Studies on immunity to Trichinella spiralis in mice

A 'dual antibody' basis for acquired immunity has been suggested for Trichinella spiralis infections. Adult T. spiralis recovered from mouse intestines were cultured for 24 hours in medium 199 with serum. Newborn larvae born during this time were injected intravenously into mice to produce infections of the parenteral stages. 'Anti-adult' immunity was produced by eliminating adult worms with methyridine before newborn larva production commenced. The immune state of the host was gauged from the numbers of muscle larvae encysting from a challenge complete infection or from the numbers and size of adult worms in the intestines. 'Anti-adult' immunity was 86-95% effective against a challenge complete infection but 0-16% effective against a parenteral challenge infection. Adult worms in immune mice were stunted and expelled earlier. 'Anti-parenteral phase' immunity was 74-100% effective against a parenteral challenge but 27-63% effective against a complete infection, and no obvious effects of immunity occured against adult worms in the intestines. Newborn larvae were shown to be antigenic by their capacity to react with antibody in in vitro culture and in the IFAT, however, attempts to immunise mice with antigen prepared from newborn larvae or by cambendazole abbreviated newborn larva infections were unsuccessful. Attempts to detect the occurence of stage specific cell mediated responses were inconclusive but IFAT and in vitro serum culture techniques indicated a stage specific difference between the three life cycle stages tested. Adult worm and newborn larva cuticular antigens appeared to cross-react and to be different from those of muscle larvae while newborn larva and muscle larva E and S antigens appeared to cross-react and to be different from those of adult worms Mice challenged with newborn larvae injected 14 days after a normal infection contained more muscle larvae than the challenge and the infected/non-chal1enged controls added together. It is speculated that the intestinal and parenteral phases could interact to partially suppress the immune response developing in a normal infection.