TY - JOUR

T1 - Genotypic variation in parasite avoidance behaviour and other mechanistic, nonlinear components of transmission

AU - Strauss, Alexander T.

AU - Hite, Jessica L.

AU - Civitello, David J.

AU - Shocket, Marta S.

AU - Cáceres, Carla E.

AU - Hall, Spencer R.

PY - 2019/11/20

Y1 - 2019/11/20

N2 - Traditional epidemiological models assume that transmission increases proportionally to the density of parasites. However, empirical data frequentlycontradict this assumption. General yet mechanistic models can explainwhy transmission depends nonlinearly on parasite density and therebyidentify potential defensive strategies of hosts. For example, hosts coulddecrease their exposure rates at higher parasite densities (via behaviouralavoidance) or decrease their per-parasite susceptibility when encounteringmore parasites (e.g. via stronger immune responses). To illustrate, wefitted mechanistic transmission models to 19 genotypes of Daphnia dentiferahosts over gradients of the trophically acquired parasite, Metschnikowia bicuspidata. Exposure rate (foraging, F) frequently decreased with parasitedensity (Z), and per-parasite susceptibility (U) frequently decreased withparasite encounters (F×Z). Consequently, infection rates (F×U×Z) oftenpeaked at intermediate parasite densities. Moreover, host genotypes variedsubstantially in these responses. Exposure rates remained constant forsome genotypes but decreased sensitively with parasite density for others(up to 78%). Furthermore, genotypes with more sensitive foraging/exposurealso foraged faster in the absence of parasites (suggesting ‘fast and sensitive’versus ‘slow and steady’ strategies). These relationships suggest that highdensities of parasites can inhibit transmission by decreasing exposure ratesand/or per-parasite susceptibility, and identify several intriguing axes forthe evolution of host defence.

AB - Traditional epidemiological models assume that transmission increases proportionally to the density of parasites. However, empirical data frequentlycontradict this assumption. General yet mechanistic models can explainwhy transmission depends nonlinearly on parasite density and therebyidentify potential defensive strategies of hosts. For example, hosts coulddecrease their exposure rates at higher parasite densities (via behaviouralavoidance) or decrease their per-parasite susceptibility when encounteringmore parasites (e.g. via stronger immune responses). To illustrate, wefitted mechanistic transmission models to 19 genotypes of Daphnia dentiferahosts over gradients of the trophically acquired parasite, Metschnikowia bicuspidata. Exposure rate (foraging, F) frequently decreased with parasitedensity (Z), and per-parasite susceptibility (U) frequently decreased withparasite encounters (F×Z). Consequently, infection rates (F×U×Z) oftenpeaked at intermediate parasite densities. Moreover, host genotypes variedsubstantially in these responses. Exposure rates remained constant forsome genotypes but decreased sensitively with parasite density for others(up to 78%). Furthermore, genotypes with more sensitive foraging/exposurealso foraged faster in the absence of parasites (suggesting ‘fast and sensitive’versus ‘slow and steady’ strategies). These relationships suggest that highdensities of parasites can inhibit transmission by decreasing exposure ratesand/or per-parasite susceptibility, and identify several intriguing axes forthe evolution of host defence.

U2 - 10.1098/rspb.2019.2164

DO - 10.1098/rspb.2019.2164

M3 - Journal article

VL - 286

JO - Proceedings of the Royal Society B: Biological Sciences

JF - Proceedings of the Royal Society B: Biological Sciences

SN - 0962-8452

IS - 1915

ER -