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Creators/Authors contains: "Miller, Debra L"

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  1. Free, publicly-accessible full text available July 11, 2026
  2. 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. 
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  3. Abstract Hellbenders ( Cryptobranchus alleganiensis ) are large, aquatic salamanders from the eastern United States. Both subspecies, eastern and Ozark hellbenders, have experienced declines resulting in federal listing of Ozark hellbenders. The globally distributed chytrid fungus, Batrachochytrium dendrobatidis (Bd) has been detected in both subspecies, and Batrachochytrium salamandrivorans ( Bsal ) poses a new threat if introduced into North America. Ozark hellbenders also suffer a high prevalence of toe lesions of unknown etiology, with changes in host immunocompetence hypothesized to contribute. Antimicrobial peptides (AMPs) secreted from dermal granular glands may play a role in hellbender health. We collected skin secretions from free-ranging hellbenders and enriched them for small cationic peptides used for growth inhibition assays against Bd and Bsal . Generalized linear mixed models revealed the presence of active toe lesions as the strongest and only significant predictor of decreased Bd inhibition by skin peptides. We also found skin secretions were more inhibitory of Bsal than Bd . MALDI-TOF mass spectrometry revealed candidate peptides responsible for anti-chytrid activity. Results support the hypothesis that hellbender skin secretions are important for innate immunity against chytrid pathogens, and decreased production or release of skin peptides may be linked to other sub-lethal effects of disease associated with toe lesions. 
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  4. 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. 
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  5. Abstract Batrachochytrium salamandrivorans ( Bsal ) is a fungal pathogen of amphibians that is emerging in Europe and could be introduced to North America through international trade or other pathways. To evaluate the risk of Bsal invasion to amphibian biodiversity, we performed dose-response experiments on 35 North American species from 10 families, including larvae from five species. We discovered that Bsal caused infection in 74% and mortality in 35% of species tested. Both salamanders and frogs became infected and developed Bsal chytridiomycosis. Based on our host susceptibility results, environmental suitability conditions for Bsal , and geographic ranges of salamanders in the United States, predicted biodiversity loss is expected to be greatest in the Appalachian Region and along the West Coast. Indices of infection and disease susceptibility suggest that North American amphibian species span a spectrum of vulnerability to Bsal chytridiomycosis and most amphibian communities will include an assemblage of resistant, carrier, and amplification species. Predicted salamander losses could exceed 80 species in the United States and 140 species in North America. 
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  6. null (Ed.)
    Batrachochytrium salamandrivorans is an emerging fungus that is causing salamander declines in Europe. We evaluated whether an invasive frog species (Cuban treefrog, Osteopilus septentrionalis) that is found in international trade could be an asymptomatic carrier when exposed to zoospore doses known to infect salamanders. We discovered that Cuban treefrogs could be infected with B. salamandrivorans and, surprisingly, that chytridiomycosis developed in animals at the two highest zoospore doses. To fulfill Koch’s postulates, we isolated B. salamandrivorans from infected frogs, exposed eastern newts (Notophthalmus viridescens) to the isolate, and verified infection and disease by histopathology. This experiment represents the first documentation of B. salamandrivorans chytridiomycosis in a frog species and substantially expands the conservation threat and possible mobilization of this pathogen in trade. 
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  7. Ariel, Ellen (Ed.)
    Ranaviruses are emerging pathogens of poikilothermic vertebrates. In 2015 the Global Ranavirus Reporting System (GRRS) was established as a centralized, open access, online database for reports of the presence (and absence) of ranavirus around the globe. The GRRS has multiple data layers (e.g., location, date, host(s) species, and methods of detection) of use to those studying the epidemiology, ecology, and evolution of this group of viruses. Here we summarize the temporal, spatial, diagnostic, and host-taxonomic patterns of ranavirus reports in the GRRS. The number, distribution, and host diversity of ranavirus reports have increased dramatically since the mid 1990s, presumably in response to increased interest in ranaviruses and the conservation of their hosts, and also the availability of molecular diagnostics. Yet there are clear geographic and taxonomic biases among the reports. We encourage ranavirus researchers to add their studies to the portal because such collation can provide collaborative opportunities and unique insights to our developing knowledge of this pathogen and the emerging infectious disease that it causes. 
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  8. Wang, Chengshu (Ed.)
    Environmental temperature is a key factor driving various biological processes, including immune defenses and host-pathogen interactions. Here, we evaluated the effects of environmental temperature on the pathogenicity of the emerging fungal pathogen, Batrachochytrium salamandrivorans ( Bsal ), using controlled laboratory experiments, and measured components of host immune defense to identify regulating mechanisms. We found that adult and juvenile Notophthalmus viridescens died faster due to Bsal chytridiomycosis at 14°C than at 6 and 22°C. Pathogen replication rates, total available proteins on the skin, and microbiome composition likely drove these relationships. Temperature-dependent skin microbiome composition in our laboratory experiments matched seasonal trends in wild N . viridescens , adding validity to these results. We also found that hydrophobic peptide production after two months post-exposure to Bsal was reduced in infected animals compared to controls, perhaps due to peptide release earlier in infection or impaired granular gland function in diseased animals. Using our temperature-dependent susceptibility results, we performed a geographic analysis that revealed N . viridescens populations in the northeastern United States and southeastern Canada are at greatest risk for Bsal invasion, which shifted risk north compared to previous assessments. Our results indicate that environmental temperature will play a key role in the epidemiology of Bsal and provide evidence that temperature manipulations may be a viable disease management strategy. 
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  9. null (Ed.)