The population genetics of the causative agent of snake fungal disease indicate recent introductions to the USA
Snake fungal disease (SFD; ophidiomycosis), caused by the pathogen Ophidiomyces ophiodiicola ( Oo ), has been documented in wild snakes in North America and Eurasia, and is considered an emerging disease in the eastern United States of America. However, a lack of historical disease data has made it...
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Published in | PLoS biology Vol. 20; no. 6; p. e3001676 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
San Francisco
Public Library of Science
23.06.2022
Public Library of Science (PLoS) |
Subjects | |
Online Access | Get full text |
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Summary: | Snake fungal disease (SFD; ophidiomycosis), caused by the pathogen
Ophidiomyces ophiodiicola
(
Oo
), has been documented in wild snakes in North America and Eurasia, and is considered an emerging disease in the eastern United States of America. However, a lack of historical disease data has made it challenging to determine whether
Oo
is a recent arrival to the USA or whether SFD emergence is due to other factors. Here, we examined the genomes of 82
Oo
strains to determine the pathogen’s history in the eastern USA.
Oo
strains from the USA formed a clade (Clade II) distinct from European strains (Clade I), and molecular dating indicated that these clades diverged too recently (approximately 2,000 years ago) for transcontinental dispersal of
Oo
to have occurred via natural snake movements across Beringia. A lack of nonrecombinant intermediates between clonal lineages in Clade II indicates that
Oo
has actually been introduced multiple times to North America from an unsampled source population, and molecular dating indicates that several of these introductions occurred within the last few hundred years. Molecular dating also indicated that the most common Clade II clonal lineages have expanded recently in the USA, with time of most recent common ancestor mean estimates ranging from 1985 to 2007 CE. The presence of Clade II in captive snakes worldwide demonstrates a potential mechanism of introduction and highlights that additional incursions are likely unless action is taken to reduce the risk of pathogen translocation and spillover into wild snake populations. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Current address: Genencor Technology Center, Palo Alto, California, United States of America The authors have declared that no competing interests exist. |
ISSN: | 1545-7885 1544-9173 1545-7885 |
DOI: | 10.1371/journal.pbio.3001676 |