GENG Yi, WANG Kai-Yu, XIAO Dan, CHEN De-Fang, HUANG Jin-Lu. PATHOLOGICAL STUDIES ON CHANNEL CATFISH INDUCED BY EXTRACELLULAR PRODUCTS OF STENOTROPHOMONAS MALTOPHILIA[J]. ACTA HYDROBIOLOGICA SINICA, 2010, 34(2): 345-352.
Citation: GENG Yi, WANG Kai-Yu, XIAO Dan, CHEN De-Fang, HUANG Jin-Lu. PATHOLOGICAL STUDIES ON CHANNEL CATFISH INDUCED BY EXTRACELLULAR PRODUCTS OF STENOTROPHOMONAS MALTOPHILIA[J]. ACTA HYDROBIOLOGICA SINICA, 2010, 34(2): 345-352.

PATHOLOGICAL STUDIES ON CHANNEL CATFISH INDUCED BY EXTRACELLULAR PRODUCTS OF STENOTROPHOMONAS MALTOPHILIA

  • Stenotrophomonas maltophiliam is an aerobic, nonfermentative, gram-negative bacterium ubiquitous in nature. It is a causative agent of the channel catfish (Ictalurus punctatus). S. maltophilia infection is capable of causing high morbidities and mortalities in channel catfish, it is considered to be the most significant factor affecting commercial catfish aquaculture. A stain of S. maltophilia, isolated from the diseased channel catfish in a fish farm in Sichuan Province, was identified by morphology, physiological and biochemical characteristics analysis, and 16srRNA gene sequence detection. In order to understand S. maltophilia pathogenetic mechanism, the pathology of channel catfish induced by extracellular products (ECPs) of S. maltophilia was studied. The ECPs of S. maltophilia was extracted with ammonium sulfate precipitation, and challenged with channel catfish by the intraperitoneal (i. p.) route. The test was conducted for 7d, with doses of 1.42mg/kg, 1.85 mg/kg, 2.40 mg/kg, 3.13 mg/kg, 4.07 mg/kg and 5.29 mg/kg body weight, respectively. The mortality was respectively 0.00%, 10.00%, 20.00%, 40.00%, 70.00% and 100.00%. The results showed that the ECPs of S. maltophilia had quite strong virulence to channel catfish, and the LD50 to channel catfish was about 3.21mg protein/kg body weight. Challenged fish showed neurosis, congestion and hemorrhage in the abdomen and lower jaw, distension of abdomen, yellowish or flooded fluid in the peritoneal cavity, congestion and hemorrhage in mucosa of gastrointestinal tract, intussusception in rectum, swelling in liver, kidney and spleen. Histopathological examination showed edema, hemorrhage, degeneration, necrosis and the inflammatory response in many organs; especially, serious lesions in brain, kidney, liver, gastrointestinal tract, spleen and skeletal muscle. The kidney showed edema, degeneration and necrosis in renal tubular epithelia, and with macrophages and neutrophi infiltration in the interstitial substance. Edema, vacuolar degeneration and necrosis were seen in liver cells. Epithelia of the gastrointestinal tract underwent degeneration and necrosis, while the lamina propria and tunica submucosa showed edema and infiltration with lymphocytes, macrophages and neutrophi. Congestion, hemorrhage and reduction of the lymphocytes were observed in spleen. Degeneration, necrosis and inflammatory cells infiltration appeared in skeletal muscles. Edema and neuronal shrinkage appeared in brain. Concentrated nucleolus, swelling mitochondria and dilatated endoplasmic reticulum were ultrastructurally observed in visceral organ (liver, spleen and kidney) cells. The lymphocytes of spleen and kidney underwent chromatin condensation and margination, forming the apoptotic bodies. These results indicated that the ECPs was an important pathogenic factor of S. maltophilia, which could induce apoptosis in the lymphocytes, miltiple organ damnification and death.
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