Predation (Including Parasites and Disease) and Herbivory


Organisms are usually both enemies and victims of ecological interactions. Even individuals within ‘top predator’ species often suffer from cannibalism (an ecological ‘self‐loop’), parasites, or disease agents. Predators capture, kill and consume their victims. Parasites either live on or within a victim and may kill their host directly or, more typically, reduce the host's growth, survival and/or reproductive potential. Parasitoids function like predators but the act of killing the host is done by offspring which, generally, hatch from an egg on or near a host and then enter the victim and consumes it from inside. Disease agents vary in their effects on victims from hardly noticeable to causing death. Finally, herbivory is that act of an animal consuming part, or the entirety, of a plant. The effect of herbivory on plants may be unquantifiable to resulting in the death of the plant.

Key Concepts:

  • Predators capture, kill and consume their prey.

  • Parasitoids lay eggs on or near victims. These eggs hatch and the larvae enter and consume their victims from within.

  • Parasites live on or within their victims and usually reduce the victim's ability to grow, survive and/or reproduce.

  • Disease agents generally reduce victim growth, survival and/or reproductive rates.

  • Herbivory is the act by an animal of consuming plant material which may reduce plant growth, survival and/or reproductive success.

  • Researchers continue to debate the relative importance of top‐down effects from enemies on victims and the effects of bottom‐up effects of resources in population dynamics.

  • Mathematical and computer models can help us to understand and predict these complex species interactions.

Keywords: predation; herbivory; plant–animal interactions; host–pathogen dynamics; models

Figure 1.

(a) The standard Lotka–Volterra predator–prey model results in oscillations when the number of predators and prey are not, simultaneously, in equilibrium. This results in oscillations that exhibit neutral stability. On the right (b) is the phase‐plane graph. The dashed lines represent zero isoclines (equilibria) for prey (horizontal, solid line, V=q/ac) and enemies at E=r/a (vertical line). In this rendering r=0.5, a=0.025, c=0.1, and d=0.1.

Figure 2.

The three predator functional responses (see text and Holling, ).

Figure 3.

The Nicholson–Bailey parasitoid model. The model follows equation with H[1]=200; P[1]=150; a=0.004; c=1; R=1.75. The equilibrium solutions would be H[1]=ln(R)/(c*a*(R−1))≈186.5 and P[1]=ln(R)/a≈139.9.

Figure 4.

The solutions to two epidemic models are shown. (a) The number of susceptible (S), infectious (I) and recovered (R) individuals over time. (b) The phase‐plane graph for the number of infectious versus susceptible individuals over time. Note that we start with mostly susceptible individuals. The peak (maximum I) occurs at the vertical dashed line which represents the threshold susceptible population which just maintains the disease agent (v/B). The lower panels (c and d) are similar but for the network model. The network used was a Watts–Strogatz graph (Watts and Strogatz, ) with k=4, p=0.05 and N=300. Note the similarity (and differences).



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Tilman D and Kareiva P (eds) (1997) Spatial Ecology: The Role of Space in Population Dynamics and Interspecific Interactions. Princeton, NJ: Princeton University Press.

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Hartvigsen, Gregg(Jun 2012) Predation (Including Parasites and Disease) and Herbivory. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1002/9780470015902.a0003310.pub2]