In chapter 1, I describe a laboratory infection experiment designed to evaluate the hematological and organ-level consequences of C. hepatica infection on deer mice. I compared a series of physiological measures between uninfected and infected littermates from two localities, and found that infection caused significant changes in all measures: Infected mice had (1) increased serum concentrations of alkaline phosphatase, which reveals bile duct obstruction; (2) reduced serum concentrations of albumin, an important liver product; (3) increased immunoglobulin concentrations; (4) increased hematocrits, which may help mice cope with impaired energy metabolism; and (5) enlarged livers and spleens, which may reflect increased energetic drain in infected animals. I also found that the consequences of infection can depend on host sex and locality; significant infection*locality interactions imply that evolved differences alter the physiological outcome of infection. The cell- and organ-level effects that I describe in Chapter 1 must produce interindividual fitness differences in order to be important to host ecology and evolution. In Chapter 2, I evaluate this requirement. I performed a second similarly-designed infection experiment to determine the effects of C. hepatic infection on oxygen consumption (and by implication, metabolic performance and fitness) in deer mice. I found that infection has a measurable negative effect under cold-stress conditions, which means this parasite may affect winter survivorship in these mice. Furthermore, negative effects were only apparent in mice that did not have a shared history with this worm. Thus, evolutionary responses in host populations can amerliorate the negative consequences of parasitic infection. In Chapter 3, I compare levels of allozyme heterozygosity and the prevalence of C. hepatica among Michigan deer mouse populations to test the prediction that more uniform populations will have higher rates of infection. To make this test, I took advantage of two attributes of some island faunas: low genetic diversity and high levels of disease. I found that the prevalence of C. hepatica is negatively correlated with average heterozygosity. This is the first evidence for such an association from conspecific animal populations. These populations differ in other attributes, however, and I also found a positive correlation between C. hepatica prevalence and host population density. Thus in northern Michigan deer mouse populations, genetic, ecological, or both kinds of factors may determine the prevalence of C. hepatica. Laboratory experiments are required to determine definitively whether genetic diversity is important in determining disease levels in this system. In summary, C. hepatica has measurable physiological effects on deer mice. Furthermore, the origin of hosts and parasites can alter the magnitude (or existence) of these effects, which implies that coevolution between these animals has taken place where they co-occur. Finally, levels of genetic diversity may play a role in determining the prevalence of C. hepatica in these P. maniculatus populations. A more complete understanding of the interaction between C. hepatica and P. maniculatus in Michigan will require field studies (e.g. mark-recapture) to complement the laboratory physiology experiments and laboratory infection experiments to complement the prevalence