Predators and Patterns of Within-Host Growth Can Mediate Both Among-Host Competition and Evolution of Transmission Potential of Parasites

Abstract

JSTOR is a not-for-profit service that helps scholars, researchers, and students discover, use, and build upon a wide range of content in a trusted digital archive. We use information technology and tools to increase productivity and facilitate new forms of scholarship. For more information about JSTOR, please contact support@jstor.org.. abstract: Parasite prevalence shows tremendous spatiotemporal variation. Theory indicates that this variation might stem from lifehistory characteristics of parasites and key ecological factors. Here, we illustrate how the interaction of an important predator and the schedule of transmission potential of two parasites can explain parasite abundance. A field survey showed that a noncastrating fungus (Metschnikowia bicuspidata) commonly infected a dominant zooplankton host (Daphnia dentifera), while a castrating bacterial parasite (Pasteuria ramosa) was rare. This result seemed surprising given that the bacterium produces many more infectious propagules (spores) than the fungus upon host death. The fungus's dominance can be explained by the schedule of within-host growth of parasites (i.e., how transmission potential changes over the course of infection) and the release of spores from "sloppy" predators (Chaoborus spp., who consume Daphnia prey whole and then later regurgitate the carapace and parasite spores). In essence, sloppy predators create a niche that the faster-schedule fungus currently occupies. However, a selection experiment showed that the slower-schedule bacterium can evolve into this faster-schedule, predator-mediated niche (but pays a cost in maximal spore yield to do so). Hence, our study shows how parasite life history can interact with predation to strongly influence the ecology, epidemiology, and evolution of infectious disease.

Sex as a strategy against rapidly evolving parasites

“…There was strong evidence for rapid parasite adaptation to grow within asexually produced offspring that were genetically identical to their mothers (figure 4). These findings convincingly support previous studies that have demonstrated evolution in the Pasteuria parasite [26,35]. Further analysis revealed there were no significant genetic correlations for parasite within-host growth comparing across parasite isolates and host reproductive modes (figure 4 b – e ).…”

Expression of parasite genetic variation changes over the course of infection: implications of within-host dynamics for the evolution of virulence

“…In this context, it has already been shown that accelerated host death is ecologically and epidemiological important. Predation on infected animals, for example, has been shown to be a modifier of infection dynamics in Daphnia [29,30], as predators shortened the infection period by releasing spores from their infected prey during feeding ('sloppy predator' [31]), thereby selecting for accelerated parasite development [30]. Indeed, Pasteuria spores are infectious as early as 14 days post-infection ( [32]; M. Clerc 2012, personal observation) and any extrinsic mortality from this moment onwards would allow transmission and alter evolutionary dynamics.…”

Starvation reveals the cause of infection-induced castration and gigantism

“…Some evidence for adaptive gigantism comes from selection experiments [34]. After five generations of selection for either fast development (early killing of hosts) or slow development (late killing of hosts), Pasteuria strains selected for fast development had higher spore loads early in infection than strains selected for slow development, but that pattern reversed later in infection.…”