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External reinfection of a fungal pathogen does not contribute to pathogen growth

TitleExternal reinfection of a fungal pathogen does not contribute to pathogen growth
Publication TypeJournal Article
Year of Publication2018
AuthorsDiRenzo G.V, Tunstall T.S, Ibanez R., deVries M.S, Longo A.V, Zamudio K.R, Lips K.R
Date Published2018/12
Type of ArticleArticle
ISBN Number1612-9202
Accession NumberWOS:000451591600012
KeywordsAbiotic reservoir; amphibian; Amphibians; assemblage; batrachochytrium-dendrobatidis; biodiversity; Biodiversity & Conservation; chytridiomycosis; community; disease; dynamics; emerging infectious-disease; Environmental Sciences & Ecology; Epizootic; extinction; imperfect; Multi-species; panama; population declines; transmission; tropical

Chytridiomycosis is an emerging infectious disease of amphibians caused by the fungal pathogen Batrachochytrium dendrobatidis (Bd), which has led to devastating declines in amphibian populations worldwide. Current theory predicts that Bd infections are maintained through both reproduction on the host's skin and reinfection from sources outside of the host. To investigate the importance of external reinfection on pathogen burden, we infected captive-bred individuals of the highly susceptible Panamanian Golden Frog, Atelopus glyphus, and wild-caught glass frogs, Espadarana prosoblepon, with Bd. We housed the animals in one of three treatments: individually, in heterospecific pairs, and in conspecific pairs. For 8 weeks, we measured the Bd load and shedding rate of all frogs. We found that Atelopus had high rates of increase in both Bd load and shedding rate, but pathogen growth rates did not differ among treatments. The infection intensity of Espadarana co-housed with Atelopus was indistinguishable from those housed singly and those in conspecific pairs, despite being exposed to a large external source of Bd zoospores. Our results indicate that Bd load in both species is driven by pathogen replication within an individual, with reinfection from outside the host contributing little to the amplification of host fungal load.

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