Bats provide important ecosystem services such as pollination of native forests; they are also a source of zoonotic pathogens for humans and domestic animals. Human-induced changes to native habitats may have created more opportunities for bats to reside in urban settings, thus decreasing pollination services to native forests and increasing opportunities for zoonotic transmission. In Australia, fruit bats ( Pteropus spp. flying foxes) are increasingly inhabiting urban areas where they feed on anthropogenic food sources with nutritional characteristics and phenology that differ from native habitats. We use optimal foraging theory to investigate the relationship between bat residence time in a patch, the time it takes to search for a new patch (simulating loss of native habitat) and seasonal resource production. We show that it can be beneficial to reside in a patch, even when food productivity is low, as long as foraging intensity is low and the expected searching time is high. A small increase in the expected patch searching time greatly increases the residence time, suggesting nonlinear associations between patch residence and loss of seasonal native resources. We also found that sudden increases in resource consumption due to an influx of new bats has complex effects on patch departure times that again depend on expected searching times and seasonality. Our results suggest that the increased use of urban landscapes by bats may be a response to new spatial and temporal configurations of foraging opportunities. Given that bats are reservoir hosts of zoonotic diseases, our results provide a framework to study the effects of foraging ecology on disease dynamics. One contribution of 14 to a theme isssue ‘Anthropogenic resource subsidies and host–parasite dynamics in wildlife’.

Modern weed science is at a crossroads. Born out of advances in chemistry, it has focused on minimizing weed competition with genetically uniform crops and heavy reliance on herbicides. Paradoxically, the success obtained with such an approach and the reluctance to conduct integrated and multidisciplinary research has resulted in unintended, but predictable, consequences, including the selection of herbicide resistant biotypes. Advances in eco-evolutionary biology, a relatively recent discipline that seeks to understand how local population dynamics arise from phenotypic variation resulting from natural selection, habitat distribution, and propagule dispersal across the landscape are transforming our understanding of the processes that regulate agroecosystems. Within this framework, complementary tactics to develop alternative weed management programs include the following: (1) weed scientists must recognize that evolution occurs within crop fields at ecologically-relevant time scales and is rooted in the inherent variation that exists in all populations; (2) weed management should recognize that the probability of a resistant mutant is directly related to the population size; (3) farmers need to acknowledge that herbicide resistance transcends any one farm and should coordinate local practices with regional actions; (4) incentives should be developed and implemented to help the adoption of eco-evolutionary management programs; and (5) risk analysis can help incorporate an eco-evolutionary perspective into integrated weed management programs.

Environmental variation has important effects on host–pathogen interactions, affecting large-scale ecological processes such as the severity and frequency of epidemics. However, less is known about how the environment interacts with host immunity to modulate virus fitness within hosts. Here, we studied the interaction between host immune responses and water temperature on the long-term persistence of a model vertebrate virus, infectious hematopoietic necrosis virus (IHNV) in steelhead trout (Oncorhynchus mykiss). We first used cell culture methods to factor out strong host immune responses, allowing us to test the effect of temperature on viral replication. We found that 15 ${}^{\circ }$C water temperature accelerated IHNV replication compared to the colder 10 and 8 ${}^{\circ }$C temperatures. We then conducted in vivo experiments to quantify the effect of 6, 10, and 15 ${}^{\circ }$C water temperatures on IHNV persistence over 8 months. Fish held at 15 and 10 ${}^{\circ }$C were found to have higher prevalence of neutralizing antibodies compared to fish held at 6 ${}^{\circ }$C. We found that IHNV persisted for a shorter time at warmer temperatures and resulted in an overall lower fish mortality compared to colder temperatures. These results support the hypothesis that temperature and host immune responses interact to modulate virus persistence within hosts. When immune responses were minimized (i.e., in vitro) virus replication was higher at warmer temperatures. However, with a full potential for host immune responses (i.e., in vivo experiments) longer virus persistence and higher long-term virulence was favored in colder temperatures. We also found that the viral RNA that persisted at later time points (179 and 270 days post-exposure) was mostly localized in the kidney and spleen tissues. These tissues are composed of hematopoietic cells that are favored targets of the virus. By partitioning the effect of temperature on host and pathogen responses, our results help to better understand environmental drivers of host–pathogen interactions within hosts, providing insights into potential host–pathogen responses to climate change.

The use of viral pathogens to control the population size of pest insects has produced both successful and unsuccessful outcomes. Here, we investigate whether those biocontrol successes and failures can be explained by key ecological and evolutionary processes between hosts and pathogens. Specifically, we examine how heterogeneity in pathogen transmission, ecological and evolutionary tradeoffs, and pathogen diversity affect insect population density and thus successful control. We first review the existing literature and then use numerical simulations of mathematical models to further explore these processes. Our results show that the control of insect densities using viruses depends strongly on the heterogeneity of virus transmission among insects. Overall, increased heterogeneity of transmission reduces the effect of viruses on insect densities and increases the long-term stability of insect populations. Lower equilibrium insect densities occur when transmission is heritable and when there is a tradeoff between mean transmission and insect fecundity compared to when the heterogeneity of transmission arises from non-genetic sources. Thus, the heterogeneity of transmission is a key parameter that regulates the long-term population dynamics of insects and their pathogens. We also show that both heterogeneity of transmission and life-history tradeoffs modulate characteristics of population dynamics such as the frequency and intensity of “boom–bust" population cycles. Furthermore, we show that because of life-history tradeoffs affecting the transmission rate, the use of multiple pathogen strains is more effective than the use of a single strain to control insect densities only when the pathogen strains differ considerably in their transmission characteristics. By quantifying the effects of ecology and evolution on population densities, we are able to offer recommendations to assess the long-term effects of classical biocontrol.

Investment in host defences against pathogens may lead to trade‐offs with host fecundity. When such trade‐offs arise from genetic correlations, rates of phenotypic change by natural selection may be affected. However, genetic correlations between host survival and fecundity are rarely quantified. To understand trade‐offs between immune responses to baculovirus exposure and fecundity in the gypsy moth (Lymantria dispar), we estimated genetic correlations between survival probability and traits related to fecundity, such as pupal weight. In addition, we tested whether different virus isolates have different effects on male and female pupal weight. To estimate genetic correlations, we exposed individuals of known relatedness to a single baculovirus isolate. To then evaluate the effect of virus isolate on pupal weight, we exposed a single gypsy moth strain to 16 baculovirus isolates. We found a negative genetic correlation between survival and pupal weight. In addition, virus exposure caused late‐pupating females to be identical in weight to males, whereas unexposed females were 2–3 times as large as unexposed males. Finally, we found that female pupal weight is a quadratic function of host mortality across virus isolates, which is likely due to trade‐offs and compensatory growth processes acting at high and low mortality levels, respectively. Overall, our results suggest that fecundity costs may strongly affect the response to selection for disease resistance. In nature, baculoviruses contribute to the regulation of gypsy moth outbreaks, as pathogens often do in forest‐defoliating insects. We therefore argue that trade‐offs between host life‐history traits may help explain outbreak dynamics.