ArticleEpidemiology and infection2015
Blowback: new formal perspectives on agriculturally driven pathogen evolution and spread.
Article in Epidemiology and infection, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- On Disease Configurations, Black-Grass Blowback, and Probiotic Pest Management.Annals of the American Association of Geographers · 2024Article
- Genotype and sex-based host variation in behaviour and susceptibility drives population disease dynamics.Proceedings. Biological sciences · 2020Article
- Emerging zoonoses: tackling the challenges.Epidemiology and infection · 2015Article
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
By their diversity in time, space, and mode, traditional and conservation agricultures can create barriers limiting pathogen evolution and spread analogous to a sterilizing temperature. Large-scale monocropping and confined animal feeding-lot operations remove such barriers, resulting, above agroecologically specific thresholds, in the development and wide propagation of novel disease strains. We apply a newly developed class of necessary-conditions statistical models of evolutionary process, first using the theory on an evolutionarily stable viral pathogen vulnerable to vaccine treatment: post-World War II poliomyelitis emerged in the UK and USA from sudden widespread adoption of automobile ownership and usage. We then examine an evolutionarily variable pathogen, swine influenza in North America. The model suggests epidemiological blowback from globalizing intensive husbandry and the raising and shipping of monoculture livestock across increasing expanses, is likely to be far more consequential, driving viral selection for greater virulence and lowered response to biomedical intervention.
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