ORCID Profile
0000-0002-0938-0017
Current Organisations
Monash University
,
Novo Nordisk
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Publisher: Wiley
Date: 08-12-2021
Abstract: The spread of infectious disease is determined by the ability of a pathogen to proliferate within and spread between susceptible hosts. Processes that limit the performance of a pathogen thus occur at two scales: varying with both the availability of energy within a host, and the number of susceptible hosts in a patch. When the rate at which a host intakes and expends energy is density‐dependent, these two processes are intimately linked. By modifying how hosts compete for and expend resources, a shift in population density may contribute to differences in the flow of energy in a host–pathogen system, both in terms of the energy available for a host to grow, reproduce and fight infection, as well as the energy available for a pathogen to exploit. Energy flux, therefore, connects the two contrasting scales of within‐ and between‐host dynamics by directly linking the proliferation of a pathogen to the number of hosts circulating within a patch. We use the host Daphnia magna to explore the relationship between energy intake and expenditure at various population densities, as estimated by feeding and metabolic rates respectively. By infecting hosts with the bacterial pathogen Pasteuria ramosa , we then explore how infection changes the relative balance of energy intake and expenditure, and how this energy scope translates into production of transmission spores. Our work demonstrates that energy intake declines at a faster rate with density than does metabolic rate, leaving more excess energy (i.e. discretionary energy) available for both hosts and their dependent pathogens at low population densities. This energetic advantage translates positively into host and pathogen growth, with the production of mature transmission spores benefiting most from correlated changes in host body size, as well as a direct connection between energy scope and spore loads. Our findings reinforce how patch quality for a pathogen operates at two contrasting scales, with the within‐host proliferation of a pathogen being optimised in energy rich, low density host populations and opportunities for between‐host transmission likely maximised in dense populations. A free Plain Language Summary can be found within the Supporting Information of this article.
Publisher: Cold Spring Harbor Laboratory
Date: 29-01-2020
DOI: 10.1101/2020.01.29.924498
Abstract: Rapid evolutionary change during range expansions can lead to erging range core and front populations, with the emergence of dispersal syndromes (coupled responses in dispersal and life-history traits). Besides intraspecific effects, range expansions may be impacted by interspecific interactions such as parasitism. Yet, despite the potentially large impact of parasites imposing additional selective pressures on the host, their role on range expansions remains largely unexplored. Using microcosm populations of the ciliate Paramecium caudatum and its bacterial parasite Holospora undulata , we studied experimental range expansions under parasite presence or absence. We found that the interaction of range expansion and parasite treatments affected the evolution of host dispersal syndromes. Namely, front populations showed different associations of population growth parameters and swimming behaviours than core populations, indicating ergent evolution. Parasitism reshaped trait associations, with hosts evolved in the presence of the parasite exhibiting overall increased resistance and reduced dispersal. Nonetheless, when comparing infected range core and front populations, we found a positive association, suggesting joint evolution of resistance and dispersal at the front. We conclude that host-parasite interactions during range expansions can change evolutionary trajectories this in turn may feed back on the ecological dynamics of the range expansion and parasite epidemics.
Publisher: Oxford University Press (OUP)
Date: 10-2019
DOI: 10.1002/EVL3.141
Abstract: Repeated extinction and recolonization events generate a landscape of host populations that vary in their time since colonization. Within this dynamic landscape, pathogens that excel at invading recently colonized host populations are not necessarily those that perform best in host populations at or near their carrying capacity, potentially giving rise to ergent selection for pathogen traits that mediate the invasion process. Rarely, however, has this contention been empirically tested. Using Daphnia magna, we explored how differences in the colonization history of a host population influence the invasion success of different genotypes of the pathogen Pasteuria ramosa. By partitioning the pathogen invasion process into a series of in idual steps, we show that each pathogen optimizes invasion differently when encountering host populations that vary in their time since colonization. All pathogen genotypes were more likely to establish successfully in recently colonized host populations, but the production of transmission spores was typically maximized in either the subsequent growth or stationary phase of host colonization. Integrating across the first three pathogen invasion steps (initial establishment, proliferation, and secondary infection) revealed that overall pathogen invasion success (and its variance) was, nonetheless, highest in recently colonized host populations. However, only pathogens that were slow to kill their host were able to maximize host-facilitated dispersal. This suggests that only a subset of pathogen genotypes—the less virulent and more dispersive—are more likely to encounter newly colonized host populations at the front of a range expansion or in metapopulations with high extinction rates. Our results suggest a fundamental trade-off for a pathogen between dispersal and virulence, and evidence for higher invasion success in younger host populations, a finding with clear implications for pathogen evolution in spatiotemporally dynamic settings.
Publisher: Cold Spring Harbor Laboratory
Date: 31-07-2020
DOI: 10.1101/2020.07.30.228742
Abstract: Dispersal is a central determinant of spatial dynamics in communities and ecosystems, and various ecological factors can shape the evolution of constitutive and plastic dispersal behaviours. One important driver of dispersal plasticity is the biotic environment. Parasites, for ex le, influence the internal condition of infected hosts and define external patch quality. Thus state-dependent dispersal may be determined by infection status and context-dependent dispersal by the abundance of infected hosts in the population. A prerequisite for such dispersal plasticity to evolve is a genetic basis on which natural selection can act. Using interconnected microcosms, we investigated dispersal in experimental populations of the freshwater protist Paramecium caudatum in response to the bacterial parasite Holospora undulata . For a collection of 20 natural host strains, we found substantial variation in constitutive dispersal, and to a lesser degree in dispersal plasticity. First, infection tended to increase or decrease dispersal relative to uninfected controls, depending on strain identity, potentially indicative of state-dependent dispersal plasticity. Infection additionally decreased host swimming speed compared to the uninfected counterparts. Second, for certain strains, there was a weak negative association between dispersal and infection prevalence, such that uninfected hosts tended to disperse less when infection was more frequent in the population, indicating context-dependent dispersal plasticity. Future experiments may test whether the observed differences in dispersal plasticity are sufficiently strong to react to natural selection. The evolution of dispersal plasticity as a strategy to mitigate parasite effects spatially may have important implications for epidemiological dynamics.
Publisher: The Royal Society
Date: 04-01-2023
Abstract: Rapid evolutionary change during range expansions can lead to erging range core and front populations, with the emergence of dispersal syndromes (coupled responses in dispersal and life-history traits). Besides intraspecific effects, range expansions may be impacted by interspecific interactions such as parasitism. Yet, despite the potentially large impact of parasites imposing additional selective pressures on the host, their role on range expansions remains largely unexplored. Using microcosm populations of the ciliate Paramecium caudatum and its bacterial parasite Holospora undulata , we studied experimental range expansions under parasite presence or absence. We found that the interaction of range expansion and parasite treatments affected the evolution of host dispersal syndromes. Namely, front populations showed different associations of population growth parameters and swimming behaviours than core populations, indicating ergent evolution. Parasitism reshaped trait associations, with hosts evolved in the presence of the parasite exhibiting overall increased resistance and reduced dispersal. Nonetheless, when comparing infected range core and front populations, we found a positive association, suggesting joint evolution of resistance and dispersal at the front. We conclude that host–parasite interactions during range expansions can change evolutionary trajectories this in turn may feedback on the ecological dynamics of the range expansion and parasite epidemics.
Publisher: Wiley
Date: 14-02-2021
DOI: 10.1111/ELE.13692
Abstract: Exploitative parasites are predicted to evolve in highly connected populations or in expanding epidemics. However, many parasites rely on host dispersal to reach new populations, potentially causing conflict between local transmission and global spread. We performed experimental range expansions in interconnected microcosms of the protozoan Paramecium caudatum , allowing natural dispersal of hosts infected with the bacterial parasite Holospora undulata . Parasites from range front treatments facilitated host dispersal and were less virulent, but also invested less in horizontal transmission than parasites from range cores. These differences were consistent with parameter estimates derived from an epidemiological model fitted on population‐level time‐series data. Our results illustrate how dispersal selection can have profound consequences for the evolution of parasite life history and virulence. Decrypting the eco‐evolutionary processes that shape parasite 'dispersal syndromes' may be important for the management of spreading epidemics in changing environments, biological invasions or in other spatial non‐equilibrium settings.
Publisher: The Royal Society
Date: 06-2019
Abstract: Pathogens often rely on their host for dispersal. Yet, maximizing fitness via replication can cause damage to the host and an associated reduction in host movement, incurring a trade-off between transmission and dispersal. Here, we test the idea that pathogens might mitigate this trade-off between reproductive fitness and dispersal by taking advantage of sexual dimorphism in their host, tailoring responses separately to males and females. Using experimental populations of Daphnia magna and its bacterial pathogen Pasteuria ramosa as a test-case, we find evidence that this pathogen can use male hosts as a dispersal vector, and the larger females as high-quality resource patches for optimized production of transmission spores. As sexual dimorphism in dispersal and body size is widespread across the animal kingdom, this differential exploitation of the sexes by a pathogen might be an unappreciated phenomenon, possibly evolved in various systems.
Publisher: Wiley
Date: 02-11-2021
DOI: 10.1111/GCB.15950
Abstract: The distribution of disease vectors such as mosquitoes is changing. Climate change, invasions and vector control strategies all alter the distribution and abundance of mosquitoes. When disease vectors undergo a range shift, so do disease burdens. Predicting such shifts is a priority to adequately prepare for disease control. Accurate predictions of distributional changes depend on how factors such as temperature and competition affect mosquito life‐history traits, particularly body size and reproduction. Direct estimates of both body size and reproduction in mosquitoes are logistically challenging and time‐consuming, so the field has long relied upon linear (isometric) conversions between wing length (a convenient proxy of size) and reproductive output. These linear transformations underlie most models projecting species' distributions and competitive interactions between native and invasive disease vectors. Using a series of meta‐analyses, we show that the relationship between wing length and fecundity are nonlinear (hyperallometric) for most mosquito species. We show that whilst most models ignore reproductive hyperallometry (with respect to wing length), doing so introduces systematic biases into estimates of population growth. In particular, failing to account for reproductive hyperallometry overestimates the effects of temperature and underestimates the effects of competition. Assuming isometry also increases the potential to misestimate the efficacy of vector control strategies by underestimating the contribution of larger females in population replenishment. Finally, failing to account for reproductive hyperallometry and variation in body size can lead to qualitative errors via the counter‐intuitive effects of Jensen's inequality. For ex le, if mean sizes decrease, but variance increases, then reproductive outputs may actually increase. We suggest that future disease vector models incorporate hyperallometric relationships to more accurately predict changes in mosquito distribution in response to global change.
No related grants have been discovered for Louise Nørgaard.