04 Jun 2019
10:00 - 10:20


Louise Rollins Smith, Vanderbilt University School of Medicine

Louise A. Rollins-Smith1, Laura K. Reinert1, Mitchell Le Sage1, Thomas Umile2, Kevin P.C. Minbiole2, E. Davis Carter3, Debra L. Miller3, and Matthew J. Gray3

1Department of Pathology, Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN
2Department of Chemistry, Villanova University, Villanova, PA
3 University of Tennessee Institute of Agriculture, Knoxville, TN

Amphibians have been declining around the world for more than four decades. Contributing to these declines are the chytrid fungi, Batrachochytrium dendrobatidis (Bd) and Batrachochytrium salamandrivorans (Bsal), which cause the disease chytridiomycosis. Amphibians have complex immune defenses against fungi, but Batrachochytrium fungi have a number of counter-defenses. Previously, we identified three small metabolites that inhibit lymphocyte proliferation. We
hypothesize that the fungi respond to stress by production and release of these mediators to evade immune destruction. Bsal is the newest amphibian pathogen that causes death as it enters new populations, and it appears to produce similar inhibitory metabolites. Here, we present preliminary evidence that innate skin secretions of Eastern newts, Notophthalmus viridescens, contain a mixture of proteins that reduce the viability of infectious Bsal zoospores. The proteins appear to be more abundant when induced from animals held in cold conditions (6 C) in comparison with warmer newts (at 14 C or 22 C). In Bsal exposure trials, pathogen loads were also reduced at 6 C in comparison with animals exposed at 14 C or 22 C. Although cold temperature did not impair production of the defensive proteins, they were only partially protective for Bsal-exposed newts. Newts at 6 C developed chytridiomycosis and died more slowly than at 14 C; however, mortality was similar between temperatures. Thus, it appears that temperature may plan a critical role in innate skin defenses against Bsal chytridiomycosis, and those defenses alone are insufficient to prevent development of chytridiomycosis in this susceptible host species.

Funding NSF IOS-1557634, IOS-155759, DEB-1814520.