Host microbiome responses to the Snake Fungal Disease pathogen (Ophidiomyces ophidiicola) are driven by changes in microbial richness

• Published in: Scientific reports Vol. 12; no. 1; p. 3078
• Main Authors: Romer, Alexander S., Grinath, Joshua B., Moe, Kylie C., Walker, Donald M.
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 23-02-2022; Nature Publishing Group; Nature Portfolio
• Subjects: 631/158/853; 631/326/421; 704/158/2452; 704/158/855; Animal Diseases - microbiology; Animals; Colubridae - microbiology; Disease Progression; Epidermis - microbiology; Fungal diseases; Host Microbial Interactions - physiology; Humanities and Social Sciences; Microbiomes; multidisciplinary; Mycoses - microbiology; Onygenales - pathogenicity; Pathogens; Science; Science (multidisciplinary); Time Factors
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-022-07042-5

Dermatophytic pathogens are a source of disturbance to the host microbiome, but the temporal progression of these disturbances is unclear. Here, we determined how Snake Fungal Disease, caused by
Ophidiomyces ophidiicola
, resulted in disturbance to the host microbiome. To assess disease effects on the microbiome, 22 Common Watersnakes (
Nerodia sipedon
) were collected and half were inoculated with
O. ophidiicola.
Epidermal swabs were collected weekly for use in microbiome and pathogen load characterization. For the inoculated treatment only, we found a significant effect of disease progression on microbial richness and Shannon diversity consistent with the intermediate disturbance hypothesis. When explicitly accounting for differences in assemblage richness, we found that β-diversity among snakes was significantly affected by the interaction of time and treatment group, with assemblages becoming more dissimilar across time in the inoculated, but not the control group. Also, differences between treatments in average microbiome composition became greater with time, but this interactive effect was not evident when accounting for assemblage richness. These results suggest that changes in composition of the host microbiome associated with disease largely occur due to changes in microbial richness related to disease progression.