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In this study, using the duck hepatitis virus standard the virulent R 85952 strains artificially infected 3-day-old ducklings through clinical observation, the incidence of routine blood and serum biochemical parameters were measured, dynamic pathology observed and DHV distribution determination designed to reveal the pathogenic mechanism of duck hepatitis virus. Provide a theoretical basis for further prevention DVH. Test the 300-day-old ducklings were randomly divided into 2 groups: control group, 60 240 test group, respectively isolation rearing. Test group each subcutaneous injection of 0.2 ml of virus solution, observe and record after challenging clinical manifestations and death situation. 6h after challenge, 12h, 16h, 20h, 24h, 28h, 32h and 36h were taken 18 test ducks and six controls duck, collecting duck's blood test and control groups do blood was measured in serum and serum was separated by centrifugation Determination of biochemical parameters. Whichever is the liver, spleen, brain, heart, lung, kidney, pancreas and small intestine, fixed in 10% neutral formalin, embedded in paraffin, sliced. Part slice pathological changes observed by HE staining, another part immunoenzyme staining method was measured DHV distribution. Sacrificing part of the liver tissue was cut into small pieces of 1mm3 4 ℃ 3% glutaraldehyde phosphate buffer fixed conventional dehydration, embedding, ultrathin sectioning, staining, set JEM-100SX transmission electron microscope observation. The clinical symptoms after artificial infection: the experimental group challenge 12h ducks feed, drinking and mental condition, with no significant difference between the control group, 18h test group 2 died, before his death showed the ground, head thrown back, The legs after kicking, typical opisthotonus symptoms, and about 20% of the ducklings performance lassitude. 12 ducklings have died to 24h 120 ducklings lassitude, 100% of the 24 to 36h test group Ap incidence, mortality was 80%, 36h after death gradually reduced duck survived five days after the test group of 17, and resistance through rehabilitation. Ducklings diet, mental condition of the control group were normal, no abnormal mortality in addition to culling outside. Routine blood measurement results show: the duck red blood cell count of infection DHV test group compared with the control group significantly reduced (P lt; 0.01); duck test group compared to the number of white blood cells infected with DHV 24h with the control group, no significant differences or declined slightly number of test group duck leukocytes after 24h compared with the control group significantly significantly reduce (P lt; 0.05); experimental group duck hemoglobin content extremely significant significantly lower than the control group (P lt; 0.01); experimental group duck's blood sedimentation rate of a very significant with high in the control group (P lt; 0.01). Serum biochemical parameters were measured results show that: the serum Na , K Ca 2 Mg 2 Cl - , the P 5 concentration of inorganic ions and urea nitrogen (BUN) content change is not obvious, and changes in plasma osmolality (OSM) is not evident; alanine aminotransferase (ALT) , aspartate aminotransferase (AST) and glutamyl transferase (GGT) compared with the control group, there was significantly higher (P lt; 0.01); concentration of glucose (GLU) after challenging 24 ~ 36h extremely significant decline (P lt; 0.01), triglyceride (TG), cholesterol (CHOL) and very low density lipoprotein (VLDL) was highly significantly higher (P lt; 0.01) changes that decrease blood sugar and elevated blood lipids; total bilirubin (TBIL ) and direct bilirubin (DBIL), respectively, from the challenge after 20h and 12h and compared with the control group significantly increased (P lt; 0.05). The above results suggest: ducklings infected with duck hepatitis virus liver damage does the most obvious, and the pathological process of acute necrotizing hepatitis. Histopathological changes: mainly liver degeneration and necrosis of the cells of various tissues and organs of the spleen, kidney, pancreas, brain, and small intestine, myocardial cells and lung lesions edema, inflammatory cell infiltration and hemorrhage based. Major ultrastructural changes of the liver tissue of liver mitochondria swelling, disintegration, glycogen reduce nucleus deformation or nuclear membrane rupture. The application immunoenzyme staining was artificially infected with type I DHV standard virulent R 85952 strains ducklings time of liver, spleen, brain, heart, lung, kidney, pancreas and small intestine tissue paraffin sections virus antigen detection, detection results to the The DHV order of: liver, kidney, spleen, small intestine, lung, pancreas, heart, brain. Thus, the authors believe that the duck viral hepatitis pathogenesis of liver damage after the virus enters the body, liver tissue bleeding, degeneration and necrosis, caused liver failure leading to death. Second, the damage to the other organs, especially damage to the brain tissue, accelerated the death of the infected ducklings.
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