Abstract:Wildlife disease surveillance and pathogen detection are fundamental for conservation, population sustainability, and public health. Detection of pathogens in snakes is often overlooked despite their essential roles as both predators and prey within their communities. Ophidiomycosis (formerly referred to as Snake Fungal Disease, SFD), an emergent disease on the North American landscape caused by the fungus
Ophidiomyces ophiodiicola
, poses a threat to snake population health and stabilit… Show more
“…However, overall, prevalence was relatively low (8.7%) when compared to studies conducted in North America. of free-ranging snakes in the USA and Canada, with 9.8% observed mortality [30,33].…”
Section: Discussionmentioning
confidence: 99%
“…However, overall, prevalence was relatively low (8.7%) when compared to studies conducted in North America. Samples collected from 31 states in the U.S. and Puerto Rico detected O. ophidiicola in 17.2% of wild snakes, and a meta-analysis of 33 studies reported overall O. ophidiicola infection in 18.5% of free-ranging snakes in the USA and Canada, with 9.8% observed mortality [30, 33].…”
Infectious diseases are influenced by interactions between host and pathogens in variable environments and are rarely homogenous across the landscape. Areas with elevated pathogen burden and transmission may indicate a disruption to steady-state disease dynamics. However, isolating processes that result in increases in infection prevalence and intensity remains a challenge. Here we elucidate the contribution of host species, and pathogen clade in disease hotspots. We examined broad-scale patterns of infection of O. ophidiicola, the pathogen that causes snake fungal disease, in 21 species of snakes across 10 countries in Europe. Disease hotspots were evident across several regions in Europe, and our analyses revealed significant differences in infection based on host species and pathogen clade. Over 80% of positive detections were from host species in the Natrix genus, indicating potential higher susceptibility in this group. The presence of O. ophidiicola genotypes that have been associated with more severe disease in North America, also resulted in high rates of infection compared to genotypes only described from Europe. Elevated infection prevalence was best explained by an interaction between host and pathogen identity which was not uniform across all species. More broadly, these findings present important mechanisms underlying disease hotspots across a disease endemic region.
“…However, overall, prevalence was relatively low (8.7%) when compared to studies conducted in North America. of free-ranging snakes in the USA and Canada, with 9.8% observed mortality [30,33].…”
Section: Discussionmentioning
confidence: 99%
“…However, overall, prevalence was relatively low (8.7%) when compared to studies conducted in North America. Samples collected from 31 states in the U.S. and Puerto Rico detected O. ophidiicola in 17.2% of wild snakes, and a meta-analysis of 33 studies reported overall O. ophidiicola infection in 18.5% of free-ranging snakes in the USA and Canada, with 9.8% observed mortality [30, 33].…”
Infectious diseases are influenced by interactions between host and pathogens in variable environments and are rarely homogenous across the landscape. Areas with elevated pathogen burden and transmission may indicate a disruption to steady-state disease dynamics. However, isolating processes that result in increases in infection prevalence and intensity remains a challenge. Here we elucidate the contribution of host species, and pathogen clade in disease hotspots. We examined broad-scale patterns of infection of O. ophidiicola, the pathogen that causes snake fungal disease, in 21 species of snakes across 10 countries in Europe. Disease hotspots were evident across several regions in Europe, and our analyses revealed significant differences in infection based on host species and pathogen clade. Over 80% of positive detections were from host species in the Natrix genus, indicating potential higher susceptibility in this group. The presence of O. ophidiicola genotypes that have been associated with more severe disease in North America, also resulted in high rates of infection compared to genotypes only described from Europe. Elevated infection prevalence was best explained by an interaction between host and pathogen identity which was not uniform across all species. More broadly, these findings present important mechanisms underlying disease hotspots across a disease endemic region.
“…O. ophidiicola is a generalist pathogen which is capable of infecting numerous snake species across the phylogeny (31, 33, 92). We acknowledge that the physiological response to this pathogen may vary among different host snake species, but we suspect that the biological mechanisms underlying host response (like immune activation, metabolism, etc.)…”
There is growing concern about infectious diseases in wildlife species caused by pathogenic fungi. Detailed knowledge exists about host pathology and the molecular mechanisms underlying host physiological response to some fungal diseases affecting amphibians and bats but is lacking for others with potentially significant impacts on large groups of animals. One such disease is ophidiomycosis (Snake Fungal Disease; SFD) which is caused by the fungus Ophidiomyces ophidiicola and impacts diverse species of snakes. Despite this potential, the biological mechanisms and molecular changes occurring during infection are unknown for any snake species. To gain this information, we performed a controlled experimental infection of captive Prairie rattlesnakes ( Crotalus viridis ) with O. ophidiicola at different temperatures. We then generated liver, kidney, and skin transcriptomes from control and infected snakes to assess tissue specific genetic responses to infection. Given previous SFD histopathological studies and the fact that snakes are ectotherms, we expected highest fungal activity on skin and a significant impact of temperature on host response. In contrast, we found that most of the differential gene expression was restricted to internal tissues and fungal-infected snakes showed transcriptome profiles indicative of long-term inflammation of specific tissues. Infected snakes at the lower temperature had the most pronounced overall host functional response whereas, infected snakes at the higher temperature had overall expression profiles similar to control snakes possibly indicating recovery from the disease. Overall, our results suggest SFD is a systemic disease with a chronic host response, unlike acute response shown by amphibians to Batrachochytrium dendrobatidis infections. Our analysis also generated a list of candidate protein coding genes that potentially mediate SFD response in snakes, providing tools for future comparative and evolutionary studies into variable species susceptibility to ophidiomycosis.
“…The emerging fungi pathogens threaten biodiversity more than any other group of microorganisms that can cause disease (Fisher et al, 2012). They are responsible for declines of many taxa, including fishes (Hatai, 2012;Rodger, 2016;Yanong, 2003), amphibians (Blaustein et al, 2018;Grogan et al, 2018;Hussain & Pandit, 2012;Rollins-Smith, 2017), and reptiles (Allender et al, 2020;Lorch et al, 2016;Schumacher, 2003). These declines are especially severe in amphibians, whose populations are declining worldwide (Blaustein et al, 2018;Collins, 2010).…”
Section: Emerging Fungal Pathogensmentioning
confidence: 99%
“…The ectotherms decline has multiple causes, emphasizing the increased prevalence and outbreaks of diseases caused by emerging pathogens, such as fungus and viruses, in amphibians (Blaustein et al, 2018;Chen & Robert, 2011;Grogan et al, 2018;Hussain & Pandit, 2012;Rollins-Smith, 2017), reptiles (Allender et al, 2020;Lorch et al, 2016;Marschang, 2019;Schumacher, 1997Schumacher, , 2003, and fishes (Hatai, 2012;Rodger, 2016;Yanong, 2003). This increase in the prevalence of pathogens and the resulting diseases, in turn, are associated with climate change and environmental contamination (Becker & Zamudio, 2011;Brem & Lips, 2008;Burrowes et al, 2004).…”
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