Browsing by Author "J. F. Levine, Committee Member"

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    Molecular Epidemiology of Outbreaks of Spring Viremia of Carp Virus in North America, Europe and Asia
    (2007-11-01) Miller, Otis Jr.; J. F. Levine, Committee Member; G. A. Lewbart, Committee Member; W. A. Gebreyes, Committee Member; F. J. Fuller, Committee Chair
    Spring Viremia of Carp Virus (SVCV) or Rhabdovirus carpio is the causative agent of the fish disease, Spring Viremia of Carp (SVC). Genetic relationships between 35 spring viremia of carp virus (SVCV) genogroup Ia isolates were determined based on the nucleotide sequence of the phosphoprotein (P) gene and glycoprotein (G) genes. Phylogenetic analysis based on P-gene sequences revealed two distinct subgroups within the SVCV genogroup Ia, designated SVCV Iai and Iaii, and suggests at least two independent introductions of the virus in the USA in 2002. Combined P - and G - sequence data support the emergence of SVCV in Illinois, USA and Lake Ontario, Canada, from the initial outbreak in Wisconsin, USA, and demonstrate a close genetic link to viruses isolated during routine import checks on fish brought into the UK from Asia. The data also showed a genetic link between SVCV isolations made in Missouri and Washington, USA, in 2004 and the earlier isolation made in North Carolina, USA, in 2002. However, based on the close relationship to a 2004 UK isolate, the data suggests that the Washington isolate represents a third introduction into the US from a common source, rather than a re-emergence from the 2002 isolate. There was strong phylogenetic support for an Asian origin for 9 of 16 UK viruses isolated either from imported fish, or shown to have been in direct contact with fish imported from Asia. In one case, there was 100% nucleotide identity in the G-gene with a virus isolated in the Peoples Republic of China. The remaining portion of this dissertation deals with biosecurity on ornamental fish farms. A good biosecurity program results in control of disease transmission by eliminating pathogen introduction onto farm(s) and dissemination between farms or between ponds on any farm. Each method of possible pathogen movement to new susceptible animals is addressed by a biosecurity plan and prevention is implemented by education and appropriate actions of employees. A biosecurity plan seeks to control: 1. people carrying pathogens on person including visitors and employees, 2. inspection and quarantine of incoming fish, 3. contaminated inanimate objects like vehicles, nets, and other equipment, 4. wild animals that may act as vectors for the pathogen, and 5. water source. Daily operations of a farm must focus on these controls to prevent disease incidence, or if disease has already occurred, its spread. This paper will introduce, through phylogenetic analyses, countries of interest for disease risk to SVCV and introduce a risk assessment tool that can identify biosecurity measures for establishing a biosecurity plan suitable for the control and prevention of one of the industries' disruptive and economical devastating infectious disease, spring viremia of carp.
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    Oxidative Stress in the Aquatic Environment: Effects of Hypoxia and Polychlorinated Biphenyls in Fish and Bivalve Molluscs
    (2006-06-13) Lehmann, Daniel Wade; J. F. Levine, Committee Member; D. Shea, Committee Member; J. M. Law, Committee Chair; G. A. LeBlanc, Committee Member
    Oxidative damage is hypothesized to be an underlying cause of many chronic disease states. Acutely, oxidative damage can lead to irreversible cell injury and pathological consequences. Reactive oxygen species, while naturally occurring at low levels in biological systems, can also be brought about by severe environmental conditions such as hypoxia or by chemical contaminants. This body of work encompasses two different areas of toxicological research into the generation of radical species and the resulting oxidative damage to organisms. The first section deals with hypoxia as a causative factor in epizootic ulcerative syndrome (EUS) in Atlantic menhaden (Brevoortia tyrannus) in the estuaries of the Atlantic coast. Menhaden have a fairly large impact on the coastal environment and on tourism for the state, being integral to food webs of the estuary, coastal shelf, and an indicator of environmental degradation. Our hypothesis was that environmental exposure to hypoxic conditions in the estuaries leads to oxidative stress in Menhaden sufficient to cause tissue damage. Specific objectives of the study were two-fold: Determination of LC50 levels for both Atlantic Menhaden and the hypoxia tolerant species, Nile Tilapia (Oreochromis niloticus), at both acute (2 hour) and medium term (96 hours) exposures to hypoxia. Results indicated that tilapia have a very high tolerance and adaptability to hypoxic conditions. We could not ascertain an LC50 for tilapia as at 0.24 mg⁄L (3% saturation) we saw only 28% mortality at 2 hours. Ca++ and K+ were the only ionic alterations to blood chemistry due to exposure. Menhaden had an LC50 of 1.2 mg⁄L (16% saturation) dissolved oxygen (at 28 ppt salinity) over 1 hour and had blood chemistry dysregulation affecting Ca++, K+, Na+, and glucose levels. In the 96 hour exposures, no alterations in lipid peroxidation, glutathione, lipid soluble antioxidants, or strand breakage were detected indicating that hypoxia and reperfusion were not sufficient to cause oxidative damage or EUS in these species. In the second portion, we evaluated the effects of PCBs in Corbicula clams as possible surrogates for endangered bivalve mollusks. The Ward Transformer site, in Wake County, North Carolina was found to have Aroclor 1260 levels as high as 1.7 mg⁄kg in fish collected miles downstream from the source. Concern over the effects of PCB exposure to the native wildlife, especially at-risk populations of native bivalves, prompted the hypothesis that oxidative damage due to Aroclor exposure would cause changes in biomarkers and pathology associated with decreased health status. Specifically, we conducted a laboratory study to determine the effects of Aroclor 1260 in order to validate common biomarkers of oxidative damage in Corbicula fluminea clams, without confounding environmental factors. Secondly, we performed field deployments of Corbicula into the polluted Brier Creek system to gauge the oxidative status of animals in the field relative to a downstream gradient of Aroclor 1260 concentrations. Results from the laboratory study at 0, 1, 10, and 100 ppb indicated that exposures were detrimental to the clams. Antioxidant biomarkers responded significantly at 3 weeks exposure and morphologic changes included inflammation, anasarca, Brown cell accumulation, severe gonad atrophy, inflammation, and necrosis. In conjunction with biomarker changes, a linear relationship was seen to exist between sediment and time-weighted average water concentrations of PCBs and total oxidant scavenging capacity (TOSC) values. These studies indicated that oxidative damage occurs as a result of exposure to Aroclor 1260.