An official website of the United States government
Abstract Disease outcomes depend heavily on infection intensity which is often heterogeneous across and within host populations. Most individuals carry low pathogen loads and a few carry high loads, a pattern known as aggregation. Although well characterized in macroparasite systems, aggregation and infection intensity are rarely incorporated into microparasite models.This raises key questions: Do similar mechanisms underlie aggregation in macro‐ and microparasite systems? Moreover, how do aggregation and load‐dependent effects shape outcomes such as host suppression and virulence–transmission trade‐offs?To address these questions, we developed a series of differential equation models that allow the pathogen load distribution across hosts to evolve dynamically, shaped by both within‐ and between‐host processes. We applied this framework to the amphibian chytrid fungus system caused byBatrachochytrium dendrobatidis(Bd), a fungal pathogen threatening amphibian populations worldwide.Our results show that both stronger load‐dependent mortality and faster within‐host replication reduce aggregation. Aggregation, in turn, weakens host suppression and flattens virulence–transmission trade‐off, shifting peak transmission to higher replication rates.Overall, our models show that similar mechanisms of infection intensity and aggregation influence host–pathogen dynamics in microparasites as in macroparasites. This work offers a framework for advancing theoretical and data‐driven understanding of how within‐host processes scale to population‐level disease dynamics, advocating for a unified approach to disease modelling that bridges the macro‐ and microparasites.
more »
« less
This content will become publicly available on July 1, 2027
Environmental detection of the amphibian chytrid fungus in water bodies is associated with host infection along a deforestation gradient
Abstract Many wildlife pathogens can persist in the environment independently of their hosts, with the habitat itself serving as a reservoir and potential source of transmission. However, reliably detecting and quantifying free‐living pathogen stages across heterogeneous landscapes using environmental DNA methods remains challenging. Understanding how landcover and habitat structure drive pathogen distribution at the environmental and host levels is critical for advancing disease surveillance and ecology.Amphibian chytridiomycosis, caused by the fungal pathogenBatrachochytrium dendrobatidis(Bd), provides a useful model system to address these broader challenges, yet most studies have focused on host–pathogen interactions, with less emphasis onBdwithin environmental reservoirs. UsingBdas a model system, we investigated whether pathogen distribution in natural aquatic environments is associated with host infection patterns across gradients of habitat loss. We sampled four tropical amphibian species across eight rainforest landscapes and quantifiedBdin paired water and host samples using a high‐capacity water filtration method coupled with digital and real‐time quantitative polymerase chain reaction detection assays.Our results revealed a strong positive correlation betweenBdDNA concentrations in water and infection loads on amphibian skin, indicating that environmentalBdDNA is associated with host infection patterns.Forest cover and habitat split (i.e. spatial separation between forests and aquatic breeding sites) were the primary predictors ofBdoccurrence, concentration and infection load across environmental and host‐associated forms, and bothBd‐GPL andBd‐Asia‐2/Brazil lineages were detected across our study landscapes.Our study introduces and validates a robust protocol for detecting environmentalBd, providing a scalable approach to quantify pathogen–environment associations across multiple landscapes and environmental gradients.Synthesis and applications: Linking environmental pathogen detection with host infection patterns can improve surveillance of diseases involving environmental transmission, particularly where direct host sampling is logistically challenging. This approach enables the identification of areas of elevated transmission risk and supports targeted monitoring and management under habitat loss and degradation. It also provides a practical tool to guide conservation actions in landscapes undergoing rapid land‐use change.
more »
« less
- Award ID(s):
- 2120084
- PAR ID:
- 10709719
- Publisher / Repository:
- Wiley
- Date Published:
- Journal Name:
- Journal of Applied Ecology
- Volume:
- 63
- Issue:
- 7
- ISSN:
- 0021-8901
- Format(s):
- Medium: X
- Sponsoring Org:
- National Science Foundation
More Like this
-
-
Abstract Host competence—the ability to acquire, harbour and transmit infections—drives pathogen spread and persistence in multi‐host communities. Evaluating species‐specific competence is critical for predicting transmission, particularly for generalist fungal pathogens likeBatrachochytrium dendrobatidis(Bd). Despite its central role in disease dynamics, we lack an epidemiologically grounded competence metric that rigorously accounts for how infection intensity affects a host's competence. This knowledge gap limits our ability to compare mechanisms across species and assess their roles in pathogen persistence. To address these challenges, we developed a novel, load‐dependent competence metric using host–pathogen Integral Projection Models (IPMs) that integrates variation in susceptibility, within‐host pathogen growth and pathogen shedding dynamics.We applied this metric to laboratory‐based challenge experiments with three common North American amphibians (Notophthalmus viridescens,Rana clamitansandRana catesbeianus) that persist endemically with Bd. Using dose–response assays and repeated pathogen shedding measurements across species, we asked: (i) is there a consistent, non‐linear relationship between infection intensity and pathogen shedding across species? and (ii) which load‐based traits best predict host competence? We quantified four of five components of host competence—susceptibility, pathogen growth, pathogen survival and load‐dependent shedding—and used these to parameterize species‐specific IPMs, integrating competence into a single relative metric across species.We found that Bd shedding increased non‐linearly with infection intensity, contradicting the standard assumption that Bd shedding is linearly related to infection intensity.Notophthalmus viridescensandR. catesbeianuswere the most competent hosts but through distinct pathways: high susceptibility inN. viridescensand elevated shedding rates inR. catesbeianus. In contrast, density‐dependent reductions in pathogen growth and shedding limitedR. clamitanscompetence. Thus, species‐level competence is not determined by a single trait, but emerges from interactions among multiple load‐based processes.Our results demonstrate that variation in competence emerges from distinct, species‐specific processes across multiple dimensions of competence. By linking individual infection dynamics to population‐level transmission potential, our integrative framework provides a more mechanistic approach to predicting host contributions to community‐level pathogen persistence. Read the freePlain Language Summaryfor this article on the Journal blog.more » « less
-
Disruption of habitat connectivity alters host movement patterns and pathogen exposure in wildlife. Changes in exposure dynamics have led to increased research interest in host-associated microbial communities (i.e., microbiomes), particularly in how repeated encounters with pathogens may drive microbial filtering processes that favor the assembly of pathogen-inhibiting microbiomes, a concept known as the adaptive microbiome principle. Understanding how habitat connectivity and pathogen exposure shape adaptive microbiomes remains a key frontier in disease ecology. For widely distributed waterborne pathogens such as the amphibian chytrid fungusBatrachochytrium dendrobatidis(Bd), sustained host exposure in contiguous terrestrial–aquatic habitats may promote selection of microbiomes with enhanced antifungal properties. In contrast, under conditions of high habitat split, where key habitats such as forests and water bodies are spatially disconnected, limited exposure to Bd during the pre-breeding and overwintering seasons may hinder the selection of Bd-inhibitory microbiomes that are critical for host protection during the subsequent breeding season, when pathogen exposure in water bodies is at its peak. Our results demonstrate that habitat split may limit recruitment of putative Bd-inhibitory skin bacteria, while Bd loads increase with habitat split for certain amphibian species. Results from Joint Species Distribution Models also indicate that habitat split is a key driver of reduced skin bacterial diversity, even after accounting for biotic and abiotic metrics. Our study provides evidence that spatial connectivity among natural habitats is essential for maintaining multiple levels of biodiversity, from host species to their associated functional microbiomes, highlighting a critical link between environmental disturbance, microbial defenses, and disease dynamics.more » « less
-
Abstract Parasites routinely persist in seasonal systems while infecting multiple host species. An important question for parasite control is whether parasite persistence is driven by particular host species, specific times of year or their interaction. We have few empirically tractable models to answer this question.We develop a data‐driven model that partitions species‐specific and temporal drivers of parasite persistence from commonly collected surveillance data. Leveraging standard epidemiological theory, our approach demonstrates a novel way to link time‐varying fluctuations in species‐level contributions to parasite persistence directly to time‐integrated parasite persistence in the community as a whole, while using real‐world field data that is tractable to obtain.We applied our approach to 3 years of parasite surveillance data in seasonal amphibian communities persisting with the fungal pathogenBatrachochytrium dendrobatidis(Bd). We asked three questions: (i) Do amphibians trade‐off in their contributions to Bd persistence across the year? (ii) What host characteristics, such as seasonally fluctuating host density or host competence, drive these trade‐offs? and (iii) what are the relative contributions of species compared to periods of high transmission for enzootic Bd persistence?We found that the identity of the amphibian species driving Bd persistence was highly variable through time. Specifically, temporal variability in host density and less so variability in host competence drove the temporal variation in species' contributions to persistence. Moreover, our model identified two distinct mechanisms of Bd persistence: (i) spillover dynamics from a dominant maintenance species and (ii) temporally asynchronous, but equal, contributions of host species to persistence. In both cases, species‐targeted interventions were as effective or more effective than temporal control for reducing the capacity of Bd to persist.Broadly, our results demonstrate that species contributions to parasite persistence can have strong, asynchronous temporal variability, potentially limiting the effectiveness of targeted seasonal parasite control. Our model is designed to link closely with standard parasite surveillance data and is broadly applicable to other host–parasite systems where it can partition who, when and what drive parasite persistence in multi‐host seasonal communities.more » « less
-
Abstract Batrachochytrium dendrobatidis(Bd), an aquatic pathogenic fungus, is responsible for the decline of hundreds of amphibian species worldwide and negatively impacts biodiversity globally. Prophylactic exposure to the metabolites produced by Bd can provide protection for naïve tree frogs and reduce subsequent Bd infection intensity.Here, we used a response surface design crossing Bd metabolite prophylaxis concentration and exposure duration to determine how these factors modulate prophylactic protection against Bd in Pacific chorus frog (Pseudacris regilla) tadpoles (5 × 5 surface design) and metamorphs (3 × 3 surface design). We exposed individuals every weekday to one of five Bd metabolite concentrations or a water control for 1–5 weeks, after which all animals were challenged with live Bd to evaluate their susceptibility.Exposure to the Bd metabolite prophylaxis reduced Bd load and prevalence compared to the control for both the tadpoles and metamorphs. Increasing Bd metabolite prophylaxis concentration did not confer additional protection for either life stage, but increasing duration of exposure did benefit metamorphs by decreasing Bd prevalence but not Bd load.On average, control tadpoles and metamorphs had 66.2% and 99.4% higher Bd loads, respectively, than tadpoles and metamorphs exposed to any Bd metabolite prophylaxis.Additionally, Bd metabolite prophylaxis reduced Bd prevalence relative to controls in both tadpoles (20.5% vs. 56.3%, respectively) and metamorphs (21.9% vs. 87.5%, respectively).Synthesis and applications: The efficacy of short‐term exposures of relatively low concentrations of Bd metabolites at reducing Bd infections suggests that this approach has the potential to be scaled up to field use to aid in disease mitigation and conservation. Our results, combined with additional research on Bd metabolite prophylaxis for other amphibian species, suggest that this strategy may represent a broadly useful tool to protect at‐risk amphibian populations.more » « less
