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Parasite variation and the evolution of virulence in a Daphnia-microparasite system

Published online by Cambridge University Press:  16 November 2007

T. J. LITTLE*
Affiliation:
Institute of Evolutionary Biology, School of Biological Sciences, University of Edinburgh, Kings Buildings, West Mains Road, EdinburghEH9 3JT, UK
W. CHADWICK
Affiliation:
Institute of Evolutionary Biology, School of Biological Sciences, University of Edinburgh, Kings Buildings, West Mains Road, EdinburghEH9 3JT, UK
K. WATT
Affiliation:
Institute of Evolutionary Biology, School of Biological Sciences, University of Edinburgh, Kings Buildings, West Mains Road, EdinburghEH9 3JT, UK
*
*Corresponding author. Tel: +0131 650 7781. Fax: +0131 650 6564. E-mail: tom.little@ed.ac.uk

Summary

Understanding genetic relationships amongst the life-history traits of parasites is crucial for testing hypotheses on the evolution of virulence. This study therefore examined variation between parasite isolates (the bacterium Pasteuria ramosa) from the crustacean Daphnia magna. From a single wild-caught infected host we obtained 2 P. ramosa isolates that differed substantially in the mortality they caused. Surprisingly, the isolate causing higher early mortality was, on average, less successful at establishing infections and had a slower growth rate within hosts. The observation that within-host replication rate was negatively correlated with mortality could violate a central assumption of the trade-off hypothesis for the evolution of virulence, but we discuss a number of caveats which caution against premature rejection of the trade-off hypothesis. We sought to test if the characteristics of these parasite isolates were constant across host genotypes in a second experiment that included 2 Daphnia host clones. The relative growth rates of the two parasite isolates did indeed depend on the host genotype (although the rank order did not change). We suggest that testing evolutionary hypotheses for virulence may require substantial sampling of both host and parasite genetic variation, and discuss how selection for virulence may change with the epidemiological state of natural populations and how this can promote genetic variation for virulence.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2007

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