Treatment of BALB/c or MF1 mice with cyclosporin A (CsA) around the time of infection with Schistosoma mansoni conferred almost complete protection. The migration kinetics of L-[75Se]selenomethionine-labelled infective cercariae were investigated by compressed tissue autoradiography. Similar levels of skin penetration were achieved by cercariae in control and drug-treated individuals. CsA arrested 87–94% of the worms in the skin and ultimately all of these died in this site. Few worms (7–14%) migrated from the skin to the lungs and none completed migration to the liver. Nevertheless, the autoradiograms revealed a limited degree of lateral cutaneous migration by the worms present in the skins of CsA-treated mice. Results of perfusion recovery experiments carried out during the course of infection reinforced the tracking data.

129/Ola mice resemble WEHI 129J mice in that around 70% of the individuals in any given population resist a primary infection with Schistosoma mansoni. Squashed-organ autoradiographic tracking of [Se]selenomethionine-labelled parasites has shown that the kinetics of worm migration in 129/Ola mice follows the expected pattern, and that all rodents harbour essentially similar numbers of worms on day 14 post-infection. Combined lung and liver worm recovery techniques have revealed, however, that segregation of mice into ‘permissive’ and ‘non-permissive’ individuals can first be detected on day 20. ‘Non-permissive’ mice are characterized by the absence of schistosome eggs at all times in the liver parenchyma and, in consequence, lack the attendant manifestations of pathology; they do, however, harbour a few stunted worms in the liver and significant numbers of adult schistosomes in the pulmonary vasculature. Histological analysis of sectioned lung tissue from such animals indicates that some lung-located schistosomes feed, pair and lay eggs. Nevertheless, eosinophil-enriched inflammatory reactions develop around such worms and the parasites themselves exhibit various manifestations of trauma, ranging from minor vacuolation to gut herniation and extrusion. The phenomenon of ‘non-permissiveness’ thus involves retardation of worm development in the liver and, in consequence, relocation of the parasites to the lungs, where they become subject to host effector responses.

Schistosomes infect the mammalian host by direct penetration of the skin and must then undergo a protracted migration to the site of parasitization, for Schistosoma mansoni the hepatic portal vasculature. This article reviews the work published roughly between 1976 and 1986 that clarified our understanding of the process in the laboratory mouse. A combination of histopathology, larval injection experiments and autoradiographic tracking revealed that migration involved one to several circuits of the pulmonary-systemic vasculature before chance delivery in cardiac output to splanchnic arteries that lead indirectly to the portal tract. The kinetics of migration through different capillary beds was established, with the lungs of naïve mice not the skin proving the greatest obstacle; a proportion of schistosomula entered the alveoli from where they did not recover. The ‘immunity’ displayed by mice with a chronic infection was shown to be an artefact of a ‘leaky’ hepatic portal system, generated as a result of egg-induced hepatic pathology. The blockade of pulmonary migration was exacerbated in mice vaccinated with irradiated cercariae by immune-mediated inflammatory foci that developed around lung schistosomula thus decreasing the proportion that matured, but parasite elimination was a prolonged process, not an acute cytolytic ‘hit.’