We examined a host system (Peromyscus maniculatus) in which a single autosomal gene controls susceptibility or resistance to infection by the cestode parasite Hymenolepis citelli. Parasite deaths of both primary and secondary (challenge) infections were examined, using a probabilistic model, to see if deaths were random and uncorrelated within each genotype. Within susceptible hosts, post-patent survival of primary worms was not random and heterogeneity was due to among-host effects rather than parasite-age effects, suggesting a second genetic or immunological process. Secondary infections in susceptible hosts appear to be lost randomly, independent of primary infection age or burden. The loss rate is similar to that for primary worms. The lack of correlation or alteration in (susceptible) host response to primary and secondary infections suggests that the latter are eliminated by a process that differs from that acting on primary worms. In resistant hosts, parasite survival rates suggest that the immunological process elicited by the primary infection also acts to eliminate the secondary infection more rapidly. Suggestions are made for improving experimental methods when dealing with mixed genotype populations. Experiments should permit direct estimation of genotype frequency and of parasite death rates within each genotype. This separation of host type is particularly important when studying correlation of successive worm burdens since any host or treatment mixture (genotype, age, sex, size or infection dose) may induce correlations that could be mistakenly interpreted.