“Predicting the thermal and allometric dependencies of disease transmission via the metabolic theory of ecology”

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Devin Kirk, Pepijn Luijckx, Andrijana Stanic, and Martin Krkošek (May 2019)

Warming temperatures associated with climate change and host body size can both alter infectious disease spread, though often in complex ways. This is because both factors can affect different components of disease transmission, namely the contact rate between uninfected and infected individuals or parasites, and the subsequent likelihood that that contact results in a new infection. To understand how warming and size will affect disease spread in a host-parasite system, we need to first predict their effects on contact and infection rates, and then tie these predictions together using classic disease models of transmission. The metabolic theory of ecology (MTE) provides a general framework for predicting how temperature and host size affect contact and infection rates. Here, the authors conducted two experiments using a Daphnia–parasite system, and then fit MTE models to the data. They show that transmission is strongly affected by temperature, and that the different rates vary with temperature and body size in distinct manners. Moreover, they show that MTE functions can capture how contact rate and the probability of infection change across temperature and size. Together these two functions can accurately predict transmission rate continuously across a wide temperature range. This represents a valuable potential tool for helping predict how disease spread will change as environmental temperatures rise.


Abstract

The metabolic theory of ecology (MTE) provides a general framework of allometric and thermal dependence that may be useful for predicting how climate change will affect disease spread. Using Daphnia magna and a microsporidian gut parasite, we conducted two experiments across a wide thermal range and fitted transmission models that utilize MTE submodels for transmission parameters. We decomposed transmission into contact rate and probability of infection, and further decomposed probability of infection into a product of gut residence time (GRT) and per-parasite infection rate of gut cells. Contact rate generally increased with temperature and scaled positively with body size, whereas infection rate had a narrow hump-shaped thermal response and scaled negatively with body size. GRT increased with host size and was longest at extreme temperatures. GRT and infection rate inside the gut combined to create a 3.5× higher probability of infection for the smallest relative to the largest individuals. Small temperature changes caused large differences in transmission. We also fit several alternative transmission models to data at individual temperatures. The more complex models, parasite antagonism or synergism and host heterogeneity, did not substantially improve the fit to the data. Our results show that transmission rate is the product of several distinct thermal and allometric functions that can be predicted continuously across temperature and host size using MTE.