At present many laboratories throughout the world are studying the chemotherapy and immunology of Schistosoma mansoni in laboratory hosts. Many workers judge the success or failure of their attempts to cure or immunize these hosts from the ratio of the number of living adult worms recovered to the number of infecting cercariae. This ratio is affected, however, not only by the efficacy of any treatment, but also by the methods used to infect the animals and to recover the worms. If these methods result in widely varying worm recoveries amongst the animals in any experimental group, then small but significant effects of treatment might well be missed. Alternatively, such large experimental groups must be used that the work becomes tedious to perform and depends upon the availability of a great deal of technical assistance. This paper describes techniques which are rapid and do not require great skill in their performance. More important, in our hands they have given very consistent results. In this respect, particularly, we believe that these techniques have advantages over others which are currently practised.The techniques described here are those which were used in other investigations reported in this journal (Smithers & Terry, 1965a, b).The strain of S. mansoni used throughout this work was isolated in Puerto Rico and was obtained through the courtesy of Dr W. B. DeWitt of the National Institutes of Health. The parasite is maintained in an albino strain of Australorbis glabratus (Newton, 1955). Snails are exposed individually to ten miracidia overnight at 27 °C.

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Schistosomes grown in mice were tested at different stages of development for susceptibility to an in vitro cytotoxic effector mechanism involving eosinophils and an antibody directed against mouse determinants. Despite the fact that 5-day lung worms and 6-week adult worms both bound the antibody to their surfaces, eosinophils attached preferentially to the adults and killed them. Complement had an enhancing effect in this system. Those eosinophils which did adhere to the lung worms degranulated onto the tegument but were unable to mediate damage or killing, even when complement was activated at the parasite surface. The resistance shown by the lung worms was shared by 2-week worms and small 3-week worms. Larger 3-week worms and older stages were, however, susceptible to cell-mediated cytotoxicity in this system. We suggest that the host antigen disguise constitutes the major protective mechanism utilized by older schistosomes to evade immunity, but that the younger stages have an additional and equally effective mechanism of resistance.

A French translation of the Memorandum will be published in a future issue of the Bulletin.

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In recent years there has been a steadily growing interest in the immunology of schistosomiasis. Much work has been carried out using a variety of experimental hosts and many attempts have been made to vaccinate these hosts against schistosomes, both by exposing them to irradiated cercariae and by injecting them with various antigens derived from the parasites. These attempts have been attended by varying degrees of success. The ultimate object of much of this work has been its possible application to the disease in man. We believe, however, that work of this kind cannot really be profitably undertaken unless there already exists a sound understanding of the basic host-parasite relations between the schistosomes and their hosts. This knowledge is essential in order to decide whether a finding in one host is likely to be applicable in others. With this idea in mind, we report here our findings on naturally acquired resistance to Schistosoma mansoni in the rhesus monkey.