Emerging infectious diseases are a major threat to biodiversity conservation, and to the health of wildlife and human populations. They are also utterly fascinating. Our disease ecology research explores how host-pathogen interactions vary with context (environmental conditions, host health, host species, etc.), and how disease ecology can be best incorporated into species recovery planning (25).
Our disease ecology research focuses largely on two pathogens: Pseudogymnoascus destructans, the fungus that causes bat white-nose syndrome, and Ophidiomyces ophidiicola, the fungus that causes ophidiomycosis (snake fungal disease).
Bat white-nose syndrome (WNS) has caused mass mortality in a number of bat species since the introduction of P. destructans to eastern North American and its subsequent spread. We are interested in understanding the genetic, physiological and demographic responses to bat populations to this strong, novel selective pressure. Is something different about the ~5% of individuals who have survived, in species where ~95% mortality occurred after the initial introduction of the pathogen? And what are the chronic effects of exposure to WNS, in survivors that are now co-existing with the pathogen? Our exploration of these questions involve frequent collaborations with Drs. Mike Donaldson, Chris Kyle, and Craig Willis, including a study characterizing the spatial genetic structure of Canadian little brown bats (31), which informed our study providing the first empirical evidence for direct selection by WNS on immune genes in affected bat populations (33).
We have also used transcriptomic analyses to understand how the response of bats to WNS differs among bat species (32, 37, 56) and how the fungus itself responds to growth under different conditions (36).
We analyzed cortisol (“stress hormone”) levels in bat claws to demonstrate that exposure to WNS during the winter has a long-term effect on physiological stress that lasts beyond recovery from the disease itself (28). To our knowledge, this is the first evidence for pathogen-linked carry-over effects in free-ranging mammals. And PhD candidate Karen Vanderwolf is currently studying the effects of bat skin chemistry (especially pH) on the microbiome of bat wings, investigating how skin chemistry affects the microbiome, and how this variation predicts host species’ susceptibility to WNS.
Of course, wildlife populations are never affected by just one stressor at a time, and pathogens rarely get the chance to infect an otherwise uninfected individual. We are interested in wildlife syndemics (interactions among diseases, or between diseases and environmental factors) and in understanding how the effects of WNS interact with other pressures on bat populations. We recently collaborated with the Misra Lab to characterize a novel coronavirus (34), and used transcriptomic analyses to demonstrate that co-infection with this coronavirus alters the systemic response of little brown bats to WNS (43).
Ophidiomyces ophidiicola is the causative agent of ophidiomycosis (snake fungal disease), a recently described disease that has been proposed as a major threat to wild snake populations. However, empirical support for this proposal is lacking, and despite frequent comparisons to bat WNS, it’s not clear that this disease has the same conservation implications for wild populations (64). Rachel Dillon recently completed her MSc testing whether ophidiomycosis affects fitness of wild eastern foxsnakes (Pantherophis vulpinus), using six years of telemetry data from the Wetlands and Reptiles Project (publications in preparation).
And we recently collaborated with the Canadian Wildlife Health Cooperative on studies characterizing the pathology of ophidiomycosis in wild snakes (54) and experimentally testing the effects of brumation on disease outcomes in infected snakes (58, led by Dr. Christina Mackenzie).