Red lip mullet Chelon haematocheilus (body weight = $468{\pm}91g$) which became sick during an outbreak of disease at mariculture facilities at Cheonsu Bay, Korea, during July-August 2013, were examined to identify the cause of the disease. Diseased mullets displayed green liver syndrome,...
Red lip mullet Chelon haematocheilus (body weight = $468{\pm}91g$) which became sick during an outbreak of disease at mariculture facilities at Cheonsu Bay, Korea, during July-August 2013, were examined to identify the cause of the disease. Diseased mullets displayed green liver syndrome, and Lactococcus garvieae were isolated from their internal organs. Argulus sp., Trichodina sp., and/or Vibrio spp. were also discovered in some infected fish. Histopathological examination revealed that fatty liver syndrome with hepatocyte degeneration, reflected in heterokaryons, inflammatory lesions, and melanomacrophage centers ($MMC_S$), had caused fibrosis around the kidney, spleen, and blood vessels. After the outbreak, visceral fat and green liver syndrome in the mullets were consistently observed throughout the year in the same mariculture facilities, indicating that the cultured mullets suffered a chronic metabolic disorder. Although Vibrio spp. were also isolated from some individuals, L. garvieae, which is known to be a causative agent of red lip mullet mortality, was isolated from all diseased individuals. This is the first report of L. garvieae infection in cultured red lip mullet.
Red lip mullet Chelon haematocheilus (body weight = $468{\pm}91g$) which became sick during an outbreak of disease at mariculture facilities at Cheonsu Bay, Korea, during July-August 2013, were examined to identify the cause of the disease. Diseased mullets displayed green liver syndrome, and Lactococcus garvieae were isolated from their internal organs. Argulus sp., Trichodina sp., and/or Vibrio spp. were also discovered in some infected fish. Histopathological examination revealed that fatty liver syndrome with hepatocyte degeneration, reflected in heterokaryons, inflammatory lesions, and melanomacrophage centers ($MMC_S$), had caused fibrosis around the kidney, spleen, and blood vessels. After the outbreak, visceral fat and green liver syndrome in the mullets were consistently observed throughout the year in the same mariculture facilities, indicating that the cultured mullets suffered a chronic metabolic disorder. Although Vibrio spp. were also isolated from some individuals, L. garvieae, which is known to be a causative agent of red lip mullet mortality, was isolated from all diseased individuals. This is the first report of L. garvieae infection in cultured red lip mullet.
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제안 방법
5 min, and a final extension at 72°C for 5 min. Direct sequencing of the amplified DNA fragment was performed using a 3730xl DNA automatic sequencer (Applied Biosystems; Foster City, CA, USA). All sequences were submitted for similarity searches with BLAST (Altschul et al.
DNA for PCR was isolated using a High Pure PCR Template Preparation Kit (Roche, Basel, Switzerland), RNA was isolated using TRIZOL® Reagent (Invitrogen, Carlsbad, CA, USA) according to the manual, and cDNA was produced using SuperScript™II Reverse Transcriptase (Invitrogen, USA). The isolated DNA was applied as a template for the analysis of RSIV PCR, and the synthesized cDNA was used for the analysis of VHSV, VNNV, HRV, and MBV PCR. PCR was conducted using ExTaq®(Takara, Shiga, Japan).
대상 데이터
5% of the total fish stock (average fish body weight 523 ± 10 g). Three moribund red lip mullet from each farm were used in this study.
성능/효과
The prevailing milky white colonies (ML-01, ML-02, and ML-03) were grown on BNA smeared with kidney and spleen samples from all fish (n = 9), and glossy colonies (MV-01, MV-02, and MV-03) were also isolated from some fish (n =3) (Table 1). The 16S rRNA gene sequences of the prevailing isolates (ML-01, ML-02, and ML-03) were 100% matched with Lactococcus garvieae ATCC49156 strains isolated from cultured Japanese yellowtail in 1974 (GenBank accession no. NR 102968.1) (Table 2). These three strains, with identical 16S RNA gene attributes, exhibited differences in acid production from mannitol and glucose according to test strains (Table 2).
참고문헌 (14)
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