In January 2007, an epizootic occurred among cultured turbot (Scophthalmus maximus) in a fish farm in Jiaonan, China. The diseased turbot exhibited hemorrhagic ulcer on the body, abundant yellowish ascetic fluid filled in the body cavity, swollen intestine, necrosis of liver and darkened cholecyst. Samples were taken aseptically from the hepatopancreas, spleen, gall bladder, kidney and brain, and inoculated immediately onto LBN (LB medium supplement with 2% NaCl) plates, which were incubated at 28 ℃ for 24 h. A predominant strain, which was designated as da3, was isolated from the gall bladder of the infected fish. Pathogenicity assays revealed that da3 was virulent to turbot by intraperitoneal injection challenge. The LD₅₀ of da3 to turbot was calculated as 2×10⁶ CFU/fish to the 25 g weight turbot. Strain da3 was a Gramnegative, curved bacterium with single polar flagellum, and could grow on TCBS medium and produce yellow colonies. Strain da3 was similar to Vibrio ichthyoenteri in morphological, most of the physiological, biochemical characteristics and 16S rDNA sequence except in lysinedecarboxylase (LDC) and the ability of using DGluconic acid. Strain da3 was identified to be V. ichthyoenteri. Portions of liver, spleen, kidney, intestine, brain and heart from the naturally diseased turbot were sampled, fixed in Davidson’s fixative for 12 h, and then were processed for paraffin embedding. Paraffin blocks of the tissues were cut at 4 μm thickness, and the sections were stained by the procedure of H.E. The slides were examined using an Olympus microscope, and images were captured with digital camera. There were distinctive histopathological changes in liver, kidney, spleen and intestine of the diseased turbot, and to a less extent in the brain. In the liver, necrosis of the hepatocytes were observed, and erythrocytopenia in the vein of the liver illustrated a septicemia. In the kidney, lesions of histocytes membrane, necrosis of some renal tubules, and decreased number of erythrocytes was observed. In the spleen, the number of erythrocytes decreased sharply, indicating the damage to the hematopoiesis. In the intestine, the intestinal villus goblet cells expanded to round, and the lumina popria necrosed severely. Examination of fixed tissues from healthy turbot showed structure integrity in liver, kidney, spleen and intestine. The histopathological changes in the diseased turbot may lead to the dysfunction of the organs. The results of this study may be important for controlling the bacterial disease of turbot.