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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 facilitate the predator, relieve stuntedness and induce recurrent epidemics.Parameters and colors are identical to Fig 2, except δ = 0, indicating that sick individuals do not effectively compete with healthy individuals. (a) Dynamics after introduction of the disease in the stunted population state for μP. = 0.45. Here, the disease causes a single epidemic, after which the host population shifts to the non-stunted equilibrium and the disease goes extinct. (b) Dynamics after introduction of the disease in the stunted population state for μP. = 0.56. After an initial large epidemic, the system settles in a limit cycle with recurrent epidemics of intermediate amplitude. Note that each epidemic is closely followed by an increase in predator density. (c) Bifurcation diagram for total juvenile prey density 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. The red lines and area indicate the amplitude of the stable limit cycles. Dashed lines are unstable equilibriums.
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pone.0132251.g003: The disease can facilitate the predator, relieve stuntedness and induce recurrent epidemics.Parameters and colors are identical to Fig 2, except δ = 0, indicating that sick individuals do not effectively compete with healthy individuals. (a) Dynamics after introduction of the disease in the stunted population state for μP. = 0.45. Here, the disease causes a single epidemic, after which the host population shifts to the non-stunted equilibrium and the disease goes extinct. (b) Dynamics after introduction of the disease in the stunted population state for μP. = 0.56. After an initial large epidemic, the system settles in a limit cycle with recurrent epidemics of intermediate amplitude. Note that each epidemic is closely followed by an increase in predator density. (c) Bifurcation diagram for total juvenile prey density 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. The red lines and area indicate the amplitude of the stable limit cycles. Dashed lines are unstable equilibriums.

Mentions: Now we consider the case that infected juveniles do not effectively compete with healthy juveniles, i.c. δ = 0. This can e.g. be due to sick individuals being in a bad condition, or shifting their diet or habitat. In Fig 3a, invasion of the disease in the stunted population is shown for intermediate predator death rate of μP = 0.45. Here, the disease causes a single epidemic, but this induces the population to shift to the non-stunted equilibrium and consequently the disease goes extinct after the epidemic. In this case, the effect of the disease on the predator is positive, as the introduction of the disease causes a roughly threefold increase in the predator density. If we introduce the disease in the stunted population for an increased predator death rate of μP = 0.56, in Fig 3b, we obtain a new type of dynamics. In this case, after a large initial epidemic, the disease almost disappears, but for this predator death rate there does not exist a stable non-stunted population equilibrium. Consequently, after the epidemic, the population slowly rebuilds to the stunted equilibrium, but this in turn allows the disease to re-enter the population and cause a secondary epidemic. This process repeats itself, resulting in limit cycle behaviour with recurrent epidemics, with prevalence varying strongly between 1% and 75%. The introduction of the disease again has a strong positive effect on the predator, increasing predator density by a factor varying between 3-fold (at the start of the epidemic) and 8-fold (during and after the epidemic). However, the interaction between the disease and the predator in this case is complex, as the highest predator densities are actually reached in the periods where the disease is almost absent. Yet, also in this case the disease acts to facilitate the predator, as it prevents the prey population from getting stuck in the stunted equilibrium. Actually, the recovery of the predator population closely follows the epidemic outbreaks.


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 facilitate the predator, relieve stuntedness and induce recurrent epidemics.Parameters and colors are identical to Fig 2, except δ = 0, indicating that sick individuals do not effectively compete with healthy individuals. (a) Dynamics after introduction of the disease in the stunted population state for μP. = 0.45. Here, the disease causes a single epidemic, after which the host population shifts to the non-stunted equilibrium and the disease goes extinct. (b) Dynamics after introduction of the disease in the stunted population state for μP. = 0.56. After an initial large epidemic, the system settles in a limit cycle with recurrent epidemics of intermediate amplitude. Note that each epidemic is closely followed by an increase in predator density. (c) Bifurcation diagram for total juvenile prey density 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. The red lines and area indicate the amplitude of the stable limit cycles. Dashed lines are unstable equilibriums.
© Copyright Policy
Related In: Results  -  Collection

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

pone.0132251.g003: The disease can facilitate the predator, relieve stuntedness and induce recurrent epidemics.Parameters and colors are identical to Fig 2, except δ = 0, indicating that sick individuals do not effectively compete with healthy individuals. (a) Dynamics after introduction of the disease in the stunted population state for μP. = 0.45. Here, the disease causes a single epidemic, after which the host population shifts to the non-stunted equilibrium and the disease goes extinct. (b) Dynamics after introduction of the disease in the stunted population state for μP. = 0.56. After an initial large epidemic, the system settles in a limit cycle with recurrent epidemics of intermediate amplitude. Note that each epidemic is closely followed by an increase in predator density. (c) Bifurcation diagram for total juvenile prey density 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. The red lines and area indicate the amplitude of the stable limit cycles. Dashed lines are unstable equilibriums.
Mentions: Now we consider the case that infected juveniles do not effectively compete with healthy juveniles, i.c. δ = 0. This can e.g. be due to sick individuals being in a bad condition, or shifting their diet or habitat. In Fig 3a, invasion of the disease in the stunted population is shown for intermediate predator death rate of μP = 0.45. Here, the disease causes a single epidemic, but this induces the population to shift to the non-stunted equilibrium and consequently the disease goes extinct after the epidemic. In this case, the effect of the disease on the predator is positive, as the introduction of the disease causes a roughly threefold increase in the predator density. If we introduce the disease in the stunted population for an increased predator death rate of μP = 0.56, in Fig 3b, we obtain a new type of dynamics. In this case, after a large initial epidemic, the disease almost disappears, but for this predator death rate there does not exist a stable non-stunted population equilibrium. Consequently, after the epidemic, the population slowly rebuilds to the stunted equilibrium, but this in turn allows the disease to re-enter the population and cause a secondary epidemic. This process repeats itself, resulting in limit cycle behaviour with recurrent epidemics, with prevalence varying strongly between 1% and 75%. The introduction of the disease again has a strong positive effect on the predator, increasing predator density by a factor varying between 3-fold (at the start of the epidemic) and 8-fold (during and after the epidemic). However, the interaction between the disease and the predator in this case is complex, as the highest predator densities are actually reached in the periods where the disease is almost absent. Yet, also in this case the disease acts to facilitate the predator, as it prevents the prey population from getting stuck in the stunted equilibrium. Actually, the recovery of the predator population closely follows the epidemic outbreaks.

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