Browsing by Author "Craig Harms, Committee Member"
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- The biology and ecology of the invasive Indo-Pacific lionfish(2009-08-07) Morris, James Adiel Jr.; Craig Harms, Committee Member; James Rice, Committee Co-Chair; Jeff Govoni, Committee Co-Chair; Kyle Shertzer, Committee Member; Craig Sullivan, Committee MemberThe Indo-Pacific lionfishes, Pterois miles and P. volitans, are now established along the Southeast U.S. and Caribbean and are expected to expand into the Gulf of Mexico and Central and South America. Prior to this invasion little was known regarding the biology and ecology of these lionfishes. I provide a synopsis of chronology, taxonomy, local abundance, reproduction, early life history and dispersal, venomology, feeding ecology, parasitology, potential impacts, and possible control and management strategies for the lionfish invasion. This information was collected by review of the literature and by direct field and experimental study. I confirm the existence of an unusual supraocular tentacle phenotype and suggest that the high prevalence of this phenotype in the Atlantic is not the result of selection, but likely ontogenetic change. To describe the trophic impacts of lionfish, I report a comprehensive assessment of diet that describes lionfish as a generalist piscivore that preys on over 40 species of teleost comprising more than 20 families. Next, I use the histology of gonads to describe both oogenesis and reproductive dynamics of lionfish. Lionfish mature relatively early and reproduce several times per month throughout the entire calendar year off North Carolina and the Bahamas. To investigate predation, an important component of natural mortality, I assessed the vulnerability of juvenile lionfish to predation by native serranids. Juvenile lionfish are not readily consumed by serranids, even after extreme periods of starvation. Last, I used a stage-based, matrix population model to estimate the scale of control that would be needed to reduce an invading population of lionfish. Together, this research provides the first comprehensive assessment on lionfish biology and ecology and explains a number of life history and ecological interactions that have facilitated the unprecedented and rapid establishment of this invasive finfish. Future research is needed to understand the scale of impacts that lionfish could cause, especially in coral reef ecosystems, which are already heavily stressed. This research further demonstrates the need for lionfish control strategies and more rigorous prevention and early detection and rapid response programs for marine non-native introductions.
- Modulation of Immune Function Parameters in Fish Caused by Sudden Environmental Changes(2005-03-06) Choi, Kyoungju; Craig Harms, Committee Member; Mac Law, Committee Co-Chair; W. Gregory Cope, Committee Co-Chair; Muquarrab Qureshi, Committee MemberThree related projects were conducted using multiple tiered bioassays to determine the effects of acute changes in salinity, low oxygen saturation (hypoxia), or triamcinolone on immune function in teleost (bony) fish using the well characterized tilapia fish model. We hypothesized that sudden changes in the aquatic environment, specifically salinity and dissolved oxygen, would compromise immune function in teleost fish leading to alterations of cytokine expression, namely increase in TGF-β and decrease in IL-1β; suppression of phagocytosis; and adverse changes in plasma chemistry and hematology. Further, we hypothesized that these immune system changes would be similar to those caused by administration of triamcinolone. Our overall hypothesis was that the total immunocompromise caused by rapid environmental changes leads to increased susceptibility to diseases such as epizootic ulcerative syndrome (EUS). To model the rapid environmental changes often experienced by fish in North Carolina estuaries, tilapia (Oreochromis niloticus) were exposed under controlled laboratory conditions to either acute salinity changes, acute drop in dissolved oxygen, or intraperitoneal injection of triamcinolone (positive control). Tiered bioassays of increasing specificity for immune function were performed on tissue samples: Tier I, histopathology; Tier II, hematology, plasma biochemistry, and plasma cortisol; Tier III, phagocytosis of peripheral blood leukocytes (PBL), and mRNA expression of transforming growth factor-β (TGF-β) & interleukin-1β (IL-1β) splenic mononuclear cells using real time PCR. While histopathology was a useful tool for assessing overall health of the test fish, no remarkable lesions were found in that could be attributed to any of the three stressors. Triamcinolone administration (i.p., 10mg/kg) for 3 days induced lymphopenia, neutrophilia with overall leukopenia, and monocytosis. Hematocrit and circulatory red blood cell count did not change with triamcinolone administration nor with acute decrease in salinity. Increase in salinity (5-20 ppt) had no effects on any of the aforementioned parameters. Hypoxia induced lymphopenia and neutrophilia without change in monocytes and additionally inhibited values of PO2, SO2, total protein, and lipase in exposed fish. Decrease in salinity (20-5 ppt) did not affect plasma cortisol levels, nor did triamcinolone administration or hypoxia treatment. Plasma protein level was not changed in response to decrease in salinity or triamcinolone administration. Triamcinolone administration suppressed phagocytosis of peripheral blood leukocytes (PBL) without a significant change in phagocytic index (P.I). Decrease in salinity elevated phagocytosis without change in P.I. in exposed tilapia. Increase in TGF-β transcription and decrease in IL-1β transcription with in vitro LPS stimulation were identified after triamcinolone administration. Acute decrease in salinity upregulated TGF-β transcription, whereas IL-1β transcription without in vitro LPS stimulation was not detectable in exposed fish. During hypoxia it was observed that changes in phagocytosis and TGF-β transcription were correlated negatively and that changes in IL-1β transcription and phagocytosis correlated positively. Taken together, these controlled laboratory experiments suggest that rapid changes in the aquatic environment can lead to increased disease susceptibility via compromise of the fish immune system. In these studies, this immunocompromise was especially evident in the modulation of the inflammatory mediators TGF-β and IL-1β, as well as in shifts in blood leukocyte distribution. It is likely that such perturbations of teleost immune system parameters have much wider implications, including in North Carolina estuaries.
