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전염성근괴사증바이러스(IMNV)를 인위감염 시킨 흰다리새우(Litopenaeus vannamei)의 근육에서 나타난 미세 손상과 염증반응에 대한 조직병리학적 특성 연구

Histopathological features of pacific whiteleg shrimp, Litopenaeus vannamei, infected with Infectious Myonecrosis Virus (IMNV) with an emphasis on micro-traumas and inflammatory responses in muscle tissues

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초록

We injected infectious myonecrosis virus (IMNV) to pacific whiteleg shrimp, Litopenaeus vannamei, and observed closely with using light microscope and transmission electron microscope (TEM) for 4-8 days post infection (dpi). As clinical signs, abdominal bodies had mild opaque muscles at 5 dpi. And the mortality was shown at 6 dpi. At 8 dpi, most injected shrimps had severe opaque muscles and humped back that cause of movement disorder. As results of histopathological examinations, local parts of abdominal body muscle had muscle fiber hyalinization, muscle fiber atrophy, rounded muscle fibers, myofibrillar hypertrophy in size, a decrease in number of myofibrils and phagocytosis from the sarcolemmas by multiple hemocytes at 4 dpi. Especially, myofibrillar hypertrophy appeared at the whole or random part of single muscle fiber not in specific locations like the center or edge of muscle fiber. At 6-7 dpi, multiple muscle necrosis, muscle fiber segmentation, myofibril lysis appeared and a few hemocytes were infiltrated at lesions. At 8 dpi, extensive muscle necrosis, multiple myofibril lysis and muscle fiber atrophy were shown, and very few hemocytes were infiltrated. In early stage of infection, local viral myositis with zenker’s degeneration were shown. These lesions appeared multiply after the early stage. In late stage of infection, extensive coagulative muscle necrosis appeared with few of inflammatory response such as hemocytes infiltration. The lack of hemocytes infiltration response at the late stage might be disadvantage for Litopenaeus vannamei to defense against IMNV and to recover, because hematocytes (granulocyte, semi-granulocyte) eliminate pathogen and damaged tissues from infection sites and help recover. As results of the TEM observation, IMNVs that had nonenveloped icosahedral capsid which was 30-40 nm diameter were in myofibril and beside tubules of sarcoplasmic reticulum and moved to the certain direction. The micro-tears and micro-traumas in myofibrils caused muscle fiber necrosis. And semi-granulocytes engulfed IMNVs to eliminate virus.

Abstract

We injected infectious myonecrosis virus (IMNV) to pacific whiteleg shrimp, Litopenaeus vannamei, and observed closely with using light microscope and transmission electron microscope (TEM) for 4-8 days post infection (dpi). As clinical signs, abdominal bodies had mild opaque muscles at 5 dpi. And the mortality was shown at 6 dpi. At 8 dpi, most injected shrimps had severe opaque muscles and humped back that cause of movement disorder. As results of histopathological examinations, local parts of abdominal body muscle had muscle fiber hyalinization, muscle fiber atrophy, rounded muscle fibers, myofibrillar hypertrophy in size, a decrease in number of myofibrils and phagocytosis from the sarcolemmas by multiple hemocytes at 4 dpi. Especially, myofibrillar hypertrophy appeared at the whole or random part of single muscle fiber not in specific locations like the center or edge of muscle fiber. At 6-7 dpi, multiple muscle necrosis, muscle fiber segmentation, myofibril lysis appeared and a few hemocytes were infiltrated at lesions. At 8 dpi, extensive muscle necrosis, multiple myofibril lysis and muscle fiber atrophy were shown, and very few hemocytes were infiltrated. In early stage of infection, local viral myositis with zenker’s degeneration were shown. These lesions appeared multiply after the early stage. In late stage of infection, extensive coagulative muscle necrosis appeared with few of inflammatory response such as hemocytes infiltration. The lack of hemocytes infiltration response at the late stage might be disadvantage for Litopenaeus vannamei to defense against IMNV and to recover, because hematocytes (granulocyte, semi-granulocyte) eliminate pathogen and damaged tissues from infection sites and help recover. As results of the TEM observation, IMNVs that had nonenveloped icosahedral capsid which was 30-40 nm diameter were in myofibril and beside tubules of sarcoplasmic reticulum and moved to the certain direction. The micro-tears and micro-traumas in myofibrils caused muscle fiber necrosis. And semi-granulocytes engulfed IMNVs to eliminate virus.

참고문헌 (32)

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