How and why parasite virulence (terms in bold font are in the Glossary) evolves are arguably some of the most important questions addressed by evolutionary biologists. The 1990s saw rich and abounding research in this area, mostly based on the 'trade-off hypothesis' (Anderson & May, 1982), which states that virulence is an unavoidable consequence of parasite transmission (see Box 1). In this review, we first briefly outline the seldomdiscussed history of virulence evolution. Then, we expose the current debate in the field, which can be summarized as a challenge to the trade-off hypothesis. Finally, to answer this challenge, we discuss the advances made in the past decade and we argue that, in the light of these advances, we need not abandon the trade-off model. Instead, we argue that these new insights ought to be incorporated into the current theory and we identify promising future directions. A history of virulenceMany, if not most, of the recent theories that attempt to explain how parasites evolve assume that there is a link between virulence and transmission, the so-called 'virulence-transmission trade-off'. However, this idea has become the focus of intense debate. To better understand the issues of current debates in the field, one should be aware that virulence evolution was studied long before the trade-off hypothesis was formulated. Our purpose here is not to present an exhaustive review of the history of the study of infectious diseases but to give a mere glimpse of the richness and originality of this field that has linked many disciplines, from ecology to molecular biology.The notion that virulence is not fixed but evolves can be traced to Pasteur and Koch in the 19th century. AbstractIt has been more than two decades since the formulation of the so-called 'trade-off' hypothesis as an alternative to the then commonly accepted idea that parasites should always evolve towards avirulence (the 'avirulence hypothesis'). The trade-off hypothesis states that virulence is an unavoidable consequence of parasite transmission; however, since the 1990s, this hypothesis has been increasingly challenged. We discuss the history of the study of virulence evolution and the development of theories towards the trade-off hypothesis in order to illustrate the context of the debate. We investigate the arguments raised against the trade-off hypothesis and argue that trade-offs exist, but may not be of the simple form that is usually assumed, involving other mechanisms (and life-history traits) than those originally considered. Many processes such as pathogen adaptation to within-host competition, interactions with the immune system and shifting transmission routes, will all be interrelated making sweeping evolutionary predictions harder to obtain. We argue that this is the heart of the current debate in the field and while species-specific models may be better predictive tools, the trade-off hypothesis and its basic extensions are necessary to assess the qualitative impacts of virulence management strategies.
Evolutionary invasion analysis is a powerful technique for modelling in evolutionary biology. The general approach is to derive an expression for the growth rate of a mutant allele encoding some novel phenotype, and then to use this expression to predict long-term evolutionary outcomes. Mathematically, such 'invasion fitness' expressions are most often derived using standard linear stability analyses from dynamical systems theory. Interestingly, there is a mathematically equivalent approach to such stability analyses that is often employed in mathematical epidemiology, and that is based on so-called 'next-generation' matrices. Although this next-generation matrix approach has sometimes also been used in evolutionary invasion analyses, it is not yet common in this area despite the fact that it can sometimes greatly simplify calculations. The aim of this article is to bring the approach to a wider evolutionary audience in two ways. First, we review the next-generation matrix approach and provide a novel, and easily intuited, interpretation of how this approach relates to more standard techniques. Second, we illustrate next-generation methods in evolutionary invasion analysis through a series of informative examples. Although focusing primarily on evolutionary invasion analysis, we provide several insights that apply to biological modelling in general.
Global climate change is a major threat to biodiversity. The most common methods for predicting the response of biodiversity to changing climate do not explicitly incorporate fundamental evolutionary and ecological processes that determine species responses to changing climate, such as reproduction, dispersal, and adaptation. We provide an overview of an emerging mechanistic spatial theory of species range shifts under climate change. This theoretical framework explicitly defines the ecological processes that contribute to species range shifts via biologically meaningful dispersal, reproductive, and climate envelope parameters. We present methods for estimating the parameters of the model with widely available species occurrence and abundance data and then apply these methods to empirical data for 12 North American butterfly species to illustrate the potential use of the theory for global change biology. The model predicts species persistence in light of current climate change and habitat loss. On average, we estimate that the climate envelopes of our study species are shifting north at a rate of 3.25 +/- 1.36 km/yr (mean +/- SD) and that our study species produce 3.46 +/- 1.39 (mean +/- SD) viable offspring per individual per year. Based on our parameter estimates, we are able to predict the relative risk of our 12 study species for lagging behind changing climate. This theoretical framework improves predictions of global change outcomes by facilitating the development and testing of hypotheses, providing mechanistic predictions of current and future range dynamics, and encouraging the adaptive integration of theory and data. The theory is ripe for future developments such as the incorporation of biotic interactions and evolution of adaptations to novel climatic conditions, and it has the potential to be a catalyst for the development of more effective conservation strategies to mitigate losses of biodiversity from global climate change.
An overlooked aspect of disease ecology is considering how and why animals come into contact with one and other resulting in disease transmission. Mathematical models of disease spread frequently assume mass-action transmission, justified by stating that susceptible and infectious hosts mix readily, and foregoing any detailed description of host movement. Numerous recent studies have recorded, analysed and modelled animal movement. These movement models describe how animals move with respect to resources, conspecifics and previous movement directions and have been used to understand the conditions for the occurrence and the spread of infectious diseases when hosts perform a type of movement. Here, we summarize the effect of the different types of movement on the threshold conditions for disease spread. We identify gaps in the literature and suggest several promising directions for future research. The mechanistic inclusion of movement in epidemic models may be beneficial for the following two reasons. Firstly, the estimation of the transmission coefficient in an epidemic model is possible because animal movement data can be used to estimate the rate of contacts between conspecifics. Secondly, unsuccessful transmission events, where a susceptible host contacts an infectious host but does not become infected can be quantified. Following an outbreak, this enables disease ecologists to identify 'near misses' and to explore possible alternative epidemic outcomes given shifts in ecological or immunological parameters.This article is part of the themed issue 'Opening the black box: re-examining the ecology and evolution of parasite transmission'.
BackgroundMovement data are frequently collected using Global Positioning System (GPS) receivers, but recorded GPS locations are subject to errors. While past studies have suggested methods to improve location accuracy, mechanistic movement models utilize distributions of turning angles and directional biases and these data present a new challenge in recognizing and reducing the effect of measurement error.MethodsI collected locations from a stationary GPS collar, analyzed a probabilistic model and used Monte Carlo simulations to understand how measurement error affects measured turning angles and directional biases.ResultsResults from each of the three methods were in complete agreement: measurement error gives rise to a systematic bias where a stationary animal is most likely to be measured as turning 180° or moving towards a fixed point in space. These spurious effects occur in GPS data when the measured distance between locations is <20 meters.ConclusionsMeasurement error must be considered as a possible cause of 180° turning angles in GPS data. Consequences of failing to account for measurement error are predicting overly tortuous movement, numerous returns to previously visited locations, inaccurately predicting species range, core areas, and the frequency of crossing linear features. By understanding the effect of GPS measurement error, ecologists are able to disregard false signals to more accurately design conservation plans for endangered wildlife.
Sea lice (Lepeophtheirus salmonis) are a significant source of monetary losses on salmon farms. Sea lice exhibit temperature-dependent development rates and salinity-dependent mortality, but to date no deterministic models have incorporated these seasonally varying factors. To understand how environmental variation and life history characteristics affect sea lice abundance, we derive a delay differential equation model and parameterize the model with environmental data from British Columbia and southern Newfoundland. We calculate the lifetime reproductive output for female sea lice maturing to adulthood at different times of the year and find differences in the timing of peak reproduction between the two regions. Using a sensitivity analysis, we find that sea lice abundance is more sensitive to variation in mean annual water temperature and mean annual salinity than to variation in life history parameters. Our results suggest that effective sea lice management requires consideration of site-specific temperature and salinity patterns and, in particular, that the optimal timing of production cycles and sea lice treatments might vary between regions.
Antimicrobials are an effective treatment for many types of infections, but their overuse promotes the spread of resistant microorganisms that defy conventional treatments and complicate patient care. In 2009, an antimicrobial stewardship program was implemented at Mount Sinai Hospital (MSH, Toronto, Canada). Components of this program were to alter the fraction of patients prescribed antimicrobials, to shorten the average duration of treatment, and to alter the types of antimicrobials prescribed. These components were incorporated into a mathematical model that was compared to data reporting the number of patients colonized with Pseudomonas aeruginosa and the number of patients colonized with antimicrobial-resistant P. aeruginosa first isolates before and after the antimicrobial stewardship program. Our analysis shows that the reported decrease in the number of patients colonized was due to treating fewer patients, while the reported decrease in the number of patients colonized with resistant P. aeruginosa was due to the combined effect of treating fewer patients and altering the types of antimicrobials prescribed. We also find that shortening the average duration of treatment was unlikely to have produced any noticeable effects and that further reducing the fraction of patients prescribed antimicrobials would most substantially reduce P. aeruginosa antimicrobial resistance in the future. The analytical framework that we derive considers the effect of colonization pressure on infection spread and can be used to interpret clinical antimicrobial resistance data to assess different aspects of antimicrobial stewardship within the ecological context of the intensive care unit.
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