Pathological Studies On Acute Peristome Edema Disease In Sea Cucumbers [Apostichopus Japonicus (Selenka)] And Muscle Atrophy Disease Of Abalones (Haliotis Discus Hannai)

Acute peristome edema disease in juvenile and adult sea cucumbers [Apostichopus japonicus (Selenka)] reared in North China. Acute peristome edema disease (APED) is a new disease that broke out in cultured sea cucumber along the Shangdong and Liaoning province coasts in China, PR, and has caused a great deal of death in Apostichopus japonicus(Selenka)since 2004. Here we report virus-like particles found in intestine epithelium of sea cucumbers reared in North China. It is the first time that sea cucumbers are reported to be infected by virus. Histological examinations showed that the viral inclusion bodies existed in intestine epithelium cells. Electron microscopic examinations show that the virions were spherical, 80—100 nm in diameter, and composed of a helical nucleocapsid within an envelope with surface projections. Detailed studies on the morphogenesis of these viruses found many characteristics previously described for coronaviruses. Virus particles always congregated, and formed a virus vesicle with an encircling membrane. The most obvious cellular pathologic feature is large granular areas of cytoplasm, relatively devoid of organelles. Tubular structures within virus-containing vesicles, nucleocapsid inclusions, and double-membrane vesicles are also found in the cytopathic cells. No rickettsia, chlamydia, bacteria, or other parasitic organisms were found.Pathology of atrophic muscle in abalones (Haliotis discus hannai) reared in North China. Severe muscle atrophy disease in cultured abalone juveniles and adults were reported in 2004 and 2005 in North China. Electromyography test shows that the atrophy of abalones is myogenetic but not neurogenetic. Comparing to the control group, the number of intact myofibrils and the diameter of myofibrils of the diseased ones significantly decreased statistically. The levels of Creatine Kinase (CK), Creatine kinase—MM(CK--MM) and Lactate Dehydrogenase (LDH) in serum of diseased abalones increased significantly comparing to the control, which suggests that damage of muscle cells occurred. Ultrathin-section electron microscopic examination was performed and paired helical filaments (PHFs) inclusion bodies were found in cytopathic cells of muscle, which is the pathologic feature reported for atrophic muscles of human patients with inclusion body myositis. It is the first time that PHFs inclusion bodies were reported found in invertebrate. Further research on myofibril damages demonstrated that two abnormal structures, Small Cylinder Structure (SCS) and Dense-Colored Particles (DCPs), proliferated in broken myofibrils, which were observed to be related directly to myofibril damage. The mechanism of the infection was discussed.Pathophysiology of muscle atrophy in abalones (Haliotis discus hanni) reared in China. Severe amyotrophy syndrome of cultured abalone was a chronic disease and the disease breaks out in North China in May every year. Ultrathin-section electron microscopic examination was performed and myofibers were observed to be damaged severely, within which most of myofibrils were broken. Large numbers of petaloid glycogen particles, some of which were encircled in membranes, were observed accumulated among broken myofibrils. It suggests that the glucose metabolism were inhibited in the disease, which is proved by the low level glucose detected in blood. Lower levels of cholesterol and triglyceride, together with high level of high-density lipoprotein in blood suggest the promotion of lipolysis. Low levels of total carbon dioxide in blood suggest acid-base disturbance, which belongs to metabolic acidosis by its etiologic analyses. Electrolytes imbalances were characterized by low levels of sodium and potassium accompanied with high levels of phosphate and magnesium in blood. Hypoproteinemia also appeared in diseased abalones, which suggest the diseased abalones were in severe dystrophia. The content uric acid and the levels of choline esterase andγ-transpeptidase in blood all decreased sharply compared to the control. It can be concluded from the results that the inhibition of glucose metabolism brings series of imbalances and disturbances to the physiological functions of the abalones, and even caused them to death.