Anthropogenic resource subsidies and host-parasite dynamics in wildlife

Peer reviewe

Climate Change and Infectious Disease Dynamics

The International Panel on Climate Change has made an unequivocal case that the earth\u27s climate is changing in profound ways, and that human activities are contributing significantly to climate disruption (IPCC 2007). The weight of evidence demonstrates warming global temperatures, changing patterns of precipitation, and increasing climate variability, with more extreme events. Thus, the physical underpinnings of ecology are changing, with pervasive effects on disease dynamics. Interactions among environment, hosts, and pathogens drive disease processes, and climate change will influence every interaction in this triad, directly and indirectly

Formation and dynamics of van der Waals molecules in buffer-gas traps

We show that weakly bound He-containing van der Waals molecules can be produced and magnetically trapped in buffer-gas cooling experiments, and provide a general model for the formation and dynamics of these molecules. Our analysis shows that, at typical experimental parameters, thermodynamics favors the formation of van der Waals complexes composed of a helium atom bound to most open-shell atoms and molecules, and that complex formation occurs quickly enough to ensure chemical equilibrium. For molecular pairs composed of a He atom and an S-state atom, the molecular spin is stable during formation, dissociation, and collisions, and thus these molecules can be magnetically trapped. Collisional spin relaxations are too slow to affect trap lifetimes. However, helium-3-containing complexes can change spin due to adiabatic crossings between trapped and untrapped Zeeman states, mediated by the anisotropic hyperfine interaction, causing trap loss. We provide a detailed model for Ag3He molecules, using ab initio calculation of Ag-He interaction potentials and spin interactions, quantum scattering theory, and direct Monte Carlo simulations to describe formation and spin relaxation in this system. The calculated rate of spin-change agrees quantitatively with experimental observations, providing indirect evidence for molecular formation in buffer-gas-cooled magnetic traps.Comment: 20 pages, 13 figure

Cyclic peptide production using a macrocyclase with enhanced substrate promiscuity and relaxed recognition determinants

This project was supported by grants from the ERC (no. 339367, MJ), BBSRC IBCatalyst (no. BB/M028526/1, MJ, WEH), BBSRC FoF (no. BB/M013669/1, MJ, WEH), IBioIC Exemplar (no. 2014-2-4, MJ, WEH), an AstraZeneca studentship (MJ, WEH, LT, KR), the Academy of Finland (no. 259505, DPF) and the SULSA leaders award (WEH). The authors like to thank the Aberdeen Proteomics Facility and the Aberdeen School of Natural and Computing Sciences MS Facility for LCMS analysis. Electronic supplementary information (ESI) available: Experimental section, Fig. S1–S60 and Tables S1–S3. See DOI: 10.1039/c7cc05913bPeer reviewedPublisher PD

Malignant Catarrhal Fever Induced by Alcelaphine herpesvirus 1 Is Associated with Proliferation of CD8+ T Cells Supporting a Latent Infection

Alcelaphine herpesvirus 1 (AlHV-1), carried by wildebeest asymptomatically, causes malignant catarrhal fever (WD-MCF) when cross-species transmitted to a variety of susceptible species of the Artiodactyla order. Experimentally, WD-MCF can be induced in rabbits. The lesions observed are very similar to those described in natural host species. Here, we used the rabbit model and in vivo 5-Bromo-2′-Deoxyuridine (BrdU) incorporation to study WD-MCF pathogenesis. The results obtained can be summarized as follows. (i) AlHV-1 infection induces CD8+ T cell proliferation detectable as early as 15 days post-inoculation. (ii) While the viral load in peripheral blood mononuclear cells remains below the detection level during most of the incubation period, it increases drastically few days before death. At that time, at least 10% of CD8+ cells carry the viral genome; while CD11b+, IgM+ and CD4+ cells do not. (iii) RT-PCR analyses of mononuclear cells isolated from the spleen and the popliteal lymph node of infected rabbits revealed no expression of ORF25 and ORF9, low or no expression of ORF50, and high or no expression of ORF73. Based on these data, we propose a new model for the pathogenesis of WD-MCF. This model relies on proliferation of infected CD8+ cells supporting a predominantly latent infection

Investigation of the Climatic and Environmental Context of Hendra Virus Spillover Events 1994–2010

Hendra virus is a recently emerged bat-borne zoonotic agent with high lethality in horses and humans in Australia. This is a rare disease and the determinants of bat to horse transmission, including the factors that bring these hosts together at critical times, are poorly understood. In this cross-disciplinary study climatic and vegetation primary productivity variables are compared for the dispersed and heterogenic 1994–2010 outbreak sites. The significant occurrence of spillover events within the dry season (p =  0.013, 95% CI (0.57–0.98)) suggests seasonal forcing of transmission across species, or seasonal forcing of virus excretion by the reservoir host. We explore the evidence for both. Preliminary investigations of the spatial determinants of Hendra disease locations are also presented. We find that postal areas in the Australian state of Queensland in which pteropid fruit bat (flying fox) roosts occur are approximately forty times more likely (OR = 40.5, (95% CI (5.16, 317.52)) to be the location of Hendra spillover events. This appears to be independent of density of horses at these locations. We consider issues of scale of host resource use, land use change and limitations of existing data that challenge analysis and limit further conclusive outcomes. This investigation of a broad range of potential climatic and environmental influences provides a good base for future investigations. Further understanding of cross-species Hendra virus transmission requires better understanding of flying fox resource use in the urban-rural landscape

Food for contagion : synthesis and future directions for studying host-parasite responses to resource shifts in anthropogenic environments

Human-provided resource subsidies for wildlife are diverse, common and have profound consequences for wildlife-pathogen interactions, as demonstrated by papers in this themed issue spanning empirical, theoretical and management perspectives from a range of study systems. Contributions cut across scales of organization, from the within-host dynamics of immune function, to population-level impacts on parasite transmission, to landscape-and regional-scale patterns of infection. In this concluding paper, we identify common threads and key findings from author contributions, including the consequences of resource subsidies for (i) host immunity; (ii) animal aggregation and contact rates; (iii) host movement and landscape-level infection patterns; and (iv) interspecific contacts and cross-species transmission. Exciting avenues for future work include studies that integrate mechanistic modelling and empirical approaches to better explore cross-scale processes, and experimental manipulations of food resources to quantify host and pathogen responses. Work is also needed to examine evolutionary responses to provisioning, and ask how diet-altered changes to the host microbiome influence infection processes. Given the massive public health and conservation implications of anthropogenic resource shifts, we end by underscoring the need for practical recommendations to manage supplemental feeding practices, limit human-wildlife conflicts over shared food resources and reduce cross-species transmission risks, including to humans. This article is part of the theme issue 'Anthropogenic resource subsidies and host-parasite dynamics in wildlife'.Peer reviewe

Ecological and evolutionary drivers of hemoplasma infection and bacterial genotype sharing in a Neotropical bat community

Most emerging pathogens can infect multiple species, underlining the importance of understanding the ecological and evolutionary factors that allow some hosts to harbour greater infection prevalence and share pathogens with other species. However, our understanding of pathogen jumps is based primarily around viruses, despite bacteria accounting for the greatest proportion of zoonoses. Because bacterial pathogens in bats (order Chiroptera) can have conservation and human health consequences, studies that examine the ecological and evolutionary drivers of bacterial prevalence and barriers to pathogen sharing are crucially needed. Here were studied haemotropic Mycoplasma spp. (i.e., haemoplasmas) across a speciesâ€rich bat community in Belize over two years. Across 469 bats spanning 33 species, half of individuals and twoâ€thirds of species were haemoplasma positive. Infection prevalence was higher for males and for species with larger body mass and colony sizes. Haemoplasmas displayed high genetic diversity (21 novel genotypes) and strong host specificity. Evolutionary patterns supported codivergence of bats and bacterial genotypes alongside phylogenetically constrained host shifts. Bat species centrality to the network of shared haemoplasma genotypes was phylogenetically clustered and unrelated to prevalence, further suggesting rare—but detectable—bacterial sharing between species. Our study highlights the importance of using fine phylogenetic scales when assessing host specificity and suggests phylogenetic similarity may play a key role in host shifts not only for viruses but also for bacteria. Such work more broadly contributes to increasing efforts to understand crossâ€species transmission and the epidemiological consequences of bacterial pathogens