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|a White plague disease dynamics in the US Virgin Islands: coupling spatial epidemiology with laboratory transmission |h [electronic resource]. |
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|a St. Thomas, Virgin Islands : |b University of the Virgin Islands, |c 2017. |
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|a 1 online resource (50 pages) |
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|a Copyright Elizabeth J. Brown. Permission granted to the University of the Virgin Islands to digitize, archive and distribute this item for non-profit research and educational purposes. Any reuse of this item in excess of fair use or other copyright exemptions requires permission of the copyright holder. |
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|a Diseases have contributed to coral mortality worldwide. While white plaque diseade (WP) is one of the most prevalent coral diseases in the Caribbean, fundamental questions remain about its etiology, virulence, and transmissibility. The aim of this thesis was to evaluate white plaque disease dynamics by 1) determining if white plaque disease clustered spatially on a mesophotic coral reef, and 2) evaluating if WP lesion expansion rates were similar among coral species and at under different temperature scenarios. To examine clustering of diseade lesions at the “reef scale”, a 7x7 grid of 50 m x 50 m cells was overlain on a continous area of mesophotic reef for a total of 2500m². Each cell was sampled with two drop camera photos. Analysis of clustering at the “colony scale” was based on radial transects counting the number of diseased corals that appeared within 5 m of a randomly-selected diseased or healthy-central coral. Two difference spatial analyses---the Spatial Analysis of Distance IndicEs (SADIE) and Moran’s I---were used to analyze whether corals showing signs of white plaque disease tended to cluster spatially. Additionally, a laboratory study was conducted to evaluate the lesion expansion rate of whire plaque disease under different temperature regimes. White plaque-infected corals of various species were exposed to low (27.8 °C ± 0.5 °C) and high (31.5 °C ± 0.8 °C) water temperatures in experimental tanks. The spatial analyses showed that white plaque disease temporarily clusters on a reef scale, but clustering at the reef scale is not necessarily reflected at the colony level. Overall, disease prevalence was lower than expected, which may have contributed to the lack of detectionof spatial structuring. Radial transects showed that more diseased corals were within 5m of diseased corals (n = 6) than healthy ones (n = 2), though this was not statistically significant, likely because of the low number of diseased corals found. Lesion progression rates of the disease varied significantly among species, but there was a significant interaction between species and temperature treatment. The high temperature treatment resulted in significantly faster rates of lesion progression on Favia fragum than the high treatment for Porites astreoides and Siderastrea siderea or the low treatment for S. radians. Results of this study can be used to inform the investigation of a causative agent of white plaque disease and inform managers about reef areas at risl of disease-related mortality. |
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|a Electronic reproduction. |c University of the Virgin Islands, |d 2017. |f (UVI Digital Library) |n Mode of access: World Wide Web. |n System requirements: Internet connectivity; Web browser software. |
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|a University of the Virgin Islands. |
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|a white plague disease -- United States Virgin Islands. |
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|a coupling spatial epidemiology . |
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|a UVI Dissertation/Theses Collection. |
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|a UVI |c UVI Dissertation/Theses Collection |
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|u http://uvi.sobeklibrary.com/AA00000032/00001 |y Electronic Resource |
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|a https:/uvi.sobeklibrary.com/content/AA/00/00/00/32/00001/Brown_Elizabeththm.jpg |
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|a UVI Dissertation/Theses Collection |