Defining the risk landscape in the context of pathogen pollution: <i>Toxoplasma gondii</i> in sea otters along the Pacific Rim. Burgess, T. L., Tim Tinker, M., Miller, M. A., Bodkin, J. L., Murray, M. J., Saarinen, J. A., Nichol, L. M., Larson, S., Conrad, P. A., & Johnson, C. K. Royal Society Open Science, 5(7):171178, July, 2018.
Defining the risk landscape in the context of pathogen pollution: <i>Toxoplasma gondii</i> in sea otters along the Pacific Rim [link]Paper  doi  abstract   bibtex   
Pathogens entering the marine environment as pollutants exhibit a spatial signature driven by their transport mechanisms. The sea otter ( Enhydra lutris ), a marine animal which lives much of its life within sight of land, presents a unique opportunity to understand land–sea pathogen transmission. Using a dataset on Toxoplasma gondii prevalence across sea otter range from Alaska to California, we found that the dominant drivers of infection risk vary depending upon the spatial scale of analysis. At the population level, regions with high T. gondii prevalence had higher human population density and a greater proportion of human-dominated land uses, suggesting a strong role for population density of the felid definitive host of this parasite. This relationship persisted when a subset of data were analysed at the individual level: large-scale patterns in sea otter T. gondii infection prevalence were largely explained by individual exposure to areas of high human housing unit density, and other landscape features associated with anthropogenic land use, such as impervious surfaces and cropping land. These results contrast with the small-scale, within-region analysis, in which age, sex and prey choice accounted for most of the variation in infection risk, and terrestrial environmental features provided little variation to help in explaining observed patterns. These results underscore the importance of spatial scale in study design when quantifying both individual-level risk factors and landscape-scale variation in infection risk.
@article{burgess_defining_2018,
	title = {Defining the risk landscape in the context of pathogen pollution: \textit{{Toxoplasma} gondii} in sea otters along the {Pacific} {Rim}},
	volume = {5},
	issn = {2054-5703},
	shorttitle = {Defining the risk landscape in the context of pathogen pollution},
	url = {https://royalsocietypublishing.org/doi/10.1098/rsos.171178},
	doi = {10.1098/rsos.171178},
	abstract = {Pathogens entering the marine environment as pollutants exhibit a spatial signature driven by their transport mechanisms. The sea otter (
              Enhydra lutris
              ), a marine animal which lives much of its life within sight of land, presents a unique opportunity to understand land–sea pathogen transmission. Using a dataset on
              Toxoplasma gondii
              prevalence across sea otter range from Alaska to California, we found that the dominant drivers of infection risk vary depending upon the spatial scale of analysis. At the population level, regions with high
              T. gondii
              prevalence had higher human population density and a greater proportion of human-dominated land uses, suggesting a strong role for population density of the felid definitive host of this parasite. This relationship persisted when a subset of data were analysed at the individual level: large-scale patterns in sea otter
              T. gondii
              infection prevalence were largely explained by individual exposure to areas of high human housing unit density, and other landscape features associated with anthropogenic land use, such as impervious surfaces and cropping land. These results contrast with the small-scale, within-region analysis, in which age, sex and prey choice accounted for most of the variation in infection risk, and terrestrial environmental features provided little variation to help in explaining observed patterns. These results underscore the importance of spatial scale in study design when quantifying both individual-level risk factors and landscape-scale variation in infection risk.},
	language = {en},
	number = {7},
	urldate = {2023-06-15},
	journal = {Royal Society Open Science},
	author = {Burgess, Tristan L. and Tim Tinker, M. and Miller, Melissa A. and Bodkin, James L. and Murray, Michael J. and Saarinen, Justin A. and Nichol, Linda M. and Larson, Shawn and Conrad, Patricia A. and Johnson, Christine K.},
	month = jul,
	year = {2018},
	keywords = {NALCMS},
	pages = {171178},
}

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