Host Metapopulation Research Articles

A pathogen's spatial range is not constrained by geographical features in the flax rust pathosystem.

Climate change and shifting environmental conditions can allow pathogens to spread into previously unburdened areas. For plant pathogens, this dynamic has the potential to disrupt natural ecosystem equilibria and human agriculture, making predicting plant pathogen range shifts increasingly important. Although such predictions will hinge on an accurate understanding of the determinants of pathogen range-namely the environmental, geographical, and host range characteristics that modulate local pathogen habitation-few studies to date have probed these in natural plant populations. Here, we characterize range determinants for the model system of Lewis flax (Linum lewisii) and its pathogen, flax rust (Melampsora lini), in the Rocky Mountains. Transect surveys were performed to assess three relationships: (i) the effect of geographical features-elevation, slope aspect, slope grade, and land cover-on flax presence and density, (ii) the effect of geographical features on flax rust presence and prevalence, and (iii) the effects of flax's local population density and metapopulation structure on flax rust presence and prevalence. We found that flax population density, but not host metapopulation structure, influences the distribution of flax rust. Additionally, we showed that, while the distribution of flax was broadly constrained to a relatively narrow range of geographical and resulting environmental features, flax rust was evenly distributed across the full range of settings measured. These results indicate that a warming environment, which is expected to modulate such features, may restrict the optimal range of the plant more than that of its pathogen. Importantly, our results also suggest that even if flax shifts its spatial range to escape increasing climatic pressures, flax rust will not face any significant barriers to track this movement.

Dispersal engendered synchronization and stability of mediated infectious diseases in the patchy environment using mean-field diffusive coupling

Mobility of humans and mediating agents significantly affects the scope of mediated infectious diseases. The spatial transmission of mediated infectious diseases ultimately depends on the movement of hosts and mediators. To comprehend the causes, predict, evaluate, and restrict epidemic transmission, it is crucial to investigate the dynamics of mediated infectious diseases in the presence of mobility. The network of mediators and the host metapopulation are related to the spatial coupling for disease dissemination. Thus, in this article, the metapopulation dynamics of the mediated infectious disease model is studied in a patchy environment where the hosts and mediators population is divided into sub-population. Two networks are used to represent the patchy environment: the hosts or humans network and the mediators network. Mean field diffusive coupling is used to connect the network patches. Both homogeneous and heterogeneous networks are investigated in terms of dynamics. Dispersal engenders the patches of corresponding networks to synchronize and reach bistable states of non-trivial amplitude death. Numerical simulations are performed to demonstrate the change from one state to another state, caused by transcritical bifurcation. The stability of disease free equilibrium and endemic equilibrium is also determined by the reproduction number R0.

Disease influences host population growth rates in a natural wild plant–pathogen association over a 30‐year period

Abstract The epidemiological and demographic dynamics of plant–pathogen interactions in natural environments are strongly affected by spatial and temporal influences. Here we assess the interaction between Filipendula ulmaria and its rust pathogen Triphragmium ulmariae by analysing a 30‐year long dataset that has followed pathogen and plant population dynamics in a metapopulation of ~230 host patches growing on islands of the Skeppsvik archipelago in northern Sweden. Over this period, the host metapopulation initially expanded in both number and size of individual patches before plateauing. In contrast, the pathogen metapopulation showed greater change. Disease incidence showed a convex pattern rising for the first decade before showing a marked decline in the last decade. At the same time, the prevalence of disease in infected populations showed a constant 30‐year long decline. At the individual host population level, each population was annually classified into one of four inter‐year states: healthy, recolonization, extinction and diseased. Host populations that were healthy from 1 year to the next were significantly smaller than all other host population categories, while host populations in which disease was constantly present were significantly larger. Host populations in which the pathogen underwent either an extinction or a recolonization event were of similar size and represented a measure of the host threshold size for long‐term pathogen survival. Host population growth rates declined as disease levels increased. The growth rate of host populations in which disease was continuously present was 75% lower than in populations that were free disease. The sensitivity of the association to climate change as demonstrated through a decline in disease incidence and prevalence and an increase in drought damage to plant populations as temperatures rise has only become apparent through analysis of an extensive long‐term dataset. Synthesis. To date wild plant–pathogen studies have focused on the epidemiology of the pathogen and its effect on individual plant fitness. Here we have established a link to the impact of the pathogen on the long‐term dynamics of host populations. This has the potential to trigger a cascade of changes in the species composition and diversity of communities.

Metacommunity of a host metapopulation: explaining patterns and structures of a fish parasite metacommunity in a Neotropical floodplain basin

Metacommunity of a host metapopulation: explaining patterns and structures of a fish parasite metacommunity in a Neotropical floodplain basin

The dynamics of evolutionary rescue from a novel pathogen threat in a host metapopulation

When a novel disease strikes a naïve host population, there is evidence that the most immediate response can involve host evolution while the pathogen remains relatively unchanged. When hosts also live in metapopulations, there may be critical differences in the dynamics that emerge from the synergy among evolutionary, ecological, and epidemiological factors. Here we used a Susceptible-Infected-Recovery model to explore how spatial and temporal ecological factors may drive the epidemiological and rapid-evolutionary dynamics of host metapopulations. For simplicity, we assumed two host genotypes: wild type, which has a positive intrinsic growth rate in the absence of disease, and robust type, which is less likely to catch the infection given exposure but has a lower intrinsic growth rate in the absence of infection. We found that the robust-type host would be strongly selected for in the presence of disease when transmission differences between the two types is large. The growth rate of the wild type had dual but opposite effects on host composition: a smaller increase in wild-type growth increased wild-type competition and lead to periodical disease outbreaks over the first generations after pathogen introduction, while larger growth increased disease by providing more susceptibles, which increased robust host density but decreased periodical outbreaks. Increased migration had a similar impact as the increased differential susceptibility, both of which led to an increase in robust hosts and a decrease in periodical outbreaks. Our study provided a comprehensive understanding of the combined effects among migration, disease epidemiology, and host demography on host evolution with an unchanging pathogen. The findings have important implications for wildlife conservation and zoonotic disease control.

The impact of host metapopulation structure on short-term evolutionary rescue in the face of a novel pathogenic threat

While most evolutionary studies of host-pathogen dynamics consider pathogen evolution alone or host-pathogen coevolution, there is evidence that hosts can evolve more rapidly than their pathogen during initial outbreaks after disease introduction, e.g. evolutionary rescue in the short term. In these cases, spatial, temporal and epidemiological factors could all affect the evolutionary dynamics of the host population. To help inform potential conservation policies in the near-term, we considered the case of one pathogen introduced into a metapopulation of hosts with two genotypes: wild type and robust in which there is a tradeoff in disease-driven mortality and spatial mobility. We employed a classic Susceptible-Infected model and explored how differences in mortality and migration affect the representation of host genotypes and total host population persistence. We find that greater difference in disease-driven mortality between the two host types increases the probability of evolutionary rescue, but there is a point after which disease-driven mortality is so high as to drive the disease prevalence below the reproductive threshold, ending the outbreak and therefore benefitting the wild type. Migration reduces the chance of evolutionary rescue by reducing the competition between the two host genotypes when the difference in disease-driven mortality is sufficiently small, but at larger differences migration acts primarily as a facilitator of disease spread, increasing the probability of evolutionary rescue, though significantly decreasing the total size of the surviving population. This study reveals that both epidemiology and metapopulation ecology can play critical roles in host evolution during the emergence of a novel infection and provide guidance for host conservation and disease control.

Bighorn sheep gut microbiomes associate with genetic and spatial structure across a metapopulation

Studies in laboratory animals demonstrate important relationships between environment, host traits, and microbiome composition. However, host-microbiome relationships in natural systems are understudied. Here, we investigate metapopulation-scale microbiome variation in a wild mammalian host, the desert bighorn sheep (Ovis canadensis nelsoni). We sought to identify over-represented microbial clades and understand how landscape variables and host traits influence microbiome composition across the host metapopulation. To address these questions, we performed 16S sequencing on fecal DNA samples from thirty-nine bighorn sheep across seven loosely connected populations in the Mojave Desert and assessed relationships between microbiome composition, environmental variation, geographic distribution, and microsatellite-derived host population structure and heterozygosity. We first used a phylogenetically-informed algorithm to identify bacterial clades conserved across the metapopulation. Members of genus Ruminococcaceae, genus Lachnospiraceae, and family Christensenellaceae R7 group were among the clades over-represented across the metapopulation, consistent with their known roles as rumen symbionts in domestic livestock. Additionally, compositional variation among hosts correlated with individual-level geographic and genetic structure, and with population-level differences in genetic heterozygosity. This study identifies microbiome community variation across a mammalian metapopulation, potentially associated with genetic and geographic population structure. Our results imply that microbiome composition may diverge in accordance with landscape-scale environmental and host population characteristics.

Spatial extinction or persistence: landscape‐temperature interactions perturb predator–prey dynamics

Recognising that species interact across a range of spatial scales, we explore how landscape structure interacts with temperature to influence persistence. Specifically, we recognise that few studies indicate thermal shifts as the proximal cause of species extinctions; rather, species interactions exacerbated by temperature result in extinctions. Using microcosm‐based experiments, as models of larger landscape processes, we test hypotheses that would be problematic to address through field work. A text‐book predator–prey system (the ciliatesDidiniumandParamecium) was used to compare three landscapes: an unfragmented landscape subjected to uniform temperatures (10, 20, 30°C); a fragmented landscape (potentially hosting metapopulations) subjected to these three temperatures; and a fragmented landscape subjected to a spatial temperature gradient (∼ 10 to 30°C) – despite the prevalence of natural temperature ecoclines this is the first time such an analysis has been conducted. Initial thermal response‐analysis (growth, mortality, and movement measured between 10 and 30°C) suggested that as temperature increased, the predator might drive the prey to extinction. Thermal preferences (measured at 5 temperatures between 10 and 30°C), indicated that both predator and prey preferred warmer temperatures, with the predator exhibiting the stronger preference, suggesting that cooler regions might act as a prey‐refuge. The landscape level observations, however, did not entirely support the predictions. First, in the unfragmented landscape, increased temperature led to extinctions, but at the highest temperature (where the predator growth can be reduced) the prey survived. Second, at high temperatures the fragmented landscape failed to host metapopulations that would allow predator–prey persistence. Third, the thermal ecocline did not provide heterogeneity that improved stability; rather it forced both species to occupy a smaller realized space, leading toward extinctions. These findings reveal that temperature‐impacted rates and temperature preferences combine to drive predator–prey dynamics and persistence across landscapes.

Explaining the geographical origins of seasonal influenza A (H3N2).

Most antigenically novel and evolutionarily successful strains of seasonal influenza A (H3N2) originate in East, South and Southeast Asia. To understand this pattern, we simulated the ecological and evolutionary dynamics of influenza in a host metapopulation representing the temperate north, tropics and temperate south. Although seasonality and air traffic are frequently used to explain global migratory patterns of influenza, we find that other factors may have a comparable or greater impact. Notably, a region's basic reproductive number (R0) strongly affects the antigenic evolution of its viral population and the probability that its strains will spread and fix globally: a 17–28% higher R0 in one region can explain the observed patterns. Seasonality, in contrast, increases the probability that a tropical (less seasonal) population will export evolutionarily successful strains but alone does not predict that these strains will be antigenically advanced. The relative sizes of different host populations, their birth and death rates, and the region in which H3N2 first appears affect influenza's phylogeography in different but relatively minor ways. These results suggest general principles that dictate the spatial dynamics of antigenically evolving pathogens and offer predictions for how changes in human ecology might affect influenza evolution.

When environmentally persistent pathogens transform good habitat into ecological traps.

Habitat quality plays an important role in the dynamics and stability of wildlife metapopulations. However, the benefits of high-quality habitat may be modulated by the presence of an environmentally persistent pathogen. In some cases, the presence of environmental pathogen reservoirs on high-quality habitat may lead to the creation of ecological traps, wherein host individuals preferentially colonize high-quality habitat, but are then exposed to increased infection risk and disease-induced mortality. We explored this possibility through the development of a stochastic patch occupancy model, where we varied the pathogen’s virulence, transmission rate and environmental persistence as well as the distribution of habitat quality in the host metapopulation. This model suggests that for pathogens with intermediate levels of spread, high-quality habitat can serve as an ecological trap, and can be detrimental to host persistence relative to low-quality habitat. This inversion of the relative roles of high- and low-quality habitat highlights the importance of considering the interaction between spatial structure and pathogen transmission when managing wildlife populations exposed to an environmentally persistent pathogen.

The impact of host metapopulation structure on the population genetics of colonizing bacteria

Many key bacterial pathogens are frequently carried asymptomatically, and the emergence and spread of these opportunistic pathogens can be driven, or mitigated, via demographic changes within the host population. These inter-host transmission dynamics combine with basic evolutionary parameters such as rates of mutation and recombination, population size and selection, to shape the genetic diversity within bacterial populations. Whilst many studies have focused on how molecular processes underpin bacterial population structure, the impact of host migration and the connectivity of the local populations has received far less attention. A stochastic neutral model incorporating heightened local transmission has been previously shown to fit closely with genetic data for several bacterial species. However, this model did not incorporate transmission limiting population stratification, nor the possibility of migration of strains between subpopulations, which we address here by presenting an extended model. We study the consequences of migration in terms of shared genetic variation and show by simulation that the previously used summary statistic, the allelic mismatch distribution, can be insensitive to even large changes in microepidemic and migration rates. Using likelihood-free inference with genotype network topological summaries we fit a simpler model to commensal and hospital samples from the common nosocomial pathogens Staphylococcus aureus, Staphylococcus epidermidis, Enterococcus faecalis and Enterococcus faecium. Only the hospital data for E. faecium display clearly marked deviations from the model predictions which may be attributable to its adaptation to the hospital environment.

An island paradigm on the mainland: host population fragmentation impairs the community of avian pathogens

Emergent infectious diseases represent a major threat for biodiversity in fragmented habitat networks, but their dynamics in host metapopulations remain largely unexplored. We studied a large community of pathogens (including 26 haematozoans, bacteria and viruses as determined through polymerase chain reaction assays) in a highly fragmented mainland bird metapopulation. Contrary to recent studies, which have established that the prevalence of pathogens increase with habitat fragmentation owing to crowding and habitat-edge effects, the analysed pathogen parameters were neither dependent on host densities nor related to the spatial structure of the metapopulation. We provide, to our knowledge, the first empirical evidence for a positive effect of host population size on pathogen prevalence, richness and diversity. These new insights into the interplay between habitat fragmentation and pathogens reveal properties of a host–pathogen system resembling island environments, suggesting that severe habitat loss and fragmentation could lower pathogen pressure in small populations.

Refugia and connectivity sustain amphibian metapopulations afflicted by disease.

Metapopulation persistence in fragmented landscapes depends on habitat patches that can support resilient local populations and sufficient connectivity between patches. Yet epidemiological theory for metapopulations has largely overlooked the capacity of particular patches to act as refuges from disease, and has suggested that connectivity can undermine persistence. Here, we show that relatively warm and saline wetlands are environmental refuges from chytridiomycosis for an endangered Australian frog, and act jointly with connectivity to sustain frog metapopulations. We coupled models of microclimate and infection probability to map chytrid prevalence, and demonstrate a strong negative relationship between chytrid prevalence and the persistence of frog populations. Simulations confirm that frog metapopulations are likely to go extinct when they lack environmental refuges from disease and lose connectivity between patches. This study demonstrates that environmental heterogeneity can mediate host-pathogen interactions in fragmented landscapes, and provides evidence that connectivity principally supports host metapopulations afflicted by facultative pathogens.

Research highlight for issue 8: disease evolution and ecology across space.

How infectious disease spreads both from individual to individual and across a landscape will depend upon many inter-related factors, including the genetic composition of host and pathogen populations, the pathogen transmission rate, host density, population connectivity, and the evolutionary response of both host and pathogen over time. As such, the study of infectious disease straddles a number of fields and approaches. A key advance in the field has come from incorporation of spatial structure into both theoretical and empirical studies of the epidemiology, evolution, and ecology of disease. Researchers taking this approach were recently brought together for a workshop entitled ‘Spatial evolutionary epidemiology’ in Montpellier, France organized by Sebastien Lion and Sylvain Gandon from the Centre d’Ecologie Fonctionnelle et Evolutive (CEFE). The workshop spanned topics from infection genetics in Daphnia, to cooperation and conflict in microbial populations, to the utility of spatial epidemiological models for designing better crop planting strategies, and emphasized the broader need to think about the importance of spatial heterogeneity in order to predict the spread and evolution of pathogens. The recent literature includes a number of studies at the cutting edge of this field. For example, a model based on interactions between bacteria and their bacteriophage parasites by Ben Ashby and collaborators has demonstrated the importance of spatial structure in shaping the breadth of host resistance. They find that hosts and parasites from spatially structured populations should be less constrained by costs associated with ‘generalism’ than those from well-mixed populations, and therefore, that spatial structure is likely to increases the breadth of host resistance/parasite infectivity, especially when this increased breadth carries a significant fitness cost (Ashby et al. 2014). Another potential effect of spatial structure on host-parasite interactions is through changing rates of infection, as opposed to infection range. A recent empirical study of bacteria and phages by Pavitra Roychoudhury and coauthors experimentally evolved phages on spatially structured agar plates for 550 phage generations and found increased phage fitness was associated with a mutation conferring slower phage adsorption rate to bacterial host cells. This is in line with theoretical work suggesting spatial structure may lead to reduced parasite infectivity (e.g., Boots and Sasaki 1999) and builds upon previous empirical work from nonmicrobial systems in support of this theory. Furthermore, the authors develop a system-specific, spatially explicit model to explain how low attachment probability might lead to increased phage fitness through higher plaque density as a result of trade-offs between phage diffusion and adsorption (Roychoudhury et al. 2014). Studying spatial structure in natural populations is of course a more challenging goal, as one loses the ability to control for the type of heterogeneity across which a study is performed. Despite these potential limitations, recent work by Jussi Jousimo, Ayco Tack, and collaborators examined the impact of connectivity among over 4000 populations of the plant, Plantago lanceolata, on resistance to a co-occurring fungal pathogen, Podosphaera plantaginis, over a 12-year period. Using this large spatial dataset, the authors were able to explain the unexpected observation that highly connected populations typically showed lower pathogen prevalence and higher pathogen extinction than more isolated populations. They demonstrate that hosts from highly connected populations are in fact more resistant to the pathogen than those from more isolated populations, most likely as a result of stronger parasite-mediated selection over time (Jousimo et al. 2014). This work highlights the importance of incorporating host and pathogen evolution into models predicting the spread of disease across space, and emphasizes the potential for differential parasite-mediated selection across a host metapopulation. Finally, work by David Rasmussen and colleagues has demonstrated the strength of incorporating spatial structure into phylodynamic (coalescent) approaches to inferring past disease dynamics from genealogies (Rasmussen et al. 2014). Motivated to explain the common discrepancy between phylodynamic inferences and those made from hospital records, the authors apply their new method to a case study of mosquito-borne dengue virus in southern Vietnam. They demonstrate that a spatially structured susceptible-infected-recovered (SIR) model resulted in similar patterns to those seen from the hospitalization data, including large seasonal fluctuations in disease, and that the incorporation of ecological complexity into coalescent models increases the accuracy of inferences to disease demography. Overall, these recent studies demonstrate the added value of incorporating spatial structure into epidemiological, phylodynamic, and evolutionary/ecological models of infectious disease. Although the current body of theory on the topic offers clear predictions for how spatial structure might influence disease evolution and spread, there remains a paucity of empirical and observational studies testing these key ideas. Moving forward, the more we understand about these eco-evolutionary feedbacks, the better we will be able to manage emerging disease in natural, agricultural, and human populations.

Evolution of pathogen specialisation in a host metapopulation: joint effects of host and pathogen dispersal.

Metapopulation processes are important determinants of epidemiological and evolutionary dynamics in host-pathogen systems, and are therefore central to explaining observed patterns of disease or genetic diversity. In particular, the spatial scale of interactions between pathogens and their hosts is of primary importance because migration rates of one species can affect both spatial and temporal heterogeneity of selection on the other. In this study we developed a stochastic and discrete time simulation model to specifically examine the joint effects of host and pathogen dispersal on the evolution of pathogen specialisation in a spatially explicit metapopulation. We consider a plant-pathogen system in which the host metapopulation is composed of two plant genotypes. The pathogen is dispersed by air-borne spores on the host metapopulation. The pathogen population is characterised by a single life-history trait under selection, the infection efficacy. We found that restricted host dispersal can lead to high amount of pathogen diversity and that the extent of pathogen specialisation varied according to the spatial scale of host-pathogen dispersal. We also discuss the role of population asynchrony in determining pathogen evolutionary outcomes.

Temporal and spatial variation in prevalence of the parasiteSyngamus tracheain a metapopulation of house sparrows (Passer domesticus)

When investigating parasite-host dynamics in wild populations, a fundamental parameter to investigate is prevalence. This quantifies the percentage of individuals infected in the population. Investigating how prevalence changes over time and space can reveal interesting aspects in the parasite-host relationship in natural populations. We investigated the dynamic between a common avian parasite (Syngamus trachea) in a host metapopulation of house sparrows (Passer domesticus) on the coast of Helgeland in northern Norway. We found that parasite prevalence varied in both time and space. In addition, the parasite prevalence was found to be different between demographic groups in the local populations. Our results reveal just how complex the dynamic between a host and its parasite may become in a fragmented landscape. Although temperature may be an important factor, the specific mechanisms causing this complexity are not fully understood, but need to be further examined to understand how parasite-host interactions may affect the ecological and evolutionary dynamics and viability of host populations.

Infectious disease in animal metapopulations: the importance of environmental transmission

Motivated by an array of infectious diseases that threaten wildlife populations, a simple metapopulation model (subpopulations connected by animal movement) is developed, which allows for both movement-based and environmental transmission. The model demonstrates that for a range of plausible parameterizations of environmental transmission, increased movement rate of animals between discrete habitats can lead to a decrease in the overall proportion of sites that are occupied. This can limit the ability of the rescue effect to ensure locally extinct populations become recolonized and can drive metapopulations down in size so that extinction by mechanisms other than disease may become more likely. It further highlights that, in the context of environmental transmission, the environmental persistence time of pathogens and the probability of acquiring infection by environmental transmission can affect host metapopulations both qualitatively and quantitatively. Additional spillover sources of infection from alternate reservoir hosts are also included in the model and a synthesis of all three types of transmission, acting alone or in combination, is performed revealing that movement-based transmission is the only necessary condition for a decline in the proportion of occupied sites with increasing movement rate, but that the presence of other types of transmission can reverse this qualitative result. By including the previously neglected role of environmental transmission, this work contributes to the general discussion of when dispersal by wild animals is beneficial or detrimental to populations experiencing infectious disease.

Trans-oceanic host dispersal explains high seabird tick diversity on Cape Verde islands

Parasites represent ideal models for unravelling biogeographic patterns and mechanisms of diversification on islands. Both host-mediated dispersal and within-island adaptation can shape parasite island assemblages. In this study, we examined patterns of genetic diversity and structure of Ornithodoros seabird ticks within the Cape Verde Archipelago in relation to their global phylogeography. Contrary to expectations, ticks from multiple, geographically distant clades mixed within the archipelago. Trans-oceanic colonization via host movements probably explains high local tick diversity, contrasting with previous research that suggests little large-scale dispersal in these birds. Although host specificity was not obvious at a global scale, host-associated genetic structure was found within Cape Verde colonies, indicating that post-colonization adaptation to specific hosts probably occurs. These results highlight the role of host metapopulation dynamics in the evolutionary ecology and epidemiology of avian parasites and pathogens.

Genetic influence on disease spread following arrival of infected carriers

Epidemiology in host meta-populations depends on parasite ability to disperse between, establish and persist in distinct sub-populations of hosts. We studied the genetic factors determining the short-term establishment, and long-term maintenance, of pathogens introduced by infected hosts (i.e. carriers) into recipient populations. We used experimental populations of the freshwater ciliate Paramecium caudatum and its bacterial parasite Holospora undulata. Parasite short-term spread (approximately one horizontal transmission cycle) was affected mainly by carrier genotype, and its interactions with parasite and recipient genotypes. By contrast, parasite longer term spread (2-3 horizontal transmission cycles) was mostly determined by parasite isolate. Importantly, measures of parasite short-term success (reproductive number, R) were not good predictors for longer term prevalence, probably because of the specific interactions between host and parasite genotypes. Analogous to variation in vectorial capacity and super-spreader occurrence, two crucial components of epidemiology, we show that carrier genotype can also affect disease spread within meta-populations.

Invasion and Persistence of Infectious Agents in Fragmented Host Populations

One of the important questions in understanding infectious diseases and their prevention and control is how infectious agents can invade and become endemic in a host population. A ubiquitous feature of natural populations is that they are spatially fragmented, resulting in relatively homogeneous local populations inhabiting patches connected by the migration of hosts. Such fragmented population structures are studied extensively with metapopulation models. Being able to define and calculate an indicator for the success of invasion and persistence of an infectious agent is essential for obtaining general qualitative insights into infection dynamics, for the comparison of prevention and control scenarios, and for quantitative insights into specific systems. For homogeneous populations, the basic reproduction ratio plays this role. For metapopulations, defining such an ‘invasion indicator’ is not straightforward. Some indicators have been defined for specific situations, e.g., the household reproduction number . However, these existing indicators often fail to account for host demography and especially host migration. Here we show how to calculate a more broadly applicable indicator for the invasion and persistence of infectious agents in a host metapopulation of equally connected patches, for a wide range of possible epidemiological models. A strong feature of our method is that it explicitly accounts for host demography and host migration. Using a simple compartmental system as an example, we illustrate how can be calculated and expressed in terms of the key determinants of epidemiological dynamics.