Mycobacteriosis causes serious economic damages to yellowtail aquaculture in Japan. ​From October to November 2020, mycobacteriosis occurred in yellowtail cultured in Owase Bay, Mie Prefecture, Japan. ​In this study, we observed the gross pathology and histopathology of the diseased fish. ​We identified mycobacteria isolated from the diseased fish and investigated their drug sensitivities against 12 antimicrobial agents. ​Diseased yellowtail exhibited abdominal swelling and many nodules in their kidney and spleen. ​The head kidney and trunk kidney presented typical granulomas with a necrotic core surrounded by epithelioid cells and fibroblasts. ​The isolates were identified as Mycobacterium pseudoshottsii based on phylogenetic analysis using the 16S rRNA gene, hsp65 and rpoB. ​Low concentrations of amikacin, ciprofloxacin, kanamycin and lincomycin inhibited growth of the isolates. ​Two of three isolates showed sensitivity to erythromycin; the other isolate was resistant to it. ​Erythromycin and lincomycin that are permitted for therapeutic use in Perciformes in Japan may be useful for treating yellowtail infected with M. pseudoshottsii. ​However, emergence of antibiotic-resistant strains of M. pseudoshottsii due to antibiotic use requires attention in yellowtail aquaculture.

Visceral adhesions are found in sockeye salmon Oncorhynchus nerka in the North Pacific Ocean and adjacent regions. ​The disease is induced as the result of a host reaction associated with the migration of the freshwater philonematid nematode Philonema oncorhynchi from the host tissues to the body cavity. ​In this paper, 928 individuals of sockeye salmon caught in the central North Pacific Ocean and central Bering Sea were examined for their biological features and the presence or absence of visceral adhesions to study the impact of the disease on the growth of the fish. ​Scale patterns were also analyzed to evaluate if the disease affected the spring-summer growth of the fish in the ocean. ​No statistically significant difference was found in frequency distributions of fork length, spring-summer ocean growth, and condition factor between the fish with and without visceral adhesions. ​This indicates that the disease has no substantial negative impact on the growth of ocean-migrating sockeye salmon. ​This paper also discusses the previously hypothesized disappearance of the disease with fish maturation and suggests that it remains in some of mature salmon.

Development of Zeuxapta seriolae (Monogenea: Polyopisthocotylea, Heteraxinidae) collected from Seriola dumerili was described and compared with that of Heteraxine heterocerca, the same heteraxinid species from Seriola quinqueradiata. ​Based on the morphology of the two monogeneans from very young with a symmetrical body to adult, specimens retrieved from the gills of cultured and wild Seriola spp. (S. quinqueradiata, S. dumerili and S. aureovittata) collected in Japan and its adjacent areas during 1975–2019 were identified. ​Heteraxine heterocerca, previously known only from S. quinqueradiata and S. dumerili, was also recorded from S. aureovittata, and Z. seriolae hitherto known only from S. dumerili and S. aureovittata, was recorded from S. quinqueradiata. ​As a result, both H. heterocerca and Z. seriolae were confirmed from all the three Seriola spp. ​Cultured S. quinqueradiata and S. aureovittata were often infected with both H. heterocerca and Z. seriolae, whereas wild Seriola spp. were infected with a single species of gill monogenean. ​Culture seeds of foreign origin should be monitored continuously, as information on the polyopisthocotylean monogenean infections of Seriola species known outside Japan is quite limited.

The virucidal effect of disinfectants on Piscine orthoreovirus 2 (PRV-2), a causative agent of erythrocytic inclusion body syndrome (EIBS), was assessed through challenge experiments with EIBS-naïve juvenile coho salmon Oncorhynchus kisutch. ​A 10-fold dilution of PRV-2 virus suspension (1.05 × 10¹⁰ copies/mL of PRV-2 L2 RNA) was completely inactivated by 50 ppm povidone-iodine (15 min), 200 ppm sodium hypochlorite (30 s), or 40% ethanol (30 s). ​A 100-fold dilution of PRV-2 (1.05 × 10⁹ copies/mL) was inactivated by 12.5 ppm povidone-iodine (15 min), or by 25 ppm sodium hypochlorite (30 s); 1,600 ppm benzalkonium chloride (30 s) did not inactivate PRV-2.