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Chytridiomycosis in the direct-developing frogs of Puerto Rico

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Epidemiological theory normally does not predict host extinction from infectious disease because of a host density threshold below which pathogens cannot persist. However, host extinction can occur when a biotic or abiotic pathogen reservoir allows for density-independent transmission. Amphibians are

Epidemiological theory normally does not predict host extinction from infectious disease because of a host density threshold below which pathogens cannot persist. However, host extinction can occur when a biotic or abiotic pathogen reservoir allows for density-independent transmission. Amphibians are facing global population decline and extinction from the emerging infectious disease chytridiomycosis, caused by the fungus Batrachochytrium dentrobatidis (Bd). I use the model species Eleutherodactylus coqui to assess the impact of Bd on terrestrial direct-developing frog species, a common life history in the tropics. I tested the importance of two key factors that might influence this impact and then used laboratory experiments and published field data to model population-level impacts of Bd on E. coqui. First, I assessed the ontogenetic susceptibility of E. coqui by exposing juvenile and adult frogs to the same pathogen strain and dose. Juveniles exposed to Bd had significantly lower survival rates compared with control juveniles, while adult frogs often cleared infection. Second, I conducted experiments to determine whether E. coqui can become infected with Bd indirectly from contact with zoospores shed onto vegetation by an infected frog and from direct exposure to an infected frog. Both types of transmission were observed, making this the first demonstration that amphibians can become infected indirectly in non-aquatic habitats. Third, I tested the hypothesis that artificially-maintained cultures of Bd attenuate in pathogenicity, an effect known for other fungal pathogens. Comparing two cultures of the same Bd strain with different passage histories revealed reduced zoospore production and disease-induced mortality rates for a susceptible frog species (Atelopus zeteki) but not for the less-susceptible E. coqui. Finally, I used a mathematical model to project the population-level impacts of chytridiomycosis on E. coqui. Model analysis showed that indirect transmission, combined with either a high rate of zoospore production or low rate of zoospore mortality, is required for Bd to drive E. coqui populations below an extinction threshold. High rates of transmission plus frequent re-infection could lead to poor recruitment of infected juveniles and population decline. My research adds further insight into how emerging infectious disease is contributing to the loss of amphibian biodiversity.

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2013

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Analysis of Global Variance of the Thermal Maxima of an Amphibian Pathogen

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Batrachochytrium dendrobatidis (Bd), the amphibian chytrid fungus causing chytridiomycosis, is the cause of massive amphibian die-offs. As with any host-pathogen relationship, it is paramount to understand the growth and reproduction of the pathogen that causes an infectious disease outbreak. The

Batrachochytrium dendrobatidis (Bd), the amphibian chytrid fungus causing chytridiomycosis, is the cause of massive amphibian die-offs. As with any host-pathogen relationship, it is paramount to understand the growth and reproduction of the pathogen that causes an infectious disease outbreak. The life-cycle of the pathogen, Bd, is strongly influenced by temperature; however, previous research has focused on Bd isolated from limited geographic ranges, and may not be representative of Bd on a global scale. My research examines the relationship between Bd and temperature on the global level to determine the actual thermal maximum of Bd. Six isolates of Bd, from three continents, were incubated at a temperature within the thermal range (21°C) and a temperature higher than the optimal thermal range (27°C). Temperature affected the growth and zoosporangium size of all six isolates of Bd. All six isolates had proliferative growth at 21°C, but at 27°C the amount and quality of growth varied per isolate. My results demonstrate that each Bd isolate has a different response to temperature, and the thermal maximum for growth varies with each isolate. Further understanding of the difference in isolate response to temperature can lead to a better understanding of Bd pathogen dynamics, as well as allow us the ability to identify susceptible hosts and environments before an outbreak.

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2016-12