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Published in

The Company of Biologists, Journal of Experimental Biology, 2016

DOI: 10.1242/jeb.151456

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Can the behaviour of threespine stickleback parasitized withSchistocephalus solidusbe replicated by manipulating host physiology?

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Data provided by SHERPA/RoMEO

Abstract

Sticklebacks infected by the parasitic flatworm Schistocephalus solidus show dramatic changes in phenotype, including a loss of species-typical behavioural responses to predators. The timing of host behaviour change coincides with the development of infectivity of the parasite to the final host (a piscivorous bird), making it an ideal model for studying the mechanisms of infection-induced behavioural modification. However, whether the loss of host anti-predator behaviour results from direct manipulation by the parasite, or is a by-product (e.g. host immune response) or side-effect of infection (e.g. energetic loss), remains controversial. To understand the physiological mechanisms that generate these behavioural changes, we quantified the behavioural profiles of experimentally infected fish and attempted to replicate these in non-parasitized fish by exposing them to treatments including immunity activation and fasting, or by pharmacologically inhibiting the stress axis. All fish were screened for the following behaviours: activity, water depth preference, sociability, phototaxis, anti-predator response and latency to feed. We were able to change individual behaviours with certain treatments. Our results suggest that the impact of S. solidus on the stickleback might be of a multifactorial nature. The behaviour changes observed in infected fish may be due to the combined effects of modifying the serotonergic axis, the lack of energy, and the activation of the immune system.