• Journal of fish pathology
• /
• v.34 no.1
• /
• pp.63-70
• /
• 2021

As a part of research to elucidate the pathogenesis of so called Soft Tunic Syndrome(STS), that caused mass mortalities in the cultured sea squirts, Halocynthia roretzi, the epidemiological and pathological analysis were done to both clinically normal and diseased groups of the farms of Tongyoung and Geoje coastal areas in southeast sea from February to July, 2008. In the histological finding of the tunic, most of individuals showed tunic softness syndromes that included the disarrangement and destruction of tunic fiber with the simultaneous presence of flagellates-like cells, recently suspected as main agents of tunic softness syndromes. Simultaneously, the intensive degenerative changes of the skeletal muscle of diseased sea squirts were recognized. The changes were characterized with the hyalinization and condensation of muscle fibril and hemocytic infiltration in the muscle fibers. Those were thought to be a kind of typical Zenker's necrosis as in the skeletal muscle of higher vertebrates. Besides of the diseased sea squirts, Zenker's necrosis of skeletal muscles were seen in the normal ones. Epidemiological inquiry for diseased groups revealed that the higher incidences of tunic softness syndrome were recorded in the fast growing groups and in the sites presuming the organic pollution. And Higher malondialadehyde(MDA) and glutathione peroxidase(GPx) activity were detected in the groups showing STS. Those results suggested that Zenker's necrosis of body muscles was a kind of"nutritional myopathy" by oxidative stress. Conclusively, it was considered that Zenker's necrosis of body muscles gives an important clue for elucidating pathogenesis of STS of cultured squirts. And it seems that the necrosis were caused by the oxidative stress to body muscle during abnormal rapid growth of sea squirts.

• Journal of fish pathology
• /
• v.35 no.2
• /
• pp.167-176
• /
• 2022

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 ap- peared 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-trau- mas in myofibrils caused muscle fiber necrosis. And semi-granulocytes engulfed IMNVs to eliminate virus.