Date of Thesis

Spring 2026

Description

Bats are known host reservoirs for communicable diseases, possessing the ability to tolerate the high pathogen loads of emerging infectious diseases (EID) without suffering negative fitness effects. However, white-nose syndrome (WNS) is challenging this preconception in North American bat populations. WNS is a cutaneous fungal infection caused by Pseudogymnoascus destructans (Pd) that has resulted in mass mortality of North American bat hibernacula since its arrival in 2006. Despite threatening extinction in some species, a comprehensive understanding of host-pathogen interactions in WNS-affected bats remains limited. This study uses differential expression analyses to reveal pathogen whole-transcriptome changes in response to differing host environments across a historical gradient of WNS exposure. We found that Pd differentially expresses transcripts when growing on Myotis lucifugus (Mylu) with 10 years, 5 years, or less than 1 year of prior WNS experience. Interestingly, Pd responds dynamically to different host immune responses by upregulating unique pathways while ultimately achieving similar pathogenic outcomes such as host tissue damage, oxidative stress evasion, and nutrient acquisition. Additionally, our results suggest that Pd is responding competitively to resistant host immune responses from all three Mylu populations, suggesting that insufficient time has passed for selective pressures to select for commensal host-pathogen interactions in North American WNS.

Keywords

White-nose syndrome, Myotis lucifugus, Pseudogymnoascus destructans, Bat immunology, Bat disease tolerance, Transcriptomics

Access Type

Honors Thesis (Bucknell Access Only)

Degree Type

Bachelor of Science

Major

Biology

First Advisor

Ken Field

Second Advisor

Janani Hariharan

Third Advisor

Sanjay Dharmavaram

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