Infectious diseases rarely end in extinction. Yet the mechanisms that explain how epidemics subside are difficult to pinpoint. We investigated host-pathogen interactions after the emergence of a lethal fungal pathogen in a tropical amphibian assemblage. Some amphibian host species are recovering, but the pathogen is still present and is as pathogenic today as it was almost a decade ago. In addition, some species have defenses that are more effective now than they were before the epidemic. These results suggest that host recoveries are not caused by pathogen attenuation and may be due to shifts in host responses. Our findings provide insights into the mechanisms underlying disease transitions, which are increasingly important to understand in an era of emerging infectious diseases and unprecedented global pandemics.

The disease chytridiomycosis is responsible for global amphibian declines. Chytridiomycosis is caused by Batrachochytrium dendrobatidis ( Bd ) and B. salamandrivorans ( Bsal ), fungal pathogens with stationary and transmissible life stages. Establishing methods that quantify growth and survival of both life stages can facilitate research on the pathophysiology and disease ecology of these pathogens. We tested the efficacy of the MTT assay, a colorimetric test of cell viability, and found it to be a reliable method for quantifying the viability of Bd and Bsal stationary life stages. This method can provide insights into these pathogens’ growth and reproduction to improve our understanding of chytridiomycosis.

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Temperature is a critically important factor in many infectious disease systems, because it can regulate responses in both the host and the pathogen. White-nose syndrome (WNS) in bats is a severe infectious disease caused by the temperature-sensitive fungus, Pseudogymnoascus destructans ( Pd ). One feature of WNS is an increase in the frequency of arousal bouts (i.e. when bat body temperatures are elevated) in Pd -infected bats during hibernation. While several studies have proposed that increased frequency of arousals may play a role in the pathophysiology of WNS, it is unknown if the temperature fluctuations might mediate Pd growth. We hypothesized that exposure to a high frequency of elevated temperatures would reduce Pd growth due to thermal constraints on the pathogen. We simulated the thermal conditions for arousal bouts of uninfected and infected bats during hibernation (fluctuating from 8 to 25°C at two different rates) and quantified Pd growth in vitro . We found that increased exposure to high temperatures significantly reduced Pd growth. Because temperature is one of the most critical abiotic factors mediating host–pathogen interactions, resolving how Pd responds to fluctuating temperatures will provide insights for understanding WNS in bats and other fungal diseases.