Models of host-parasite coevolution assume the presence of genetic variation for host resistance and parasite infectivity, as well as genotype-specific interactions. We used the freshwater crustacean Daphnia magna and its bacterial microparasite Pasteuria ramosa to study genetic variation for host susceptibility and parasite infectivity within each of two populations. We sought to answer the following questions: Do host clones differ in their susceptibility to parasite isolates? Do parasite isolates differ in their ability to infect different host clones? Are there host clone-parasite isolate interactions? The analysis revealed considerable variation in both host resistance and parasite infectivity. There were significant host clone-parasite isolate interactions, such that there was no single host clone that was superior to all other clones in the resistance to every parasite isolate. Likewise, there was no parasite isolate that was superior to all other isolates in infectivity to every host clone. This form of host clone-parasite isolate interaction indicates the potential for coevolution based on frequency-dependent selection. Infection success of original host clone-parasite isolate combinations (i.e., those combinations that were isolated together) was significantly higher than infection success of novel host clone-parasite isolate combinations (i.e., those combinations that were created in the laboratory). This finding is consistent with the idea that parasites track specific host genotypes under natural conditions. In addition, correspondence analysis revealed that some host clones, although distinguishable with neutral genetic markers, were susceptible to the same set of parasite isolates and thus probably shared resistance genes.
It has been suggested that the harm parasites cause to their hosts is an unavoidable consequence of parasite reproduction with costs not only for the host but also for the parasite. Castrating parasites are thought to minimize their costs by reducing host fecundity, which may minimize the chances of killing both host and parasite prematurely. We conducted a series of experiments to understand the evolution of virulence of a castrating bacterium in the planktonic crustacean Daphnia magna. By manipulating food levels during the infection of D. magna with the bacterium Pasteuria ramosa, we showed that both antagonists are resource-limited and that a negative correlation between host and parasite reproduction exists, indicating resource competition among the antagonists. Pasteuria ramosa also induces enhanced growth of its hosts (gigantism), which we found to be negatively correlated with host fecundity but positively correlated with parasite reproduction. Because infected hosts never recovered from infections, we concluded that gigantism is beneficial only for the parasite. Hosts, however, have evolved counteradaptations. We showed that infected hosts have enhanced reproduction before castration. This shift to earlier reproduction increases overall host fecundity and compromises parasite reproduction. Finally, we showed that this resource conflict is subject to genetic variation among host and parasite genotypes within a population and is therefore likely to be an important force in the coevolution of virulence in this system. A verbal model is presented and suggests that the adaptive value of gigantism is to store host resources, which are liberated after parasitic castration for later use by the growing parasite. This hypothesis assumes that infections are long lasting, that is, that they have a high life expectancy.
Genetic variation among hosts for resistance to parasites is an important assumption underlying evolutionary theory of host and parasite evolution. Using the castrating bacterial parasite Pasteuria ramosa and its cladoceran host Daphnia magna, we examined both within-and between-population genetic variation for resistance. First, we tested hosts from four populations for genetic variation for resistance to three parasite isolates. Allozyme analysis revealed signi¢cant host population divergence and that genetic distance corresponds to geographic distance. Host and parasite ¢tness components showed strong genetic di¡erences between parasite isolates for host population by parasite interactions and for clones within populations, whereas host population e¡ects were signi¢cant for only a few traits. In a second experiment we tested explicitly for within-population di¡erences in variation for resistance by challenging nine host clones from a single population with four di¡erent parasite spore doses. Strong clone and dose e¡ects were evident. More susceptible clones also su¡ered higher costs once infected. The results indicate that within-population variation for resistance is high relative to between-population variation. We speculate that P. ramosa adapts to individual host clones rather than to its host population.
Individual hosts constitute a limited resource for parasites, suggesting that density-dependent effects may play a role in within-host growth and parasite regulation. This hypothesis has been tested for several helminth parasites, but not for microparasites. We therefore examined dose-response patterns for the microparasitic bacterium Pasteuria ramosa and the fungus Metschnikowiella biscuspidata infecting the planktonic crustacean Daphnia magna. With increasing numbers of transmission stages administered to the host we found that host fecundity and survival and parasite transmission-stage production declined. Using a k-value analysis, a method that quantifies the strength of density dependence, we found for both parasites that density dependence acted at all doses, indicating the absence of a minimum density below which parasite fitness is density- independent. At low doses density was exactly compensated, but it was overcompensated at high doses. Overcompensation at high doses was weak for P. ramosa, but high for M. biscuspidata. At the two highest doses M. biscuspidata killed its hosts before any transmission stages were produced. Our data indicate that density dependence is expressed through retarded spore development in P. ramosa, but through both host mortality and reduced parasite fecundity in M. biscuspidata. A further experiment (P. ramosa only) revealed that in well-fed hosts more parasite transmission stages are produced than in poorly fed hosts, suggesting that competition for host resources retards P. ramosa development. Our data for P. ramosa, but not for M. biscuspidata, are largely consistent with assumptions made in models on microparasite epidemiology. We draw attention to the relevance of dose effects and within-host competition for the evolution of virulence.
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