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Mycoviruses may influence the pathogenicity of disease-causing fungi. Although mycoviruses have been found in some chytrid fungi, limited testing has not detected them in Batrachochytrium dendrobatidis (Bd), the cause of the devastating amphibian disease, chytridiomycosis. Here we conducted a survey for mycovirus presence in 38 Bd isolates from Australia (n = 31), Brazil (n = 5) and South Korea (n = 2) with a combination of modern high-throughput sequencing and conventional dsRNA cellulose chromatography. Mycoviruses were not detected in any isolates. This result was unexpected, given the long evolutionary history of Bd, as well as the high prevalence of mycoviruses in related fungal species. Given our widespread sampling in Australia and the limited number of Bd introductions, we suggest that mycoviruses are uncommon or absent from Australian Bd. Testing more isolates from regions where Bd originated, as well as regions with high diversity or low fungal virulence may identify mycoviruses that could aid in disease control.

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.

Chytridiomycosis is among several recently emerged fungal diseases of wildlife that have caused decline or extinction of naïve populations. Despite recent advances in understanding pathogenesis, host response to infection remains poorly understood. Here we modelled a total of 162 metabolites across skin and liver tissues of 61 frogs from four populations (three long-exposed and one naïve to the fungus) of the Australian alpine tree frog (Litoria verreauxii alpina) throughout a longitudinal exposure experiment involving both infected and negative control individuals. We found that chytridiomycosis dramatically altered the organism-wide metabolism of clinically diseased frogs. Chytridiomycosis caused catastrophic failure of normal homeostatic mechanisms (interruption of biosynthetic and degradation metabolic pathways), and pronounced dysregulation of cellular energy metabolism. Key intermediates of the tricarboxylic acid cycle were markedly depleted, including in particular α-ketoglutarate and glutamate that together constitute a key nutrient pathway for immune processes. This study was the first to apply a non-targeted metabolomics approach to a fungal wildlife disease and specifically to dissect the host-pathogen interface of Bd-infected frogs. The patterns of metabolite accumulation we have identified reveal whole-body metabolic dysfunction induced by a fungal skin infection, and these findings have broad relevance for other fungal diseases.

The fungal skin disease chytridiomycosis has caused the devastating decline and extinction of hundreds of amphibian species globally, yet the potential for evolving resistance, and the underlying pathophysiological mechanisms remain poorly understood. We exposed 406 naïve, captive-raised alpine tree frogs (Litoria verreauxii alpina) from multiple populations (one evolutionarily naïve to chytridiomycosis) to the aetiological agent Batrachochytrium dendrobatidis in two concurrent and controlled infection experiments. We investigated (A) survival outcomes and clinical pathogen burdens between populations and clutches, and (B) individual host tissue responses to chytridiomycosis. Here we present multiple interrelated datasets associated with these exposure experiments, including animal signalment, survival and pathogen burden of 355 animals from Experiment A, and the following datasets related to 61 animals from Experiment B: animal signalment and pathogen burden; raw RNA-Seq reads from skin, liver and spleen tissues; de novo assembled transcriptomes for each tissue type; raw gene expression data; annotation data for each gene; and raw metabolite expression data from skin and liver tissues. These data provide an extensive baseline for future analyses.

Globalized infectious diseases are causing species declines worldwide, but their source often remains elusive. We used whole-genome sequencing to solve the spatiotemporal origins of the most devastating panzootic to date, caused by the fungus Batrachochytrium dendrobatidis, a proximate driver of global amphibian declines. We traced the source of B. dendrobatidis to the Korean peninsula, where one lineage, BdASIA-1, exhibits the genetic hallmarks of an ancestral population that seeded the panzootic. We date the emergence of this pathogen to the early 20th century, coinciding with the global expansion of commercial trade in amphibians, and we show that intercontinental transmission is ongoing. Our findings point to East Asia as a geographic hotspot for B. dendrobatidis biodiversity and the original source of these lineages that now parasitize amphibians worldwide.

Biodiversity is declining at an alarming rate, especially among vertebrates. Disease is commonly ignored or dismissed in investigations of wildlife declines, partly because there is often little or no obvious clinical evidence of illness. We argue that disease has the potential to cause many species declines and extinctions and that there is mounting evidence that this is a more important cause of declines than has been appreciated. We summarise case studies of diseases that have affected wildlife to the point of extinction and bring together the experiences of wildlife managers, veterinarians, epidemiologists, infectious disease specialists, zoologists and ecologists to provide an investigation framework to help ecologists and wildlife managers address disease as a factor in wildlife declines. Catastrophic declines of wildlife may be the result of single or multiple synergistic causes, and disease should always be one factor under consideration, unless proven otherwise. In a rapidly changing world where emerging infectious diseases have become increasingly common, the need to consider diseases has never been more important.

Ancylostoma ceylanicum is the common hookworm of domestic dogs and cats throughout Asia, and is an emerging but little understood public health risk in tropical northern Australia. We investigated the prevalence of A. ceylanicum in soil and free-ranging domestic dogs at six rainforest locations in Far North Queensland that are Indigenous Australian communities and popular tourist attractions within the Wet Tropics World Heritage Area. By combining PCR-based techniques with traditional methods of hookworm species identification, we found the prevalence of hookworm in Indigenous community dogs was high (96.3% and 91.9% from necropsy and faecal samples, respectively). The majority of these infections were A. caninum. We also observed, for the first time, the presence of A. ceylanicum infection in domestic dogs (21.7%) and soil (55.6%) in an Indigenous community. A. ceylanicum was present in soil samples from two out of the three popular tourist locations sampled. Our results contribute to the understanding of dogs as a public health risk to Indigenous communities and tourists in the Wet Tropics. Dog health needs to be more fully addressed as part of the Australian Government's commitments to “closing the gap” in chronic disease between Indigenous and other Australians, and encouraging tourism in similar locations.

Background Avian influenza viruses (AIVs) are found worldwide in numerous bird species, causing significant disease in gallinaceous poultry and occasionally other species. Surveillance of wild bird reservoirs provides an opportunity to add to the understanding of the epidemiology of AIVs. Methods This study examined key findings from the National Avian Influenza Wild Bird Surveillance Program over a 5‐year period (July 2007–June 2012), the main source of information on AIVs circulating in Australia. Results The overall proportion of birds that tested positive for influenza A via PCR was 1.9 ± 0.1%, with evidence of widespread exposure of Australian wild birds to most low pathogenic avian influenza (LPAI) subtypes (H1–13, H16). LPAI H5 subtypes were found to be dominant and widespread during this 5‐year period. Conclusion Given Australia's isolation, both geographically and ecologically, it is important for Australia not to assume that the epidemiology of AIV from other geographic regions applies here. Despite all previous highly pathogenic avian influenza outbreaks in Australian poultry being attributed to H7 subtypes, widespread detection of H5 subtypes in wild birds may represent an ongoing risk to the Australian poultry industry.

The parasitic nematode Ancylostoma ceylanicum is common in dogs, cats and humans throughout Asia, inhabiting the small intestine and possibly leading to iron-deficient anaemia in those infected. It has previously been discovered in domestic dogs in Australia and this is the first report of A. ceylanicum in wild canids. Wild dogs (dingoes and dingo hybrids) killed in council control operations (n = 26) and wild dog scats (n = 89) were collected from the Wet Tropics region around Cairns, Far North Queensland. All of the carcasses (100%) were infected with Ancylostoma caninum and three (11.5%) had dual infections with A. ceylanicum. Scats, positively sequenced for hookworm, contained A. ceylanicum, A. caninum and Ancylostoma braziliense, with A. ceylanicum the dominant species in Mount Windsor National Park, with a prevalence of 100%, but decreasing to 68% and 30.8% in scats collected from northern and southern rural suburbs of Cairns, respectively. Due to the ability of A. ceylanicum to cause a patent infection in humans, the zoonotic risk arising from this wild dog reservoir to communities in the Wet Tropics should be determined.

The ability to monitor the abundance and diversity of tabanid flies over wide areas requires effective and low-cost surveillance methods. Such monitoring activities help to quantify the risk of transmission of pathogens by tabanids. Here we examine the effectiveness and practicality of two types of trap (canopy traps and Nzi traps) and two types of attractant (octenol and carbon dioxide) for monitoring tabanid flies in tropical Australia. The Nzi trap consistently caught more tabanids and more species of tabanids than the canopy trap. It was also more robust and therefore required less maintenance in remote locations. The use of attractants substantially increased capture rates, both of individuals and species, and traps using both attractants were consistently the most effective. However, in remote locations, where it is not possible to check traps frequently, the use of attractants may not be feasible. When attractants were not used, the canopy trap caught very few tabanids, but the Nzi trap remained effective enough to be useful as a monitoring device. In addition, the number of tabanid species caught by the Nzi traps remained high, and included those that were most abundant. We therefore conclude that, in this region, Nzi traps are preferable for tabanid monitoring and that attractants greatly improve their effectiveness. However, for longterm monitoring, especially in remote locations, Nzi traps without attractants are a satisfactory option.