RESUMEN
Genetic resistance forms the foundation of infectious disease management in crops. However, rapid pathogen evolution is causing the breakdown of resistance and threatening disease control. Recent research efforts have identified strategies for resistance gene deployment that aim to disrupt pathogen adaptation and prevent breakdown. To date, there has been limited practical uptake of such strategies. In this paper, we focus on the socio-economic challenges associated with translating applied evolutionary research into scientifically informed management strategies to control pathogen adaptation. We develop a conceptual framework for the economic valuation of resistance and demonstrate that in addition to various direct benefits, resistance delivers considerable indirect and non-market value to farmers and society. Incentives for stakeholders to engage in stewardship strategies are complicated by the uncertain timeframes associated with evolutionary processes, difficulties in assigning ownership rights to genetic resources and lack of governance. These interacting biological, socio-economic and institutional complexities suggest that resistance breakdown should be viewed as a wicked problem, with often conflicting imperatives among stakeholders and no simple cause or solution. Promoting the uptake of scientific research outcomes that address complex issues in sustainable crop disease management will require a mix of education, incentives, legislation and social change. This article is part of the theme issue 'Infectious disease ecology and evolution in a changing world'.
Asunto(s)
Agricultura , Productos Agrícolas , Productos Agrícolas/genética , Factores SocioeconómicosRESUMEN
Reciprocal interactions between hosts and pathogens drive ecological, epidemiological and co-evolutionary trajectories, resulting in complex patterns of diversity at population, species and community levels. Recent results confirm the importance of negative frequency-dependent rather than 'arms-race' processes in the evolution of individual host-pathogen associations. At the community level, complex relationships between species abundance and diversity dampen or alter pathogen impacts. Invasive pathogens challenge these controls reflecting the earliest stages of evolutionary associations (akin to arms-race) where disease effects may be so great that they overwhelm the host's and community's ability to respond. Viewing these different stabilization/destabilization phases as a continuum provides a valuable perspective to assessment of the role of genetics and ecology in the dynamics of both natural and invasive host-pathogen associations.
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Interacciones Huésped-Patógeno , Fenómenos Fisiológicos de las Plantas , Plantas/microbiología , Agricultura , Evolución Biológica , Ecosistema , Especies Introducidas , Plantas/virologíaRESUMEN
Variation in host resistance and in the ability of pathogens to infect and grow (i.e. pathogenicity) is important as it provides the raw material for antagonistic (co)evolution and therefore underlies risks of disease spread, disease evolution and host shifts. Moreover, the distribution of this variation in space and time may inform us about the mode of coevolutionary selection (arms race vs. fluctuating selection dynamics) and the relative roles of G × G interactions, gene flow, selection and genetic drift in shaping coevolutionary processes. Although variation in host resistance has recently been reviewed, little is known about overall patterns in the frequency and scale of variation in pathogenicity, particularly in natural systems. Using 48 studies from 30 distinct host-pathogen systems, this review demonstrates that variation in pathogenicity is ubiquitous across multiple spatial and temporal scales. Quantitative analysis of a subset of extensively studied plant-pathogen systems shows that the magnitude of within-population variation in pathogenicity is large relative to among-population variation and that the distribution of pathogenicity partly mirrors the distribution of host resistance. At least part of the variation in pathogenicity found at a given spatial scale is adaptive, as evidenced by studies that have examined local adaptation at scales ranging from single hosts through metapopulations to entire continents and - to a lesser extent - by comparisons of pathogenicity with neutral genetic variation. Together, these results support coevolutionary selection through fluctuating selection dynamics. We end by outlining several promising directions for future research.
Asunto(s)
Bacterias/genética , Bacterias/patogenicidad , Evolución Biológica , Enfermedades de las Plantas/microbiología , Plantas/genética , Plantas/microbiología , Animales , DemografíaRESUMEN
Founder populations of fungal plant pathogens are expected to have low levels of genetic diversity coupled with further genetic drift due to, e.g., limited host availability, which should result in additional population bottlenecks. This study used microsatellite markers in the interaction between Cakile maritima and the fungal pathogen Alternaria brassicicola to explore genetic expectations associated with such situations. The host, C. maritima, was introduced into Australia approximately 100 years ago, but it is unknown whether the pathogen was already present in Australia, as it has a wide occurrence, or whether it was introduced to Australia on brassicaceous hosts. Eleven A. brassicicola populations were studied, and all showed moderate levels of gene and genotypic diversity. Chi-square tests of the frequencies of mating type alleles, a large number of genotypes, and linkage equilibrium among microsatellite loci all suggest A. brassicicola reproduces sexually. Significant genetic differentiation was found among populations, but there was no evidence for isolation by distance effects. Bayesian analyses identified eight clusters where the inferred clusters did not represent geographical populations but instead consisted of individuals admixed from all populations. Further analysis indicated that fungal populations were more likely to have experienced a recent population expansion than a population bottleneck. It is suggested that A. brassicicola has been introduced into Australia multiple times, potentially increasing the diversity and size of any A. brassicola populations already present there. Combined with its ability to reproduce sexually, such processes appear to have increased the evolutionary potential of the pathogen through recent population expansions.
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Alternaria/clasificación , Alternaria/genética , Brassicaceae/microbiología , Variación Genética , Alternaria/aislamiento & purificación , Australia , Análisis por Conglomerados , Dermatoglifia del ADN , ADN de Hongos/genética , Evolución Molecular , Repeticiones de Microsatélite , Recombinación GenéticaRESUMEN
The extent to which the distribution of soil bacteria is controlled by local environment vs. spatial factors (e.g. dispersal, colonization limitation, evolutionary events) is poorly understood and widely debated. Our understanding of biogeographic controls in microbial communities is likely hampered by the enormous environmental variability encountered across spatial scales and the broad diversity of microbial life histories. Here, we constrained environmental factors (soil chemistry, climate, above-ground plant community) to investigate the specific influence of space, by fitting all other variables first, on bacterial communities in soils over distances from m to 10² km. We found strong evidence for a spatial component to bacterial community structure that varies with scale and organism life history (dispersal and survival ability). Geographic distance had no influence over community structure for organisms known to have survival stages, but the converse was true for organisms thought to be less hardy. Community function (substrate utilization) was also shown to be highly correlated with community structure, but not to abiotic factors, suggesting nonstochastic determinants of community structure are important Our results support the view that bacterial soil communities are constrained by both edaphic factors and geographic distance and further show that the relative importance of such constraints depends critically on the taxonomic resolution used to evaluate spatio-temporal patterns of microbial diversity, as well as life history of the groups being investigated, much as is the case for macro-organisms.
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Bacterias/clasificación , Biodiversidad , Microbiología del Suelo , ADN Bacteriano/genética , Nueva Gales del Sur , Filogeografía , Polimorfismo de Longitud del Fragmento de Restricción , ARN Ribosómico 16S/genética , Suelo/química , Análisis EspacialRESUMEN
Studies of disease in relation to animal mating systems have focused on sexual selection and the evolution of sexual reproduction. Relatively little work has examined other aspects of ecological and evolutionary relationships between host social and sexual behaviour, and dynamics and prevalence of infectious diseases; this is particularly evident with respect to sexually transmitted diseases (STDs). Here, we use a simulation approach to investigate rates of STD spread in host mating systems ranging from permanent monogamy to serial polygyny or polyandry and complete promiscuity. The model assumes that one sex (female) is differentially attracted to the other, such that groups of varying size are formed within which mating and disease transmission occur. The results show that equilibrium disease levels are generally higher in females than males and are a function of variance in male mating success and the likelihood of a female switching groups between mating seasons. Moreover, initial rates of disease spread (determining whether an STD establishes in a population) depend on patterns of host movement between groups, variance in male mating success and host life history (e.g. mortality rates). Male reproductive success can be reduced substantially by a sterilizing STD and this reduction is greater in males that are more 'attractive' to females. In contrast, females that associate with more attractive males have lower absolute fitness than females associating with less attractive males. Thus, the potential for STDs to act as a constraint on directional selection processes leading to polygyny (or polyandry) is likely to depend on the details of mate choice and group dynamics.
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Reproducción/fisiología , Conducta Sexual Animal , Enfermedades de Transmisión Sexual/veterinaria , Animales , Simulación por Computador , Femenino , Masculino , Modelos Biológicos , Prevalencia , Enfermedades de Transmisión Sexual/epidemiología , Enfermedades de Transmisión Sexual/transmisiónAsunto(s)
Poliploidía , Programas Informáticos , Procesamiento Automatizado de Datos , Genotipo , HeterocigotoRESUMEN
Hybridization between locally adapted plant populations has been postulated to have significant evolutionary consequences, and, in particular, may influence host-pathogen interactions with respect to resistance and virulence structure. This study investigated patterns of resistance and virulence in a hybrid zone between "bog" and "hill" ecotypes of the native Australian flax, Linum marginale, where the host is subject to attack by the rust pathogen, Melampsora lini. Analysis of the resistance structure of adjoining bog, hill and hybrid populations found that bog plants were generally susceptible to pathogen isolates taken from all these sites, but that hybrids exhibited resistance levels similar to the more resistant hill plants. Similarly, the virulence structure of rust isolates collected from the hybrid population was more similar to that of the hill isolates than the bog. Controlled crosses between bog and hill plants showed that crosses in one direction (bog females×hill males) were much more successful than the other. A multi-year reciprocal transplant study further indicated that bog plants had significantly higher survivorship than hill plants, regardless of site. It is suggested that likelihood of differential gene flow and survivorship for bog and hill plants may at least partially explain the maintenance of a relatively narrow hybrid zone.
RESUMEN
Different patterns of resistance to six pathotypes of Melampsora lini were detected in 11 populations of Linum marginale distributed across two metapopulations. The two metapopulations (mountains and plains of New South Wales, Australia) differed in the annual cycle of disease development, which barely overlapped, and in the growth cycle and mating system of the host. Host populations in the mountains metapopulation were highly inbred, whereas those on the plains showed appreciable levels of outcrossing. Within each metapopulation there was significant variation among component populations in (1) levels of host resistance to individual pathogen isolates; (2) mean levels of resistance to all six isolates; (3) the number of resistance phenotypes present and the evenness of their distribution within the population; and (4) the average number of pathogen lines to which individual hosts were resistant. A more limited comparison of pathogen populations from the two metapopulations (two from each) found greater similarities in the structure of populations and particular virulence frequencies within, rather than among, the two metapopulations. Differences in host outcrossing rates between the two metapopulations are reflected in marked differences in the overall level of resistance, its partitioning within and among populations, the number and distribution of resistance phenotypes in the two areas, and the level of polymorphism for specific virulence factors in the pathogen, with the plains metapopulation showing consistently higher values. However, these differences were not significant. In general, variation for all parameters was just as great among populations within a metapopulation as between the two metapopulations.
RESUMEN
Spatial structuring is important in understanding the ecological and evolutionary dynamics of natural populations since local demes are rarely, if ever, completely isolated from neighboring demes. Plant host-pathogen interactions provide good examples of coevolutionary systems where both numerical and genetic dynamics have been explicitly investigated in a spatial context and where genes under selection can be unambiguously identified. In this article, we focus on long-term studies of several natural host-pathogen interactions that span a range of life histories and taxa. We use these studies to evaluate some predictions for numerical and genetic patterns at local and regional scales. Specifically, we examine the degree of among-population asynchrony in disease presence/absence and abundance, and the extent to which this is a function of isolation. For one host-pathogen interaction (Linum-Melampsora), we focus on whether there is local correspondence between resistance and virulence genes (as would be predicted by single-population coevolutionary models) or whether such correspondence occurs at larger spatial scales. Finally, we discuss the implications of these studies with respect to the impact of host and pathogen life-history variation on the spatial scale of coevolutionary interactions. Understanding coevolutionary interactions in nature requires a multidisciplinary approach, including long-term empirical studies of multiple populations and computer modeling.
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Predictions that infectious diseases would be eliminated as a major threat to human health have been shattered by emerging and reemerging infections, among them acquired immunodeficiency syndrome (AIDS), hemorrhagic fevers, marked increases in infections caused by antimicrobial-resistant bacteria, and the resurgence of tuberculosis and malaria. Understanding the dynamics of emerging and reemerging infections is critical to efforts to reduce the morbidity and mortality of such infections, to establish policy related to preparedness for infectious threats, and for decisions on where to use limited resources in the fight against infections. In order to offer a multidisciplinary perspective, 23 infectious disease specialists, epidemiologists, geneticists, microbiologists, and population biologists participated in an open forum at Emory University on emerging and reemerging infectious diseases. As summarized below, the group addressed questions about the definition, the identification, the factors responsible for, and multidisciplinary approaches to emerging and reemerging infections.
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Enfermedades Transmisibles/epidemiología , Investigación/organización & administración , Síndrome de Inmunodeficiencia Adquirida/epidemiología , Bacterias/genética , Infecciones Bacterianas/epidemiología , Evolución Biológica , Enfermedades Transmisibles/transmisión , Humanos , Malaria/epidemiología , Modelos Teóricos , Proyectos de Investigación , Tuberculosis/epidemiología , Virulencia , Virosis/epidemiología , Virus/genéticaRESUMEN
Many diseases have both sexual and nonsexual transmission routes, and closely related diseases often differ in their degree of sexual transmission. We investigate the evolution of transmission mode as a function of host social and mating structure using a model in which disease transmission is explicitly dependent on the numbers of sexual and nonsexual contacts (which are themselves a function of population density) and per-contact infection probabilities. Most generally, and in the absence of trade-offs between the degree of sexual transmission and effects on host fecundity and mortality, nonsexual transmission is favored above the social-sexual crossover point (the host density at which the number of nonsexual contacts exceeds the number of sexual contacts), while sexual transmission is favored below this point. When changes in allocation to the two transmission modes are accompanied by changes in mortality or fecundity, both mixed and pure transmission strategies can be favored. If invading genotypes differ substantially from resident genotypes, genetic polymorphism in transmission mode is possible. The evolutionary outcomes are predictable from a knowledge of the equilibrium population sizes in relation to the social-sexual crossover point. Our results also show that predictions about dynamic outcomes, based on rates of invasion for single pathogens into healthy populations, do not adequately describe the resulting disease prevalence nor predict the subsequent evolutionary dynamics; once invasion of a pathogen has occurred, the conditions for spread of a second pathogen are themselves altered. If the host is considered as a single resource, our results show that two pathogens may coexist on a single resource if they use that resource differentially and have differential feedbacks on resource abundance; such resource feedback effects may be present in other biological systems.
RESUMEN
Sexually transmitted diseases (STDs) have been generally thought of as a small subset of infectious diseases, rather than as an important group of diseases that occur in numerous species. In this paper, we have (1) briefly reviewed theoretical studies on the dynamics of STDs; (2) documented the distribution of STDs in the animal kingdom; and (3) investigated whether STDs have characteristics which distinguish them from other infectious diseases. The dynamics of STDs should differ from those of ordinary infectious diseases because their transmission depends on the frequency rather than density of infectives. With this type of transmission, there is no threshold density for disease spread, and the conditions for host-pathogen coexistence are more restrictive. Nevertheless, a wide variety of disease characteristics may allow a sexually transmitted pathogen to coexist with its host. We found over 200 diseases for which there was evidence of sexual transmission. They occurred in groups as diverse as mammals, reptiles, arachnids, insects, molluscs and nematodes. Sexually transmitted pathogens included protozoans, fungi, nematodes, helminths, and cancerous cell lines, as well as bacteria and viruses. Detailed comparison of the characteristics of sexually transmitted mammalian diseases with those that are transmitted by non-sexual means, showed that STDs cause less mortality, are longer-lived in their hosts, are less likely to invoke strong immune responses, have narrower host-ranges, and show less fluctuation in prevalence over time. These shared features are related to mode of transmission rather than either host or pathogen taxonomic affiliation. This suggests an evolutionary explanation based on shared ecologies rather than one based on phylogenetic history.