Predators and parasites are critical, interconnected members of the community and have the potential to shape host populations. Predators, in particular, can have direct and indirect impacts on disease dynamics. By removing hosts and their parasites, predators alter both host and parasite populations and ultimately shape disease transmission. Selective predation of infected hosts has received considerable attention as it is recognized to have important ecological implications. The occurrence and consequences of preferential consumption of uninfected hosts, however, has rarely been considered. Here, we synthesize current evidence suggesting this strategy of selectively predating uninfected individuals is likely more common than previously anticipated and address how including this predation strategy can change our understanding of the ecology and evolution of disease dynamics. Selective predation strategies are expected to differentially impact ecological dynamics and therefore, consideration of both strategies is required to fully understand the impact of predation on prey and host densities. In addition, given that different strategies of prey selectivity by predators change the fitness payoffs both for hosts and their parasites, we predict amplified coevolutionary rates under selective predation of infected hosts compared to uninfected hosts. Using recent work highlighting the critical role that predators play in disease dynamics, we provide insights into the potential mechanisms by which selective predation on healthy individuals can directly affect ecological outcomes and impact long‐term host–parasite coevolution. We contrast the consequences of both scenarios of selective predation while identifying current gaps in the literature and future research directions.
more »
« less
The visual ecology of selective predation: Are unhealthy hosts less stealthy hosts?
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 a
- Award ID(s):
- 1655856
- PAR ID:
- 10366412
- Publisher / Repository:
- Wiley Blackwell (John Wiley & Sons)
- Date Published:
- Journal Name:
- Ecology and Evolution
- Volume:
- 11
- Issue:
- 24
- ISSN:
- 2045-7758
- Page Range / eLocation ID:
- p. 18591-18603
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
More Like this
-
-
more » « less
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. -
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.more » « less
-
more » « less
Abstract Predation on parasites is a common interaction with multiple, concurrent outcomes. Free‐living stages of parasites can comprise a large portion of some predators' diets and may be important resources for population growth. Predation can also reduce the density of infectious agents in an ecosystem, with resultant decreases in infection rates. While predator–parasite interactions likely vary with parasite transmission strategy, few studies have examined how variation in transmission mode influences contact rates with predators and the associated changes in consumption risk.
To understand how transmission mode mediates predator–parasite interactions, we examined associations between an oligochaete predator
Chaetogaster limnaei that lives commensally on freshwater snails and nine trematode taxa that infect snails.Chaetogaster is hypothesized to consume active (i.e. mobile), free‐living stages of trematodes that infect snails (miracidia), but not the passive infectious stages (eggs); it could thus differentially affect transmission and infection prevalence of parasites, including those with medical or veterinary importance. Alternatively, when infection does occur,Chaetogaster can consume and respond numerically to free‐living trematode stages released from infected snails (cercariae). These two processes lead to contrasting predictions about whetherChaetogaster and trematode infection of snails correlate negatively (‘protective predation’) or positively (‘predator augmentation’).Here, we tested how parasite transmission mode affected
Chaetogaster –trematode relationships using data from 20,759 snails collected across 4 years from natural ponds in California. Based on generalized linear mixed modelling, snails with moreChaetogaster were less likely to be infected by trematodes that rely on active transmission. Conversely, infections by trematodes with passive infectious stages were positively associated with per‐snailChaetogaster abundance.Our results suggest that trematode transmission mode mediates the net outcome of predation on parasites. For trematodes with active infectious stages, predatory
Chaetogaster limited the risk of snail infection and its subsequent pathology (i.e. castration). For taxa with passive infectious stages, no such protective effect was observed. Rather, infected snails were associated with higherChaetogaster abundance, likely owing to the resource subsidy provided by cercariae. These findings highlight the ecological and epidemiological importance of predation on free‐living stages while underscoring the influence of parasite life history in shaping such interactions. -
more » « less
Abstract Predators may create healthier prey populations by selectively removing diseased individuals. Predators typically prefer some ages of prey over others, which may, or may not, align with those prey ages that are most likely to be diseased.
The interaction of age‐specific infection and predation has not been previously explored and likely has sizable effects on disease dynamics. We hypothesize that predator cleansing effects will be greater when the disease and predation occur in the same prey age groups.
We examine the predator cleansing effect using a model where both vulnerability to predators and pathogen prevalence vary with age. We tailor this model to chronic wasting disease (CWD) in mule deer and elk populations in the Greater Yellowstone Ecosystem, with empirical data from Yellowstone grey wolves and cougars.
Model results suggest that under moderate, yet realistic, predation pressure from cougars and wolves independently, predators may decrease CWD outbreak size substantially and delay the accumulation of symptomatic deer and elk. The magnitude of this effect is driven by the ability of predators to selectively remove late‐stage CWD infections that are likely the most responsible for transmission, but this may not be the age class they typically select. Thus, predators that select for infected young adults over uninfected juveniles have a stronger cleansing effect, and these effects are strengthened when transmission rates increase with increasing prey morbidity. There are also trade‐offs from a management perspective—that is, increasing predator kill rates can result in opposing forces on prey abundance and CWD prevalence.
Our modelling exploration shows that predators have the potential to reduce prevalence in prey populations when prey age and disease severity are considered, yet the strength of this effect is influenced by predators' selection for demography or body condition. Current CWD management focuses on increasing cervid hunting as the primary management tool, and our results suggest predators may also be a useful tool under certain conditions, but not necessarily without additional impacts on host abundance and demography. Protected areas with predator populations will play a large role in informing the debate over predator impacts on disease.
