The combined effects of pathogens and predators on insect outbreaks

Dwyer, Greg; Dushoff, Jonathan; Yee, Susan H.

doi:10.1038/nature02569

Cited by 229 publications

(271 citation statements)

References 29 publications

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“…The densitydependent interaction of LdNPV with gypsy moth populations has previously been identified as the dominant process responsible for quasi-periodic oscillations in gypsy moth populations (Dwyer et al 2004, Bjørnstad et al 2010, although the data on which this was based were largely collected before the establishment of E. maimaiga. Given that generation-long mortality caused by E. maimaiga is consistently high, typically exceeding that of LdNPV, it is remarkable that this mortality has apparently not altered the numerical interaction between LdNPV and host populations.…”

Section: Discussionmentioning

confidence: 99%

Emergent fungal entomopathogen does not alter density dependence in a viral competitor

Liebhold

Plymale

Elkinton

et al. 2013

Ecology

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Abstract. Population cycles in forest Lepidoptera often result from recurring densitydependent epizootics of entomopathogens. While these systems are typically dominated by a single pathogen species, insects are often infected by multiple pathogens, yet little is known how pathogens interact to affect host dynamics. The apparent invasion of northeastern North America by the fungal entomopathogen Entomophaga maimaiga some time prior to 1989 provides a unique opportunity to evaluate such interactions. Prior to the arrival of E. maimaga, the oscillatory dynamics of host gypsy moth, Lymantria dispar, populations were apparently driven by epizootics of a nucleopolyhedrovirus. Subsequent to its emergence, E. maimaiga has caused extensive mortality in host populations, but little is known about how it has altered multigenerational dynamics of the gypsy moth and its virus. Here we compared demographic data collected in gypsy moth populations prior to vs. after E. maimaiga's invasion. We found that the recently invading fungal pathogen virtually always causes greater levels of mortality in hosts than does the virus, but fungal mortality is largely density independent. Moreover, the presence of the fungus has apparently not altered the gypsy mothvirus density-dependent interactions that were shown to drive periodic oscillations in hosts before the arrival of the fungus.

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Section: Discussionmentioning

confidence: 99%

Emergent fungal entomopathogen does not alter density dependence in a viral competitor

Liebhold

Plymale

Elkinton

et al. 2013

Ecology

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“…Support for this hypothesis comes first of all from observational data showing that defoliators experience high rates of infection by specialist pathogens and parasitoids in peak populations (2,4) and high rates of attack by generalist predators and parasitoids in trough populations (5). Second, experimental data have confirmed key assumptions of defoliator-natural-enemy models, and the models produce longperiod, large-amplitude cycles resembling time series of insect densities and defoliation levels (6).…”

mentioning

confidence: 84%

Induced plant defenses, host–pathogen interactions, and forest insect outbreaks

Elderd

Rehill

Haynes

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Cyclic outbreaks of defoliating insects devastate forests, but their causes are poorly understood. Outbreak cycles are often assumed to be driven by density-dependent mortality due to natural enemies, because pathogens and predators cause high mortality and because natural-enemy models reproduce fluctuations in defoliation data. The role of induced defenses is in contrast often dismissed, because toxic effects of defenses are often weak and because induceddefense models explain defoliation data no better than naturalenemy models. Natural-enemy models, however, fail to explain gypsy moth outbreaks in North America, in which outbreaks in forests with a higher percentage of oaks have alternated between severe and mild, whereas outbreaks in forests with a lower percentage of oaks have been uniformly moderate. Here we show that this pattern can be explained by an interaction between induced defenses and a natural enemy. We experimentally induced hydrolyzable-tannin defenses in red oak, to show that induction reduces variability in a gypsy moth's risk of baculovirus infection. Because this effect can modulate outbreak severity and because oaks are the only genus of gypsy moth host tree that can be induced, we extended a natural-enemy model to allow for spatial variability in inducibility. Our model shows alternating outbreaks in forests with a high frequency of oaks, and uniform outbreaks in forests with a low frequency of oaks, matching the data. The complexity of this effect suggests that detecting effects of induced defenses on defoliator cycles requires a combination of experiments and models. host-pathogen model | Lymantria dispar | complex population dynamics | spatial model | hydrolyzable tannins P eriodic outbreaks of forest-defoliating insects severely damage valuable timber and increase atmospheric CO 2 levels by converting forests from carbon sinks to carbon sources (1). Decades of research have produced multiple hypotheses to explain defoliator outbreak cycles (2), but a decisive experiment to choose between competing hypotheses faces almost insurmountable logistical difficulties, because outbreaks occur at 5-30 y intervals and typically cover thousands of square kilometers (3). Efforts to support particular hypotheses have therefore instead relied on a mixture of observational field data, small-scale field and laboratory experiments, and mathematical models.For example, the most widely accepted hypothesis is that defoliator cycles are driven by natural enemies. Support for this hypothesis comes first of all from observational data showing that defoliators experience high rates of infection by specialist pathogens and parasitoids in peak populations (2, 4) and high rates of attack by generalist predators and parasitoids in trough populations (5). Second, experimental data have confirmed key assumptions of defoliator-natural-enemy models, and the models produce longperiod, large-amplitude cycles resembling time series of insect densities and defoliation levels (6).Neither data nor models have provided meani...

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“…[90], and the examples mentioned above. Although models can potentially identify what might cause cyclic dynamics, the simulated population trends are often unrealistic.…”

Section: The Role Of Models In Understanding Cyclic Dynamicsmentioning

confidence: 99%

Population cycles: generalities, exceptions and remaining mysteries

Myers¹

2018

Proc. R. Soc. B.

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Population cycles are one of nature's great mysteries. For almost a hundred years, innumerable studies have probed the causes of cyclic dynamics in snowshoe hares, voles and lemmings, forest Lepidoptera and grouse. Even though cyclic species have very different life histories, similarities in mechanisms related to their dynamics are apparent. In addition to high reproductive rates and density-related mortality from predators, pathogens or parasitoids, other characteristics include transgenerational reduced reproduction and dispersal with increasing-peak densities, and genetic similarity among populations. Experiments to stop cyclic dynamics and comparisons of cyclic and noncyclic populations provide some understanding but both reproduction and mortality must be considered. What determines variation in amplitude and periodicity of population outbreaks remains a mystery.

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The combined effects of pathogens and predators on insect outbreaks

Cited by 229 publications

References 29 publications

Emergent fungal entomopathogen does not alter density dependence in a viral competitor

Emergent fungal entomopathogen does not alter density dependence in a viral competitor

Induced plant defenses, host–pathogen interactions, and forest insect outbreaks

Population cycles: generalities, exceptions and remaining mysteries

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