Nearly every species on the planet has at least one parasite, which, by definition, incurs a cost in the host. Therefore, organisms must resist parasites - preventing or reducing infections - or tolerate parasites - reducing the costs of infection - in order to maintain their fitness despite the presence of parasites. Here, I investigated: 1) whether parasitic, larval trematodes (cercariae) can detect the least resistant tadpole host species, 2) a hypothetical framework for how host life history impacts the utilization of inflammation and thus, resistance and tolerance, 3) whether a common anesthesia technique used in experimental infections immunocompromises tadpoles, 4) the relationship between tadpole host life history, tolerance, and behavioral resistance to cercarial infection, 5) how tadpole behavior affects trematode infection location, and 6) how host life history impacts trematode infection location and the implications of this for host tolerance. In the first chapter, I investigated whether trematode cercariae could discriminate among several tadpole host species to identify the most susceptible hosts. Cercariae were consistently more attracted to Bufo terrestris tadpoles, which was the most susceptible host species. Other tadpole species varied in attractiveness in an order similar to their susceptibility to infection. Furthermore, there was consistent and significant variation among individual attractiveness and susceptibility within host species. If susceptibility to infection is heritable, chemical cues used by cercariae to identify susceptible hosts could represent a substrate on which natural selection acts, setting up a "Red Queen" arms race between host cues and parasite detection of those cues. In the second chapter, I proposed a framework which outlined the cost-benefit relationship between host life history and immune responses. Because inflammatory immune responses are known to cause self-damage to hosts, anti-inflammatory immune responses should vi be used for long-lived, slowly-developing ("slow-paced") hosts, those infected with relatively less virulent parasites, and/or ongoing but ineffective inflammatory responses. Conversely, the cost of inflammation might be less expensive than the cost of infection among shortlived, rapidly-developing ("fast-paced") hosts, those infected with virulent parasites, and/or those undergoing protracted but ineffective anti-inflammatory immune responses. In the third research chapter, I investigated whether two common anesthesia agents, benzocaine and tricaine mesylate (MS-222), immunocompromise tadpoles. These chemicals are used extensively to study the behavioral resistance of tadpoles to cercariae; if treatment increases infections not only by removing these behaviors but also by suppressing the immune system, behavior might appear artificially effective at preventing trematode infection. I found that neither benzocaine nor MS-222 affected the abundance of circulating white blood cells relative to waterexposed control tadpoles. Furthermore, there was no difference in trematode infection success when tadpoles were anesthetized, allowed to recover from anesthesia, and subsequently experimentally infected. The results of this experiment indicate that benzocaine and MS-222 are both practical, non-immunosuppressive anesthesia agents to use when studying trematode infections in amphibians. In the fourth research chapter, I quantified tadpole hosts' use of behavioral resistance (parasite-induced behaviors) and tolerance of exposure to cercariae. Across seven host species, parasite-induced behaviors were negatively correlated with pace-of-life, with rapidly-developing ("fast-paced") tadpoles exhibiting significantly more behavior than slowly-developing ("slowpaced") tadpoles. The opposite pattern was true of tolerance, where fast-paced species had poorer tolerance of cercarial exposure than slow-paced species. Given that slow-paced species are more likely to be exposed to cercariae because they 1) occur in water more likely to harbor cercariae and 2) have longer developmental times, tolerance to trematode exposure might be an vii evolutionary adaptation that circumvents the costs of behavioral - and, possibly, immunological - resistance to infection. In the fifth research chapter, I investigated whether parasite-induced behaviors were capable of affecting encystment location of trematode cercariae in Hyla femoralis tadpoles and whether the resulting encystment location affected tolerance of infection. Benzocaineanesthetized and control tadpoles had similar infection intensities. However, among benzocaineanesthetized tadpoles, the majority of cercarial infections occurred in tadpoles' heads, but unanesthetized control tadpoles were predominantly tail-infected. Furthermore, the number of head infections were negatively associated with mass change (poor tolerance), whereas the number of tail infections was positively associated with mass change (good tolerance). These results suggest that parasite-induced behavior is not only an important mechanism of resistance to trematodes, as other researchers have described, but also a mechanism of tolerance, whereby tadpoles can prevent the deleterious effects of trematode infection by controlling infection location. The sixth research chapter extends the work of the fifth and investigates whether host life history predicts encystment location of cercariae and whether encystment location affects tolerance of infection. Among seven host species, fast-paced species had significantly more infections in the head and body, whereas slow-paced species had the majority of infections in their tails. Slow-paced species were also less resistant to trematode infections in any body location than fast-paced species. These patterns were partially explained by surface area, with a slow-paced species having more surface area (making them more likely to be contacted and infected by cercariae) and a larger proportion of slow-paced species' surface area was comprised by tail than heady and body. Tail infections were less expensive than head and body infections; slow-paced species were more tolerant of infection and across species, tail infections had no effect on tolerance (mass change) whereas head infections were negatively associated with tolerance. These results suggest that slow-paced tadpoles, which are relatively more likely to viii become infected by cercariae and probably have more evolutionary history with these parasites, have invested in a morphology that improves their tolerance to parasites. The body of work that I have produced demonstrates that variation in resistance and tolerance to trematode parasites is ubiquitous among tadpole hosts. Furthermore, this variation is predictable based on host life history. Because tadpole life history can dramatically impact the likelihood of exposure to cercariae and encounters are necessary for host-parasite selective pressure to occur, life history can predict the adaptations of hosts and parasites. Given amphibians' status as the most rapidly declining taxon on the planet and the ubiquity of emerging infectious diseases for amphibians and other organisms, these findings should inform future research on host- and parasite-mediated mechanisms of disease.