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Abstract The relationship between infection prevalence and host age is informative because it can reveal processes underlying disease dynamics. Most prior work has assumed that age‐prevalence curves are shaped by infection rates, host immunity and/or infection‐induced mortality. Interactions between parasites within a host have largely been overlooked as a source of variation in age‐prevalence curves.We used field survey data and models to examine the role of interspecific interactions between parasites in shaping age‐prevalence curves. The empirical dataset included quantification of parasite infection prevalence for eight co‐occurring trematodes in over 15,000 snail hosts. We characterized age‐prevalence curves for each taxon, examined how they changed over space in relation to co‐occurring trematodes and tested whether the shape of the curves aligned with expectations for the frequencies of coinfections by two taxa in the same host. The models explored scenarios that included negative interspecific interactions between parasites, variation in the force‐of‐infection (FOI) and infection‐induced mortality that varied with host age, which were mechanisms hypothesized to be important in the empirical dataset.In the empirical dataset, four trematode parasites had monotonic increasing age‐prevalence curves and four had unimodal age‐prevalence curves. Some of the curves remained consistent in shape in relation to the prevalence of other potentially interacting trematodes, while some shifted from unimodal to monotonic increasing, suggesting release from negative interspecific interactions. The most common taxa with monotonic increasing curves had lower co‐infection frequencies than expected, suggesting they were competitively dominant. Taxa with unimodal curves had coinfection frequencies that were closer to those expected by chance.The model showed that negative interspecific interactions between parasites can cause a unimodal age‐prevalence curve in the subordinate taxon. Increases in the FOI and/or infection‐induced mortality of the dominant taxon cause shifts in the peak prevalence of the subordinate taxon to a younger host age. Infection‐induced mortality that increased with host age was the only scenario that caused a unimodal curve in the dominant taxon.Results indicated that negative interspecific interactions between parasites contributed to variation in the shape of age‐prevalence curves across parasite taxa and support the growing importance of incorporating interactions between parasites in explaining population‐level patterns of host infection over space and time. Read the freePlain Language Summaryfor this article on the Journal blog.
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Beyond single host, single parasite interactions: Quantifying competence for complete multi‐host, multi‐parasite communities
Abstract Understanding parasite transmission in communities requires knowledge of each species' capacity to support transmission. This property, ‘competence’, is a critical currency for modelling transmission under community change and for testing diversity–disease theory. Despite the central role of competence in disease ecology, we lack a clear understanding of the factors that generate competence and drive its variation.We developed novel conceptual and quantitative approaches to systematically quantify competence for a multi‐host, multi‐parasite community. We applied our framework to an extensive dataset: five amphibian host species exposed to four parasitic trematode species across five ecologically realistic exposure doses. Together, this experimental design captured 20 host–parasite interactions while integrating important information on variation in parasite exposure. Using experimental infection assays, we measured multiple components of the infection process and combined them to produce competence estimates for each interaction.With directly estimated competence values, we asked which components of the infection process best explained variation in competence: barrier resistance (the initial fraction of administered parasites blocked from infecting a host), internal clearance (the fraction of established parasites lost over time) or pre‐transmission mortality (the probability of host death prior to transmission). We found that variation in competence among the 20 interactions was best explained by differences in barrier resistance and pre‐transmission mortality, underscoring the importance of host resistance and parasite pathogenicity in shaping competence.We also produced dose‐integrated estimates of competence that incorporated natural variation in exposure to address questions on the basis and extent of variation in competence. We found strong signals that host species identity shaped competence variation (as opposed to parasite species identity). While variation in infection outcomes across hosts, parasites, individuals and doses was considerable, individual heterogeneity was limited compared to among‐species differences. This finding highlights the robustness of our competence estimates and suggests that species‐level values may be strong predictors for community‐level transmission in natural systems.Competence emerges from distinct underlying processes and can have strong species‐level characteristics; thus, this property has great potential for linking mechanisms of infection to epidemiological patterns. Read the freePlain Language Summaryfor this article on the Journal blog.
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- Award ID(s):
- 1754171
- PAR ID:
- 10380728
- Publisher / Repository:
- Wiley-Blackwell
- Date Published:
- Journal Name:
- Functional Ecology
- Volume:
- 36
- Issue:
- 8
- ISSN:
- 0269-8463
- Page Range / eLocation ID:
- p. 1845-1857
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
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