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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

The disease can suppress the predator and enhance bistability and population stuntedness.(a) Dynamics after introduction of the disease in the stunted population state for μP. = 0.45. Density of infected juveniles JI are shown in light blue. Disease parameters are β = 0.06, α = 0.05, and δ = 1, indicating that sick individuals have full competitive ability. For other colors and parameters see Fig 1. Note the strong reduction in predator density after introduction of the disease. (b) Bifurcation diagram for total juvenile prey density (i.c. JS+JI) as a function of predator death rate μP. The solid blue line indicates the stable disease free state, and the solid purple line denotes the endemic state. Dashed lines indicate unstable equilibriums. Note that the introduction of the disease considerably increases the region of bistability.
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pone.0132251.g002: The disease can suppress the predator and enhance bistability and population stuntedness.(a) Dynamics after introduction of the disease in the stunted population state for μP. = 0.45. Density of infected juveniles JI are shown in light blue. Disease parameters are β = 0.06, α = 0.05, and δ = 1, indicating that sick individuals have full competitive ability. For other colors and parameters see Fig 1. Note the strong reduction in predator density after introduction of the disease. (b) Bifurcation diagram for total juvenile prey density (i.c. JS+JI) as a function of predator death rate μP. The solid blue line indicates the stable disease free state, and the solid purple line denotes the endemic state. Dashed lines indicate unstable equilibriums. Note that the introduction of the disease considerably increases the region of bistability.

Mentions: We first consider the case of δ = 1, which implies that sick juveniles have full competitive ability against healthy juveniles. Because sick individuals compete with healthy individuals, but do not mature themselves, they can act to reinforce the stunted juvenile population bottleneck. In Fig 2a we show a typical example of the dynamics after introduction of the disease in the stunted population equilibrium. The disease quickly spreads through the juvenile population, and the system settles in an endemic equilibrium. The prevalence of the disease in this equilibrium is high at 64% of all juveniles being infected. Furthermore, the introduction of the disease strongly reduces the predator abundance, causing a roughly 4-fold reduction. This seems surprising, as the adult prey density does not change, and this is the food source for the predator. However, the adult prey density is now mainly controlled by the maturation bottleneck, which causes the predator equilibrium to be strongly reduced.


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

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

The disease can suppress the predator and enhance bistability and population stuntedness.(a) Dynamics after introduction of the disease in the stunted population state for μP. = 0.45. Density of infected juveniles JI are shown in light blue. Disease parameters are β = 0.06, α = 0.05, and δ = 1, indicating that sick individuals have full competitive ability. For other colors and parameters see Fig 1. Note the strong reduction in predator density after introduction of the disease. (b) Bifurcation diagram for total juvenile prey density (i.c. JS+JI) as a function of predator death rate μP. The solid blue line indicates the stable disease free state, and the solid purple line denotes the endemic state. Dashed lines indicate unstable equilibriums. Note that the introduction of the disease considerably increases the region of bistability.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0132251.g002: The disease can suppress the predator and enhance bistability and population stuntedness.(a) Dynamics after introduction of the disease in the stunted population state for μP. = 0.45. Density of infected juveniles JI are shown in light blue. Disease parameters are β = 0.06, α = 0.05, and δ = 1, indicating that sick individuals have full competitive ability. For other colors and parameters see Fig 1. Note the strong reduction in predator density after introduction of the disease. (b) Bifurcation diagram for total juvenile prey density (i.c. JS+JI) as a function of predator death rate μP. The solid blue line indicates the stable disease free state, and the solid purple line denotes the endemic state. Dashed lines indicate unstable equilibriums. Note that the introduction of the disease considerably increases the region of bistability.
Mentions: We first consider the case of δ = 1, which implies that sick juveniles have full competitive ability against healthy juveniles. Because sick individuals compete with healthy individuals, but do not mature themselves, they can act to reinforce the stunted juvenile population bottleneck. In Fig 2a we show a typical example of the dynamics after introduction of the disease in the stunted population equilibrium. The disease quickly spreads through the juvenile population, and the system settles in an endemic equilibrium. The prevalence of the disease in this equilibrium is high at 64% of all juveniles being infected. Furthermore, the introduction of the disease strongly reduces the predator abundance, causing a roughly 4-fold reduction. This seems surprising, as the adult prey density does not change, and this is the food source for the predator. However, the adult prey density is now mainly controlled by the maturation bottleneck, which causes the predator equilibrium to be strongly reduced.

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