When is a parasite not a parasite? Effects of larval tick burdens on white-footed mouse survival

Many animal species can carry considerable burdens of ectoparasites: parasites living on the outside of a host's body. Ectoparasite infestation can decrease host survival, but the magnitude and even direction of survival effects can vary depending on the type of ectoparasite and the nature and duration of the association. When ectoparasites also serve as vectors of pathogens, the effects of ectoparasite infestation on host survival have the potential to alter disease dynamics by regulating host populations and stabilizing transmission. We quantified the impact of larval Ixodes scapularis tick burdens on both within-season and overwinter survival of white-footed mice (Peromyscus leucopus) using a hierarchical Bayesian capture-mark-recapture model. I. scapularis and P. leucopus are, respectively, vectors and competent reservoirs for the causative agents of Lyme disease, anaplasmosis, and babesiosis. Using a data set of 5587 individual mouse capture histories over sixteen years, we found little evidence for any effect of tick burdens on either within-season or overwinter mouse survival probabilities. In male mice, tick burdens were positively correlated with within-season survival probabilities. Mean maximum tick burdens were also positively correlated with population rates of change during the concurrent breeding season. The apparent indifference of mice to high tick burdens may contribute to their effectiveness as reservoir hosts for several human zoonotic pathogens.Fil: Hersh, Michelle H.. Cary Institute of Ecosystem Studies; Estados Unidos. Bard College. Program in Biology; Estados Unidos. Sarah Lawrence College; Estados UnidosFil: LaDeau, Shannon L.. Cary Institute of Ecosystem Studies; Estados UnidosFil: Previtali, Maria Andrea. Universidad Nacional del Litoral. Facultad de Humanidades y Ciencias. Departamento de Ciencias Naturales; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Santa Fe; ArgentinaFil: Ostfeld, Richard S.. Cary Institute of Ecosystem Studies; Estados Unido

Defining the Risk of Zika and Chikungunya Virus Transmission in Human Population Centers of the Eastern United States

The recent spread of mosquito-transmitted viruses and associated disease to the Americas motivates a new, data-driven evaluation of risk in temperate population centers. Temperate regions are generally expected to pose low risk for significant mosquito-borne disease; however, the spread of the Asian tiger mosquito (Aedes albopictus) across densely populated urban areas has established a new landscape of risk. We use a model informed by field data to assess the conditions likely to facilitate local transmission of chikungunya and Zika viruses from an infected traveler to Ae. albopictus and then to other humans in USA cities with variable human densities and seasonality. Mosquito-borne disease occurs when specific combinations of conditions maximize virus-to-mosquito and mosquito-to-human contact rates. We develop a mathematical model that captures the epidemiology and is informed by current data on vector ecology from urban sites. The model demonstrates that under specific but realistic conditions, fifty-percent of introductions by infectious travelers to a high human, high mosquito density city could initiate local transmission and 10% of the introductions could result in 100 or more people infected. Despite the propensity for Ae. albopictus to bite non-human vertebrates, we also demonstrate that local virus transmission and human outbreaks may occur when vectors feed from humans even just 40% of the time. Inclusion of human behavioral changes and mitigations were not incorporated into the models and would likely reduce predicted infections. This work demonstrates how a conditional series of non-average events can result in local arbovirus transmission and outbreaks of human disease, even in temperate cities

Mycobiome of the Bat White Nose Syndrome (WNS) Affected Caves and Mines reveals High Diversity of Fungi and Local Adaptation by the Fungal Pathogen Pseudogymnoascus (Geomyces) destructans

The investigations of the bat White Nose Syndrome (WNS) have yet to provide answers as to how the causative fungus Pseudogymnoascus (Geomyces) destructans (Pd) first appeared in the Northeast and how a single clone has spread rapidly in the US and Canada. We aimed to catalogue Pd and all other fungi (mycobiome) by the culture-dependent (CD) and culture-independent (CI) methods in four Mines and two Caves from the epicenter of WNS zoonotic. Six hundred sixty-five fungal isolates were obtained by CD method including the live recovery of Pd. Seven hundred three nucleotide sequences that met the definition of operational taxonomic units (OTUs) were recovered by CI methods. Most OTUs belonged to unidentified clones deposited in the databases as environmental nucleic acid sequences (ENAS). The core mycobiome of WNS affected sites comprised of 46 species of fungi from 31 genera recovered in culture, and 17 fungal genera and 31 ENAS identified from clone libraries. Fungi such as Arthroderma spp., Geomyces spp., Kernia spp., Mortierella spp., Penicillium spp., and Verticillium spp. were predominant in culture while Ganoderma spp., Geomyces spp., Mortierella spp., Penicillium spp. and Trichosporon spp. were abundant is clone libraries. Alpha diversity analyses from CI data revealed that fungal community structure was highly diverse. However, the true species diversity remains undetermined due to under sampling. The frequent recovery of Pd indicated that the pathogen has adapted to WNS-afflicted habitats. Further, this study supports the hypothesis that Pd is an introduced species. These findings underscore the need for integrated WNS control measures that target both bats and the fungal pathogen.Comment: 59 pages, 7figure

Elevated Atmospheric Carbon Dioxide Concentrations Amplify Alternaria alternata Sporulation and Total Antigen Production

Background Although the effect of elevated carbon dioxide (CO2) concentration on pollen production has been established in some plant species, impacts on fungal sporulation and antigen production have not been elucidated. Objective Our purpose was to examine the effects of rising atmospheric CO2 concentrations on the quantity and quality of fungal spores produced on timothy (Phleum pratense) leaves. Methods Timothy plants were grown at four CO2 concentrations (300, 400, 500, and 600 μmol/mol). Leaves were used as growth substrate for Alternaria alternata and Cladosporium phlei. The spore abundance produced by both fungi, as well as the size (microscopy) and antigenic protein content (ELISA) of A. alternata, were quantified. Results Leaf carbon-to-nitrogen ratio was greater at 500 and 600 μmol/mol, and leaf biomass was greater at 600 μmol/mol than at the lower CO2 concentrations. Leaf carbon-to-nitrogen ratio was positively correlated with A. alternata spore production per gram of leaf but negatively correlated with antigenic protein content per spore. At 500 and 600 μmol/mol CO2 concentrations, A. alternata produced nearly three times the number of spores and more than twice the total antigenic protein per plant than at lower concentrations. C. phlei spore production was positively correlated with leaf carbon-to-nitrogen ratio, but overall spore production was much lower than in A. alternata, and total per-plant production did not vary among CO2 concentrations. Conclusions Elevated CO2 concentrations often increase plant leaf biomass and carbon-to-nitrogen ratio. Here we demonstrate for the first time that these leaf changes are associated with increased spore production by A. alternata, a ubiquitous allergenic fungus. This response may contribute to the increasing prevalence of allergies and asthma

Emerging Infectious Disease leads to Rapid Population Decline of Common British Birds

Emerging infectious diseases are increasingly cited as threats to wildlife, livestock and humans alike. They can threaten geographically isolated or critically endangered wildlife populations; however, relatively few studies have clearly demonstrated the extent to which emerging diseases can impact populations of common wildlife species. Here, we report the impact of an emerging protozoal disease on British populations of greenfinch Carduelis chloris and chaffinch Fringilla coelebs, two of the most common birds in Britain. Morphological and molecular analyses showed this to be due to Trichomonas gallinae. Trichomonosis emerged as a novel fatal disease of finches in Britain in 2005 and rapidly became epidemic within greenfinch, and to a lesser extent chaffinch, populations in 2006. By 2007, breeding populations of greenfinches and chaffinches in the geographic region of highest disease incidence had decreased by 35% and 21% respectively, representing mortality in excess of half a million birds. In contrast, declines were less pronounced or absent in these species in regions where the disease was found in intermediate or low incidence. Also, populations of dunnock Prunella modularis, which similarly feeds in gardens, but in which T. gallinae was rarely recorded, did not decline. This is the first trichomonosis epidemic reported in the scientific literature to negatively impact populations of free-ranging non-columbiform species, and such levels of mortality and decline due to an emerging infectious disease are unprecedented in British wild bird populations. This disease emergence event demonstrates the potential for a protozoan parasite to jump avian host taxonomic groups with dramatic effect over a short time period

Unifying the spatial epidemiology and molecular evolution of emerging epidemics

We introduce a conceptual bridge between the previously unlinked fields of phylogenetics and mathematical spatial ecology, which enables the spatial parameters of an emerging epidemic to be directly estimated from sampled pathogen genome sequences. By using phylogenetic history to correct for spatial autocorrelation, we illustrate how a fundamental spatial variable, the diffusion coefficient, can be estimated using robust nonparametric statistics, and how heterogeneity in dispersal can be readily quantified. We apply this framework to the spread of the West Nile virus across North America, an important recent instance of spatial invasion by an emerging infectious disease. We demonstrate that the dispersal of West Nile virus is greater and far more variable than previously measured, such that its dissemination was critically determined by rare, long-range movements that are unlikely to be discerned during field observations. Our results indicate that, by ignoring this heterogeneity, previous models of the epidemic have substantially overestimated its basic reproductive number. More generally, our approach demonstrates that easily obtainable genetic data can be used to measure the spatial dynamics of natural populations that are otherwise difficult or costly to quantify

Infectious Offspring: How Birds Acquire and Transmit an Avian Polyomavirus in the Wild

Detailed patterns of primary virus acquisition and subsequent dispersal in wild vertebrate populations are virtually absent. We show that nestlings of a songbird acquire polyomavirus infections from larval blowflies, common nest ectoparasites of cavity-nesting birds, while breeding adults acquire and renew the same viral infections via cloacal shedding from their offspring. Infections by these DNA viruses, known potential pathogens producing disease in some bird species, therefore follow an ‘upwards vertical’ route of an environmental nature mimicking horizontal transmission within families, as evidenced by patterns of viral infection in adults and young of experimental, cross-fostered offspring. This previously undescribed route of viral transmission from ectoparasites to offspring to parent hosts may be a common mechanism of virus dispersal in many taxa that display parental care

Avian cholera, a threat to the viability of an Arctic seabird colony?

© The Author(s), 2012. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in PLoS One 7 (2012): e29659, doi:10.1371/journal.pone.0029659.Evidence that infectious diseases cause wildlife population extirpation or extinction remains anecdotal and it is unclear whether the impacts of a pathogen at the individual level can scale up to population level so drastically. Here, we quantify the response of a Common eider colony to emerging epidemics of avian cholera, one of the most important infectious diseases affecting wild waterfowl. We show that avian cholera has the potential to drive colony extinction, even over a very short period. Extinction depends on disease severity (the impact of the disease on adult female survival) and disease frequency (the number of annual epidemics per decade). In case of epidemics of high severity (i.e., causing >30% mortality of breeding females), more than one outbreak per decade will be unsustainable for the colony and will likely lead to extinction within the next century; more than four outbreaks per decade will drive extinction to within 20 years. Such severity and frequency of avian cholera are already observed, and avian cholera might thus represent a significant threat to viability of breeding populations. However, this will depend on the mechanisms underlying avian cholera transmission, maintenance, and spread, which are currently only poorly known.The study was supported by the Canadian Wildlife Service-Environment Canada (http://www.ec.gc.ca/), Nunavut Wildlife Management Board (http:// www.nwmb.com/), Greenland Institute of Natural Resources (http://www.natur.gl/), Polar Continental Shelf Project (http://polar.nrcan.gc.ca/), Fonds Que´be´cois de la Recherche sur la Nature et les Technologies (http://www.fqrnt.gouv.qc.ca/), Canadian Network of Centres of Excellence ArcticNet (http://www.arcticnet.ulaval. ca/), Natural Sciences and Engineering Research Council of Canada (http://www.nserc-crsng.gc.ca/), and the Department of Indian Affairs and Northern Canada (http://www.ainc-inac.gc.ca/)

Marine fish traits follow fast-slow continuum across oceans

A fundamental challenge in ecology is to understand why species are found where they are and predict where they are likely to occur in the future. Trait-based approaches may provide such understanding, because it is the traits and adaptations of species that determine which environments they can inhabit. It is therefore important to identify key traits that determine species distributions and investigate how these traits relate to the environment. Based on scientific bottom-trawl surveys of marine fish abundances and traits of >1,200 species, we investigate trait-environment relationships and project the trait composition of marine fish communities across the continental shelf seas of the Northern hemisphere. We show that traits related to growth, maturation and lifespan respond most strongly to the environment. This is reflected by a pronounced “fast-slow continuum” of fish life-histories, revealing that traits vary with temperature at large spatial scales, but also with depth and seasonality at more local scales. Our findings provide insight into the structure of marine fish communities and suggest that global warming will favour an expansion of fast-living species. Knowledge of the global and local drivers of trait distributions can thus be used to predict future responses of fish communities to environmental change.Postprint2,92

An Emerging Infectious Disease Triggering Large-Scale Hyperpredation

Hyperpredation refers to an enhanced predation pressure on a secondary prey due to either an increase in the abundance of a predator population or a sudden drop in the abundance of the main prey. This scarcely documented mechanism has been previously studied in scenarios in which the introduction of a feral prey caused overexploitation of native prey. Here we provide evidence of a previously unreported link between Emergent Infectious Diseases (EIDs) and hyperpredation on a predator-prey community. We show how a viral outbreak caused the population collapse of a host prey at a large spatial scale, which subsequently promoted higher-than-normal predation intensity on a second prey from shared predators. Thus, the disease left a population dynamic fingerprint both in the primary host prey, through direct mortality from the disease, and indirectly in the secondary prey, through hyperpredation. This resulted in synchronized prey population dynamics at a large spatio-temporal scale. We therefore provide evidence for a novel mechanism by which EIDs can disrupt a predator-prey interaction from the individual behavior to the population dynamics. This mechanism can pose a further threat to biodiversity through the human-aided disruption of ecological interactions at large spatial and temporal scales.MM and JASZ were partially supported by a project of the Spanish Ministerio de Educación y Ciencia (reference CGL-2006-10689/BOS)