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Genotypic variation in parasite avoidance behaviour and other mechanistic, nonlinear components of transmission

Research output: Contribution to Journal/MagazineJournal articlepeer-review

Published
  • Alexander T. Strauss
  • Jessica L. Hite
  • David J. Civitello
  • Marta S. Shocket
  • Carla E. Cáceres
  • Spencer R. Hall
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<mark>Journal publication date</mark>20/11/2019
<mark>Journal</mark>Proceedings of the Royal Society B: Biological Sciences
Issue number1915
Volume286
Publication StatusPublished
<mark>Original language</mark>English

Abstract

Traditional epidemiological models assume that transmission increases proportionally to the density of parasites. However, empirical data frequently
contradict this assumption. General yet mechanistic models can explain
why transmission depends nonlinearly on parasite density and thereby
identify potential defensive strategies of hosts. For example, hosts could
decrease their exposure rates at higher parasite densities (via behavioural
avoidance) or decrease their per-parasite susceptibility when encountering
more parasites (e.g. via stronger immune responses). To illustrate, we
fitted mechanistic transmission models to 19 genotypes of Daphnia dentifera
hosts over gradients of the trophically acquired parasite, Metschnikowia bicuspidata. Exposure rate (foraging, F) frequently decreased with parasite
density (Z), and per-parasite susceptibility (U) frequently decreased with
parasite encounters (F×Z). Consequently, infection rates (F×U×Z) often
peaked at intermediate parasite densities. Moreover, host genotypes varied
substantially in these responses. Exposure rates remained constant for
some genotypes but decreased sensitively with parasite density for others
(up to 78%). Furthermore, genotypes with more sensitive foraging/exposure
also foraged faster in the absence of parasites (suggesting ‘fast and sensitive’
versus ‘slow and steady’ strategies). These relationships suggest that high
densities of parasites can inhibit transmission by decreasing exposure rates
and/or per-parasite susceptibility, and identify several intriguing axes for
the evolution of host defence.