Cutured carangid, Seriola purpurascens, infected with sanguinicolid trematodes, Paradeontacylix spp. were examined histopathologically. Fish were sampled bimonthly in Shikoku from March 1984, when mortalities of heavily infected fish occurred, until January 1985. Pathological changes related to the blood fluke infection were limited in the heart and gills. They were summerized as hyperplasia of gills, encapsulation of eggs in the gills and ventricle, and papillate proliferation of the endothelium in the afferent branchial arteries. No necrosis was found in any organs at any stages of infection. The infection had seasonality, and the host reaction changed with it. Survived fish (1+) got milder infection next year than 0+ fish. It is probable from the histological changes in the heart and gills that the cause of mass mortalities among 0+ fish from December 1983 to March 1984 was physical blockage of the blood flow due to accumulation of the eggs in the gill filaments and to papillae formation in the afferent branchial arteries.
Minimal inhibitory concentration (MIC) of amoxicillin (AMPC) against Pateurella piscicida, Edwardsiella tarda, Aeromonas salmonicida, A.hydrophila, Vibrio anguillarum, and Streptococcus sp. were investigated. AMPC showed the highest antibacterial activity to P.piscicida. MICs of AMPC against 30 strains of P.piscicida isolated from cultured yellowtail (Seriola quinqueradiata) in 1985 were almost as high as that of ampicillin (ABPC), ranging from 0.025 to 0.1μg/ml. Furthermore, bactericidal activity of AMPC to P.piscicida was higher than that of ABPC. Sensitivity of P.piscicida, Streptococcus sp. or E.tarda to AMPC was kept almost the same level during the culture of 20 times transfer. These results suggest that AMPC can be applied for therapy of bacterial pseudotuberculosis of cultured yellowtail.
The cytopathology and virogenesis of monodon-type baculovirus (MBV) in the hepatopancreatic cells of the cultured shrimps, giant tiger prawn (Penaeus monodon) and red tail prawn (P.penicillatus), were investigated. In the hepatopancreatocytes of infected giant tiger prawns, F, B, R and M cells were found to be susceptible to MBV. Detailed virogenesis of MBV including formation of nucleic acid, capsid substance, envelopment and formation of occlusion bodies in hepatopancreatocytes of the giant tiger prawn was also noted. The main cytopathogenic changes accompanying MBV infection observed on membranes of the hepatopancreatocytes, and nuclear hypertrophy were due to virogenesis and polyhedrin formation.Virus particles and occlusion bodies released from lysed cells entered the intestinal tract via the hepatopancreatic lumen. In addition to the giant tiger prawn, the red tail prawn, P.penicillatus, were also found to be infected by MBV. This is a new reported host for MBV. Average size of the viron and diameter of the nucleocapsid observed in red tail prawn was signilcantly smaller than those present in giant tiger prawn. However, no significant differences were obtained when the length of nucleocapsids and size of the polyhedrin subunits were compared.
Various staining methods (the Gram and periodic acid stains;the indirect fluorescence antibody technique and the indirect peroxidase procedure) were compared for their ability to detect the kidney disease bacterium (Renibacterium salmoninarum) in the tissues of rainbow trout (Salmo gairdneri) fixed by various methods (fresh frozen tissue, frozen formalin-fixed tissue, formalin-or Bouin's-fixed paraffin-embedded tissue). The results demonstrated that only the indirect peroxidase technique gave positive results regardless of the fixation method used to prepare the tissue. The other methods were either less sensitive or yielded negative results after some tissue fixation methods.
Effects of the time-lag between the exposures of fish (loach) to Flexibacter columnaris and a competitive bacterium, Citrobacter freundii on the invasion by F.columnaris were investigated.It was found that the competitor could prevent invasion of the fish by F.columnaris if it was added within 1/2h after exposure to F.columnaris. In this case, F.columnaris failed to increase in number on the body surface of fish and water environment. The invasion of fish by F.columnaris did not occur when C.freundii was added prior to F.columnaris. On the other hand, F.columnbris was able to establish itself on the body of fish and successfully invaded fish when the competitor was added 1h or later after exposure of the fish to F.columnaris. In that case, the number of F.columnaris on the body surface as well as in the water environment gradually increased. The number of C.freundii on the body surface increased initially but decreased after 48h of exposure. In the water environment, C.freundii did not significantly vary in number.
Our previous investigation revealed that a new disease prevailing in Japanese flounder larvae (Paralichthys olivaceus) in Hiroshima Prefecture, Japan was a herpesvirus infection.Present paper describes the effects of water temperature and fish age on experimental infection of flounder larvae with the causative virus, and the susceptibility of other 5 species of marine fishes to the virus. When exposed to the 0.45μm-filtrate of the diseased fish homogenate and kept at 20°C or 25°C, flounder larvae showed high mortalities (90-94%) within 9 days, while mortality was considerably delayed at 15°C. Larvae younger than 20 day-old (smaller than 9.5mm in total length) were highly susceptible but an abrupt decrease of susceptibility was found in fish of 23 day-old or older (bigger than 11.0mm). Any larvae and juveniles of other 5 marine fishes employed were not susceptible to the virus.
Inactivation of BMN virus by ultraviolet (U.V.) irradiation, sunlight exposure, heating and drying treatment was investigated by means of the infection method of the author using larval and post-larval kuruma shrimp, Penaeus japonicus. Test shrimp sampled on day 4 after waterborne inoculation were examined for nuclear hypertrophy of the mid-gut gland epithelial cells in fresh squash preparations under the dark field microscope. The results obtained are summarized as follows; U.V. irradiation (15 W U.V. lamp, 30cm in distance) : BMN virus was inactivated within 20 minutes post-irradiation. The U.V. dosage during this period was measured to 4.1×105μW·sec/cm2. Summer sunlight exposure : The virus was inactivated within 3 hours post-exposure at about 30°C. Heating : The virus was inactivated within 120 minutes at 45°C, 30 minutes at 50 and 55°C, 5 minutes at 60°C. Drying : The virus absorbed in a filter paper was inactivated within 1.5 hours postdrying at about 30°C.