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The amphibian chytrid fungal pathogen (Batrachochytrium dendrobatidis, henceforth Bd) has had a devastating impact on biodiversity, causing the decline or extinction of over 500 amphibian species. Yet, our understanding of Bd transmission pathways remains incomplete, in particular for host species with weak aquatic associations, and between reservoir and susceptible host species. We examined Bd transmission from a potential reservoir host to a potentially susceptible critically endangered host; directly assessing the capacity of the former to transmit Bd, and the susceptibility of the latter as a Bd host. Using cohousing versus sequential use of the same enclosure by the two species, we distinguished the effects of direct versus indirect (environmental) transmission. Our study provides clear evidence that both direct and indirect terrestrial transmission from a reservoir to susceptible host species results in fatal chytridiomycosis. Transmission mode had no effect on overall morbidity or disease progression in the susceptible species. Our results demonstrate that reservoir and susceptible hosts do not need to be in the same place at the same time, or within an aquatic environment for transmission to occur. Our demonstration of indirect terrestrial transmission from a reservoir to susceptible host identifies mechanisms by which Bd may drive ongoing declines in populations where the pathogen is now endemic. Identifying these transmission pathways is important for understanding long‐term extinction vulnerability of remnant populations of declining species challenged by disease.

Emerging infectious diseases have caused many species declines, changes in communities and even extinctions. There are also many species that persist following devastating declines due to disease. The broad mechanisms that enable host persistence following declines include evolution of resistance or tolerance, changes in immunity and behaviour, compensatory recruitment, pathogen attenuation, environmental refugia, density-dependent transmission and changes in community composition. Here we examine the case of chytridiomycosis, the most important wildlife disease of the past century. We review the full breadth of mechanisms allowing host persistence, and synthesise research on host, pathogen, environmental and community factors driving persistence following chytridiomycosis-related declines and overview the current evidence and the information required to support each mechanism. We found that for most species the mechanisms facilitating persistence have not been identified. We illustrate how the mechanisms that drive long-term host population dynamics determine the most effective conservation management strategies. Therefore, understanding mechanisms of host persistence is important because many species continue to be threatened by disease, some of which will require intervention. The conceptual framework we describe is broadly applicable to other novel disease systems.

Hundreds of amphibian species have declined worldwide after the emergence of the amphibian fungal pathogen Batrachochytrium dendrobatidis (Bd). Despite captive breeding efforts, it is unlikely that wild populations for many species will be reestablished unless Bd resistance increases. We performed a Bd‐challenge study in the functionally extinct southern corroboree frog Pseudophryne corroboree to investigate differences in Bd susceptibility among individuals and populations, identify genetic [major histocompatibility complex (MHC) class I] and genome‐wide variants associated with Bd resistance, and measure genetic diversity and population genetic structure. We found three MHC variants and one MHC supertype associated with Bd infection load and survival along with a suggestively associated single nucleotide polymorphism. We also showed that genome‐wide heterozygosity is associated with increased survival. Additionally, we found evidence of significant population structure among the four P. corroboree populations studied and high MHC genetic diversity. Our results indicate that there are immunogenetic differences among captive southern corroboree frogs; such differences could be manipulated to increase disease resistance and mitigate the significant threat of chytridiomycosis. These results demonstrate a potential long‐term solution to chytridiomycosis that could include breeding more resistant individuals and returning them to the wild.

The many and varied effects of human‐induced environmental change have the potential to threaten animal biodiversity and species abundance. Importantly, human land use and global climate change are predicted to reduce water availability, which might have negative consequences for freshwater organisms. In this study, we tested for an effect of a shortened hydroperiod on larval growth and development, and post‐metamorphic survival and immune function in a temperate frog, Rana pipiens. Animals developing under pond drying conditions metamorphosed at a smaller size and had lower survival after metamorphosis. We found sex‐specific differences in larval period in our fastest drying treatment, with males metamorphosing more quickly than females. Individuals that developed under drying conditions also showed reduced skin swelling after phytohaemagglutinin injection, indicating a compromised immune response. We found support for trade‐offs between growth, development and post‐metamorphic immune function across hydroperiod treatments. Whole blood from animals with shorter larval periods had lower bacterial killing ability, and small‐bodied juveniles had lower antibody titres. Overall, our results indicate that a shortened hydroperiod can affect the rate of larval amphibian growth and development, and might negatively impact the condition of species that rely on freshwater for development. Our work improves understanding of the complex impacts that environmental stressors might have on the health of animal populations.

A great diversity of parasites, from viruses and bacteria to a range of remarkable eukaryotic organisms, exploit reptile and amphibian hosts. Recent increases in the emergence of infectious disease have revealed the importance of understanding the effects of interactions between hosts and their parasites. Here we review the effects of parasite infection on a range of demographic, behavioural, genomic and physiological factors in reptile and amphibian species. Reviewing these parasite roles collectively, and prioritising areas for research, advances our ecological understanding and guides direction for conservation in a time of rapid species decline. Poorly resolved systems include Gymnophionan amphibians and Crocodilian hosts, in addition to viral and bacterial parasites. Future research should seek to understand processes enabling population recovery and examining synergistic interactions of parasites with fragmentation, climate change and other processes that threaten species persistence.

Chytridiomycosis, caused by the fungus Batrachochytrium dendrobatidis (Bd), is a skin disease responsible for the global decline of amphibians. Frog species and populations can vary in susceptibility, but this phenomenon remains poorly understood. Here, we investigated serotonin in the skin of infected and uninfected frogs. In more susceptible frog populations, skin serotonin rose with increasing infection intensity, but decreased in later stages of the disease. The more resistant population maintained a basal level of skin serotonin. Serotonin inhibited both Bd sporangial growth and Jurkat lymphocyte proliferation in vitro. However, serotonin accumulates in skin granular glands, and this compartmentalisation may prevent inhibition of Bd growth in vivo. We suggest that skin serotonin increases in susceptible frogs due to pathogen excretion of precursor tryptophan, but that resistant frogs are able to control the levels of serotonin. Overall, the immunosuppressive effects of serotonin may contribute to the susceptibility of frogs to chytridiomycosis.

Amphibian chytridiomycosis, caused by infection with Batrachochytrium dendrobatidis (Bd), is the most devastating vertebrate disease on record. Reservoir hosts are likely to be important in the Bd‐amphibian system because many amphibian species can carry infections without experiencing mortality. However, while a variety of reservoirs have been proposed, few have been empirically demonstrated to act as competent reservoir hosts. In this study, we investigate whether the common eastern froglet, Crinia signifera, a non‐declining species that is widespread in eastern Australia, is a reservoir host for Bd infection. We conducted a long‐term, large‐scale field survey to investigate disease dynamics in C. signifera at sites where four sympatric, threatened anuran species have severely declined. We also monitored Bd‐infected C. signifera in the laboratory to determine susceptibility and survivorship. Finally, we assessed population age structure to investigate disease impact in the wild. We found that C. signifera is a competent reservoir host, maintaining high prevalence and infection intensities in the wild and in the laboratory, with no signs of sub‐lethal effects or clinical disease. In the wild, the modal age is 4 years with individuals living up to 6 years, indicating that adults can survive across multiple years despite high infection prevalence and intensity. The occurrence of C. signifera at sites with remnant populations of threatened species likely contributes to ongoing disease impact in declining species decades after the arrival of Bd. The presence of C. signifera at sites where threatened species have become extinct inhibits effective reintroductions, and we recommend avoiding sites with high reservoir host abundance when planning reintroductions.

Emerging wildlife pathogens are an increasing threat to biodiversity. One of the most serious wildlife diseases is chytridiomycosis, caused by the fungal pathogen, Batrachochytrium dendrobatidis (Bd), which has been documented in over 500 amphibian species. Amphibians vary greatly in their susceptibility to Bd; some species tolerate infection, whereas others experience rapid mortality. Reservoir hosts-species that carry infection while maintaining high abundance but are rarely killed by disease-can increase extinction risk in highly susceptible, sympatric species. However, whether reservoir hosts amplify Bd in declining amphibian species has not been examined. We investigated the role of reservoir hosts in the decline of the threatened northern corroboree frog (Pseudophryne pengilleyi) in an amphibian community in southeastern Australia. In the laboratory, we characterized the response of a potential reservoir host, the (nondeclining) common eastern froglet (Crinia signifera), to Bd infection. In the field, we conducted frog abundance surveys and Bd sampling for both P. pengilleyi and C. signifera. We built multinomial logistic regression models to test whether Crinia signifera and environmental factors were associated with P. pengilleyi decline. C. signifera was a reservoir host for Bd. In the laboratory, many individuals maintained intense infections (>1000 zoospore equivalents) over 12 weeks without mortality, and 79% of individuals sampled in the wild also carried infections. The presence of C. signifera at a site was strongly associated with increased Bd prevalence in sympatric P. pengilleyi. Consistent with disease amplification by a reservoir host, P. pengilleyi declined at sites with high C. signifera abundance. Our results suggest that when reservoir hosts are present, population declines of susceptible species may continue long after the initial emergence of Bd, highlighting an urgent need to assess extinction risk in remnant populations of other declined