Effects of Structural Refuge and Density on Foraging Behaviour and Mortality of Hungry Tadpoles Subject to Predation Risk

Abstract

Theoretical models of prey behaviour predict that food‐limited prey engage in risk‐prone foraging and thereby succumb to increased mortality from predation. However, predation risk also may be influenced by factors including prey density and structural cover, such that the presumed role of prey hunger on predation risk may be obfuscated in many complex predator–prey systems. Using a tadpole (prey) – dragonfly larva (predator) system, we determined relative risk posed to hungry vs. sated prey when both density and structural cover were varied experimentally. Overall, prey response to perceived predation risk was primarily restricted to increased cover use, and hungry prey did not exhibit risk‐prone foraging. Surprisingly, hungry prey showed lower activity than sated prey when exposed to predation risk, perhaps indicating increased effort in search of refuge or spatial avoidance of predator cues among sated animals. An interaction between hunger level and predation risk treatments indicated that prey state affected sensitivity to perceived risk. We also examined the lethal implications of prey hunger by allowing predators to select directly between hungry and sated prey. Although predators qualitatively favoured hungry prey when density was elevated and structural cover was sparse, the overall low observed variation in mortality risk between hunger treatments suggests that preferential selection of hungry prey was weak. This implies that hunger effects on prey mortality risk may not be readily observed in complex landscapes with additional factors influencing risk. Thus, current starvation‐predation trade‐off theory may need to be broadened to account for other mechanisms through which undernourished prey may cope with predation risk.

Assessing behavioural and morphological responses of frog tadpoles to temporal variability in predation risk

“…Yet, this approach was critical because we assessed differential expression of plastic traits across environments and needed to control the extent of genetic differences among treatments. Further, this approach has the benefit of reducing within‐treatment variability and should increase our ability to detect fine‐scale responses to predation risk (Hossie & Murray, ). As such, variation in our data represents variation in plastic response among full‐sib individuals, rather than among genetically independent individuals.…”

The Rate of Degradation of Chemical Cues Indicating Predation Risk: An Experiment and Review

“…The presence or absence of tadpoles in the water during the aging process was manipulated because tadpoles themselves may contribute to cue breakdown by filtering particles from the water or by inoculation with microbes. Indeed, the response to predator cues is known to decline at high prey density (Hossie & Murray 2011;Van Buskirk et al 2011). The mechanism underlying this pattern is proposed to involve density-dependent risk assessment (Peacor 2003), but our experiment tests whether cue decomposition depends on prey density as well.…”

“…The presence or absence of tadpoles in the water during the aging process was manipulated because tadpoles themselves may contribute to cue breakdown by filtering particles from the water or by inoculation with microbes. Indeed, the response to predator cues is known to decline at high prey density (Hossie & Murray ; Van Buskirk et al. ).…”

Lesser of Two Evils? Foraging Choices in Response to Threats of Predation and Parasitism

“…Larval amphibians provide a good model system for examining the pre-encounter effects of predators and parasites as they have been demonstrated to exhibit defensive behaviours in response to both types of natural enemy. In the presence of predators such as larval odonates and fish, tadpoles usually alter the levels and timing of their activities, seek refuges, and abandon high resource patches [ 30 , 31 , 32 ]. With respect to pathogen avoidance, adult amphibians avoid laying eggs in water bodies containing snails that are host to trematode (flatworm) parasites, and tadpoles avoid contact with conspecifics infected by a directly-transmitted pathogenic yeast [ 33 , 34 ].…”