Schistosoma mansoni: changes in the outer membrane of the tegument during development from cercaría to adult worm.

Schistosoma mansoni: Defined system for stepwise transformation of cercaria to schistosomule in vitro

The effects of immune rhesus monkey serum on schistosomula of Schistosoma mansoni during cultivation in vitro.

Surface ultrastructure and cytochemistry of parasitic helminths.

Publisher Summary This chapter discusses the immunology of schistosomiasis. The only developments relating to innate immunity refer to the death of cercariae in the skin. Concomitant immunity has been shown to operate in a number of experimental systems, and there are encouraging reports that it may operate in human infections. A good deal of circumstantial evidence implicates host antigens as playing a role in concomitant immunity, but more direct evidence is needed to show that they indeed serve to protect the mature parasite from immune attack. The use of small animals, particularly those where syngeneic strains are available and in vitro cultivation, has increased the understanding of the immune mechanisms. In particular, a number of in vitro systems have been described in which antibodies and cells combine to damage and kill young schistosomules. It is essential to determine whether the differences described for these several systems truly reflect a multiplicity of host responses or merely represent differences in technical approach to a single system. Much work has concerned the immunopathology of the disease, particularly granuloma formation. Although the granuloma contributes significantly to the pathology, it does seem to protect the host liver from the toxic secretion of the egg. A number of approaches for the immunological control of schistosomiasis are currently under investigation, including the use of live cercariae and schistosomules and the use of more or less purified antigens.

The immunology of schistosomiasis.

A large percentage of the cercariae of Schistosoma mansoni die while penetrating the abdominal skin of rats or mice but relatively few cercariae die in the skin of hamsters.Comparison of hamsters and mice infected from the same pool of cercariae showed that the higher percentage of cercariae recovered as adult worms from hamsters than from mice was due to the lower percentage of cercariae which died during penetration of hamster skin.In similar comparisons of rats with mice the lower percentage of adult worms recovered from rats was not entirely accounted for by the higher percentage of cercariae which died in rat skin. Losses of schistosomula at later stages of development are apparently higher in rats than in mice.Cercariae die within 10 min after beginning to penetrate the skin of mice. At this stage the cercariae, which are now termed schistosomula, are attempting to penetrate the Malpighian layer of the epidermis. Five minutes later many schistosomula have entered the dermis.The cause of death of cercariae has not been determined. It is not related to the development of sensitivity to water which accompanies the transition from cercaria to schistosomulum. Sensitivity to water appears much sooner after penetration in some cercariae than in others; even after 30 min in the skin some cercariae can tolerate a return to water.In rats, hyper-immunized by a series of infections with cercariae through the abdominal skin, the percentage of challenging cercariae which die in the abdominal skin shows a slight increase over controls. No further mortality of schistosomula occurs during the next 24 h.Age resistance to infection with S. mansoni could not be demonstrated in comparisons of young mice (1 month) with old mice (1 year) of the Parkes and CBA strain.We should like to thank Dr F. Hawking for performing the skin biopsies on the dogs and Mrs P. Clark and Miss J. Marsh for their excellent technical assistance.

S. R. Smithers

Papers

Death of schistosome cercariae during penetration of the skin. II. Penetration of mammalian skin by Schistosoma mansoni.