RESUMEN
Parasites have been shown to reduce host density and to induce host population extinction in some cases but not in others. Epidemiological models suggest that variable effects of parasites on individual hosts can explain this variability on the population level. Here, we aim to support this hypothesis with a specific epidemiological model using a cross-parasite species approach. We compared the effect of six parasites on host fecundity and survival to their effects on density and risk of extinction of clonal host populations. We contrast our empirical results of population density with predictions from a deterministic model and contrast our empirical results of host and parasite extinction rates with those predicted by a stochastic model. Five horizontally transmitted microparasites (two bacteria: white bacterial disease, Pasteuria ramosa; two microsporidia: Glugoides intestinalis, Ordospora colligata; one fungus: Metschnikowiella biscuspidata); and six strains of a vertically transmitted microsporidium (Flabelliforma magnivora) of the planktonic crustacean Daphnia magna were used. In life table experiments, we quantified fecundity and survival in individual parasitized and healthy hosts and compared these with the effect of the parasites on host population density and on the likelihood of host population extinction in microcosm populations. Parasite species varied strongly in their effects on host fecundity, host survival, host density reduction, and the frequency with which they drove host populations to extinction. The fewer offspring an infected host produced, the lower the density of an infected host population. This effect on host density was relatively stronger for the vertically transmitted parasite strains than for the horizontally transmitted parasites. As predicted by the stochastic simulations, strong effects of a parasite on individual host survival and fecundity increased the risk of host population extinction. The same was true for parasite extinctions. Our results have implications for the use of microparasites in biological control programs and for the role parasites play in driving small populations to extinction.
RESUMEN
It is predicted that host exploitation should evolve to maximize parasite fitness and that virulence (= parasite-induced host mortality) evolves along with the rate of host exploitation. If the life expectancy of a parasite is short, it is expected to evolve a higher rate of host exploitation and therefore higher virulence because the penalty to the parasite for killing the host is reduced. We tested this hypothesis by keeping for 14 months the horizontally transmitted microsporidian parasite Glugoides intestinalis in mono-clonal host cultures (Daphnia magna) under conditions of high and low host background mortality. High host mortality, and thus parasite mortality, was achieved by replacing weekly 70-80% of all hosts in a culture with uninfected hosts from stock cultures (Replacement lines). In the low-mortality treatment no replacement took place. Contrary to our expectation, parasites from the Replacement lines evolved a lower within-host growth rate and virulence than parasites from the Nonreplacement lines. Across lines we found a strong positive correlation between within-host growth rate and virulence. We did further experiments to answer the question why our data did not support the predictions. Sporophorous vesicles (SVs, spore clusters) were smaller in doubly infected than in singly infected host-gut cells, indicating that competition within cells bears costs for the parasite. Due to our experimental protocol, the average life span of infections had been much higher in the Nonreplacement lines. Since the number of parasites inside a host increases with the time since infection, long-lasting infections led to high frequencies of multiply infected host-gut cells. Therefore, we speculated that within-cell competition was more severe in the Nonreplacement lines and may have led to selection for accelerated within-host growth. SVs in the Nonreplacement lines were indeed significantly larger. Our results point out that single-factor explanations for the evolution of virulence can lead to wrong predictions and that multiple infections are an important factor in virulence evolution.