Abstract

Hosts are armed with several lines of defence in the battle against parasites: they may prevent the establishment of infection, reduce parasite growth once infected or persevere through mechanisms that reduce the damage caused by infection, called tolerance. Studies on tolerance in animals have focused on mortality, and sterility tolerance has not been investigated experimentally. Here, we tested for genetic variation in the multiple steps of defence when the invertebrate Daphnia magna is infected with the sterilizing bacterial pathogen Pasteuria ramosa: anti-infection resistance, anti-growth resistance and the ability to tolerate sterilization once infected. When exposed to nine doses of a genetically diverse pathogen inoculum, six host genotypes varied in their average susceptibility to infection and in their parasite loads once infected. How host fecundity changed with increasing parasite loads did not vary between genotypes, indicating that there was no genetic variation for this measure of fecundity tolerance. However, genotypes differed in their level of fecundity compensation under infection, and we discuss how, by increasing host fitness without targeting parasite densities, fecundity compensation is consistent with the functional definition of tolerance. Such infection-induced life-history shifts are not traditionally considered to be part of the immune response, but may crucially reduce harm (in terms of fitness loss) caused by disease, and are a distinct source of selection on pathogens.

Highlights

  • Amidst the widespread threat of parasitism, hosts persist with the help of several lines of defence (Frank, 2002)

  • Resistance mechanisms that target pathogens directly have been widely investigated, but it is becoming increasingly clear that alternative ways of improving host fitness, such as tolerance, play an important role in reducing the harm caused during within-host growth

  • Genetic variation was present in several stages of defence when D. magna is infected with sterilizing pathogen P. ramosa

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Summary

Introduction

Amidst the widespread threat of parasitism, hosts persist with the help of several lines of defence (Frank, 2002). 25 (2012) 1888–1896 JOURNAL OF EVOLUTIONARY BIOLOGY a 2012 EUROPEAN SOCIETY FOR EVOLUTIONARY BIOLOGY mechanisms that interfere with infection-derived toxins (Feingold et al, 1995; Pamplona et al, 2007; Rasko & Sperandio, 2010) result in tolerance because they reduce the severity of disease that arises from infection, without directly reducing the total density of pathogens Other mechanisms, such as wound repair during infection (Reece et al, 2006; Ayres & Schneider, 2008), or those that reduce immunopathology (Graham et al, 2005), have been proposed as potential promoters of tolerance to infection, because parasite growth is not directly targeted but the net result is a fitter host

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