Factors affecting the acquisition of resistance against Schistosoma mansoni in the mouse. Evidence that the mechanisms which mediate resistance during early patent infections may lack immunological specificity

Abstract

SUMMARYMice infected with 25 to 35 unsexed Schistosoma mansoni cercariae became resistant to homologous challenge by 8 weeks, and the degree of resistance that was acquired correlated with the size of the worm burden and the tissue egg burden. Mice given 100 male or 100 female cercariae alone failed to become resistant even after 30–40 weeks of infection. When a super-infection of 100 male or 100–300 female cercariae was given to mice with 25 unsexed cercariae, the degree of resistance that was acquired was generally lower than in mice given 25 unsexed cercariae alone. In the super-infected mice there was no correlation between the size of the worm burden (mainly unpaired male or female worms) and the degree of acquired resistance. In mice super-infected with male worms there was an inverse correlation between the number of male worms and the number of eggs deposited in the liver and intestine by each mature worm pair. A positive correlation was, however, still found between the degree of acquired resistance and total tissue egg counts in mice super-infected with single sex cercariae. Mice injected intraperitoneally or subcutaneously with intact S. mansoni eggs failed to become resistant to S. mansoni challenge. Transfer of lymphoid cells or serum, separately or together, from heavily infected and demonstrably resistant donor mice to naive normal or T-cell deprived recipients failed to render the recipients resistant to S. mansoni challenge. The results indicate that resistance to re-infection in mice with recently patent S. mansoni infections is dependent on the number of S. mansoni eggs entrapped in the tissues, and that excessive numbers of unpaired S. mansoni male or female worms can inhibit the fecundity of established worm pairs. The apparent acquired resistance to S. mansoni that has been observed in this model system may be largely a consequence of non-specific factors interfering with normal patterns of challenge worm migration and maturation.