The duration of primary infections with T. spiralis was dose-dependent with greater proportional loss of worms from heavily infected hamsters and longer persistence of worms in syngeneic DSN hamsters carrying initially low intensity infections. Intestinal worms were lost more rapidly from challenged immunized animals with over 80% loss of established worms by day 6 post infection, but survival of residual worms for a further 2 weeks. Hamsters carrying initially more than 140 intestinal worms began to lose weight during the second week indicating severe pathology at this stage of infection. Mucosal mast cell numbers increased from 50 cells/20 villus crypt units in uninfected animals to a peak in excess of 150 during week 4 pi, although intestinal mastocytosis persisted long after the loss of the majority of adult worms. Serum antibody responses to muscle stage larval antigen were detected in week 3 and increased subsequently. Both mastocytosis and antibody responses were more intense on secondary exposure to infection. Hamsters vaccinated with muscle stage larval antigen showed only a moderately accelerated loss of the intestinal phase but the fecundity of worms was severely suppressed. Overall it was concluded that the hamster host provided a model of trichinellosis that, in many respects was closer than mice and rats to the pattern of infection seen in economically and clinically important host species.