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Abstract Vast alteration of the biosphere by humans is causing a sixth mass extinction, driven in part by an increase in infectious diseases. The emergence of the lethal fungal pathogenBatrachochytrium dendrobatidis(Bd) has devastated global amphibian biodiversity. Given the lack of any broadly applicable methods to reverse these impacts, the future of many amphibians appears grim. The Sierra Nevada yellow-legged frog (Rana sierrae) is highly susceptible to Bd infection and mostR. sierraepopulations are extirpated following disease outbreaks. However, some populations persist and eventually recover, and frogs in these recovering populations have increased resistance against infection. Here, we conduct a 15-year reintroduction study and show that frogs collected from recovering populations and reintroduced to vacant habitats can reestablish populations despite the presence of Bd. In addition, the likelihood of establishment is influenced by site, cohort, and frog attributes. Results from viability modeling suggest that many reintroduced populations have a low probability of extinction over 50 years. These results provide a rare example of how reintroduction of resistant individuals can allow the landscape-scale recovery of disease-impacted species, and have broad implications for amphibians and other taxa that are threatened with extinction by novel pathogens. 

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. 

Most hosts contain few parasites, whereas few hosts contain many. This pattern, known as aggregation, is well-documented in macroparasites where parasite intensity distribution among hosts affects host–parasite dynamics. Infection intensity also drives fungal disease dynamics, but we lack a basic understanding of host–fungal aggregation patterns, how they compare with macroparasites and if they reflect biological processes. To begin addressing these gaps, we characterized aggregation of the fungal pathogenBatrachochytrium dendrobatidis(Bd) in amphibian hosts. Utilizing the slope of Taylor’s Power law, we found Bd intensity distributions were more aggregated than many macroparasites, conforming closely to lognormal distributions. We observed that Bd aggregation patterns are strongly correlated with known biological processes operating in amphibian populations, such as epizoological phase (i.e. invasion, post-invasion and enzootic), and intensity-dependent disease mortality. Using intensity-dependent mathematical models, we found evidence of evolution of host resistance based on aggregation shifts in systems persisting with Bd following disease-induced declines. Our results show that Bd aggregation is highly conserved across disparate systems and contains signatures of potential biological processes of amphibian–Bd systems. Our work can inform future modelling approaches and be extended to other fungal pathogens to elucidate host–fungal interactions and unite host–fungal dynamics under a common theoretical framework. 

IntroductionBatrachochytrium salamandrivorans(Bsal) poses a major threat to global amphibian biodiversity. It is essential we understandBsaltransmission to develop better-informed management strategies. Infected carcasses are an important source of transmission for several human and wildlife disease systems; however, they have not been examined as sources forBsalexposure. Here, we evaluated whether infected newt carcasses could contribute toBsaltransmission dynamics. MethodsWe cohoused infected carcasses with susceptible newts in two cohousing chamber types (partitioned or non-partitioned) at three timepoints post-mortem ([0,24[, [24,48, [48,72] hrs). The partitioned chamber prevented newt-to-newt contact hence only allowed indirect, waterborne transmission of zoospores. We measured shedding rates of infected carcasses at each post-mortem timepoint and monitored infection status and mortality of susceptible newts which were exposed during cohousing events. ResultsOur results indicate carcasses are capable of transmittingBsalto susceptible newts up to at least 72 hrs post-mortem, even without live newts directly contacting carcasses. All susceptible newts in each chamber type and post-mortem period became infected and >90% experienced disease-induced mortality.Bsalgenomic copies/uL in skin swabs taken from infected carcasses were high, averaging 7.4x10⁵, 8.6x10⁵, and 2.0x10⁶at 24, 48, and 72 hrs post-mortem, respectively. Water samples collected from cohousing chambers averaged 2743Bsalgenomic copies/uL (approximately 1357 zoospores) and did not decline over 72 hrs. DiscussionOur results indicateBsalinfection can occur rapidly between infected carcasses and susceptible aquatic salamanders via indirect and direct transmission pathways, and carcasses may prolong outbreaks by increasing the duration that infected individuals remain infectious. Carcass removal may be a strategy to reduceBsaltransmission and the impacts of outbreaks. 

Synopsis Antimicrobial peptides (AMPs) play a fundamental role in the innate defense against microbial pathogens, as well as other immune and non-immune functions. Their role in amphibian skin defense against the pathogenic fungus Batrachochytrium dendrobatidis (Bd) is exemplified by experiments in which depletion of host’s stored AMPs increases mortality from infection. Yet, the question remains whether there are generalizable patterns of negative or positive correlations between stored AMP defenses and the probability of infection or infection intensity across populations and species. This study aims to expand on prior field studies of AMP quantities and compositions by correlating stored defenses with an estimated risk of Bd exposure (prevalence and mean infection intensity in each survey) in five locations across the United States and a total of three species. In all locations, known AMPs correlated with the ability of recovered secretions to inhibit Bd in vitro. We found that stored AMP defenses were generally unrelated to Bd infection except in one location where the relative intensity of known AMPs was lower in secretions from infected frogs. In all other locations, known AMP relative intensities were higher in infected frogs. Stored peptide quantity was either positively or negatively correlated with Bd exposure risk. Thus, future experiments coupled with organismal modeling can elucidate whether Bd infection affects secretion/synthesis and will provide insight into how to interpret amphibian ecoimmunology studies of AMPs. We also demonstrate that future AMP isolating and sequencing studies can focus efforts by correlating mass spectrometry peaks to inhibitory capacity using linear decomposition modeling. 

Introduction One of the most important emerging infectious diseases of amphibians is caused by the fungal pathogen Batrachochytrium salamandrivorans (Bsal) . Bsal was recently discovered and is of global concern due to its potential to cause high mortality in amphibians, especially salamander species. To date, little has been reported on the pathophysiological effects of Bsal ; however, studies of a similar fungus, B. dendrobatidis (Bd) , have shown that electrolyte losses and immunosuppression likely play a key role in morbidity and mortality associated with this disease. The goal of this study was to investigate pathophysiological effects and immune responses associated with Bsal chytridiomycosis using 49 rough-skinned newts ( Taricha granulosa ) as the model species. Methods Taricha granulosa were exposed to a 1 × 10 7 per 10 mL dose of Bsal zoospores and allowed to reach various stages of disease progression before being humanely euthanized. At the time of euthanasia, blood was collected for biochemical and hematological analyses as well as protein electrophoresis. Ten standardized body sections were histologically examined, and Bsal -induced skin lesions were counted and graded on a scale of 1–5 based on severity. Results Results indicated that electrolyte imbalances and dehydration induced by damage to the epidermis likely play a major role in the pathogenesis of Bsal chytridiomycosis in this species. Additionally, Bsal -infected, clinically diseased T. granulosa exhibited a systemic inflammatory response identified through alterations in complete blood counts and protein electrophoretograms. Discussion Overall, these results provide foundational information on the pathogenesis of this disease and highlight the differences and similarities between Bsal and Bd chytridiomycosis. 

The emerging fungal amphibian pathogen, Batrachochytrium salamandrivorans (Bsal), is currently spreading across Europe and given its estimated invasion potential, has the capacity to decimate salamander populations worldwide. Fungicides are a promising in situ management strategy for Bsal due to their ability to treat the environment and infected individuals. However, antifungal drugs or pesticides could adversely affect the environment and non-target hosts, thus identifying safe, effective candidate fungicides for in situ treatment is needed. Here, we estimated the inhibitory fungicidal efficacy of five plant-derived fungicides (thymol, curcumin, allicin, 6-gingerol, and Pond Pimafix®) and one chemical fungicide (Virkon® Aquatic) against Bsal zoospores in vitro. We used a broth microdilution method in 48-well plates to test the efficacy of six concentrations per fungicide on Bsal zoospore viability. Following plate incubation, we performed cell viability assays and agar plate growth trials to estimate the minimum inhibitory concentration (MIC) and minimum fungicidal concentration (MFC) of each fungicide. All six fungicides exhibited inhibitory and fungicidal effects against Bsal growth, with estimated MIC concentrations ranging from 60 to 0.156 μg/mL for the different compounds. Allicin showed the greatest efficacy (i.e., lowest MIC and MFC) against Bsal zoospores followed by curcumin, Pond Pimafix®, thymol, 6-gingerol, and Virkon® Aquatic, respectively. Our results provide evidence that plant-derived fungicides are effective at inhibiting and killing Bsal zoospores in vitro and may be useful for in situ treatment. Additional studies are needed to estimate the efficacy of these fungicides at inactivating Bsal in the environment and treating Bsal-infected amphibians.