate that a proportion of a challenge infection is killed in the lungs or at an earlier point in the pathway of migration.Immunity in the Sprague–Dawley rat can first be shown by the lung recovery technique 3 weeks after an immunizing exposure of 500 cercariae. Immunity reaches a peak between weeks 6 and 7 but then declines to zero by week 12. The PVG inbred Hooded rat shows a similar but delayed development and decline of immunity. When the lung recovery technique shows immunity to be declining, hepatic perfusion demonstrates that immunity to reinfection is partially retained, indicating that at this stage the challenge is killed after the first 5 days.Re-exposure of rats in which immunity has declined induces an anamnestic lung recovery response. There appears to be a relationship between spontaneous cure and the decline of immunity. A factor in the serum of infected rats which kills young schistosomula in culture develops in parallel with immunity, but high titres of this factor are maintained during the decline of immunity.

Metacercariae of Fasciola hepatica were excysted in a simple system based on the stimuli determined by Dixon (1966). Reproducibly high levels of excystment (70-80%) were obtained within 3h. Equal volumes of human serum and medium RPMI 1640 with 2% washed human red blood cells supported better growth in vitro than human serum diluted with ELac or NCTC 135. Reduced rates of growth were observed with serum concentrations lower than 50%. During culture over a period of 14 weeks some organisms in every culture grew to a length of 3 mm at a linear rate approximately one quarter of the growth rate in vivo (mouse). A few parasites suddenly began to develop more rapidly after six weeks in culture and reached 6-7 mm in length, comparable to the size of sexually mature Fasciola grown in mice. These cultured worms showed extensive development of the uterus, vitellaria, and testes with spermatozoa. The ovary remained rudimentary and egg formation did not occur.

Surface components of Schistosoma mansoni have been identified by lactoperoxidasecatalyzed iodination. Cercariae have a simple labeling pattern in comparison to schistosomula. Transformation of cercariae to schistosomula results in the loss of a low molecular weight material which may be the glycocalyx, and the appearance of many more labeled proteins. Mechanical conversion of cercariae to schistosomula requires subsequent incubation at 37 degrees C for more than 1 h to give the full surface-labeling pattern of schistosomula. The majority of proteins found on schistosomula appear to be present throughout the remaining part of the developmental cycle, although adult male worms had only low levels of these antigens, and female worms had virtually no detectable surface antigens. The low level of expression of schistosome antigen could be caused by adsorbed host antigen, although no evidence for adsorbed host protein was found, or by a reduced level of antigens present on the worm surface. The low level of schistosome antigen could have a role in the resistance of adult worms to the host's immune response.