Elemental iron (Fe) plays an essential role as a catalytic cofactor in several basic cellular reactions employed by nearly all known life forms. Surprisingly, while Fe is the fourth most abundant element on earth, it is often biologically limiting due to its scarce solubility in aqueous solution. Parasitic organisms face a unique challenge in terms of Fe acquisition because their host environment actively sequesters free Fe. To obtain Fe, parasites must scavenge Fe from host tissues, overcoming an array of host defense molecules that serve to bind and store free Fe intracellularly. This atomic battle has been termed a precious metal heist and is a taxonomically broad phenomenon documented in both invertebrate and vertebrate hosts. Perturbations to host Fe levels alter the competitive dynamics of this struggle for Fe; there is an overwhelming tendency for elevated host Fe levels to lead to increased parasite virulence across a variety of disease systems. In order to understand what (if any) role Fe plays in the dynamics of an emerging infectious amphibian disease, chytridiomycosis, this dissertation has begun to investigate the biological effects of host Fe bioaccumulation on both the host and parasite organisms independently, as well as the host-parasite system. Furthermore, this research explores whether individual-level host/parasite outcomes scale up to explain observed population-level disease dynamics. While the importance of Fe availability has already been documented in numerous host/parasite systems, the role that Fe plays in the biology of the amphibian chytrid fungus has not been investigated to date. Furthermore, previous studies investigating host Fe availability and disease in other systems were conducted in the laboratory on individual organisms. This project is the first to evaluate if these individuallevel host/parasite dynamics can explain population-level outbreaks of infectious disease in the wild. Finally, this project is novel in that it explores a broad mechanism (aerosol Fe deposition) through which host Fe levels can become elevated simultaneously in populations of diverse organisms across space and time. This perturbation to host Fe status could potentially explain the recent emergence of a suite of infectious wildlife diseases, if Fe is, as has been suggested, increasing in aquatic and terrestrial ecosystems globally.
|Effective start/end date||6/1/12 → 5/31/15|
- NSF: Directorate for Biological Sciences (BIO): $15,000.00