Parasites destabilize host populations by shifting stage‐structured interactions

Hite, Jessica L.; Penczykowski, Rachel M.; Shocket, Marta S.; Strauss, Alexander T.; Orlando, Paul A.; Duffy, Meghan A.; Cáceres, Carla E.; Hall, Spencer R.

doi:10.1890/15-1065.1

Cited by 21 publications

(17 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the high nutrient treatment, infection prevalence was slightly higher (Hite et al. ) and male production was of longer duration (Fig. C,D) relative to the low nutrient treatment (Appendix , Fig.…”

Section: Resultsmentioning

confidence: 90%

See 1 more Smart Citation

Allocation, not male resistance, increases male frequency during epidemics: a case study in facultatively sexual hosts

Hite

Penczykowski

Shocket

et al. 2017

Ecology

Self Cite

View full text Add to dashboard Cite

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 natural populations of a facultative parthenogenetic host during fungal epidemics. In a multi-year survey of 32 lakes, the frequency of males (an index of sex) was higher in populations of zooplankton hosts with larger epidemics. A lake mesocosm experiment established causality: experimental epidemics produced a higher frequency of males relative to disease-free controls. One common explanation for such a pattern involves Red Queen (RQ) dynamics. However, this particular system lacks key genetic specificity mechanisms required for the RQ, so we evaluated two other hypotheses. First, individual females, when stressed by infection, could increase production of male offspring vs. female offspring (a tenant of the "Abandon Ship" theory). Data from a life table experiment supports this mechanism. Second, higher male frequency during epidemics could reflect a purely demographic process (illustrated with a demographic model): males could resist infection more than females (via size-based differences in resistance and mortality). However, we found no support for this resistance mechanism. A size-based model of resistance, parameterized with data, revealed why: higher male susceptibility negated the lower exposure (a size-based advantage) of males. These results suggest that parasite-mediated increases in allocation to sex by individual females, rather than male resistance, increased the frequency of sex during larger disease epidemics.

show abstract

Section: Resultsmentioning

confidence: 90%

“…However, there was no effect of nutrients (N, v 2 = 0.165, P = 0.685) or their interaction (v 2 = 1.52, P = 0.218). In the high nutrient treatment, infection prevalence was slightly higher (Hite et al 2016) and male production was of longer duration ( Fig. 3C,D) relative to the low nutrient treatment (Appendix S2, Fig.…”

Section: Resultsmentioning

confidence: 94%

Allocation, not male resistance, increases male frequency during epidemics: a case study in facultatively sexual hosts

Hite

Penczykowski

Shocket

et al. 2017

Ecology

Self Cite

View full text Add to dashboard Cite

show abstract

“…In a comparable amphibian system in California, multi-season larvae with high infection loads also serve as intraspecific reservoirs that maintain Bd infections [2]. Furthermore, this result adds to mounting evidence that stage structure of hosts matters for disease more broadly [54][55][56][57]. Here, as in other systems, larger hosts produce more parasites, which can increase disease [58][59][60].…”

Section: Discussionmentioning

confidence: 76%

Joint effects of habitat, zooplankton, host stage structure and diversity on amphibian chytrid

Hite

Bosch

Fernández-Beaskoetxea

et al. 2016

Proc. R. Soc. B.

Self Cite

View full text Add to dashboard Cite

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 on parasites and indirect effects on parasite predators (zooplankton), host diversity and key life stages of hosts. We used a case study of amphibian hosts and the chytrid fungus, Batrachochytrium dendrobatidis, in a set of permanent and ephemeral alpine ponds. A field experiment showed that ultraviolet radiation (UVR) killed the free-living infectious stage of the parasite. Yet, permanent ponds with more UVR exposure had higher infection prevalence. Two habitat-related indirect effects worked together to counteract parasite losses from UVR: (i) UVR reduced the density of parasite predators and (ii) permanent sites fostered multi-season host larvae that fuelled parasite production. Host diversity was unlinked to hydroperiod or UVR but counteracted parasite gains; sites with higher diversity of host species had lower prevalence of infection. Thus, while habitat structure explained considerable variation in infection prevalence through two indirect pathways, it could not account for everything. This study demonstrates the importance of creating mechanistic, food web-based links between multiple habitat dimensions and disease.

show abstract

“…One system where these insights could prove especially important is in Bd ( Batrachochytrium dendrobatidis , or chytrid fungus) infection in frogs, which has been causing catastrophic worldwide declines in frog populations (Kilpatrick et al ). Bd infection has been shown to have different virulence effects in the different frog life stages (Briggs et al ; Medina et al ; Hite et al ) and these effects also vary by frog species (Berger et al ; Blaustein et al ). Recent work has shown that adult virulence in several frog populations has not decreased even after 20 years of Bd presence (Voyles et al ).…”

Section: Discussionmentioning

confidence: 99%

The evolution of stage-specific virulence: Differential selection of parasites in juveniles

Iritani

Visher²,

Boots

2019

Evolution Letters

View full text Add to dashboard Cite

The impact of infectious disease is often very different in juveniles and adults, but theory has focused on the drivers of stage‐dependent defense in hosts rather than the potential for stage‐dependent virulence evolution in parasites. Stage structure has the potential to be important to the evolution of pathogens because it exposes parasites to heterogeneous environments in terms of both host characteristics and transmission pathways. We develop a stage‐structured (juvenile–adult) epidemiological model and examine the evolutionary outcomes of stage‐specific virulence under the classic assumption of a transmission‐virulence trade‐off. We show that selection on virulence against adults remains consistent with the classic theory. However, the evolution of juvenile virulence is sensitive to both demography and transmission pathway with higher virulence against juveniles being favored either when the transmission pathway is assortative (juveniles preferentially interact together) and the juvenile stage is long, or in contrast when the transmission pathway is disassortative and the juvenile stage is short. These results highlight the potentially profound effects of host stage structure on determining parasite virulence in nature. This new perspective may have broad implications for both understanding and managing disease severity.

show abstract

Parasites destabilize host populations by shifting stage‐structured interactions

Cited by 21 publications

References 45 publications

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

Joint effects of habitat, zooplankton, host stage structure and diversity on amphibian chytrid

The evolution of stage-specific virulence: Differential selection of parasites in juveniles

Contact Info

Product

Resources

About