Natural killer (NK) activity of head kidney leucocytes of rainbow trout (Oncorhynchus mykiss) against IPN virus-infected and uninfected RTG-2 cells was examined by 51Cr release assay. Fish leucocytes were classified into four groups by cytotoxic activities : Type I, cytotoxic activity against uninfected RTG-2 cells was higher than that against infected cells; Type II, cytotoxic activity against infected cells was higher than that against uninfected cells; Type III, cytotoxic activity was low against both infected and uninfected cells; Type IV, cytotoxic activity was high against both cells. These results indicate that there are individual variations in NK activity of rainbow trout against allogenic and viral antigens.
The monogenean Anoplodiscus tai sp. nov. collected from the fins of red sea bream Pagrus major cultured in Nagasaki Prefecture, Japan is described. The new species is most similar to A. richiardii Sonsino, from Pagrus orphus in the Mediterranean reported in 1890, from which it can be distinguished by a considerably smaller body size and a larger cirrus accessory piece. Gross signs of heavily infected fish included emaciation of body and partial loss of fins. Histologically, the parasite attached firmly to the basal membrane, and the epithelium was eroded at the site of attachment. Epithelial hyperplasia was evident around the parasite. Elevation of host tissue, associated with massive cell infiltration, beneath the haptor was a common feature. This was due to sucking and pinching function of the haptor. In some cases, a portion of dermal tissues which the parasite grasped was partly torn off, and remaining tissues were distorted and necrotic. Such pathological changes may eventually lead to partial loss of fins.
Postlarval tiger shrimp (Penaeus monodon) were immersed in aerated beta-glucan suspensions for 3 h. Enhanced growth was observed in shrimp immersed in glucan at concentrations of 0.5, 1, and 2 mg/ml, but not at 0.25 mg/ml. Shrimp gill tissue became shrunken immediately after immersion in the 2 mg/ml suspension. On days 10, 18, and 43 after beta-glucan treatment, shrimp were immersed in a bacterial suspension containing Vibrio vulnificus cells at a concentration of 5×107 CFU/ml for 12 h at a density of 25 individuals per liter; deaths were recorded for one month following experimental infection. The protective effect of glucan treatment was observed in those shrimp treated with 0.5 and 1 mg/ml glucan, but not in shrimp treated with 0.25 and 2 mg/ml glucan. The protective effect lasted until day 18 following immersion. In vitro, beta-glucan treatment enhanced the phenoloxidase activity in shrimp hemocytes. It therefore appears that beta-glucan is a short-term immunostimulant for shrimp.
The present paper describes epizootiological features of VNN in larval striped jack Pseudocaranx dentex in the seed production process. This disease, caused by a nodavirus named striped jack nervous necrosis virus (SJNNV), occurred repeatedly at the two Japan Sea-Farming Association stations, Goto (Nagasaki Prefecture) and Kamiura (Oita Pref.) from 1989 to 1992. The outbreaks of the disease were observed in the larvae from 2 to 20 days old. The noticeable signs of this disease were loss of appetite and skinny body. All of the affected larvae younger than 10 days old died within 2 to 4 days after they showed clinical signs. When the larvae older than 11 days old were affected, they showed enlargement of swim bladder, and vertebral deformity, but some of them survived. ELISA tests revealed that SJNNV increased rapidly in the younger larvae, but slowly in older larvae. VNN occurred at any water temperatures from 20°C to 26°C at which seed production of striped jack is generally conducted, and SJNNV increased most rapidly at 24°C. Striped jack were induced to spawn repeatedly in one spawning season. In each spawning season, VNN rarely occurred in the larvae obtained from the early period of spawning, but the incidence of VNN became higher in the larvae obtained from late period of the season.
The present investigation was conducted to determine optimal cultural conditions of the causative bacterium of jaundice in yellowtail. This microorganism grew in L-15 medium, Eagle MEM, 0.85% NaCl solution and 1/3 sea water, each supplemented with 10% of fetal bovine serum (FBS). FBS was essential for growth of the bacterium. The bacterium did not grow in any other media usually used for bacterial isolation or culture. The optimal growth conditions for culture of the agent causing jaundice determined from this study are at temperature of 23-26°C using L-15 medium at pH 7.0-7.5 supplemented with more than 10% of FBS and 1.6-2.0% of NaCl.
Eleven fish cell lines were compared for susceptibility to red sea bream iridovirus (RSIV). Cytopathic effect was produced in BF-2, CHSE-214, FHM, JSKG, KRE-3, RTG-2 and YTF cell lines among the cell lines examined. The titers of the virus on BF-2 and KRE-3 were higher than those on the other cell lines.The pretreatment of BF-2 and KRE-3 cells with polyethylene glycol (PEG) or addition of PEG to the sample increased the virus titers. RSIV replicated at 15°C, 20°C, 25°C and 30°C but not at 37°C. The suitable temperature for viral growth was 20°C or 25°C. The virus was sensitive to acid (pH 3), chloroform and ether and unstable to heat but stable to ultrasonic treatment and repeated freezing and thawing. Treatment with 5-iodo-2-deoxyuridine (IUdR) reduced the titers of the virus.
Histopathology of the disease, which was reported to be characterized by intense congestion in central venus sinuses of gill filaments found in cultured eel was studied with spontaneously diseased fish and exprimentally infected fish by light and electron microscopy. Experimental infection produced similar histopathological changes to those observed in the spontaneously diseased fish. In gill filaments of diseased fish, dilatation of the central venous sinuses was observed. In the liver, hemorrhage in the parenchyma and destruction of blood vessels were observed. Furthermore, hemorrhage in the haematopoietic tissue and degeneration of blood vessels and glomeruli were observed in the kidney. These pathological changes were always accompanied by degeneration of endothelial cell nuclei of blood vessels. The degeneration of the nuclei were characterized by swelling, intense staining of the nuclear rim with hematoxylin, and a homogenous appearance of the nucleoplasm. Electron microscopy revealed hexagonal viral particles in the nuclei of the degenerated endothelial cells. Each virion measured about 80 nm in diameter. The virions were observed only in the degenerated endothelial cells. These results suggest that the disease of cultured eel is a systemic viral infection, which is characterized by the necrosis of endothelial cells of blood vessels.