21st Century Guidebook to Fungi, SECOND EDITION, by David Moore, Geoffrey D. Robson and Anthony P. J. Trinci

Table of Contents

1. Chapter 15: Fungi as symbionts and predators of animals
2. Chapter 16: Fungi as pathogens of animals, including man
   1. Pathogens of insects
   2. Microsporidia
   3. Trichomycetes
   4. Laboulbeniales
   5. Entomogenous fungi
   6. Biological control of arthropod pests
   7. Cutaneous chytridiomycosis: an emerging disease of amphibians
   8. Aspergillosis disease of coral
   9. Snake fungal disease
   10. White-nose syndrome of bats
   11. Mycoses: the fungus diseases of humans
   12. Clinical groupings for human fungal infections
   13. Fungi within the home and their effects on health: allergens and toxins
   14. Comparison of animal and plant pathogens and the essentials of epidemiology
   15. Mycoparasitic and fungicolous fungi
   16. Chapter 16 References and further reading
   17. Buy a PDF of Chapter 16
3. Chapter 17: Whole organism biotechnology

16.10 White-nose syndrome of bats

White-Nose Syndrome (WNS) of bats, caused by the fungal pathogen Pseudogymnoascus destructans, has decimated North American hibernating bats since its emergence in 2006 and is predicted to drive several species extinct. WNS was first detected in New York state in 2006 and was detected in Washington state in March 2016. Pseudogymnoascus destructans is endemic to Eurasia, where the disease is less severe, and it has a much lesser impact on bat populations.

Mortality from WNS differs substantially between North American species, even when they hibernate at the same sites. Some species declined more than 90% in the first year following WNS detection, whereas population growth rates in other species only decreased 8%.

Research has shown that in areas where the disease has been present for several years, bats first became infected when they returned to their winter quarters (their hibernacula) in the autumn, and both transmission and fungal growth on bats occurs primarily during winter once bats lower their body temperature and begin to hibernate. Despite markedly different mortality rates, most bat populations experience greater than 50% infection incidence; suggesting that variation in mortality is due to variation in response to infection. Mortality is thought to be due to a cascade of physiological disruptions which are reactions to tissue damage from fungal invasion. Deaths occurred approximately 70 to 120 days after infection. Variation between species in mortality was correlated with fungal loads of individual animals.

The fungal load is essentially the amount of fungus present in the animal; it can be measured by measuring the quantity of Pseudogymnoascus destructans DNA on bat skin using quantitative PCR on skin swab samples. It had already been established that there is a strong correlation between the abundance of P. destructans on bat skin measured from a swab and the extent of tissue invasion determined by histology. Although infection incidence was uniformly high in all species, fungal load varied a thousand-fold between species and statistically accounted for 98% of the differences in mortality rates. Fungal loads increased with hibernating roosting temperatures, with bats roosting at warmer temperatures having higher fungal loads and suffering greater WNS impacts. Pseudogymnoascus destructans growth increases with temperature across the range of hibernation temperatures commonly used by bats (approximately 1 to 12°C).

Consequently, differences in behavioural preferences between bat species, in particular their preferred roosting microclimate, determines the impact of a new pathogen. Understanding these behavioural/environmental influences on disease may allow control options that permit minimum intervention. Another interesting aspect of this story is that comparative genomics has demonstrated that the pathogen, Pseudogymnoascus destructans, is extremely sensitive to ultraviolet (UV) light, and to DNA alkylating mutagens. The reason for this being that the pathogen’s genome has lost a key enzyme in the repair pathway that normally contributes to repair of DNA damage induced by UV light. This feature might be exploited for treatment of bats with WNS (Langwig et al., 2016; Palmer et al., 2018).

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Updated July, 2019