Coping with crowds: Density-dependent disease resistance in desert locusts

  1. Kenneth Wilson*,,
  2. Matthew B. Thomas,
  3. Simon Blanford,
  4. Matthew Doggett,
  5. Stephen J. Simpson§, and
  6. Sarah L. Moore*
  1. *Institute of Biological Sciences, University of Stirling, Stirling FK9 4LA, United Kingdom; Natural Environmental Research Council Centre for Population Biology and CABI Bioscience, Silwood Park, Ascot, Berkshire SL5 7PY, United Kingdom; and §Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, United Kingdom
  1. Edited by May R. Berenbaum, University of Illinois at Urbana−Champaign, Urbana, IL, and approved February 8, 2002 (received for review August 31, 2001)

Abstract

Parasite transmission generally exhibits some form of positive density dependence. Thus, as population density increases, so too does the per capita risk of becoming infected. Under such circumstances, natural selection should favor individuals that use cues associated with population density to determine the optimal allocation of resources to disease resistance mechanisms. As a consequence, individuals experiencing crowded conditions are predicted to be more resistant to parasites and pathogens than those experiencing low-density conditions. This phenomenon (termed “density-dependent prophylaxis”) [Wilson, K. & Reeson, A. F. (1998) Ecol. Entomol. 23, 100–101] is predicted to be particularly prevalent in outbreak pest species and in species exhibiting density-dependent phase polyphenism, such as the desert locust, Schistocerca gregaria. Here we show that, as predicted, desert locusts reared under crowded conditions are significantly more resistant than solitary locusts to the entomopathogenic fungus, Metarhizium anisopliae var. acridum, a key natural disease of acridids and an important agent in locust and grasshopper biocontrol. Moreover, enhanced pathogen resistance in crowded locusts is associated with elevated antimicrobial activity, but not with any difference in thermal preferences or behavioral fever response. These results have implications for understanding the development and biocontrol of locust plagues.

Footnotes

  • To whom reprint requests should be addressed. E-mail: ken.wilson{at}stirling.ac.uk.

  • This paper was submitted directly (Track II) to the PNAS office.

  • Abbreviation:
    PO,
    phenoloxidase
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