| Summary: | 碩士 === 國立臺灣海洋大學 === 水產養殖學系 === 94 === Photobacterium. damselae subsp. piscicida has been proven to be a pathogenic for various fish, and has also been identified as one of the commonly found pathogen for cultured cobia. This thesis mainly investigated the influence of Ph. damselae subsp. piscicida on cobia tissue and also investigated whether it could induce onset of Apoptosis or not. The strain 9205 (Ph. damselae subsp. piscicida) isolated from moribund cobia in Pingtung were used in this experiment
The most common symptoms of fish infected by Ph. damselae subsp. piscicida naturally in the field were bleeding on the skin and deep color, but those challenged by bacteria in the lab are only deep color and no bleeding observed. From histopathological studies on the fish tissues infected by Ph. damselae subsp. piscicida naturally or challenged in the lab, the tissues severly affected in order were posterior-kidney, spleen, liver, head-kidney, and heart. Posterior-kidney were infected by the bacterium the occurrence of granuloma lesion. The common pathological changes in cobia tissue included necrosis and cloudy swelling of renal epithelial cells in poserior-kidney, necrosis of a part of hematopoeitic cells, fatty changes of parenchyma in liver, cytoplasm vacuoles and cloudy in liver, cell boundary blur among hepatocytes, and the accumulation of abnormal acidophilus matters in cytoplasm or fat globule in hepatocytes. There were pathological changes of necrosis and inflammation together with liquefactive necrosis in the spleen. In addition, necrosis and inflammation were also bound in head-kidney.
This experiment also investigated the influence of extracellular products (ECP) of Ph. damselae subsp. piscicida（strain 9205）and two types of purified phospholipase on cobia tissues. Pathological changes, such as bleeding, necrosis, and fatty changes, were observed in livers from cobia challenged by ECP. There were pathological changes observed like the accumulation of acidophilus matters in fat globule, increment of granular cells in spleen, inflammation, cataplasia of red pulp, and necrosis of white pulp. Both the injection of phospholipase A2 (58 KDa) (added LPS) and phospholipase C (27 KDa) (added LPS) into cobia intraperitoneally all caused necrosis of liver tissue, and there were fatty changes in parenchyma of hepatocytes. Away from necrosis sites, a cytoplasmic cloudines of hepatocytes were also observed. Except cloudiness, a lot of vesicles or vacuolesobserved in the cytoplasm. Furthermore, phospholipase C (27 KDa) would result in heavily bleeding in hepatocytes.
There were abnormal changes in nucleus in the histopathological observation a symptom of apoptosis. The ECP of Ph. damselae subsp. piscicida （strain 9205）could induce apoptosis of cobia as measured by TUNEL stain.
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