Preventive and therapeutic effects of oxolinic acid (OA) against the vibrio disease of cultured rainbow trout were examined. The experiment was carried out in two culture ponds (A and B) in Shizuoka prefecture from September to December in 1973. The fish in pond A (1370 fish, 50kg total body weigh) were administered OA (2.5mg/kg) in the diet once a day for 3 months. The fish in pond B (1370 fish, 50kg total body weight) were fed the normal diet for the first 9 days, and then the fish were administered OA (20mg/kg) on 10th day, 10 mg/kg on 11th and 12th days in the diet. The number of dead fish was 14 in pond A after 3 months, and the number of dead fish in pond B steadily increased until several days after the start of medication, whereafter the death rate leveled off. Causative organisms were isolated from the liver and digestive tract of the infected fish in pond B. One of organisms was identified as a genus Vibrio, and the sensitivities of this organism to teracycline, chloramphenicol and OA were 0.19, 0.19 and 0.01mcg/ml, respectively, in terms of MIC. No behavioral and histological abnormalities were found in the alive fish either from pond A or B after 3 months.
Studies were made on levels of CP in tissues of yellowtails (Seriola quinqueraaiata) which received the drug once orally in three different ways of dosing as shown in Table 1. The experimental animals received no food after drug treatment. Levels of CP in blood, liver and kidney were almost the same in groups A and C for the initial 2-6 hours after treatment despite the difference in expected dose between the two, and tissue levels of the drug in group B were lower than those in group A, though the expected doses in both the group were same. These results suggested that the rate of loss of feed was higher in feeds containing raw fish meat at a higher ratio.
A new species of acanthocephalan, Pseudorhadinorhynchus samegaiensis (Echinorhynchidea, Illosentidae), was found from the intestine of 2 years old rainbow trout cultured at Samegai Trout Experimental Station, Shiga Prefecture, in May, 1974. Sixty-seven males and 101 females were collected from 29 of 35 fishes examined. Acanthocephalans were fixed in 70% ethanol under pressure, stained with Heidenhain's hematoxylin and mounted in balsam. Type specimens are deposited in the collection of the National Science Museum, Tokyo.
A histopathological study was made on a marine gliding-bacterial infection of yellowtail broke out at Tsuruga area in winter, 1973.Gross characteristics of diseased fish were erosion and shallow ulcer formation in the body surface and fins. In the site of erosion small numbers of flexible rods were found through the epithelial basement membrane and the dermal loose connective tissue in the earlier stages. In advanced stages large numbers of flexible rods were observed to invade into the extensive loose connective tissue and the superficial layer of the dense connective tissue, in which considerable necrosis occurred. In far advanced stages the dermis and scales were destroyed and a wide dermal ulcer was developed. From the histopathological obsevasions, the dermal lesions were thought to be produced by a percutaneous infection of a marine flexible bacterium. Invasiveness to the dermal collagenous tissues was an important characteristic of this bacterium.
Recently, cultured yellow tails with black spots, less than some mm in diameter oll thefins and the dody surface have been noticed in culture farms in Shizuoka, Ehime and Kochiprefectures. The condition is named“Black Spot Disease”. Histylogical examinations of affected fishesshowed that the condition is lymphocystis, and the black spots are caused by the developmentof melanophore cells around lymphocystis cells.