Geology topics

Julia S. Lankton

Publications and source records attributed to Julia S. Lankton.

39 records · Page 3Linked to original sources

USGS2017

Pre-mining trace element and radiation exposure to biota from a breccia pipe uranium mine in the Grand Canyon (Arizona, USA) watershed

The risks to wildlife and humans from uranium (U) mining in the Grand Canyon watershed are largely unknown. In addition to U, other co-occurring ore constituents contribute to risks to biological receptors depending on their toxicological profiles. This study characterizes the pre-mining concentrations of total arsenic (As), cadmium (Cd), copper (Cu), lead (Pb), mercury (Hg), nickel (Ni), selenium (Se), thallium (Tl), U, and zinc (Zn); radiation levels; and histopathology in biota (vegetation, invertebrates, amphibians, birds, and mammals) at the Canyon Mine. Gross alpha levels were below the reporting limit (4 pCi/g) in all samples, and gross beta levels were indicative of background in vegetation (<10–17 pCi/g) and rodents (<10–43.5 pCi/g). Concentrations of U, Tl, Pb, Ni, Cu, and As in vegetation downwind from the mine were likely the result of aeolian transport. Chemical concentrations in rodents and terrestrial invertebrates indicate that surface disturbance during mine construction has not resulted in statistically significant spatial differences in fauna concentrations adjacent to the mine. Chemical concentrations in egg contents and nestlings of non-aquatic birds were less than method quantification limits or did not exceed toxicity thresholds. Bioaccumulation of As, Pb, Se, Tl, and U was evident in Western spadefoot ( Spea multiplicata ) tadpoles from the mine containment pond; concentrations of As (28.9–31.4 μg/g) and Se (5.81–7.20 μg/g) exceeded toxicity values and were significantly greater than in tadpoles from a nearby water source. Continued evaluation of As and Se in biota inhabiting and forging in the mine containment pond is warranted as mining progresses.

Arizona↗

USGS2016

Snake fungal disease: An emerging threat to wild snakes

Since 2006, there has been a marked increase in the number of reports of severe and often fatal fungal skin infections in wild snakes in the eastern USA. The emerging condition, referred to as snake fungal disease (SFD), was initially documented in rattlesnakes, where the infections were believed to pose a risk to the viability of affected populations. The disease is caused by Ophidiomyces ophiodiicola , a fungus recently split from a complex of fungi long referred to as the Chrysosporium anamorph of Nannizziopsis vriesii (CANV). Here we review the current state of knowledge about O. ophiodiicola and SFD. In addition, we provide original findings which demonstrate that O. ophiodiicola is widely distributed in eastern North America, has a broad host range, is the predominant cause of fungal skin infections in wild snakes and often causes mild infections in snakes emerging from hibernation. This new information, together with what is already available in the scientific literature, advances our knowledge of the cause, pathogenesis and ecology of SFD. However, additional research is necessary to elucidate the factors driving the emergence of this disease and develop strategies to mitigate its impacts.

Philosophical Transactions of the Royal Society B:↗

USGS2015

Experimental infection of snakes with Ophidiomyces ophiodiicola causes pathological changes that typify snake fungal disease

Snake fungal disease (SFD) is an emerging skin infection of wild snakes in eastern North America. The fungus Ophidiomyces ophiodiicola is frequently associated with the skin lesions that are characteristic of SFD, but a causal relationship between the fungus and the disease has not been established. We experimentally infected captive-bred corn snakes ( Pantherophis guttatus ) in the laboratory with pure cultures of O. ophiodiicola . All snakes in the infected group ( n = 8) developed gross and microscopic lesions identical to those observed in wild snakes with SFD; snakes in the control group ( n = 7) did not develop skin infections. Furthermore, the same strain of O. ophiodiicola used to inoculate snakes was recovered from lesions of all animals in the infected group, but no fungi were isolated from individuals in the control group. Monitoring progression of lesions throughout the experiment captured a range of presentations of SFD that have been described in wild snakes. The host response to the infection included marked recruitment of granulocytes to sites of fungal invasion, increased frequency of molting, and abnormal behaviors, such as anorexia and resting in conspicuous areas of enclosures. While these responses may help snakes to fight infection, they could also impact host fitness and may contribute to mortality in wild snakes with chronic O. ophiodiicola infection. This work provides a basis for understanding the pathogenicity of O. ophiodiicola and the ecology of SFD by using a model system that incorporates a host species that is easy to procure and maintain in the laboratory. IMPORTANCE Skin infections in snakes, referred to as snake fungal disease (SFD), have been reported with increasing frequency in wild snakes in the eastern United States. While most of these infections are associated with the fungus Ophidiomyces ophiodiicola , there has been no conclusive evidence to implicate this fungus as a primary pathogen. Furthermore, it is not understood why the infections affect different host populations differently. Our experiment demonstrates that O. ophiodiicola is the causative agent of SFD and can elicit pathological changes that likely impact fitness of wild snakes. This information, and the laboratory model we describe, will be essential in addressing unresolved questions regarding disease ecology and outcomes of O. ophiodiicola infection and helping to conserve snake populations threatened by the disease. The SFD model of infection also offers utility for exploring larger concepts related to comparative fungal virulence, host response, and host-pathogen evolution.

mBio↗