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Competition and Facilitation between a Disease and a Predator in a Stunted Prey Population.

Boerlijst MC, de Roos AM - PLoS ONE (2015)

Bottom Line: In contrast to predators, parasites do not necessarily kill their host but instead they may change host life history.Here, the disease facilitates the predator, and predator density will be substantially increased.We discuss the implications of our results for the dynamics and structure of the natural Ligula-Roach system.

View Article: PubMed Central - PubMed

Affiliation: Theoretical Ecology, Institute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, P.O. Box 94248, 1090 GE, Amsterdam, The Netherlands.

ABSTRACT
The role of diseases and parasites has received relatively little attention in modelling ecological dynamics despite mounting evidence of their importance in structuring communities. In contrast to predators, parasites do not necessarily kill their host but instead they may change host life history. Here, we study the impact of a parasite that selectively infects juvenile prey individuals and prevents them from maturing into adults. The model is inspired by the Ligula intestinalis tape worm and its cyprinid fish host Rutilis rutilis. We demonstrate that the parasite can promote as well as demote the so-called stunting in its host population, that is, the accumulation of juvenile prey, which leads to strong exploitation competition and consequently to a bottleneck in maturation. If competition between infected and uninfected individuals is strong, stunting will be enhanced and bistability between a stunted and non-stunted prey population occurs. In this case, the disease competes with the predator of its host species, possibly leading to predator extinction. In contrast, if the competition between infected and uninfected individuals is weak, the stunting is relieved, and epi-zoonotic cycles will occur, with recurrent epidemic outbreaks. Here, the disease facilitates the predator, and predator density will be substantially increased. We discuss the implications of our results for the dynamics and structure of the natural Ligula-Roach system.

No MeSH data available.


Related in: MedlinePlus

Bistability in the absence of disease.Bifurcation diagram as a function of predator death rate μP. (a) Equilibrium prey density, juveniles JS in solid line (blue), and adults A in dashed line (green), and (b) Equilibrium predator density P (red). The equilibrium curves exhibit a so-called catastrophe fold, with a bistable region for 0.435 < μP < 0.553. The unstable (saddle node) state is indicated with the dotted lines. Model parameters are b = 1, c = 1, d = 1, n = 1, φ = 1, μJ = 0.05, μA = 0.1, and μP variable.
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pone.0132251.g001: Bistability in the absence of disease.Bifurcation diagram as a function of predator death rate μP. (a) Equilibrium prey density, juveniles JS in solid line (blue), and adults A in dashed line (green), and (b) Equilibrium predator density P (red). The equilibrium curves exhibit a so-called catastrophe fold, with a bistable region for 0.435 < μP < 0.553. The unstable (saddle node) state is indicated with the dotted lines. Model parameters are b = 1, c = 1, d = 1, n = 1, φ = 1, μJ = 0.05, μA = 0.1, and μP variable.

Mentions: We first show the dynamics of our model in the absence of the disease. In Fig 1a and 1b, the equilibrium density of, respectively, prey and predator is plotted as a function of the predator death rate μP. For intermediate predator death rate (i.c. 0.435 < μP < 0.553) there exists a region of bistability. Interestingly, in both alternative steady states the adult prey density is identical, as it is uniquely determined by the predator equilibrium; i.c. putting Eq (4) to zero gives for both alternative steady states. In the equilibrium with high juvenile density, the corresponding predator density is small. Here, the prey population is stunted in the juvenile class and, consequently, maturation is strongly reduced. Consequently, the adult prey population in this case is mainly limited by the low maturation. In contrast, in the low juvenile equilibrium, the predator density is much larger. In this equilibrium, the total maturation into the adult population is increased, but this is balanced by the larger predation rate. In conclusion, in the absence of the disease the prey population can be caught in a stunted equilibrium, where high abundance of juvenile prey causes strong competition amongst juveniles, resulting in stunted growth and a maturation bottleneck. However, such a large juvenile prey population could serve as a target for a disease, which could potentially act to relieve the stuntedness of the prey population.


Competition and Facilitation between a Disease and a Predator in a Stunted Prey Population.

Boerlijst MC, de Roos AM - PLoS ONE (2015)

Bistability in the absence of disease.Bifurcation diagram as a function of predator death rate μP. (a) Equilibrium prey density, juveniles JS in solid line (blue), and adults A in dashed line (green), and (b) Equilibrium predator density P (red). The equilibrium curves exhibit a so-called catastrophe fold, with a bistable region for 0.435 < μP < 0.553. The unstable (saddle node) state is indicated with the dotted lines. Model parameters are b = 1, c = 1, d = 1, n = 1, φ = 1, μJ = 0.05, μA = 0.1, and μP variable.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4492505&req=5

pone.0132251.g001: Bistability in the absence of disease.Bifurcation diagram as a function of predator death rate μP. (a) Equilibrium prey density, juveniles JS in solid line (blue), and adults A in dashed line (green), and (b) Equilibrium predator density P (red). The equilibrium curves exhibit a so-called catastrophe fold, with a bistable region for 0.435 < μP < 0.553. The unstable (saddle node) state is indicated with the dotted lines. Model parameters are b = 1, c = 1, d = 1, n = 1, φ = 1, μJ = 0.05, μA = 0.1, and μP variable.
Mentions: We first show the dynamics of our model in the absence of the disease. In Fig 1a and 1b, the equilibrium density of, respectively, prey and predator is plotted as a function of the predator death rate μP. For intermediate predator death rate (i.c. 0.435 < μP < 0.553) there exists a region of bistability. Interestingly, in both alternative steady states the adult prey density is identical, as it is uniquely determined by the predator equilibrium; i.c. putting Eq (4) to zero gives for both alternative steady states. In the equilibrium with high juvenile density, the corresponding predator density is small. Here, the prey population is stunted in the juvenile class and, consequently, maturation is strongly reduced. Consequently, the adult prey population in this case is mainly limited by the low maturation. In contrast, in the low juvenile equilibrium, the predator density is much larger. In this equilibrium, the total maturation into the adult population is increased, but this is balanced by the larger predation rate. In conclusion, in the absence of the disease the prey population can be caught in a stunted equilibrium, where high abundance of juvenile prey causes strong competition amongst juveniles, resulting in stunted growth and a maturation bottleneck. However, such a large juvenile prey population could serve as a target for a disease, which could potentially act to relieve the stuntedness of the prey population.

Bottom Line: In contrast to predators, parasites do not necessarily kill their host but instead they may change host life history.Here, the disease facilitates the predator, and predator density will be substantially increased.We discuss the implications of our results for the dynamics and structure of the natural Ligula-Roach system.

View Article: PubMed Central - PubMed

Affiliation: Theoretical Ecology, Institute for Biodiversity and Ecosystem Dynamics, University of Amsterdam, P.O. Box 94248, 1090 GE, Amsterdam, The Netherlands.

ABSTRACT
The role of diseases and parasites has received relatively little attention in modelling ecological dynamics despite mounting evidence of their importance in structuring communities. In contrast to predators, parasites do not necessarily kill their host but instead they may change host life history. Here, we study the impact of a parasite that selectively infects juvenile prey individuals and prevents them from maturing into adults. The model is inspired by the Ligula intestinalis tape worm and its cyprinid fish host Rutilis rutilis. We demonstrate that the parasite can promote as well as demote the so-called stunting in its host population, that is, the accumulation of juvenile prey, which leads to strong exploitation competition and consequently to a bottleneck in maturation. If competition between infected and uninfected individuals is strong, stunting will be enhanced and bistability between a stunted and non-stunted prey population occurs. In this case, the disease competes with the predator of its host species, possibly leading to predator extinction. In contrast, if the competition between infected and uninfected individuals is weak, the stunting is relieved, and epi-zoonotic cycles will occur, with recurrent epidemic outbreaks. Here, the disease facilitates the predator, and predator density will be substantially increased. We discuss the implications of our results for the dynamics and structure of the natural Ligula-Roach system.

No MeSH data available.


Related in: MedlinePlus