Over the past decade, millions of North American bats have perished from a fungal infection known as white-nose syndrome. As its name suggests, the most conspicuous manifestation of the disease is the development of fuzzy white fungus on the muzzle, which strikes during hibernation. Beyond this superficial symptom, the fungus causes nasty lesions on the wings and disrupts blood chemistry prior to death. The disease also causes bats to wake up more frequently during hibernation and the increased energy expenditure causes the animals to wither away.
Whilst it is clear that the fungus wreaks physiological havoc, exactly how the pathology progresses is unclear. To investigate how the initially innocuous-looking infection causes death and population demise, Liam McGuire and his colleagues, then at the University of Winnipeg (Canada), devised a series of experiments on wild-caught little brown bats. Half of the (initially healthy) animals were inoculated with the fungus that causes white-nose syndrome before hibernating in captivity.
Over the initial 4 months, the hibernating bats were filmed with an infrared camera, and the team observed that infected bats woke up considerably more often than healthy animals. After this period, the authors moved the bats into chambers in which they could record the animals’ metabolic rate (by measuring carbon dioxide excretion) and water loss. Even whilst dormant, the infected bats were spending more energy. The researchers also measured evaporative water loss when the bats were exposed to either humidified or dry air. The bats inoculated with the fungus lost more water than healthy animals in both circumstances, and they were especially vulnerable to desiccation in dry air.
At the end of their experiment, McGuire and colleagues measured the severity of the infection by taking photographs of the bats’ wings under UV light. The fluorescent fungus covered up to almost half the wing surface area in inoculated animals (but was confirmed to be absent in uninfected animals). The authors then looked for correlations between the extent of the individuals’ infection and their metabolic rate or water loss. There was a clear relationship between water loss and wing damage; the individuals with extensive wing lesions became most dehydrated. This indicates that water probably seeps directly through the wounds. However, there was no correlation between torpid metabolic rate and severity of wing lesions, which suggests that factors other than water loss are elevating metabolic rate.
This timely study demonstrates that increased evaporative water loss and elevated metabolic rate independently endanger bats infected with white-nose syndrome. The finding that dry air exacerbates the dehydration is particularly pertinent and may influence how infected animals are treated. Thus, this study neatly exemplifies how a mechanistic understanding of how emerging pathogens disrupt animal physiology may provide a key bedrock to developing successful conservation programmes.
