A healthy but depleted herd: Predators decrease prey disease and density.

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.

Exploring how ecological and epidemiological processes shape multi-host disease dynamics using global sensitivity analysis.

We use global sensitivity analysis (specifically, Partial Rank Correlation Coefficients) to explore the roles of ecological and epidemiological processes in shaping the temporal dynamics of a parameterized SIR-type model of two host species and an environmentally transmitted pathogen. We compute the sensitivities of disease prevalence in each host species to model parameters. Sensitivity rankings are calculated, interpreted biologically, and contrasted for cases where the pathogen is introduced into a disease-free community and cases where a second host species is introduced into an endemic single-host community.

Exploring How a Generalist Pathogen and Within-Host Priority Effects Alter the Risk of Being Infected by a Specialist Pathogen.

AbstractIn multihost-multipathogen communities, a focal host's risk of being infected by a particular pathogen can be influenced by the presence of other host and pathogen species. We explore how indirect interactions between pathogens at the within-host level (through coinfecting the same individual) and the between-host level (through altered susceptible host densities) affect the focal host's risk of infection. We use an SI-type epidemiological model of two host species and two environmentally transmitted pathogens where one pathogen is a specialist on the focal host and the other pathogen is a generalist.

The Context-Dependent Effects of Host Competence, Competition, and Pathogen Transmission Mode on Disease Prevalence.

AbstractBiodiversity in communities is changing globally, including the gain and loss of host species in host-pathogen communities. Increased host diversity can cause infection prevalence in a focal host to increase (amplification) or decrease (dilution). However, it is unclear what general rules govern the context-dependent effects, in part because theories for pathogens with different transmission modes have developed largely independently.

Dose relationships can exacerbate, mute, or reverse the impact of heterospecific host density on infection prevalence.

The likelihood an individual becomes infected depends on the community in which it is embedded. For environmentally transmitted parasites, host community composition can alter host density, the density of parasites that hosts encounter in the environment, and the dose to which hosts are subsequently exposed. While some multi-host theory incorporates some of these factors (e.

Using sensitivity analysis to identify factors promoting higher versus lower infection prevalence in multi-host communities.

Relationships between host species richness and levels of disease in a focal host are likely to be context-dependent, depending on the characteristics of which particular host species are present in a community. I use a multi-host epidemiological model with environmental transmission to explore how the characteristics of the host species (e.g.

Evolutionary and Plastic Phenotypic Change Can Be Just as Fast as Changes in Population Densities.

AbstractEvolution and plasticity can drive population-level phenotypic change (e.g., changes in the mean phenotype) on timescales comparable to changes in population densities.

Comparing the Indirect Effects between Exploiters in Predator-Prey and Host-Pathogen Systems.

AbstractIn multipredator and multipathogen systems, exploiters interact indirectly via shared victim species. Interspecific prey competition and the degree of predator specialization are known to influence whether predators have competitive (i.e.

When to be temperate: on the fitness benefits of lysis vs. lysogeny.

Bacterial viruses, that is 'bacteriophage' or 'phage', can infect and lyse their bacterial hosts, releasing new viral progeny. In addition to the lytic pathway, certain bacteriophage (i.e.

Destabilizing evolutionary and eco-evolutionary feedbacks drive empirical eco-evolutionary cycles.

We develop a method to identify how ecological, evolutionary, and eco-evolutionary feedbacks influence system stability. We apply our method to nine empirically parametrized eco-evolutionary models of exploiter-victim systems from the literature and identify which particular feedbacks cause some systems to converge to a steady state or to exhibit sustained oscillations. We find that ecological feedbacks involving the interactions between all species and evolutionary and eco-evolutionary feedbacks involving only the interactions between exploiter species (predators or pathogens) are typically stabilizing.

How (co)evolution alters predator responses to increased mortality: extinction thresholds and hydra effects.

Population responses to environmental change depend on both the ecological interactions between species and the evolutionary responses of all species. In this study, we explore how evolution in prey, predators, or both species affect the responses of predator populations to a sustained increase in mortality. We use an eco-evolutionary predator-prey model to explore how evolution alters the predator extinction threshold (defined as the minimum mortality rate that prevents population growth at low predator densities) and predator hydra effects (increased predator abundance in response to increased mortality).

Viral invasion fitness across a continuum from lysis to latency.

The prevailing paradigm in ecological studies of viruses and their microbial hosts is that the reproductive success of viruses depends on the proliferation of the 'predator', that is, the virus particle. Yet, viruses are obligate intracellular parasites, and the virus genome-the actual unit of selection-can persist and proliferate from one cell generation to the next without lysis or the production of new virus particles. Here, we propose a theoretical framework to quantify the invasion fitness of viruses using an epidemiological cell-centric metric that focuses on the proliferation of viral genomes inside cells instead of virus particles outside cells.

The Effects of Predator Evolution and Genetic Variation on Predator-Prey Population-Level Dynamics.

This paper explores how predator evolution and the magnitude of predator genetic variation alter the population-level dynamics of predator-prey systems. We do this by analyzing a general eco-evolutionary predator-prey model using four methods: Method 1 identifies how eco-evolutionary feedbacks alter system stability in the fast and slow evolution limits; Method 2 identifies how the amount of standing predator genetic variation alters system stability; Method 3 identifies how the phase lags in predator-prey cycles depend on the amount of genetic variation; and Method 4 determines conditions for different cycle shapes in the fast and slow evolution limits using geometric singular perturbation theory. With these four methods, we identify the conditions under which predator evolution alters system stability and shapes of predator-prey cycles, and how those effect depend on the amount of genetic variation in the predator population.

Predator-Prey Coevolution Drives Productivity-Richness Relationships in Planktonic Systems.

The relationship between environmental productivity and species richness often varies among empirical studies, and despite much research, simple explanations for this phenomenon remain elusive. We investigated how phytoplankton and zooplankton coevolution shapes productivity-richness relationships in both phytoplankton and zooplankton, using a simple nutrient-phytoplankton-zooplankton model that incorporates size-dependent metabolic rates summarized from empirical studies. The model allowed comparisons of evolved species richness across productivity levels and at different evolutionary times.

Population Density, Not Host Competence, Drives Patterns of Disease in an Invaded Community.

Generalist parasites can strongly influence interactions between native and invasive species. Host competence can be used to predict how an invasive species will affect community disease dynamics; the addition of a highly competent, invasive host is predicted to increase disease. However, densities of invasive and native species can also influence the impacts of invasive species on community disease dynamics.

Hydra effects in discrete-time models of stable communities.

A species exhibits a hydra effect when, counter-intuitively, increased mortality of the species causes an increase in its abundance. Hydra effects have been studied in many continuous time (differential equation) multispecies models, but only rarely have hydra effects been observed in or studied with discrete time (difference equation) multispecies models. In addition most discrete time theory focuses on single-species models.

How the Magnitude of Prey Genetic Variation Alters Predator-Prey Eco-Evolutionary Dynamics.

Evolution can alter the stability and dynamics of ecological communities; for example, prey evolution can drive cyclic dynamics in predator-prey systems that are not possible in the absence of evolution. However, it is unclear how the magnitude of additive genetic variation in the evolving species mediates those effects. In this study, I explore how the magnitude of prey additive genetic variation determines what effects prey evolution has on the dynamics and stability of predator-prey systems.

Hydra effects in stable communities and their implications for system dynamics.

A hydra effect occurs when the mean density of a species increases in response to greater mortality. We show that, in a stable multispecies system, a species exhibits a hydra effect only if maintaining that species at its equilibrium density destabilizes the system. The stability of the original system is due to the responses of the hydra-effect species to changes in the other species' densities.

Multiple regimes of robust patterns between network structure and biodiversity.

Ecological networks such as plant-pollinator and host-parasite networks have structured interactions that define who interacts with whom. The structure of interactions also shapes ecological and evolutionary dynamics. Yet, there is significant ongoing debate as to whether certain structures, e.

Is competition needed for ecological character displacement? Does displacement decrease competition?

Interspecific competition for resources is generally considered to be the selective force driving ecological character displacement, and displacement is assumed to reduce competition. Skeptics of the prevalence of character displacement often cite lack of evidence of competition. The present article uses a simple model to examine whether competition is needed for character displacement and whether displacement reduces competition.

Coevolution can reverse predator-prey cycles.

A hallmark of Lotka-Volterra models, and other ecological models of predator-prey interactions, is that in predator-prey cycles, peaks in prey abundance precede peaks in predator abundance. Such models typically assume that species life history traits are fixed over ecologically relevant time scales. However, the coevolution of predator and prey traits has been shown to alter the community dynamics of natural systems, leading to novel dynamics including antiphase and cryptic cycles.

The virus of my virus is my friend: ecological effects of virophage with alternative modes of coinfection.

Virophages are viruses that rely on the replication machinery of other viruses to reproduce within eukaryotic hosts. Two different modes of coinfection have been posited based on experimental observation. In one mode, the virophage and the virus enter the host independently.

Mechanisms of multi-strain coexistence in host-phage systems with nested infection networks.

Bacteria and their viruses (bacteriophages) coexist in natural environments forming complex infection networks. Recent empirical findings suggest that phage-bacteria infection networks often possess a nested structure such that there is a hierarchical relationship among who can infect whom. Here we consider how nested infection networks may affect phage and bacteria dynamics using a multi-type Lotka-Volterra framework with cross-infection.

Distinguishing between indirect and direct modes of transmission using epidemiological time series.

Pathogen transmission can involve direct and/or indirect pathways. Using theoretical models, in this study we ask, "do directly and indirectly transmitted pathogens yield different population-level epidemiological dynamics?" and "can the transmission pathway be inferred from population-level epidemiological data?" Our approach involves comparing the continuous-time dynamics of a class of compartmental epidemiological models with direct versus environmentally mediated indirect transmission pathways. Combing analytical theory and numerical simulations we show that models with direct and indirect transmission can produce quantitatively similar time series when the pathogen cannot reproduce in the environment, particularly when the environmental pathogen dynamics are fast.