Disease progression model for bat white-nose syndrome (WNS). We propose a mechanistic multi-stage disease model for WNS in a hibernating bat that encompasses current knowledge on the progression of fungal-induced wing pathology and physiologic sequelae leading to mortality from disease. Initial colonization and invasion of the wing epidermis by Pseudogymnoascus destructans (Pd) results in increased energy expenditure, chronic respiratory acidosis (elevated blood pCO2 and bicarbonate), and hyperkalemia (elevated blood potassium). Erosion and ulceration of the epidermis stimulate increased frequencies of arousal from torpor, which remove excess CO2 and normalize blood pH, but contribute to dehydration and depletion of fat reserves. As wing pathology becomes more extensive and severe, these effects are exacerbated by water and electrolyte loss across the epidermis (hypotonic dehydration), which stimulate more frequent arousals and create a positive feedback loop that ultimately leads to mortality when energy reserves and compensatory mechanisms become exhausted.