Adult S. mansoni from a recently infected rhesus monkey (Macaca mulatta) were transferred into the hepatic portal systems of a normal rhesus and of a rhesus which had acquired complete resistance to the parasite. The worms were recovered after 2 days and examined by light and electron microscopy.

The worms recovered from the normal monkey were undamaged. Most of the worms recovered from the hyperimmune monkey were alive but had localized aggregations of host cells on their surfaces. Small areas of the tegument of these worms showed structural and degenerative changes, namely an increase in density and vacuolation of the tegument; the formation of small, round, membrane-bounded cytoplasmic bodies within vacuoles in the tegument; the breakdown of the outer membrane of the tegument and release of the cytoplasmic contents; and finally the complete disappearance of the tegument exposing the underlying muscle fibres. Host monocytes and polymorphonuclear leucocytes were closely applied to severely damaged parts of the tegument; the host cells appeared to be phagocytic. The other tissues of the worms were normal. Apparently the above damage is a result of the host's immune reaction which is directed against the tegument of the worms. Worms grown in mice and subsequently transferred to monkeys immunized against mouse antigens are similarly damaged, but in this case the damage occurs more rapidly.