Warming and top-down control of stage-structured prey: Linking theory to patterns in natural systems.

Warming has broad and often nonlinear impacts on organismal physiology and traits, allowing it to impact species interactions like predation through a variety of pathways that may be difficult to predict. Predictions are commonly based on short-term experiments and models, and these studies often yield conflicting results depending on the environmental context, spatiotemporal scale, and the predator and prey species considered. Thus, the accuracy of predicted changes in interaction strength, and their importance to the broader ecosystems they take place in, remain unclear. Here, we attempted to link one such set of predictions generated using theory, modeling, and controlled experiments to patterns in the natural abundance of prey across a broad thermal gradient. To do so, we first predicted how warming would impact a stage-structured predator-prey interaction in riverine rock pools between Pantala spp. dragonfly nymph predators and Aedes atropalpus mosquito larval prey. We then described temperature variation across a set of hundreds of riverine rock pools (n = 775) and leveraged this natural gradient to look for evidence for or against our model's predictions. Our model's predictions suggested that warming should weaken predator control of mosquito larval prey by accelerating their development and shrinking the window of time during which aquatic dragonfly nymphs could consume them. This was consistent with data collected in rock pool ecosystems, where the negative effects of dragonfly nymph predators on mosquito larval abundance were weaker in warmer pools. Our findings provide additional evidence to substantiate our model-derived predictions while emphasizing the importance of assessing similar predictions using natural gradients of temperature whenever possible.

Spatial distribution of damage affects the healing, growth, and morphology of coral.

Many predators and herbivores do not kill their prey, but rather remove or damage tissue. Prey are often able to heal or regenerate this lost tissue. If the prey are modular organisms (e.g., some plants and cnidarians), regeneration is frequently influenced by other modules interconnected to damaged ones. For example, many coral predators remove tissue from colonies consisting of many polyps, and these polyps often share resources with their neighbors. Thus, the distribution of tissue loss on a coral colony could affect the coral's response. I hypothesized that spatially aggregated damage might be slow to heal due to competing demands on nearby polyps. To explore the spatial patterns of corallivory and their implications, I conducted: (1) field surveys documenting the spatial distribution of lesions on corals; (2) field experiments testing the effect of the distance between lesions on coral tissue healing, skeletal growth, and morphology; and (3) field surveys relating corallivore presence to coral growth and morphology. In the field surveys, lesions were aggregated at multiple spatial scales, and most lesions had other lesions within 2 cm. When lesions were near one another, coral tissue regeneration was depressed, although there was no effect on whole colony growth. After a year, however, linear extension was lower in the neighborhood of the lesions. Additionally, gastropod corallivores (Coralliophila violacea) with low movement decreased coral growth and increased coral topographical complexity. These results suggest that corallivores that create clusters of coral damage have a greater effect on coral growth and recovery from damage than corallivores that spread damage throughout the colony.

Top-down pulses reduce prey population sizes and persistence.

Resource pulses are well documented and have important consequences for population dynamics relative to continuous inputs. However, pulses of top-down factors (e.g. predation) are less explored and appreciated in the ecological literature. Here, we use a simple differential equation population model to show how pulsed removals of individuals from a population alter population size relative to continuous dynamics. Pulsed removals result in lower equilibrium population sizes relative to continuous removals, and the differences are greatest at low population growth rates, high removal rates, and with large, infrequent pulses. Furthermore, the timing of the removal pulses (either stochastic or cyclic) affects population size. For example, cyclic removals are less likely than stochastic removals to result in population eradication, but when eradication occurs, the time until eradication is shorter for cyclic than with stochastic removals.

Optimal sampling strategies for detecting zoonotic disease epidemics.

The early detection of disease epidemics reduces the chance of successful introductions into new locales, minimizes the number of infections, and reduces the financial impact. We develop a framework to determine the optimal sampling strategy for disease detection in zoonotic host-vector epidemiological systems when a disease goes from below detectable levels to an epidemic. We find that if the time of disease introduction is known then the optimal sampling strategy can switch abruptly between sampling only from the vector population to sampling only from the host population. We also construct time-independent optimal sampling strategies when conducting periodic sampling that can involve sampling both the host and the vector populations simultaneously. Both time-dependent and -independent solutions can be useful for sampling design, depending on whether the time of introduction of the disease is known or not. We illustrate the approach with West Nile virus, a globally-spreading zoonotic arbovirus. Though our analytical results are based on a linearization of the dynamical systems, the sampling rules appear robust over a wide range of parameter space when compared to nonlinear simulation models. Our results suggest some simple rules that can be used by practitioners when developing surveillance programs. These rules require knowledge of transition rates between epidemiological compartments, which population was initially infected, and of the cost per sample for serological tests.