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Abstract The healthy herds hypothesis proposes that predators can reduce parasite prevalence and thereby increase the density of their prey. However, evidence for such predator‐driven reductions in the prevalence of prey remains mixed. Furthermore, even less evidence supports increases in prey density during epidemics. Here, we used a planktonic predator–prey–parasite system to experimentally test the healthy herds hypothesis. We manipulated density of a predator (the phantom midge,Chaoborus punctipennis) and parasitism (the virulent fungusMetschnikowia bicuspidata) in experimental assemblages. Because we know natural populations of the prey (Daphnia dentifera) vary in susceptibility to both predator and parasite, we stocked experimental populations with nine genotypes spanning a broad range of susceptibility to both enemies. Predation significantly reduced infection prevalence, eliminating infection at the highest predation level. However, lower parasitism did not increase densities of prey; instead, prey density decreased substantially at the highest predation levels (a major density cost of healthy herds predation). This density result was predicted by a model parameterized for this system. The model specifies three conditions for predation to increase prey density during epidemics: (i) predators selectively feed on infected prey, (ii) consumed infected prey release fewer infectious propagules than unconsumed prey, and (iii) sufficiently low infection prevalence. While the system satisfied the first two conditions, prevalence remained too high to see an increase in prey density with predation. Low prey densities caused by high predation drove increases in algal resources of the prey, fueling greater reproduction, indicating that consumer–resource interactions can complicate predator–prey–parasite dynamics. Overall, in our experiment, predation reduced the prevalence of a virulent parasite but, at the highest levels, also reduced prey density. Hence, while healthy herds predation is possible under some conditions, our empirical results make it clear that the manipulation of predators to reduce parasite prevalence may harm prey density. 

Abstract Transmission from one host to another is a crucial component of parasite fitness. For some aquatic parasites, transmission occurs via a free‐living stage that spends time in the water, awaiting an encounter with a new host. These parasite transmission stages can be impacted by biotic and abiotic factors that influence the parasite's ability to successfully infect or grow in a new host.Here we tested whether time spent in the water column and/or exposure to common cyanobacterial toxins impacted parasite transmission stages. More specifically, we tested whether the infectivity, within host growth, and virulence of the fungal parasiteMetschnikowia bicuspidatachanged as a result of time spent in the water or from exposure to cyanotoxins in the water column. We exposed parasite transmission spores to different levels of one of two ecologically important cyanotoxins, microcystin‐LR and anatoxin‐a, and factorially manipulated the amount of time spores were incubated in water. We removed the toxins and used those same spores to infect one genotype of the common lake zooplanktonDaphnia dentifera.We found that cyanotoxins did not impact parasite fitness (infection prevalence and spore yield per infected host) or virulence (host lifetime reproduction and survivorship) at the tested concentrations (10 and 30 μg/L). However, we found that spending longer as a transmission spore decreased a spore's chances for successful infection: spores that were only incubated for 24 hr infected approximately 75% of exposed hosts, whereas spores incubated for 10 days infected less than 50% of exposed hosts.We also found a negative relationship between the final spore yield from infected hosts and the proportion of hosts that became infected. In treatments where spores spent longer in the water column prior to encountering a host, infection prevalence was lower (indicating lower per spore infectivity), but each infected host yielded more spores at the end of infection. We hypothesise that this pattern may result from intraspecific parasite competition within the host.Overall, these results suggest that transmission spores of this parasite are not strongly influenced by cyanotoxins in the water column, but that other aspects of spending time in the water strongly influence parasite fitness. 

Abstract Predators can strongly influence disease transmission and evolution, particularly when they prey selectively on infected hosts. Although selective predation has been observed in numerous systems, why predators select infected prey remains poorly understood. Here, we use a mathematical model of predator vision to test a long‐standing hypothesis about the mechanistic basis of selective predation in aDaphnia–microparasite system, which serves as a model for the ecology and evolution of infectious diseases. Bluegill sunfish feed selectively onDaphniainfected by a variety of parasites, particularly in water uncolored by dissolved organic carbon. The leading hypothesis for selective predation in this system is that infection‐induced changes in the transparency ofDaphniarender them more visible to bluegill. Rigorously evaluating this hypothesis requires that we quantify the effect of infection on the visibility of prey from the predator's perspective, rather than our own. Using a model of the bluegill visual system, we show that three common parasites,Metschnikowia bicuspidata,Pasteuria ramosa, andSpirobacillus cienkowskii, decrease the transparency ofDaphnia, rendering infectedDaphniadarker against a background of bright downwelling light. As a result of this increased brightness contrast, bluegill can see infectedDaphniaat greater distances than uninfectedDaphnia—between 19% and 33% further, depending on the parasite.PasteuriaandSpirobacillusalso increase the chromatic contrast ofDaphnia. These findings lend support to the hypothesis that selective predation by fish on infectedDaphniacould result from the effects of infection onDaphnia's visibility. However, contrary to expectations, the visibility ofDaphniawas not strongly impacted by water color in our model. Our work demonstrates that models of animal visual systems can be useful in understanding ecological interactions that impact disease transmission. 

Parasites exert strong selective pressure on their hosts, and many hosts can evolve rapidly in response. As such, host-parasite interactions have a special place in the study of contemporary evolution. However, these interactions are often considered in isolation from the ecological contexts in which they occur. Here we review different ways in which the ecological context of host-parasite interactions can modulate their evolutionary outcomes in important and sometimes unexpected ways. Specifically, we highlight how predation, competition, and abiotic factors change the outcome of contemporary evolution for both hosts and parasites. In doing so, we focus on insights gained from the Daphnia-microparasite system. This system has emerged as a model system for understanding the ecology and evolution of host-parasite interactions, and has provided important insights into how ecological context influences contemporary evolution. 

How and why do predators sometimes fuel disease outbreaks but other times thwart them? Answering this could help explain spatial and temporal variation in disease and could explain why attempts to control disease by manipulating predators sometimes fail. We give eight mechanisms by which predators can suppress/spread disease in prey populations, exploring each generally and reviewing evidence from the study system that has been the focus of much of our research. This system focuses on Daphnia dentifera, a dominant herbivore in lake food webs in the Midwestern United States. D. dentifera is prey to bluegill sunfish and phantom midge larvae, as well as host to a virulent fungal pathogen. We review evidence for bluegill sunfish as ‘healthy herds’ predators that reduce disease, and for midge larvae as ‘predator spreaders’ that fuel disease outbreaks. We find that both predators can impact disease via multiple mechanisms. Bluegill feed selectively on infected hosts and also depress disease in Daphnia by reducing the density of midge larvae which spread disease. They also increase the abundance of Ceriodaphnia, which reduce disease. Midge larvae increase disease in their hosts, in part by releasing spores into the water column where they can be consumed by additional hosts.