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Interactions between plants and herbivores are central in most ecosystems, but their strength is highly variable. The amount of variability within a system is thought to influence most aspects of plant-herbivore biology, from ecological stability to plant defense evolution. Our understanding of what influences variability, however, is limited by sparse data. We collected standardized surveys of herbivory for 503 plant species at 790 sites across 116° of latitude. With these data, we show that within-population variability in herbivory increases with latitude, decreases with plant size, and is phylogenetically structured. Differences in the magnitude of variability are thus central to how plant-herbivore biology varies across macroscale gradients. We argue that increased focus on interaction variability will advance understanding of patterns of life on Earth.

Disease ecologists now recognize the limitation behind examining host-parasite interactions in isolation: community members-especially predators-dramatically affect host-parasite dynamics. Although the initial paradigm was that predation should reduce disease in prey populations ("healthy herds hypothesis"), researchers have realized that predators sometimes increase disease in their prey. These "predator-spreaders" are now recognized as critical to disease dynamics, but empirical research on the topic remains fragmented. In a narrow sense, a "predator-spreader" would be defined as a predator that mechanically spreads parasites via feeding. However, predators affect their prey and, subsequently, disease transmission in many other ways such as altering prey population structure, behavior, and physiology. We review the existing evidence for these mechanisms and provide heuristics that incorporate features of the host, predator, parasite, and environment to understand whether or not a predator is likely to be a predator-spreader. We also provide guidance for targeted study of each mechanism and quantifying the effects of predators on parasitism in a way that yields more general insights into the factors that promote predator spreading. We aim to offer a better understanding of this important and underappreciated interaction and a path toward being able to predict how changes in predation will influence parasite dynamics., (© 2023 The Authors. Ecology and Evolution published by John Wiley & Sons Ltd.)

Cannibalism, while prevalent in the natural world, is often viewed as detrimental to a cannibal's health, especially when they consume pathogen-infected conspecifics. The argument stems from the idea that cannibalizing infected individuals increases the chance of coming into contact with a pathogen and subsequently becoming infected. Using an insect pest, the fall armyworm (Spodoptera frugiperda), that readily cannibalizes at the larval stage and its lethal pathogen, we experimentally examined how cannibalism affects viral transmission at both an individual and population level. Prior to death, the pathogen in the system stops the larval host from growing, resulting in infected individuals being smaller than healthy individuals. This leads to size-structured cannibalism of infected individuals with the larger healthy larvae consuming the smaller infected larvae, which is commonly observed. At the individual level, we show that the probability of cannibalism is relatively high for both infected and uninfected individuals especially when the cannibal is larger than the victim. However, the probability of the cannibal becoming infected given that a pathogen-infected individual has been cannibalized is relatively low. On a population level, when cannibalism is allowed to occur transmission rates decline. Additionally, by cannibalizing infected larvae, cannibals lower the infection risk for non-cannibals. Thus, cannibalism can decrease infection prevalence and, therefore, may not be as deleterious as once thought. Under certain circumstances, cannibalizing infected individuals, from the uninfected host's perspective, may even be advantageous, as one obtains a meal and decreases competition for resources with little chance of becoming infected., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Objective: More similar locations may have similar infectious disease dynamics. There is clear overlap in putative causes for epidemic similarity, such as geographic distance, age structure, and population size. We compare the effects of these potential drivers on epidemic similarity compared to a baseline assumption that differences in the basic reproductive number ( R 0 ) will translate to differences in epidemic trajectories., Methods: Using COVID-19 case counts from United States counties, we explore the importance of geographic distance, population size differences, and age structure dissimilarity on resulting epidemic similarity., Results: We find clear effects of geographic space, age structure, population size, and R 0 on epidemic similarity, but notably the effect of age structure was stronger than the baseline assumption that differences in R 0 would be most related to epidemic similarity., Conclusions: Together, this highlights the role of spatial and demographic processes on SARS-CoV2 epidemics in the United States., Competing Interests: The authors have no conflicts of interest to declare., (© 2022 The Authors.)

The large spatial scale, geographical overlap, and similarities in transmission mode between the 1918 H1N1 influenza and 2020 SARS-CoV-2 pandemics together provide a novel opportunity to investigate relationships between transmission of two different diseases in the same location. To this end, we use initial exponential growth rates in a Bayesian hierarchical framework to estimate the basic reproductive number, R 0 , of both disease outbreaks in a common set of 43 cities in the United States. By leveraging multiple epidemic time series across a large spatial area, we are able to better characterize the variation in R 0 across the United States. Additionally, we provide one of the first city-level comparisons of R 0 between these two pandemics and explore how demography and outbreak timing are related to R 0 . Despite similarities in transmission modes and a common set of locations, R 0 estimates for COVID-19 were uncorrelated with estimates of pandemic influenza R 0 in the same cities. Also, the relationships between R 0 and key population or epidemic traits differed between diseases. For example, epidemics that started later tended to be less severe for COVID-19, while influenza epidemics exhibited an opposite pattern. Our results suggest that despite similarities between diseases, epidemics starting in the same location may differ markedly in their initial progression., (© The Author(s) 2022. Published by Oxford University Press on behalf of National Academy of Sciences.)

AbstractOver the past few decades, it has become clear that ecological and evolutionary dynamics are influenced by processes operating across spatial and temporal scales. Processes that operate on small spatial scales have the potential to influence dynamics at much larger scales; for example, a change in the physiology of a primary producer can alter primary productivity in an ecosystem. Similarly, evolution-a process that historically was thought of as occurring at longer timescales-can influence ecological dynamics and vice versa. The importance of considering multiple scales is broadly true in ecology and evolution, and it is especially important for studies of disease ecology and evolution. Yet characterizing the scales at which individual studies operate is surprisingly challenging, as we (re)discovered while trying to characterize articles published in this journal over the past three decades. However, while it is difficult to determine where one scale ends and another begins, it is also clear that work that spans across a spectrum can yield insights that could not be gleaned from a narrower focus. To demonstrate this, we highlight studies previously published in this journal that show the value of working across scales. We then introduce the six articles that comprise this Focused Topic section. Together, these articles present systems, theory, and methods that provide important insights that could not have been obtained from studying a single scale in isolation.

Plant vascular systems can translocate the entomopathogen Bacillus thuringiensis from the soil into plant tissues. However, whether other soil dwelling entomopathogens utilize plant vascular tissue for movement has not yet been fully explored. We used Spodoptera frugiperda multiple nucleopolyhedrovirus (SfMNPV) to evaluate whether baculoviruses, a common entomopathogen and bioinsecticide, can be transported through the plant vascular pathways of Zea mays . We found that our treatments did not allow a sufficient virus translocation into the plant to induce a lethal infection in insects, which was confirmed by a molecular analysis. While other entomopathogens translocate, baculoviruses may not be one of them.

As an essential micronutrient for many organisms, sodium plays an important role in ecological and evolutionary dynamics. Although plants mediate trophic fluxes of sodium, from substrates to higher trophic levels, relatively little comparative research has been published about plant growth and sodium accumulation in response to variation in substrate sodium. Accordingly, we carried out a systematic review of plants' responses to variation in substrate sodium concentrations.We compared biomass and tissue-sodium accumulation among 107 cultivars or populations (67 species in 20 plant families), broadly expanding beyond the agricultural and model taxa for which several generalizations previously had been made. We hypothesized a priori response models for each population's growth and sodium accumulation as a function of increasing substrate NaCl and used Bayesian Information Criterion to choose the best model. Additionally, using a phylogenetic signal analysis, we tested for phylogenetic patterning of responses across taxa.The influence of substrate sodium on growth differed across taxa, with most populations experiencing detrimental effects at high concentrations. Irrespective of growth responses, tissue sodium concentrations for most taxa increased as sodium concentration in the substrate increased. We found no strong associations between the type of growth response and the type of sodium accumulation response across taxa. Although experiments often fail to test plants across a sufficiently broad range of substrate salinities, non-crop species tended toward higher sodium tolerance than domesticated species. Moreover, some phylogenetic conservatism was apparent, in that evolutionary history helped predict the distribution of total-plant growth responses across the phylogeny, but not sodium accumulation responses.Our study reveals that saltier plants in saltier soils proves to be a broadly general pattern for sodium across plant taxa. Regardless of growth responses, sodium accumulation mostly followed an increasing trend as substrate sodium levels increased., Competing Interests: The authors have no competing interest to declare., (© 2021 The Authors. Ecology and Evolution published by John Wiley & Sons Ltd.)

Autographa californica Multiple Nucleopolyhedrovirus (AcMNPV) is a baculovirus that causes systemic infections in many arthropod pests. The specific molecular processes underlying the biocidal activity of AcMNPV on its insect hosts are largely unknown. We describe the transcriptional responses in two major pests, Spodoptera frugiperda (fall armyworm) and Trichoplusia ni (cabbage looper), to determine the host-pathogen responses during systemic infection, concurrently with the viral response to the host. We assembled species-specific transcriptomes of the hemolymph to identify host transcriptional responses during systemic infection and assessed the viral transcript abundance in infected hemolymph from both species. We found transcriptional suppression of chitin metabolism and tracheal development in infected hosts. Synergistic transcriptional support was observed to suggest suppression of immune responses and induction of oxidative stress indicating disease progression in the host. The entire AcMNPV core genome was expressed in the infected host hemolymph with a proportional high abundance detected for viral transcripts associated with replication, structure, and movement. Interestingly, several of the host genes that were targeted by AcMNPV as revealed by our study are also targets of chemical insecticides currently used commercially to control arthropod pests. Our results reveal an extensive overlap between biological processes represented by transcriptional responses in both hosts, as well as convergence on highly abundant viral genes expressed in the two hosts, providing an overview of the host-pathogen transcriptomic landscape during systemic infection.

Predators and pathogens often regulate the population dynamics of their prey or hosts. When species interact with both their predators and their pathogens, understanding each interaction in isolation may not capture the system's dynamics. For instance, predators can influence pathogen transmission via consumptive effects, such as feeding on infected prey, or non-consumptive effects, such as changing the prey's susceptibility to infection. A prey species' infection status can, in turn, influence predator's choice of prey and have negative fitness consequences for the predator. To test how intraguild predation (IGP), when predator and pathogen share the same prey/host, affects pathogen transmission, predator preference, and predator fitness, we conducted a series of experiments using a crop pest (Pseudoplusia includens), a generalist predator (Podisus maculiventris), and a generalist pathogen (Autographa californica multicapsid nuclear polyhedrovirus, AcMNPV). Using a field experiment, we quantified the effects of consumptive and non-consumptive predators on pathogen transmission. We found that a number of models provided similar fits to the data. These models included null models showing no effects of predation and models that included a predation effect. We also found that predators consumed infected prey more often when choosing between live infected or live healthy prey. Infected prey also reduced predator fitness. Developmental times of predators fed infected prey increased by 20% and longevity decreased by 45%, compared with those that consumed an equivalent number of non-infected prey. While this research shows an effect of the pathogen on intraguild predator fitness, we found no support that predators affected pathogen transmission.

The commonly observed negative correlation between the number of species in an ecological community and disease risk, typically referred to as "the dilution effect", has received a substantial amount of attention over the past decade. Attempts to test this relationship experimentally have revealed that, in addition to the mean disease risk decreasing with species number, so too does the variance of disease risk. This is referred to as the "variance reduction effect", and has received relatively little attention in the disease-diversity literature. Here, we set out to clarify and quantify some of these relationships in an idealized model of a randomly assembled multi-species community undergoing an epidemic. We specifically investigate the variance of the community disease reproductive ratio, a multi-species extension of the basic reproductive ratio [Formula: see text], for a family of random-parameter community SIR models, and show how the variance of community [Formula: see text] varies depending on whether transmission is density or frequency-dependent. We finally outline areas of further research on how changes in variance affect transmission dynamics in other systems.

When plants establish outside their native range, their ability to adapt to the new environment is influenced by both demography and dispersal. However, the relative importance of these two factors is poorly understood. To quantify the influence of demography and dispersal on patterns of genetic diversity underlying adaptation, we used data from a globally distributed demographic research network comprising 35 native and 18 nonnative populations of Plantago lanceolata Species-specific simulation experiments showed that dispersal would dilute demographic influences on genetic diversity at local scales. Populations in the native European range had strong spatial genetic structure associated with geographic distance and precipitation seasonality. In contrast, nonnative populations had weaker spatial genetic structure that was not associated with environmental gradients but with higher within-population genetic diversity. Our findings show that dispersal caused by repeated, long-distance, human-mediated introductions has allowed invasive plant populations to overcome environmental constraints on genetic diversity, even without strong demographic changes. The impact of invasive plants may, therefore, increase with repeated introductions, highlighting the need to constrain future introductions of species even if they already exist in an area., Competing Interests: The authors declare no competing interest., (Copyright © 2020 the Author(s). Published by PNAS.)

The virulence-transmission trade-off hypothesis proposed more than 30 years ago is the cornerstone in the study of host-parasite co-evolution. This hypothesis rests on the premise that virulence is an unavoidable and increasing cost because the parasite uses host resources to replicate. This cost associated with replication ultimately results in a deceleration in transmission rate because increasing within-host replication increases host mortality. Empirical tests of predictions of the hypothesis have found mixed support, which cast doubt about its overall generalizability. To quantitatively address this issue, we conducted a meta-analysis of 29 empirical studies, after reviewing over 6000 published papers, addressing the four core relationships between (1) virulence and recovery rate, (2) within-host replication rate and virulence, (3) within-host replication and transmission rate, and (4) virulence and transmission rate. We found strong support for an increasing relationship between replication and virulence, and replication and transmission. Yet, it is still uncertain if these relationships generally decelerate due to high within-study variability. There was insufficient data to quantitatively test the other two core relationships predicted by the theory. Overall, the results suggest that the current empirical evidence provides partial support for the trade-off hypothesis, but more work remains to be done., (© 2019 The Author(s). Evolution © 2019 The Society for the Study of Evolution.)

A plant's induction of secondary defenses helps to decrease herbivore damage by changing resource quality. While these chemical or physical defenses may directly decrease herbivory, they can also have indirect consequences. In a tritrophic system consisting of a plant, an insect herbivore, and an insect pathogen, plant based trait-mediated indirect effects (TMIEs) can alter host-pathogen interactions and, thereby, indirectly affect disease transmission. In a series of field experiments, individual soybean plants (Glycine max) were sprayed with either a jasmonic acid (JA) solution to trigger induction of plant defenses or a similar control compound. Fall armyworm (Spodoptera frugiperda) larvae along with varying amounts of a lethal baculovirus were placed on the plants to measure transmission. Induction of plant defenses decreased viral transmission due to increased population heterogeneity arising from changes in individual susceptibility. The change in susceptibility via TMIEs was driven by a decrease in feeding rates and an increase viral dose needed to infect larvae. While the induction against herbivore attack may decrease herbivory, it can also decrease the efficacy of the herbivore's pathogen potentially to the plant's detriment. While TMIEs have been well-recognized for being driven by top-down forces, bottom-up interactions can dictate community dynamics and, here, epizootic severity., (© 2018 by the Ecological Society of America.)

While it is well established that climate change affects species distributions and abundances, the impacts of climate change on species interactions has not been extensively studied. This is particularly important for specialists whose interactions are tightly linked, such as between the monarch butterfly (Danaus plexippus) and the plant genus Asclepias, on which it depends. We used open-top chambers (OTCs) to increase temperatures in experimental plots and placed either nonnative Asclepias curassavica or native A. incarnata in each plot along with monarch larvae. We found, under current climatic conditions, adult monarchs had higher survival and mass when feeding on A. curassavica. However, under future conditions, monarchs fared much worse on A. curassavica. The decrease in adult survival and mass was associated with increasing cardenolide concentrations under warmer temperatures. Increased temperatures alone reduced monarch forewing length. Cardenolide concentrations in A. curassavica may have transitioned from beneficial to detrimental as temperature increased. Thus, the increasing cardenolide concentrations may have pushed the larvae over a tipping point into an ecological trap; whereby past environmental cues associated with increased fitness give misleading information. Given the ubiquity of specialist plant-herbivore interactions, the potential for such ecological traps to emerge as temperatures increase may have far-reaching consequences., (© 2018 by the Ecological Society of America.)

Spatial patterning is a key natural history attribute of sessile organisms that frequently emerges from and dictates potential for interactions among organisms. We tested whether bunchgrasses, the dominant plant functional group in longleaf pine savanna groundcover communities, are nonrandomly patterned by characterizing the spatial dispersion of three bunchgrass species across six sites in Louisiana and Florida. We mapped bunchgrass tussocks of >5.0 cm basal diameter in three [Formula: see text] plots at each site. We modeled tussocks as two-dimensional objects to analyze their spatial relationships while preserving sizes and shapes of individual tussocks. Tussocks were overdispersed (more regularly spaced than random) for all species and sites at the local interaction scale (<0.3 m). This general pattern likely arises from a tussock-centered, distance-dependent mechanism, for example, intertussock competition. Nonrandom spatial patterns of dominant species have implications for community assembly and ecosystem function in tussock-dominated grasslands and savannas, including those characterized by extreme biodiversity.

The appendix has been hypothesized to protect the colon against Clostridium difficile infection (CDI) by providing a continuous source of commensal bacteria that crowd out the potentially unhealthy bacteria and/or by contributing to defensive immune dynamics. Here, a series of deterministic systems comprised of ordinary differential equations, which treat the system as an ecological community of microorganisms, model the dynamics of colon microbiome. The first model includes migration of commensal bacteria from the appendix to the gut, while the second model expands this to also include immune dynamics. Simulations and simple analytic techniques are used to explore dynamics under biologically relevant parameters values. Both models exhibited bistability with steady states of a healthy state and of fulminant CDI. However, we find that the appendix size was much too small for migration to affect the stability of the system. Both models affirm the use of fecal transplants in conjunction with antibiotic use for CDI treatment, while the second model also suggests that anti-inflammatory drugs may protect against CDI. Ultimately, in general neither the appendiceal migration rate of commensal microbiota nor the boost to antibody production could exert an appreciable impact on the stability of the system, thus failing to support the proposed protective role of the appendix against CDI., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Plant-mediated variations in the outcomes of host-pathogen interactions can strongly affect epizootics and the population dynamics of numerous species, including devastating agricultural pests such as the fall armyworm. Most studies of plant-mediated effects on insect pathogens focus on host mortality, but few have measured pathogen yield, which can affect whether or not an epizootic outbreak occurs. Insects challenged with baculoviruses on different plant species and parts can vary in levels of mortality and yield of infectious stages (occlusion bodies; OBs). We previously demonstrated that soybean genotypes and induced anti-herbivore defenses influence baculovirus infectivity. Here, we used a soybean genotype that strongly reduced baculovirus infectivity when virus was ingested on induced plants (Braxton) and another that did not reduce infectivity (Gasoy), to determine how soybean genotype and induced defenses influence OB yield and speed of kill. These are key fitness measures because baculoviruses are obligate-killing pathogens. We challenged fall armyworm, Spodoptera frugiperda, with the baculovirus S. frugiperda multi-nucleocapsid nucleopolyhedrovirus (SfMNPV) during short or long-term exposure to plant treatments (i.e., induced or non-induced genotypes). Caterpillars were either fed plant treatments only during virus ingestion (short-term exposure to foliage) or from the point of virus ingestion until death (long-term exposure). We found trade-offs of increasing OB yield with slower speed of kill and decreasing virus dose. OB yield increased more with longer time to death and decreased more with increasing virus dose after short-term feeding on Braxton compared with Gasoy. OB yield increased significantly more with time to death in larvae that fed until death on non-induced foliage than induced foliage. Moreover, fewer OBs per unit of host tissue were produced when larvae were fed induced foliage than non-induced foliage. These findings highlight the potential importance of plant effects, even at the individual plant level, on entomopathogen fitness, which may impact epizootic transmission events and host population dynamics., (Copyright © 2017 Elsevier Inc. All rights reserved.)

Cannibalism occurs in a majority of both carnivorous and noncarnivorous animal taxa from invertebrates to mammals. Similarly, infectious parasites are ubiquitous in nature. Thus, interactions between cannibalism and disease occur regularly. While some adaptive benefits of cannibalism are clear, the prevailing view is that the risk of parasite transmission due to cannibalism would increase disease spread and, thus, limit the evolutionary extent of cannibalism throughout the animal kingdom. In contrast, surprisingly little attention has been paid to the other half of the interaction between cannibalism and disease, that is, how cannibalism affects parasites. Here we examine the interaction between cannibalism and parasites and show how advances across independent lines of research suggest that cannibalism can also reduce the prevalence of parasites and, thus, infection risk for cannibals. Cannibalism does this by both directly killing parasites in infected victims and by reducing the number of susceptible hosts, often enhanced by the stage-structured nature of cannibalism and infection. While the well-established view that disease should limit cannibalism has held sway, we present theory and examples from a synthesis of the literature showing how cannibalism may also limit disease and highlight key areas where conceptual and empirical work is needed to resolve this debate.

Population cycling is a widespread phenomenon, observed across a multitude of taxa in both laboratory and natural conditions. Historically, the theory associated with population cycles was tightly linked to pairwise consumer-resource interactions and studied via deterministic models, but current empirical and theoretical research reveals a much richer basis for ecological cycles. Stochasticity and seasonality can modulate or create cyclic behaviour in non-intuitive ways, the high-dimensionality in ecological systems can profoundly influence cycling, and so can demographic structure and eco-evolutionary dynamics. An inclusive theory for population cycles, ranging from ecosystem-level to demographic modelling, grounded in observational or experimental data, is therefore necessary to better understand observed cyclical patterns. In turn, by gaining better insight into the drivers of population cycles, we can begin to understand the causes of cycle gain and loss, how biodiversity interacts with population cycling, and how to effectively manage wildly fluctuating populations, all of which are growing domains of ecological research., (© 2017 John Wiley & Sons Ltd/CNRS.)

While rising global temperatures are increasingly affecting both species and their biotic interactions, the debate about whether global warming will increase or decrease disease transmission between individuals remains far from resolved. This may stem from the lack of empirical data. Using a tractable and easily manipulated insect host-pathogen system, we conducted a series of field and laboratory experiments to examine how increased temperatures affect disease transmission using the crop-defoliating pest, the fall armyworm (Spodoptera frugiperda) and its species-specific baculovirus, which causes a fatal infection. To examine the effects of temperature on disease transmission in the field, we manipulated baculovirus density and temperature. As infection occurs when a host consumes leaf tissue on which the pathogen resides, baculovirus density was controlled by placing varying numbers of infected neonate larvae on experimental plants. Temperature was manipulated by using open-top chambers (OTCs). The laboratory experiments examined how increased temperatures affect fall armyworm feeding and development rates, which provide insight into how host feeding behaviour and physiology may affect transmission. Disease transmission and outbreak intensity, measured as the cumulative fraction infected during an epizootic, increased at higher temperatures. However, there was no appreciable change in the mean transmission rate of the disease, which is often the focus of empirical and theoretical research. Instead, the coefficient of variation (CV) associated with the transmission rate shrunk. As the CV decreased, heterogeneity in disease risk across individuals declined, which resulted in an increase in outbreak intensity. In the laboratory, increased temperatures increased feeding rates and decreased developmental times. As the host consumes the virus along with the leaf tissue on which it resides, increased feeding rate is likely to increase the probability of an individual consuming virus-infected leaf tissue. On the other hand, decreased developmental time increases the sloughing of midgut cells, which is predicted to hinder viral infection. Increases in outbreak intensity or epizootic severity, as the climate warms, may lead to changes in the long-term dynamics of pests whose populations are strongly affected by host-pathogen interactions. Overall, this work demonstrates that the usual assumptions governing these effects, via changes in the mean transmission rate alone, may not be correct., (© 2013 The Authors. Journal of Animal Ecology © 2013 British Ecological Society.)

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 induced-defense models explain defoliation data no better than natural-enemy 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.

Estimates of a disease's basic reproductive rate R0 play a central role in understanding outbreaks and planning intervention strategies. In many calculations of R0, a simplifying assumption is that different host populations have effectively identical transmission rates. This assumption can lead to an underestimate of the overall uncertainty associated with R0, which, due to the non-linearity of epidemic processes, may result in a mis-estimate of epidemic intensity and miscalculated expenditures associated with public-health interventions. In this paper, we utilize a Bayesian method for quantifying the overall uncertainty arising from differences in population-specific basic reproductive rates. Using this method, we fit spatial and non-spatial susceptible-exposed-infected-recovered (SEIR) models to a series of 13 smallpox outbreaks. Five outbreaks occurred in populations that had been previously exposed to smallpox, while the remaining eight occurred in Native-American populations that were naïve to the disease at the time. The Native-American outbreaks were close in a spatial and temporal sense. Using Bayesian Information Criterion (BIC), we show that the best model includes population-specific R0 values. These differences in R0 values may, in part, be due to differences in genetic background, social structure, or food and water availability. As a result of these inter-population differences, the overall uncertainty associated with the "population average" value of smallpox R0 is larger, a finding that can have important consequences for controlling epidemics. In general, Bayesian hierarchical models are able to properly account for the uncertainty associated with multiple epidemics, provide a clearer understanding of variability in epidemic dynamics, and yield a better assessment of the range of potential risks and consequences that decision makers face., (Copyright © 2013 Elsevier B.V. All rights reserved.)

Classical epidemic theory focuses on directly transmitted pathogens, but many pathogens are instead transmitted when hosts encounter infectious particles. Theory has shown that for such diseases pathogen persistence time in the environment can strongly affect disease dynamics, but estimates of persistence time, and consequently tests of the theory, are extremely rare. We consider the consequences of persistence time for the dynamics of the gypsy moth baculovirus, a pathogen transmitted when larvae consume foliage contaminated with particles released from infectious cadavers. Using field-transmission experiments, we are able to estimate persistence time under natural conditions, and inserting our estimates into a standard epidemic model suggests that epidemics are often terminated by a combination of pupation and burnout rather than by burnout alone, as predicted by theory. Extending our models to allow for multiple generations, and including environmental transmission over the winter, suggests that the virus may survive over the long term even in the absence of complex persistence mechanisms, such as environmental reservoirs or covert infections. Our work suggests that estimates of persistence times can lead to a deeper understanding of environmentally transmitted pathogens and illustrates the usefulness of experiments that are closely tied to mathematical models.

1. Studies of variability in host resistance to disease generally emphasize variability in susceptibility given exposure, neglecting the possibility that hosts may vary in behaviours that affect the risk of exposure. 2. In many insects, horizontal transmission of baculoviruses occurs when larvae consume foliage contaminated by the cadavers of virus-infected conspecific larvae; so, host behaviour may have a strong effect on the risk of infection. 3. We studied variability in the behaviour of gypsy moth (Lymantria dispar) larvae, which are able to detect and avoid virus-contaminated foliage. 4. Our results show that detection ability can be affected by the family line that larvae originate from, even at some distance from a virus-infected cadaver, and suggest that cadaver-detection ability may be heritable. 5. There is thus the potential for natural selection to act on cadaver-detection ability, and thereby to affect the dynamics of pathogen-driven cycles in gypsy moth populations. 6. We argue that host behaviour is a neglected component in studies of variability in disease resistance.

The theory of insect population dynamics has shown that heterogeneity in natural-enemy attack rates is strongly stabilizing. We tested the usefulness of this theory for outbreaking insects, many of which are attacked by infectious pathogens. We measured heterogeneity among gypsy moth larvae in their risk of infection with a nucleopolyhedrovirus, which is effectively heterogeneity in the pathogen's attack rate. Our data show that heterogeneity in infection risk in this insect is so high that it leads to a stable equilibrium in the models, which is inconsistent with the outbreaks seen in North American gypsy moth populations. Our data further suggest that infection risk declines after epidemics, in turn suggesting that the model assumption of constant infection risk is incorrect. We therefore constructed an alternative model in which natural selection drives fluctuations in infection risk, leading to reductions after epidemics because of selection for resistance and increases after epidemics because of a cost of resistance. This model shows cycles even for high heterogeneity, and experiments confirm that infection risk is indeed heritable. The model is very general, and so we argue that natural selection for disease resistance may play a role in many insect outbreaks.

Concerns over bioterrorism and emerging diseases have led to the widespread use of epidemic models for evaluating public health strategies. Partly because epidemic models often capture the dynamics of prior epidemics remarkably well, little attention has been paid to how uncertainty in parameter estimates might affect model predictions. To understand such effects, we used Bayesian statistics to rigorously estimate the uncertainty in the parameters of an epidemic model, focusing on smallpox bioterrorism. We then used a vaccination model to translate the uncertainty in the model parameters into uncertainty in which of two vaccination strategies would provide a better response to bioterrorism, mass vaccination, or vaccination of social contacts, so-called "trace vaccination." Our results show that the uncertainty in the model parameters is remarkably high and that this uncertainty has important implications for vaccination strategies. For example, under one plausible scenario, the most likely outcome is that mass vaccination would save approximately 100,000 more lives than trace vaccination. Because of the high uncertainty in the parameters, however, there is also a substantial probability that mass vaccination would save 200,000 or more lives than trace vaccination. In addition to providing the best response to the most likely outcome, mass vaccination thus has the advantage of preventing outcomes that are only slightly less likely but that are substantially more horrific. Rigorous estimates of uncertainty thus can reveal hidden advantages of public health strategies, suggesting that formal uncertainty estimation should play a key role in planning for epidemics.

Disturbances, such as flooding, play important roles in determining community structure. Most studies of disturbances focus on the direct effects and, hence, the indirect effects of disturbances are poorly understood. Within terrestrial riparian areas, annual flooding leads to differences in the arthropod community as compared to non-flooded areas. In turn, these differences are likely to alter the survival, growth, and reproduction of plant species via an indirect effect of flooding (i.e., changes in herbivory patterns). To test for such effects, an experiment was conducted wherein arthropod predators and herbivores were excluded from plots in flooded and non-flooded areas and the impact on a common riparian plant, Mimulus guttatus was examined. In general, the direct effect of flooding on M. guttatus was positive. The indirect effects, however, significantly decreased plant survival for both years of the experiment, regardless of predator presence, because of an increased exposure to grasshoppers, the most abundant herbivore in the non-flooded sites. Leafhoppers, which were more abundant in the flooded sites, had much weaker and varying effects. During 2000, when the leafhopper herbivory was high, arthropod predators did not significantly reduce damage to plants. In 2001, the mean herbivory damage was lower and predators were able to significantly reduce overall leafhopper damage. The effects of predators on leafhoppers, however, did not increase plant survival, final weight, or the reproduction potential and, thus, did not initiate a species-level trophic cascade. Overall, it was the differences in the herbivore community that led to a significant decrease in plant survival. While flooding certainly alters riparian plant survival through direct abiotic effects, it also indirectly affects riparian plants by changing the arthropod community, in particular herbivores, and hence trophic interactions.