Spencer R. Hall
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View article: On the Cause and Consequences of Coinfection: A General Mechanistic Framework of Within‐Host Parasite Competition
On the Cause and Consequences of Coinfection: A General Mechanistic Framework of Within‐Host Parasite Competition Open
Coinfections pose serious threats to health and exacerbate parasite burden. If coinfection is detrimental, then what within‐host factors facilitate it? Equally importantly, what hinders it, say via exclusion or priority effects? Such inter…
View article: <i>On the cause and consequences of coinfection:</i>A general mechanistic framework of within-host parasite competition
<i>On the cause and consequences of coinfection:</i>A general mechanistic framework of within-host parasite competition Open
Coinfections pose serious threats to health and exacerbate parasite burden. If coinfection is detrimental, then what within-host factors facilitate it? Equally importantly, what hinders it, say via exclusion or priority effects? Such inter…
View article: A healthy but depleted herd: Predators decrease prey disease and density
A healthy but depleted herd: Predators decrease prey disease and density Open
The healthy herds hypothesis proposes that predators can reduce parasite prevalence and thereby increase the density of their prey. However, evidence for such predator‐driven reductions in the prevalence of prey remains mixed. Furthermore,…
View article: Niche theory for within‐host parasite dynamics: Analogies to food web modules via feedback loops
Niche theory for within‐host parasite dynamics: Analogies to food web modules via feedback loops Open
Why do parasites exhibit a wide dynamical range within their hosts? For instance, why does infecting dose either lead to infection or immune clearance? Why do some parasites exhibit boom‐bust, oscillatory dynamics? What maintains parasite …
View article: A paradox of parasite resistance: Disease-driven trophic cascades increase the cost of resistance, selecting for lower resistance with parasites than without them
A paradox of parasite resistance: Disease-driven trophic cascades increase the cost of resistance, selecting for lower resistance with parasites than without them Open
Most evolutionary theory predicts that, during epidemics, hosts will evolve higher resistance to parasites that kill them. Here, we provide an alternative to that typical expectation, with an explanation centered on resource feedbacks. Whe…
View article: Niche theory for within-host parasite dynamics: Analogies to food web modules via feedback loops
Niche theory for within-host parasite dynamics: Analogies to food web modules via feedback loops Open
Why do parasites exhibit a wide dynamical range within their hosts? For instance, why can a parasite only sometimes successfully infect its host? Why do some parasites exhibit large fluctuations? Why do two parasites coinfect, exclude each…
View article: Genotypic variation in an ecologically important parasite is associated with host species, lake and spore size
Genotypic variation in an ecologically important parasite is associated with host species, lake and spore size Open
View article: Shedding light on environmentally transmitted parasites: lighter conditions within lakes restrict epidemic size
Shedding light on environmentally transmitted parasites: lighter conditions within lakes restrict epidemic size Open
Parasite fitness depends on a successful journey from one host to another. For parasites that are transmitted environmentally, abiotic conditions might modulate the success of this journey. Here we evaluate how light, a key abiotic factor,…
View article: Virulent disease epidemics can increase host density by depressing foraging of hosts
Virulent disease epidemics can increase host density by depressing foraging of hosts Open
All else equal, parasites that harm host fitness should depress densities of their hosts. However, parasites that alter host traits may increase host density via indirect ecological interactions. Here, we show how depression of infected ho…
View article: Genotypic variation in parasite avoidance behaviour and other mechanistic, nonlinear components of transmission
Genotypic variation in parasite avoidance behaviour and other mechanistic, nonlinear components of transmission Open
Traditional epidemiological models assume that transmission increases proportionally to the density of parasites. However, empirical data frequently contradict this assumption. General yet mechanistic models can explain why transmission de…
View article: Why Do Phytoplankton Evolve Large Size in Response to Grazing?
Why Do Phytoplankton Evolve Large Size in Response to Grazing? Open
Phytoplankton are among the smallest primary producers on Earth, yet they display a wide range of cell sizes. Typically, small phytoplankton species are stronger nutrient competitors than large phytoplankton species, but they are also more…
View article: Can hot temperatures limit disease transmission? A test of mechanisms in a zooplankton–fungus system
Can hot temperatures limit disease transmission? A test of mechanisms in a zooplankton–fungus system Open
Thermal ecology theory predicts that transmission of infectious diseases should respond unimodally to temperature, that is be maximized at intermediate temperatures and constrained at extreme low and high temperatures. However, empirical e…
View article: Variation in Immune Defense Shapes Disease Outcomes in Laboratory and Wild Daphnia
Variation in Immune Defense Shapes Disease Outcomes in Laboratory and Wild Daphnia Open
Host susceptibility may be critical for the spread of infectious disease, and understanding its basis is a goal of ecological immunology. Here, we employed a series of mechanistic tests to evaluate four factors commonly assumed to influenc…
View article: Can hot temperatures limit disease transmission? A test of mechanisms in a zooplankton-fungus system
Can hot temperatures limit disease transmission? A test of mechanisms in a zooplankton-fungus system Open
unimodally to temperature, i.e., be maximized at intermediate temperatures and constrained at extreme low and high temperatures. However, empirical evidence linking hot temperatures to decreased transmission in nature remains limited. We t…
View article: Supplementary material from "Genotypic variation in parasite avoidance behaviour and other mechanistic, nonlinear components of transmission"
Supplementary material from "Genotypic variation in parasite avoidance behaviour and other mechanistic, nonlinear components of transmission" Open
Traditional epidemiological models assume that transmission increases proportionally to the density of parasites. However, empirical data frequently contradict this assumption. General yet mechanistic models can explain why transmission de…
View article: Linking host traits, interactions with competitors and disease: Mechanistic foundations for disease dilution
Linking host traits, interactions with competitors and disease: Mechanistic foundations for disease dilution Open
The size of disease epidemics remains difficult to predict, especially when parasites interact with multiple species. Traits of focal hosts like susceptibility could directly predict epidemic size, while other traits including competitive …
View article: Rapid evolution rescues hosts from competition and disease but—despite a dilution effect—increases the density of infected hosts
Rapid evolution rescues hosts from competition and disease but—despite a dilution effect—increases the density of infected hosts Open
Virulent parasites can depress the densities of their hosts. Taxa that reduce disease via dilution effects might alleviate this burden. However, ‘diluter’ taxa can also depress host densities through competition for shared resources. The c…
View article: Allocation, not male resistance, increases male frequency during epidemics: a case study in facultatively sexual hosts
Allocation, not male resistance, increases male frequency during epidemics: a case study in facultatively sexual hosts Open
Why do natural populations vary in the frequency of sexual reproduction? Virulent parasites may help explain why sex is favored during disease epidemics. To illustrate, we show a higher frequency of males and sexually produced offspring in…
View article: Supplementary material from "Rapid evolution rescues hosts from competition and disease but—despite a dilution effect—increases the density of infected hosts"
Supplementary material from "Rapid evolution rescues hosts from competition and disease but—despite a dilution effect—increases the density of infected hosts" Open
Virulent parasites can depress the densities of their hosts. Taxa that reduce disease via dilution effects might alleviate this burden. However, ‘diluter’ taxa can also depress host densities through competition for shared resources. The c…
View article: Issue Information
Issue Information Open
Two male mountain goats photographed by
View article: Joint effects of habitat, zooplankton, host stage structure and diversity on amphibian chytrid
Joint effects of habitat, zooplankton, host stage structure and diversity on amphibian chytrid Open
Why does the severity of parasite infection differ dramatically across habitats? This question remains challenging to answer because multiple correlated pathways drive disease. Here, we examined habitat–disease links through direct effects…
View article: Habitat, predators, and hosts regulate disease in <i>Daphnia</i> through direct and indirect pathways
Habitat, predators, and hosts regulate disease in <i>Daphnia</i> through direct and indirect pathways Open
Community ecology can link habitat to disease via interactions among habitat, focal hosts, other hosts, their parasites, and predators. However, complicated food web interactions (i.e., trophic interactions among predators and their impact…
View article: Appendix C. Seasonal dynamics of host populations.
Appendix C. Seasonal dynamics of host populations. Open
Seasonal dynamics of host populations.
View article: Appendix A. Details on the experiments used to parameterize the S-I-Z model with predation, along woth statistical methods used to estimate these parameters.
Appendix A. Details on the experiments used to parameterize the S-I-Z model with predation, along woth statistical methods used to estimate these parameters. Open
Details on the experiments used to parameterize the S-I-Z model with predation, along woth statistical methods used to estimate these parameters.
View article: Supplement 1. Data files to be used with annotated R code presented in Appendix E.
Supplement 1. Data files to be used with annotated R code presented in Appendix E. Open
File List DentInfections.txt – data on infections in Daphnia dentifera DentPulInfections.txt – data on infections in both Daphnia pulicaria and Daphnia dentifera Description Appendix E presents R code for analyzing infection prevalence in …
View article: Appendix A. More data, derivation of the DEB model, and further development of the conversion efficiency mechanism.
Appendix A. More data, derivation of the DEB model, and further development of the conversion efficiency mechanism. Open
More data, derivation of the DEB model, and further development of the conversion efficiency mechanism.
View article: Appendix B. Description of model system.
Appendix B. Description of model system. Open
Description of model system.
View article: Appendix E. Annotated R code and output for analyses presented in the article .
Appendix E. Annotated R code and output for analyses presented in the article . Open
Annotated R code and output for analyses presented in the article .
View article: Appendix B. Description of the stability of the equilibria produced by modeling the dynamics of susceptible hosts (S), infected hosts (I), and free-floating spores (Z) (i.e., the S–I–Z model) with predators (P).
Appendix B. Description of the stability of the equilibria produced by modeling the dynamics of susceptible hosts (S), infected hosts (I), and free-floating spores (Z) (i.e., the S–I–Z model) with predators (P). Open
Description of the stability of the equilibria produced by modeling the dynamics of susceptible hosts (S), infected hosts (I), and free-floating spores (Z) (i.e., the S–I–Z model) with predators (P).
View article: Appendix A. A table presenting results of nonparametric univariate analyses of edible seston C, P, and C:P ratio.
Appendix A. A table presenting results of nonparametric univariate analyses of edible seston C, P, and C:P ratio. Open
A table presenting results of nonparametric univariate analyses of edible seston C, P, and C:P ratio.