Abstract

Host density can increase infection rates and reduce host fitness as increasing population density enhances the risk of becoming infected either through increased encounter rate or because host condition may decline. Conceivably, potential hosts could take high host density as a cue to up-regulate their defence systems. However, as host density usually covaries with food availability, it is difficult to examine the importance of host density in isolation. Thus, we performed two full-factorial experiments that varied juvenile densities of Daphnia magna (a freshwater crustacean) and food availability independently. We also included a simulated high-density treatment, where juvenile experimental animals were kept in filtered media that previously maintained Daphnia at high-density. Upon reaching adulthood, we exposed the Daphnia to their sterilizing bacterial parasite, Pasteuria ramosa, and examined how the juvenile treatments influenced the likelihood and severity of infection (Experiment I) and host immune investment (Experiment II). Neither juvenile density nor food treatments affected the likelihood of infection; however, well-fed hosts that were well-fed as juveniles produced more offspring prior to sterilization than their less well-fed counterparts. By contrast, parasite growth was independent of host juvenile resources or host density. Parasite-exposed hosts had a greater number of circulating haemocytes than controls (i.e., there was a cellular immune response), but the magnitude of immune response was not mediated by food availability or host density. These results suggest that density dependent effects on disease arise primarily through correlated changes in food availability: low food could limit parasitism and potentially curtail epidemics by reducing both the host’s and parasite’s reproduction as both depend on the same food.

Highlights

  • Host fitness decline due to parasitism is commonly context dependent [1,2,3,4]

  • Recent theoretical studies suggest that the expression of virulence depends on host population density, such that infected hosts have a higher sensitivity to density, and reach their carrying capacity earlier than uninfected hosts [5,6]

  • The present study analysed the effects of varying juvenile host densities and food availability on D. magna fitness under infection with the sterilizing parasite P. ramosa

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Summary

Introduction

Host fitness decline due to parasitism (often termed virulence) is commonly context dependent [1,2,3,4]. Recent theoretical studies suggest that the expression of virulence depends on host population density, such that infected hosts have a higher sensitivity to density, and reach their carrying capacity earlier than uninfected hosts [5,6]. Since increased host density is thought to enhance the potential of parasite transmission [4,7], elevated juvenile host densities may predict increased likelihood of infection at the adult stage, and act as a cue for hosts to shift investment into immune defences. Increased immune preparedness can potentially come with costs - either energetic cost of investment or immunopathological cost when responses are launched [8]. Survival was reduced in bumblebees and beetles with challenged immune systems [9,10], and in Indian meal moths and sticklebacks, an increase in resistance was correlated with longer development time [11,12]

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