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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. 

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.