Showing papers by "Kevin Gross published in 1999"
TL;DR: An extensive body of theoretical work has shown that variability in risk across host patches can be stabilizing when risk is concentrated in patches with many hosts, in patch with few hosts, or in a particular subset of patches regardless of host distribution.
Abstract: A central result of host-parasitoid theory is that hostparasitoid dynamics in simple models can be stabilized by aggregation of risk among hosts (Chesson and Murdoch 1986). Aggregation of risk describes the degree of variability in the distribution of attack probabilities over all hosts in the population; the more variable this distribution is, the more aggregated risk is said to be. For example, if all hosts have an equal probability of being parasitized, risk is equally spread among hosts, but if some hosts have a greater chance of being parasitized, risk of parasitism is aggregated in a subset of the population. When the distribution of risk is sufficiently aggregated, this aggregation stabilizes host-parasitoid dynamics through pseudointerference among foraging parasitoids (Free et al. 1977; Walde and Murdoch 1988). Pseudointerference decreases the number of hosts killed per parasitoid as parasitoid densities rise above equilibrium, thereby squelching the onset of unstable oscillations that ultimately result in the extinction of the parasitoid. Aggregation of risk is often envisioned as arising from differences in risk among patches of hosts. An extensive body of theoretical work has shown that variability in risk across host patches can be stabilizing when risk is concentrated in patches with many hosts (host densitydependent aggregation; Hassell and May 1973), in patches with few hosts (inverse density-dependent aggregation; Hassell 1984), or in a particular subset of patches regardless of host distribution (density-independent aggregation; Chesson and Murdoch 1986). Variability in risk among patches is not the only pathway to a variable distribution
18 citations