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When environmentally persistent pathogens transform good habitat into ecological traps.

ABSTRACT: 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.

SUBMITTER: Leach CB

PROVIDER: S-EPMC4821283 | biostudies-literature | 2016 Mar

REPOSITORIES: biostudies-literature

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When environmentally persistent pathogens transform good habitat into ecological traps.

Leach Clinton B CB Webb Colleen T CT Cross Paul C PC

Royal Society open science 20160323 3

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 mort ...[more]

PMID: 27069672

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Project description:Variants of the susceptible-infected-removed (SIR) model of Kermack & McKendrick (1927) enjoy wide application in epidemiology, offering simple yet powerful inferential and predictive tools in the study of diverse infectious diseases across human, animal and plant populations. Direct transmission models (DTM) are a subset of these that treat the processes of disease transmission as comprising a series of discrete instantaneous events. Infections transmitted indirectly by persistent environmental pathogens, however, are examples where a DTM description might fail and are perhaps better described by models that comprise explicit environmental transmission routes, so-called environmental transmission models (ETM). In this paper we discuss the stochastic susceptible-exposed-infected-removed (SEIR) DTM and susceptible-exposed-infected-removed-pathogen (SEIR-P) ETM and we show that the former is the timescale separation limit of the latter, with ETM host-disease dynamics increasingly resembling those of a DTM when the pathogen's characteristic timescale is shortened, relative to that of the host population. Using graphical posterior predictive checks (GPPC), we investigate the validity of the SEIR model when fitted to simulated SEIR-P host infection and removal times. Such analyses demonstrate how, in many cases, the SEIR model is robust to departure from direct transmission. Finally, we present a case study of white spot disease (WSD) in penaeid shrimp with rates of environmental transmission and pathogen decay (SEIR-P model parameters) estimated using published results of experiments. Using SEIR and SEIR-P simulations of a hypothetical WSD outbreak management scenario, we demonstrate how relative shortening of the pathogen timescale comes about in practice. With atttempts to remove diseased shrimp from the population every 24h, we see SEIR and SEIR-P model outputs closely conincide. However, when removals are 6-hourly, the two models' mean outputs diverge, with distinct predictions of outbreak size and duration.

Project description:BackgroundBillions of people living in poverty are at risk of environmentally mediated infectious diseases-that is, pathogens with environmental reservoirs that affect disease persistence and control and where environmental control of pathogens can reduce human risk. The complex ecology of these diseases creates a global health problem not easily solved with medical treatment alone.MethodsWe quantified the current global disease burden caused by environmentally mediated infectious diseases and used a structural equation model to explore environmental and socioeconomic factors associated with the human burden of environmentally mediated pathogens across all countries.FindingsWe found that around 80% (455 of 560) of WHO-tracked pathogen species known to infect humans are environmentally mediated, causing about 40% (129 488 of 359 341 disability-adjusted life years) of contemporary infectious disease burden (global loss of 130 million years of healthy life annually). The majority of this environmentally mediated disease burden occurs in tropical countries, and the poorest countries carry the highest burdens across all latitudes. We found weak associations between disease burden and biodiversity or agricultural land use at the global scale. In contrast, the proportion of people with rural poor livelihoods in a country was a strong proximate indicator of environmentally mediated infectious disease burden. Political stability and wealth were associated with improved sanitation, better health care, and lower proportions of rural poverty, indirectly resulting in lower burdens of environmentally mediated infections. Rarely, environmentally mediated pathogens can evolve into global pandemics (eg, HIV, COVID-19) affecting even the wealthiest communities.InterpretationThe high and uneven burden of environmentally mediated infections highlights the need for innovative social and ecological interventions to complement biomedical advances in the pursuit of global health and sustainability goals.FundingBill & Melinda Gates Foundation, National Institutes of Health, National Science Foundation, Alfred P. Sloan Foundation, National Institute for Mathematical and Biological Synthesis, Stanford University, and the US Defense Advanced Research Projects Agency.

Project description:While the effect of habitat connectivity on local and regional diversity has been analysed in a number of studies, time-dependent dynamics in metacommunities have received comparatively little consideration. When local patches of a metacommunity are identical in environmental conditions but differ in initial community composition, dispersal among patches may result in homogenization of local communities. In a microcosm experiment with benthic ciliates, we tested the hypothesis that the effect of connectivity on diversity is time-dependent and only transitory, with the degree of connectivity affecting the time to homogenization but not the final outcome. Six microcosms were connected to a metacommunity with one of three levels of connectivity. The six patches differed in initial community composition but were identical in environmental conditions. We found a time-dependent and transitory effect of connectivity on local and regional richness and on local Shannon diversity, while Bray-Curtis dissimilarity and regional Shannon diversity were persistently affected by connectivity. Local richness increased and regional richness decreased with connectivity during the initial phase of the experiment but soon converged to similar values in all three connectivity treatments. Local Shannon diversity was unimodally related to time, with maximum diversity reached sooner with high than with medium or low connectivity. Eventually, however, local diversity converged to similar values irrespective of connectivity. At the regional scale, Shannon diversity was persistently lower with high than with low connectivity. While initial differences in community composition vanished with medium and high connectivity, they were maintained with low connectivity resulting in persistently high beta and regional diversity. The effect of connectivity on ciliate community composition translated down to the algal resource, as stronger dominance of the superior competitor with high and medium connectivity resulted in stronger depletion of the resource.

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When environmentally persistent pathogens transform good habitat into ecological traps.

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When environmentally persistent pathogens transform good habitat into ecological traps.

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