Trichinella spiralis: evidence that mice do not express rapid expulsion

The rapid expulsion of Trichinella spiralis by mice of a variety of inbred and F1 mouse strains was examined. Mice were reinfected once with T. spiralis during and immediately after the natural termination of a primary infection and worm rejection was measured less than or equal to 24 hr after the challenge. The results showed that the challenge (super)infection was consistently rejected by all mouse strains before rejection of the adult worms from the primary infection commenced. Rejection of the challenge infection began at different times after the primary infection with NFS (2 days) less than C3H less than or equal to B10.Q approximately B10.BR (greater than 5 days). In all strains, rejection of the challenge infection preceded adult worm rejection from the primary infection by 5-8 days. At its peak, the loss of challenge worms related directly to the strength of the primary rejection process NFS greater than or equal to 98%, C3H 90-98%, and B10 mice 80-90%. Furthermore, loss of the capacity to reject the challenge followed approximately 7 days after the complete loss of the primary infection in each strain examined. Thus, the sooner worms from the primary infection were lost, the earlier the capacity to promptly reject the challenge infection disappeared. B10.Br mice still partially rejected a superinfection 35 days after the primary infection began, whereas NFS mice lost this capacity around 25 days. However, premature termination of the primary infection in B10.BR mice with methyridine at the same time that NFS mice naturally terminated their infection (15 days) abrogated the capacity of B10.BR mice to reject the superinfection at 24 days. Passive transfer of protective rat IgG monoclonal antibody to mice did not lead to rapid expulsion. Transfer of mouse immune serum to intestinally primed rats did result in rapid expulsion, suggesting that mouse antibody responses were adequate. The expression of superinfection rejection was susceptible to the administration in vivo of GK1.5, anti-mouse L3T4 antibody. The data indicate that the principal determinant of the strength, time of initiation, and longevity of rejection of a challenge infection was the response to the primary infection of that individual mouse strain. The genetic determinants of challenge infection rejection were seen to be identical to those that determined rejection of the primary infection. Since no evidence could be found to support the identity of this response with rapid expulsion, as defined in rats, a new term, "associative expulsion," is proposed.(ABSTRACT TRUNCATED AT 400 WORDS)