4.7 Article

Parasite exposure and host susceptibility jointly drive the emergence of epidemics

Journal

ECOLOGY
Volume 102, Issue 2, Pages -

Publisher

WILEY
DOI: 10.1002/ecy.3245

Keywords

Daphnia; disease; epidemic; exposure; host trait; immune; infection stage; Metschnikowia; susceptibility; transmission

Categories

Funding

  1. National Science Foundation [DGE 1144245, DGE 1069157, NSF 1354407, 1655665, NSF 1701515, NSF 1655656]
  2. Division Of Environmental Biology
  3. Direct For Biological Sciences [1655665, 1655656] Funding Source: National Science Foundation

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The study on interactions between an aquatic host and its fungal parasite revealed that epidemics are driven by the interaction of parasite exposure and host susceptibility. Epidemics only emerged when a host population's level of exposure exceeded its individuals' capacity for recovery, and host internal clearance traits were critical in regulating epidemics. Individual host traits can play a significant role in influencing broad epidemiological patterns.
Parasite transmission is thought to depend on both parasite exposure and host susceptibility to infection; however, the relative contribution of these two factors to epidemics remains unclear. We used interactions between an aquatic host and its fungal parasite to evaluate how parasite exposure and host susceptibility interact to drive epidemics. In six lakes, we tracked the following factors from pre-epidemic to epidemic emergence: (1) parasite exposure (measured observationally as fungal spores attacking wild-caught hosts), (2) host susceptibility (measured experimentally as the number of fungal spores required to produce terminal infection), (3) host susceptibility traits (barrier resistance and internal clearance, both quantified with experimental assays), and (4) parasite prevalence (measured observationally from wild-caught hosts). Tracking these factors over 6 months and in almost 7,000 wild-caught hosts provided key information on the drivers of epidemics. We found that epidemics depended critically on the interaction of exposure and susceptibility; epidemics only emerged when a host population's level of exposure exceeded its individuals' capacity for recovery. Additionally, we found that host internal clearance traits (the hemocyte response) were critical in regulating epidemics. Our study provides an empirical demonstration of how parasite exposure and host susceptibility interact to inhibit or drive disease in natural systems and demonstrates that epidemics can be delayed by asynchronicity in the two processes. Finally, our results highlight how individual host traits can scale up to influence broad epidemiological patterns.

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