Over the last few days several members of our team (Mariel Familiar Lopez, myself, Thais Sasso Lopes, Harry Hines, Dave Newell and Liam Bolitho) attended the combined meeting of the Australian Society of Herpetologists and the Society for Research on Amphibians and Reptiles in New Zealand, held at Kindilan Camp, Redland Bay, Queensland, Australia.
It was a great conference with an impressive selection of research presented in two parallel sessions over 2.5 days. Below are the abstracts from our team members.
Chytridiomycosis causes catastrophic organism-wide metabolic dysregulation including profound failure of cellular energy pathways
Grogan, Laura F. (1), Skerratt, L.F. (2), Berger, L. (2), Cashins, S.D. (2), Trengove, R.D. (3, 4) and Gummer, J.P.A. (3, 4)
(1) Griffith Wildlife Disease Ecology Group, Environmental Futures Research Institute, School of Environment, Griffith University, Nathan, Queensland 4111, Australia; (2) One Health Research Group, College of Public Health, Medical and Veterinary Sciences, James Cook University, Townsville, Queensland 4811, Australia; (3) Separation Science and Metabolomics Laboratory, Murdoch University, Perth, Western Australia 6150, Australia; (4) Metabolomics Australia, Murdoch University Node, Murdoch University, Perth, Western Australia 6150, Australia.
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.