Species diversity concurrently dilutes and amplifies transmission in a zoonotic host–pathogen system through competing mechanisms

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Abstract

In this era of unprecedented biodiversity loss and increased zoonotic disease emergence, it is imperative to understand the effects of biodiversity on zoonotic pathogen dynamics in wildlife. Whether increasing biodiversity should lead to a decrease or increase in infection prevalence, termed the dilution and amplification effects, respectively, has been hotly debated in disease ecology. Sin Nombre hantavirus, which has an ∼35% mortality rate when it spills over into humans, occurs at a lower prevalence in the reservoir host, the North American deermouse, in areas with higher small mammal diversity—a dilution effect. However, the mechanism driving this relationship is not understood. Using a mechanistic mathematical model of infection dynamics and a unique long-term, high-resolution, multisite dataset, it appears that the observed dilution effect is a result of increasing small-mammal diversity leading to decreased deermouse population density and, subsequently, prevalence (a result of density-dependent transmission). However, once density is taken into account, there is an increase in the transmission rate at sites with higher diversity—a component amplification effect. Therefore, dilution and amplification are occurring at the same time in the same host–pathogen system; there is a component amplification effect (increase in transmission rate), but overall a net dilution because the effect of diversity on reservoir host population density is stronger. These results suggest we should focus on how biodiversity affects individual mechanisms that drive prevalence and their relative strengths if we want to make generalizable predictions across host–pathogen systems.

Original languageEnglish
Pages (from-to)7979-7984
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Volume115
Issue number31
DOIs
StatePublished - Jul 31 2018

Funding

tional Development Award (IDeA) Networks of Biomedical Research Excellence (INBRE) program in Montana. A.D.L. was supported by the Research and Policy for Infectious Disease Dynamics (RAPIDD) program of the Science and Technology Directorate (US Department of Homeland Security) and the Fogarty International Center (NIH); the University of Montana, University Grant Program; and NSF Established Program to Stimulate Competitive Research (EPSCoR). Long-term data collection was supported by the US Centers for Disease Control and Prevention, Atlanta and the NIH Institutional Development Award (IDeA) Networks of Biomedical Research Excellence (INBRE) program in Montana. A.D.L. was supported by the Research and Policy for Infectious Disease Dynamics (RAPIDD) program of the Science and Technology Directorate (US Department of Homeland Security) and the Fogarty International Center (NIH); the University of Montana, University Grant Program; and NSF Established Program to Stimulate Competitive Research (EPSCoR). ACKNOWLEDGMENTS. Long-term data collection was supported by the US Centers for Disease Control and Prevention, Atlanta and the NIH Institu-

Funders
Indiana University-Purdue University Indianapolis
Centers for Disease Control and Prevention

    Keywords

    • Amplification effect
    • Dilution effect
    • Hantavirus
    • SIR modeling
    • Zoonotic disease

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