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The application of a recently developed mathematical model for predicting the spread of chronic wasting disease (CWD) in wild deer was assessed under different scenarios where harvesting is employed in disease management. A process-based mathematical model for CWD transmission in wild deer populations was recently developed and parameterized by Al-arydah et al. (2011) to provide a scientific basis for understanding the factors that affect spread of CWD and evaluate concomitant disease-control strategies. The impact of gender on CWD transmission was shown to have a significant influence on the spread of the disease in the wild. Our model demonstrates a range of harvesting rates in which CWD is controlled and deer populations survive. However, if harvesting rates are too low, the disease remains endemic for decades. Conversely, the Canadian deer population is eradicated if harvesting rates are excessive. Future investigation includes building the model to assess the spread of CWD under different disease-management scenarios.

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Many studies have considered recent increases in ultraviolet B radiation (UVBR) and endocrine disrupting chemicals polluting the environment as possible contributing factors to the reduction in amphibian populations. It has been demonstrated that exposure of amphibians to estrogenic chemicals or UVBR can affect the timing of larval development and metamorphosis. However, amphibians in the wild are exposed to multiple environmental stressors simultaneously. Therefore, our study examines the effects of UVBR and the estrogenic chemical 4-tert-octylphenol (OP), alone and in combination, on the thyroid system of Rana pipiens tadpoles, which is the main regulator of amphibian metamorphosis. Results demonstrate that thyroid gland histomorphology measurements in Gosner stage 31 tadpoles continuously exposed to UVBR (0.21W/m(2)) were not different than those measured in animals from the control group. In a separate experiment, tadpoles exposed to environmentally relevant levels of UVBR (0.22W/m(2)) and/or OP (0.01nM or 10nM) exhibited significantly delayed development starting from Gosner stage 29, given that fewer tadpoles developed past stage 29 in these groups. In addition, significantly fewer UVBR-treated tadpoles developed past stage 34 and metamorphosed. Samples were collected from stages 29 and 34 tadpoles for gene expression analysis in tail tissue and measurements of T3 (triiodothyronine) whole body levels (minus tail). UVBR and/or OP exposure did not affect T3 levels in stages 29 and 34 tadpoles. However, a decrease in deiodinase type 2 (D2) or increase in deiodinase type 3 (D3) mRNA levels was observed in groups of tadpoles with slowed developmental rates at those developmental stages. Given that D2 activates and D3 inactivates thyroid hormones (TH), UVBR/OP mediated disruptions in development are likely caused by dysfunctions in the localized metabolism of THs through alterations in the expression of these enzymes in peripheral tissues. This is the first study to our knowledge reporting a potential thyroid-based mechanism of action for the developmental delays in amphibians exposed to UVBR and/or OP.

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Levels of ultraviolet B radiation (UVBR) reaching the Earth's surface have increased since the 1970s as a result of stratospheric ozone depletion caused by the emission of ozone-depleting substances (ODSs) such as chlorofluorocarbons. Despite international agreements to phase out harmful ODSs, these substances are persistent, and even under the most optimistic scenarios, stratospheric ozone levels will not return to pre-1980 levels for several decades. Furthermore, climate change may enhance chemical stratospheric ozone depletion. Global phenomena such as climate change, ozone depletion, and acidification of aquatic ecosystems interact to modify dissolved organic carbon levels in aquatic systems, thereby increasing the penetration of UVBR. Since amphibians inhabit both aquatic and terrestrial habitats and have unshelled eggs and permeable skin, they are vulnerable to changes in environmental conditions and habitat quality. Increased exposure of amphibians to UVBR can produce lethal and sublethal effects, especially in individuals that do not possess adequate defense mechanisms to protect themselves. In this article, we discuss worldwide increases in UVBR and the adverse effects of UVBR exposure on amphibians. Specifically, studies on the effects of UVBR on amphibian development and metamorphosis are summarized, and possible mechanisms of thyroid system disruption caused by UVBR exposure are considered.

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Biosolids produced from pulp and paper mill wastewater treatment have excellent properties as soil conditioners, but often contain high levels of Escherichia coli. E. coli are commonly used as indicators of fecal contamination and health hazard; therefore, their presence in biosolids causes concern and has lead to restrictions in land-spreading. The objectives of this study were to determine the following: (1) if E. coli from the biosolids of a wastewater-free pulp and paper mill were enteric pathogens, and (2) if other waterborne microbial pathogens were present. E. coli were screened for heat-labile and heat-stable enterotoxin and verocytotoxin virulence genes using a polymerase chain reaction. Ten isolates were also screened for invasion-associated locus and invasion plasmid antigen H genes. None of the 120 isolates carried these genes. Tests for seven other microbial pathogens were negative. Effluents and biosolids from this mill do not contain common microbial pathogens and are unlikely to pose a health hazard.

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