A Reevaluation of Density-Dependent Population Cycles in Open Systems

2000 ◽  
Vol 155 (1) ◽  
pp. 36
Author(s):  
Johnson
2016 ◽  
Vol 110 (7) ◽  
pp. 1648-1660 ◽  
Author(s):  
Jan Ribbe ◽  
Berenike Maier

1978 ◽  
Vol 110 (5) ◽  
pp. 513-518 ◽  
Author(s):  
Alan A. Berryman

AbstractA simple population model is used to test the hypothesis that Douglas-fir tussock moth population cycles are caused by time-delays in the responses of density-dependent (negative feedback) processes. The limited data that are available do not seriously conflict with this hypothesis.


Author(s):  
Louis W. Botsford ◽  
J. Wilson White ◽  
Alan Hastings

This chapter examines age-structured models with density-dependent recruitment. In particular, it focuses on populations with over-compensatory density dependence, such as may occur due to cannibalism or some types of space competition. When the slope (at the equilibrium point) of the relationship between egg production and subsequent recruitment is declining in an over-compensatory way, the population may exhibit unstable limit cycles with period twice the generation time (2T). These cycles occur when that slope is steeply negative and the spawning age distribution has a high mean and low width. These results are applied to study the behavior of cycles in the U.S. west coast Dungeness crab fishery, variability in populations of an intertidal barnacle, and cycles in populations of a pest, the flour beetle. Additionally, it is shown how single-sex harvesting and compensatory growth affect population cycles and equilibria.


2006 ◽  
Vol 167 (5) ◽  
pp. 695
Author(s):  
Smith ◽  
White ◽  
Lambin ◽  
Sherratt ◽  
Begon

2006 ◽  
Vol 167 (5) ◽  
pp. 695-704 ◽  
Author(s):  
Matthew J. Smith ◽  
Andrew White ◽  
Xavier Lambin ◽  
Jonathan A. Sherratt ◽  
Michael Begon

2021 ◽  
Author(s):  
Adam Pepi ◽  
Vincent Pan ◽  
Richard Karban

AbstractInfectious disease is an important potential driver of population cycles, but this must occur through delayed density-dependent infection and resulting fitness effects. Delayed density-dependent infection by baculoviruses can be caused by environmental persistence of viral occlusion bodies, which can be influenced by environmental factors. In particular, ultraviolet radiation is potentially important in reducing the environmental persistence of viruses by inactivating viral occlusion bodies.Delayed density-dependent viral infection has rarely been observed empirically at the population level although theory predicts that it is necessary for these pathogens to drive population cycles. Similarly, field studies have not examined the potential effects of ultraviolet radiation on viral infection rates in natural animal populations. We tested if viral infection is delayed density-dependent with the potential to drive cyclic dynamics and if ultraviolet radiation influences viral infection.We censused 18 moth populations across nearly 9° of latitude over two years and quantified the effects of direct and delayed density and ultraviolet radiation on granulovirus infection rate, infection severity, and survival to adulthood. Caterpillars were collected from each population in the field and reared in the laboratory.We found that infection rate, infection severity, and survival to adulthood exhibited delayed density-dependence. Ultraviolet radiation in the previous summer decreased infection severity, and increased survival probability of the virus. Structural equation modelling found that the effect of lagged density on moth survival was mediated through infection rate and infection severity, and was 2.5 fold stronger than the effect of ultraviolet radiation on survival through infection severity.Our findings provide clear evidence that delayed density dependence can arise through viral infection rate and severity in insects, which supports the role of viral disease as a potential mechanism, among others, that may drive insect population cycles. Furthermore, our findings support predictions that ultraviolet radiation can modify viral disease dynamics in insect populations, most likely through attenuating viral persistence in the environment.


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