The fecundity of Schistosoma mansoni in chronic nonhuman primate infections and after transplantation into naive hosts.
Adult Schistosoma mansoni worms were transplanted from 8 nonhuman primates with chronic infections into 8 naive recipients, in an effort to test the hypothesis that worm fecundity reduction in chronic infections is the result of host immunity or some other host effect. Techniques for perfusing living donors without the added use of anti-schistosomal drugs and for reducing the likelihood of post-operative bacterial endotoxemia and septic shock are described. Fecundity values in terms of eggs per day per female worm were obtained for the worms in their original and in their new hosts and compared. In 3 experiments, perfusions were incomplete and the donors were saved, enabling direct comparisons of fecundity to be made in subpopulations of worms in both their original and new hosts, after equal life spans. In only 1 of the 8 transplantations was there a clear increase in fecundity after surgical introduction into a naive host. Therefore, these experiments fail to support the hypothesis that reduced fecundity of S. mansoni worms in permissive nonhuman primate hosts is a reversible result of host immunity or some other host-derived factor. Despite this negation, further evidence for reduced worm fecundity in older infections was obtained. In the absence of in vivo evidence for immune-mediated antifecundity, worm senescence is the most likely explanation for this finding, with irreversible immune damage to the worms being a less attractive alternative hypothesis.
D000818:Animals; D002908:Chronic Disease; D005260:Female; D005298:Fertility; D008252:Macaca fascicularis; D008297:Male; D010215:Papio; D010270:Parasite Egg Count; D012550:Schistosoma mansoni / Q000502:physiology*; D012555:Schistosomiasis mansoni / Q000276:immunology / Q000469:parasitology*