Abstract
Summary: Acquired resistance to Schistosoma japonicum was evident after the lung phase of migration of challenge schistosomula. ‘Trickle’ infections which gave similar primary worm burdens to single infections stimulated similar levels of resistance. There was a strong correlation between the size of the primary worm burden of individual mice and their ability to resist infection 8 weeks after exposure to S. japonicum. However, acquired resistance did not develop until 6 weeks, that is after the primary infection had become patent, and was maximal some 12 weeks after infection; thereafter resistance declined. The numbers of parasite eggs deposited in the tissues increased during acute infection (duration of 12 weeks or less) and tended to stabilize or decrease during chronic infection (longer than 12 weeks). There were good correlations between the resistance of mice to challenge and the numbers of eggs deposited in their livers, guts or lungs during acute infection, but these correlations were not evident during chronic infection. The inflammatory responses to tissue-bound eggs regress during chronic infection and this may influence the relationship between acquired resistance and egg burden. Comparable primary infections of S. japonicum or S. mansoni protected equally well against both heterologous and homologous challenges. However, unisexual infections of S. mansoni, which produced no overt pathology, failed to confer protection against a challenge of S. japonicum.

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