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The parotid lymph nodes of naive and previously infected Balb/c mice were studied after, respectively, infection and re-infection with cercariae of Schistosoma mansoni via the ears. Schistosomula were able to pass through the lymph node by following the lymph flow or by penetrating the veins of the medullary cords. The number of nodal mast cells was higher from day 2 to 6 of primary infection; and from day 5 to 11 of re-infection. The amount of degranulating mast cells was significantly higher at day 4 of infection and at day 1 of re-infection. Eosinophils characterized the nodal inflammatory processes observed after day 5 in both primarily-infected and re-infected mice. However, only in the latter the eosinophils were able to adhere to the larval surface. In primarily-infected mice, no intranodal larva presented signs of degeneration. In contrast, in re-infected animals, some degenerating larvae were found inside eosinophilic infiltrates. The eosinophils reached the nodal tissue by migrating through the high endothelial venules and their collecting veins.

Mice transcutaneously infected with about 400 cercariae were submitted to treatment with oxamniquine (400 mg/kg), 24 hours after infection. The recovery of schistosomules, at 4, 24, 48 and 72 hours and 35 days after treatment, showed the activity of the drug on the parasites, thus practically preventing their migration from the skin to the lungs. Worm recovery performed in the lungs (96 hours after treatment) showed recovery means of 0.6 worms/mouse in the treated group and 53.8 in the control group (untreated). The perfusion of the portal system carried out at 35 days after treatment clearly showed the elimination of all the parasites in the treated group, whereas a recovery mean of 144.7 worms/mouse was detected in the control group (untreated). These findings confirm the efficacy of oxamniquine at the skin phase of infection, and also show similarity with the immunization method that uses irradiated cercariae. The practical application of these findings in the medical clinic is discussed too.

Mice infected with 350 cercariae of Schistosoma mansoni (LE strain) were treated with oxamniquine, at the dose of 400 mg/kg, 24, 48, 72, and 96 h after infection. Forty days after the treatment, the animals were submitted to a challenge infection with 80 cercariae, through the abdominal and ear skins. The number of immature worms in the animal groups treated 24 and 96 h after the first infection was found to be lower than that in the control group, thus showing that the death of schistosomes by chemotherapy, at the skin and pulmonary phases, causes an acquired resistance state.

1. In order to study local tissue anaphylactic responses to infection with Schistosoma mansoni cercariae, mice of three different strains (C57BL/10J, Balb/cJ and CBA/J) were infected by subcutaneous injection of 15 to 20 cercariae. Eleven to 16 weeks later the animals were reinfected through one ear with 250 to 350 cercariae. 2. Throughout the infection period, the histamine content of the ears increased up to 150% of control values. Upon reinfection, the penetration of cercariae through the ear reduced its histamine content to near normal values. 3. Reinfection causes inflammation as judged by a 1.5 to 2.3-fold increase in the amounts of plasma leaking through the ear vessels as measured by leakage of Evans blue dye. 4. These results suggest that the local inflammatory reaction mediated by mast cells is important in the resistance of mice to reinfection with S. mansoni.

The hind-body region of Schistosoma mansoni cercariae observed in the scanning electron microscope demonstrates various stages of contraction which may be compared with those of living larvae which are secreting the acetabular gland contents. No evidence for an extensive lesion was found in cercarial bodies which had shed their tails under experimental conditions. Experiments on the permeability of the larvae to sodium fluoride, methylene blue and amino acids demonstrated that tail loss significantly affects the permeability of the bodies although the effect is greater immediately after decaudation than at later times. Subsequent increases in permeability may be correlated with a change in the general body surface.

Normal and S. mansoni-infected mice were exposed to the penetration of 250-350 cercariae through one ear. Two days later, when the ear was removed and chopped, 30 to 50% more schistosomula were recovered from the ears of normal mice than from the ears of infected (immune) mice. Administration of cyproheptadine, a histamine-serotonin antagonist (2 mg/kg), 30 min before challenge infection rendered immune mice indistinguishable from normal mice. Partial depletion of histamine by pretreatment with compound 48-80, a histamine releaser (1 mg/kg) 2 days before challenge infection increased the numbers of schistosomula recovered from the ears of both normal and immune mice. These results are interpreted to mean that vasoactive amines released by skin mast cells play an important role in hindering the viable passage of schistosomula through the skin of normal and immune mice.