You have full text access to this OnlineOpen article

Multiple infections alter density dependence in host–pathogen interactions

  1. MICHAEL B. BONSALL1,3,*,
  2. REBECCA BENMAYOR2,3

Article first published online: 1 SEP 2005

DOI: 10.1111/j.1365-2656.2005.00991.x

Issue

Journal of Animal Ecology

Journal of Animal Ecology

Volume 74, Issue 5, pages 937–945, September 2005

Additional Information

How to Cite

BONSALL, M. B. and BENMAYOR, R. (2005), Multiple infections alter density dependence in host–pathogen interactions. Journal of Animal Ecology, 74: 937–945. doi: 10.1111/j.1365-2656.2005.00991.x

Author Information

  1. 1

    Department of Biological Sciences, Imperial College London, Silwood Park Campus, Ascot, Berks SL5 7PY, UK;

  2. 2

    CEH Oxford, Mansfield Road, Oxford OX1 3SR, UK; and

  3. 3

    Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK

* Dr Mike Bonsall, Department of Zoology, University of Oxford, South Parks Road, Oxford, OX1 3PS, UK. E-mail: michael.bonsall@zoo.ox.ac.uk

Publication History

  1. Issue published online: 1 SEP 2005
  2. Article first published online: 1 SEP 2005
  3. Received 20 October 2004; accepted 15 March 2005

SEARCH

SEARCH BY CITATION

ARTICLE TOOLS

View Full Article (HTML) Get PDF (240K)

Keywords:

  • baculoviruses;
  • diseases;
  • maximum likelihood;
  • model choice;
  • model selection;
  • population dynamics;
  • time series

Summary

  • 1
    The hypothesis that multiple infections might disrupt or alter the density-dependent processes regulating a host–pathogen interaction is explored using time series from a well-known laboratory insect–pathogen model system.
  • 2
    We compare the population dynamics of the same host (Plodia interpunctella) infected with a single (granulovirus) or multiple (granulovirus and nucleopolyhedrovirus) pathogens and show how the dynamical fluctuations are altered by the presence of this second pathogen.
  • 3
    Using a maximum likelihood-based approach, we explore the density-dependent mechanisms underpinning the host–pathogen interaction. These regulatory processes differ between single and multiple infections. In singly infected systems, the density-dependent mechanisms of regulation operate through birth rate while in doubly infected systems, density dependence is mediated through death rate.
  • 4
    Further, these deterministic dynamics are modulated by the effects of demographic stochasticity. This stochastic process, the overall sum of individual probabilities of births, deaths and infection influence the changes in population size. In the Plodia–granulovirus system, nonlinear density-dependent births coupled with demographic noise is the necessary prerequisite for the observed dynamics. In the multiple infection system, noise acts together with disease transmission and mortality to affect the population dynamics.
  • 5
    We discuss the implication of these differing regulatory processes in the different-sized species assemblages in the presence of noise for understanding the ecologies of host–pathogen interactions.
View Full Article (HTML) Get PDF (240K)