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ABSTRACT Batrachochytrium dendrobatidiscontinues to cause declines in amphibian populations worldwide, and it remains unclear why skin defenses often fail to control the infection. Although amphibians have a complex, multifunctional immune system, the chytridiomycosis agent seems to have evolved countermeasures that enable it to survive and eventually impair critical skin functions. Previous studies show thatB. dendrobatidiscells or cell-free supernatants inhibit lymphocytes by inducing apoptosis, suggesting impaired local cell killing. However, there is little evidence of lymphocyte recruitment to chytrid-infected skin, implying the fungus may also inhibit the functions of antigen-presenting cells. Here, we demonstrate that phagocytosis by peritoneal macrophages is significantly reduced by co-culture with live or heat-killedB. dendrobatidiszoosporangia, freeze-thawed zoospores, fungal cell-free supernatants, or cell-wall fragments. The phagocytic capacity of frog bone marrow-derived macrophages, differentiated by colony-stimulating factor-1 (CSF-1) or interleukin-34 (IL-34) (key macrophage growth factors), as well as immortalized mammalian macrophages, is also impaired. Inhibition of mammalian macrophages suggests that these inhibitory factors are not restricted to amphibian cells. Overall, these studies indicate thatB. dendrobatidiscells and their components can hinder the recognition and function of macrophages that reside in or enter the skin to clear infections. This disabling of host phagocytosis is undoubtedly central to howB. dendrobatidisprevents effective innate and adaptive immune responses in the skin. 

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. 

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. 

ABSTRACT Infectious diseases can cause severe population declines, reducing genetic diversity, ecological function, and prospects for long‐term survival. Such declines often result in genetic bottlenecks, with small, isolated populations that are especially vulnerable to extinction due to genetic drift and inbreeding. Chytridiomycosis, caused byBatrachochytrium dendrobatidis(Bd), has led to global amphibian declines. Yet, some populations now show signs of recovery, even thoughBdis present and pathogenic. In this study, we use a genomic approach to investigate the genetic patterns underlying recoveries in three amphibian species from Panama that experiencedBd‐related declines followed by apparent recoveries:Colostethus panamansis,Lithobates warszewitschiiandSachatamia albomaculata. These species differ in life history traits and dispersal capacities, allowing us to examine how such differences influence genetic signatures of recovery. Here, we employed a frog‐specific genomic capture assay to analyse the effective population sizes, population structures, and both genome‐wide and immune‐specific genetic diversity. Our results reveal recent genetic bottlenecks and low effective population sizes across all three species, consistent with evidence of past disease‐driven declines. However, we found distinct patterns of gene flow and immune genetic diversity among species. These findings suggest that gene flow may serve as a key demographic and adaptive contributor of recovery in some species by introducing novel genetic variation. Understanding how populations recover from infectious disease impacts is critical for informing conservation efforts. Our study provides insights into the genetic signatures associated with recovery and highlights the importance of species‐specific traits in shaping evolutionary responses to emerging diseases. 

ABSTRACT In our rapidly changing world, evolution is likely to play an important role in facilitating the resilience of wildlife populations. The Sierra Nevada yellow‐legged frog (Rana sierrae) provides a rare example of recovery following severe declines caused by the amphibian chytrid fungus (Batrachochytrium dendrobatidis). However, the role of evolution in facilitating this recovery remains circumstantial. In this study, we sought to gain insights into the potential role of evolution by comparing genomes of frogs from naive and recovering populations located in close proximity. Using multiple methods to scan frog genomes for signatures of selection, our study reveals several genomic variants associated with frog recovery. Specifically, we identify outlier gene variants across genes related to skin integrity and intracellular regulation, an interferon‐related gene and a recovery‐associated variant in RIN3—a gene that may play a critical role in disease defence and wound healing. Finally, we report no differences in genetic diversity between naive and recovering populations. Our study provides a rare example from natural populations that suggests that evolution can produce individuals that harbour adaptive alleles and allow population recovery in the presence of novel stressors. These findings complement recent research on rapid amphibian evolution in response to disease and provide mechanistic hypotheses for how individuals can prove resilient to disease outbreaks. 

ABSTRACT AimSpecies distribution models (SDMs) are an important tool for conservation efforts, and when constructed using high‐quality predictor and response data could be useful for identifying portions of a species' range that could serve as refugia from risks that are influenced by environmental conditions, such as pathogens.Batrachochytrium dendrobatidis(Bd) is a fungal pathogen that causes lethal disease in amphibians but is also sensitive to environmental factors including temperature and humidity. SDMs built using high spatial and temporal resolution environmental data may be able to help identify environmental refugia fromBdfor amphibians. In this study, we create our own high‐resolution remotely sensed environmental dataset and use high‐quality presence/absence survey data to build newBdSDMs of Panama. LocationPanama. TaxaThe amphibian chytrid fungusBdand amphibian communities. MethodsWe used environmental values from various time periods prior toBdtesting (lag of 2, 7, 15, 30 days) and levels ofBdinfection intensity from survey swabs (present, medium intensity, high intensity) to run multiple Boosted Regression Trees to model environmental suitability forBdand evaluated their performance. ResultsOur results indicated that the 15‐day period prior to testing was the most predictive time‐period forBdenvironmental suitability in Panama. Additionally, we found that we could not only model the distribution of the pathogen itself but discern unique spatial and temporal patterns of high infection intensities often associated with disease outbreaks. We created daily predictive maps of the probability ofBdoccurrence and of medium and high infection intensities in Panama from 2005 to 2018 and averaged them by season. Main ConclusionsHigher environmental suitability forBdtended to be found at higher elevations, a pattern observed in previousBdfield studies and consistent withBd's physiological requirements. The high temporal and spatial resolution of these maps gives a unique insight into exploring temporal patterns ofBdintensity in specific locations and to identify environmental refugia fromBdfor amphibian reintroduction efforts and surveys for relict populations. 

Abstract Individual heterogeneity, in number of parasites, size, etc., interacts critically with population dynamics. We tease this out in a model case study of microparasite load with empirically supported assumptions to investigate how variance in load interacts with population dynamics, We show how the mean and variance of load vary throughout an epidemic. Further, we show how mean and variance have mutual negative feedbacks on each other mediated by high death rates at high loads. Helpfully, we find that mean and variance provide information into underlying processes as well. Population trends in the mean and variance reveal underlying trends in within-host processes, e.g. differentiating host evolution of defence that manifests as tolerance, constitutive resistance, inducible resistance or acquired resistance. Our findings apply to many microparasites, including fungal pathogens which show large variance in infection load. As a case study, we consider endangered frog populations recovering from fungal epidemics and find that the mean and variance guide management actions. Lastly, we demonstrate the impact of load variance on host fitness, pathogen fitness and host population suppression. Our results demonstrate the importance of trait heterogeneity and the insights available from relatively simple models, both for microparasite load and possibly other traits. 

ABSTRACT Chytridiomycosis is a contributor to amphibian population declines. Diseased amphibians show symptoms of lethargy and loss of righting reflexes, likely due to an ion imbalance across the skin. However, it is possible developing zoosporangia release toxins that affect neuromuscular activity. Using Xenopus laevis as a model, we hypothesized that locomotor performance would be affected by injection of Bd supernatant factors. X. laevis were injected and then filmed performing a swimming escape response with high-speed cameras at 4 h, 24 h, and 1-week post-injection. Average maximum swimming velocity and escape latency were digitized using high-speed video. Despite no difference in escape velocity, there was a significant difference in escape latency 24 h post injection at both concentrations tested, 106 and 107 cell equivalents, though only differences at 106 cell equivalents/ml supernatant persisted 1 week post injection. Changes in specific locomotor function suggest that there may be neurotoxins present, though the potential neurotoxins may exhibit neural circuit specificity across escape behavior. This study provides a method to test more purified extracts to determine whether Bd produces neurotoxic factors that could enter the blood stream and alter locomotion during a natural skin infection. 

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. 

ABSTRACT Pathogens often exploit ecological and evolutionary opportunities created by anthropogenic change, with profound consequences for host communities. In Brazil's Atlantic Forest, the amphibian chytrid fungusBatrachochytrium dendrobatidis(Bd) exemplifies this dynamic, with two co‐occurring lineages: the enzootic Bd‐Brazil lineage and the invasive Global Panzootic Lineage (Bd‐GPL), implicated in historical amphibian declines and Bd hybridization events. To investigate how host taxonomy and habitat use influence Bd lineage distribution, we sampled 3836 amphibians representing 42 species across paired aquatic and terrestrial transects over a two‐year period. We successfully genotypedn = 252 out of 777 Bd‐positive samples using nuclear and mitochondrial SNP assays to differentiate between Bd‐GPL, Bd‐Brazil, hybrids, and coinfections. Our results reveal that Bd lineage distribution is nonrandomly associated with host genus and habitat type. Stream‐dwelling frogs, particularly those in the genusHylodes, had higher rates of coinfection with Bd‐GPL and Bd‐Brazil than most other genera. This pattern may reflect their lifelong association with streams, which might increase their exposure to zoospores from multiple Bd lineages. In contrast, terrestrial transects were dominated by single‐lineage Bd‐GPL infections, even when accounting for differences in amphibian species composition and host genus among transect types. These findings suggest that aquatic habitats could serve as refugia for Bd‐Brazil, while Bd‐GPL may exhibit more desiccation tolerance. Methodological limitations of this study, including biases towards successfully genotyping high‐load infections and limited genomic resolution, underscore the need for more high‐resolution sequencing approaches to fully understand pathogen dynamics in the Atlantic Forest.