Infectious pancreatic necrosis (IPN) was first reported in freshwater trout in 1940’s in Canada and in 1950’s in the USA, and subsequently spread around the world. The causative agent, infectious pancreatic necrosis virus (IPNV), which was the first fish-virus isolated in a cell culture, is a double-stranded RNA virus in the family Birnaviridae. In 1960’s, Japanese rainbow trout aquaculture suffered a lot of fish losses at the fry stage, and the cause was confirmed to be IPNV by the virological study. In 1980’s, IPN in Japan has gradually calmed down due to being worked synergistically with hatchery biosecurity practice, increase of host resistance and decrease of virus virulence. However, it is still one of the obstacles in the Atlantic salmon industry in the world.
Beko disease is derived from the concave body surface of fish infected with microsporidians in the myocytes. In this paper, several fish microsporidians including Microsporidium seriolae from Seriola spp. (S. quinqueradiata, S. dumerili and S. lalandi), Microsporidium spp. from three other cultured fish, and Heterosporis anguillarum from Japanese eel Anguilla japonica are reviewed. A shift of eel-farming method from open field ponds to house-type heating culture systems has emerged the beko disease in cultured Japanese eel. Considering the successful transmission of H. anguillarum to uninfected juveniles, frequent screening in eel size seems to reduce the incidence of the disease in eel farms. Previously, beko disease of yellowtail S. quinqueradiata was not been considered as a serious problem, because yellowtail juveniles infected with M. seriolae usually recover from the disease until the time of adult stage. However, serious condition of the disease in cultured yellowtail has recently received attention as a re-emerging disease. Unknown life-cycle of M. seriolae makes the control measures difficult. As diagnostic methods, microscopic examination with Uvitex 2B staining and molecular tools with PCR have been developed. Furthermore, other related microsporidians have been reported in cultured red sea bream Pagrus major, hatchery-bred spotted halibut Verasper variegatus and juvenile Pacific bluefin tuna Thunnus orientalis.
Capsalid monogeneans infect the skin of marine fish; among them, Benedenia seriolae and Neobenedenia girellae are most important pathogens of cultured fish. The former infects the skin of amberjacks, Seriola spp., while the latter, being not host specific, has been found from the skin of 15 fishes in Japan. Feeding epithelial cells and mucous of the host results in skin abrasion, causing growth retardation and secondary bacterial infection, even leading to the death of the host fish. Eggs entangle on the culture net, which is prone to heavy infection of fish cultured in net cages. Prevention of infection is practically impossible as its life cycle has been established in fish farms. Chemotherapy with hydrogen peroxide or praziquantel is effective but repeated treatment is required, as immunity is not acquired by infected fish. Development of new control measures such as biological control and selective breeding of a resistant strain against these monogeneans are in progress.
Blood fluke infection among diseased Japanese amberjack Seriola quinqueradiata (n = 9,470) cultured in Oita Prefecture was monitored from 1992 to 2001. Infection was confirmed by the presence of parasite eggs accumulated in the gills. Amberjack with parasite eggs were found in all culture areas except for Usuki Bay. Eggs in the gills of 0-year-old fish started to be observed from early July, with the minimum body weight (BW) of 130 g in Yonouzu Bay, whereas in Nyuzu Bay egg-positive fish was first found in late August with the minimum BW of 296 g. Amberjack were cultured in the inner part of Nyuzu Bay up to the size of 200-250 g in BW, suggesting that infection occurred when fish were later moved to the mouth of the bay for further growth. In the inner part of Nyuzu Bay, hypoxia and conspicuously high dissolved inorganic nitrogen in the water near the bottom and acid volatile sulfides in the sediment were recorded every summer in the present survey. It is speculated that such extraordinary environment is unfavorable for the propagation of the intermediate host of the causative organism in the inner part, but not at the mouth, of the bay.
Enteric redmouth disease caused by Yersinia ruckeri, is one of the most important aquaculture diseases worldwide. In this study, the effects of 11 disinfectants on Y. ruckeri ATCC29473 (2.8 × 108 CFU/mL) and Y. ruckeri FPC1215 (2.9 × 108 CFU/mL), were examined at 20°C. Nine disinfectants exhibited minimum bactericidal concentrations against both strains after 30 s exposure: 40% ethanol, 30% isopropanol, 4 mg/L povidone iodine, 1.25 mg/L sodium hypochlorite, 1:15,000 Rontect®, 1:3,840 Acecide®, 1:100 Hibiten®, 1:1,000 Osuban® and 1:1,000 Hyamine®. However, no disinfection effects were observed for Saponated cresol solution® or Pyceze®.
We investigated possible infection with Perkinsus olseni and/or P. honshuensis in Manila clams in Korean waters using Perkinsus species-specific PCR. Ray’s fluid thioglycollate medium assay revealed that 97.3% of the clams examined were infected with Perkinsus sp., with the mean intensity ranging from 2.2 × 104 to 6.8 × 106 cells/g gill. In the Perkinsus species-specific PCR assay, all the amplified Perkinsus-positive bands were identified as P. olseni, while none of P. honshuensis-specific band was amplified. Our survey results indicate that P. olseni is the main causative agent of perkinsosis in Manila clam populations in Korean waters, while more extensive survey must be carried out.
A disease outbreak occurred in hatchery-reared devil stinger Inimicus japonicus (approximately 2 g). Abnormally enlarged cells specific for red sea bream iridoviral disease (RSIVD) were observed in the moribund fish. Red sea bream iridovirus (RSIV) genome (106.1-8.9 copies/mg tissue) were detected from the dead fish. The nucleotide sequence of the MCP gene of the isolated virus was identical to those of the RSIV isolates previously reported in Japan. In an infection trial, all of devil stinger intraperitoneally inoculated with the virus (102.3 TCID50/fish) died and the viral genome was detected from the dead fish at 106.9-9.2 copies/mg tissue. This is the first report of RSIVD in devil stinger.
Rock bream Oplegnathus fasciatus were immersed in cultured RSIV suspension at 17°C for 30 min, and reared for 80 days without controlling temperature. Fish rearing temperature naturally increased at approximately 0.1°C/day from 17°C. Mortalities of fish without and with RSIV at 105.8, 103.8 and 101.8 TCID50/mL were 5.8%, 30.8%, 22.5% and 6.7%, respectively. Surviving fish were reared at 26°C, and intramuscularly injected with RSIV at 101.8 or 100.8 TCID50/fish. Survivors from RSIV-immersion at ≥ 103.8 TCID50/mL were strongly protected against RSIV challenge whereas those at ≤ 101.8 TCID50/mL died, suggesting that fish immunization with live RSIV at low temperature could be conducted by immersion route.