Presenting my research at the Amphibian Disease Meeting in Phoenix, Arizona!
I was recently awarded a 2018 Griffith Sciences Early Career Researcher Travel Grant ($3000) to attend the Amphibian Disease Meeting in Phoenix, Arizona - the pre-eminent international gathering of researchers working in the field of amphibian diseases, held at Arizona State University by Prof. James Collins and Dr. Elizabeth Davidson.
I first made a trip out to Rochester, New York, to visit collaborator Prof. Jacques Robert, before attending the Amphibian Disease Meeting in Arizona. The meeting convenor, Prof. James Collins recommended four of my recently published first-author papers as research highlights since the last meeting in his opening summary presentation (thanks Jim!).
I then presented my work on the metabolic response of amphibians to chytridiomycosis:
Title: "Chytridiomycosis causes catastrophic organism-wide metabolic dysregulation includingvprofound failure of cellular energy pathways"
Authors: Laura F. Grogan, Lee F. Skerratt, Lee Berger, Scott D. Cashins, Robert D. Trengove & Joel P. A. Gummer
Abstract: 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.
I followed this up with a meeting with collaborators Prof. Cherie Briggs and Assoc. Prof. Marm Kilpatrick, to discuss progress on the ARC Discovery Project.
All in all it was a very successful trip!