新型鸭病毒性肝炎病理学的动态研究
|
摘要
7日龄健康麻鸭166只随机分成两组：试验组100只，对照组66只。试验组经右腿部肌肉注射新型鸭肝炎病毒鸭肝匀浆0.2ml／只，复制新型鸭病毒性肝炎病理模型。对所建立的病理模型进行临床症状观察、病理组织学检查，同时在接种后12h、24h、48h、96h、168h、336h、504h和672h测定感染后血清生化指标，运用淋巴细胞-酸性非特异性酯酶组织化学染色法(ANAE)、白细胞分类计数等方法对所建立的病理模型进行动态研究。
人工感染后其临床症状为：接种后12-24h，精神沉郁、缩颈弓背，出现划水样姿势，随后开始出现死亡，死后呈典型的角弓反张姿势。雏鸭死亡高峰为接种后48-72h，死亡率为41％。死亡鸭剖检可见：肝显著肿大、出血；脾肿大，表面呈红白相间的斑驳状；肾脏肿大，淤血，尿酸盐沉积；法氏囊肿大。其他脏器无明显眼观变化。
剖杀鸭组织学检查结果显示：肝脏：接种后24h，肝细胞发生肿胀，水泡变性，48h后出现脂肪变性及局灶性出血，96h后呈现严重的气球样变，直至672h仍有轻度空泡样变和小胆管增生；脾脏：接种后48h，脾小体外围淋巴细胞数目明显减少，网状细胞增生；肾脏：接种后24h至96h，近曲小管上皮细胞核固缩，胞浆内出现大小不一的空泡；胰脏：接种后48-96h，表现为局灶性脂肪变性；法氏囊：接种后48h，淋巴小结髓质部淋巴细胞数目明显减少。
透射电镜对肝、脑、肾、胰四种组织超微结构观察表明：肝脏接种12h后肝糖原溶解，胞浆内细胞器溶解至消失，细胞核固缩；发生神经症状后剖杀雏鸭表现在肝细胞广泛严重的脂肪变性及坏死，胞浆内细胞器溶解至消失；脾脏内淋巴细胞肿胀，坏死(核固缩、核溶解)，胞核和胞浆内细胞器溶解甚至消失；大脑主要表现为神经细胞核固缩或核溶解；胰脏主要表现在胰腺细胞胞浆内线粒体肿胀，空泡样变，内质网极度扩张，胞浆内脂质样物质聚集。
血清生化指标测定结果表明：雏鸭感染新型DHV后，GOT和GPT活性升高，并在接种后96h达到最高值；TP和ALB含量降低，并于接种后96h降至最低值；UA含量在接种后168h下降；ChE、CRE在感染后无明显变化。
华中农业大学硕士学位论文
试验组血液中ANAE十淋巴细胞比例(%)从接种后48h开始持续阳氏，直到接种后
504h恢复正常。白细胞分类计数结果表明:异嗜性白细胞比例降低，淋巴细胞和单核细
胞比例升高。嗜酸性和嗜碱性白细胞比例在感染后无明显变化。
由此作者认为，新型鸭病毒性肝炎在组织病理学变化上和I型鸭病毒幽干炎存在不同
之处，新型DHV引起的肝脏、脾脏、法氏囊及脑等组织的病变较I型DHV明显。病毒
对脑组织的直接损伤可能是使雏鸭出现神经症状的原因之一。
166,7-days old healthy ducklings were divided randomly into 2 groups, 100 for the tested group and 66 for the control group. The pathological model of New Duck Viral Hepatitis (NDVH) was duplicated through inoculating New Duck Hepatitis Vims (NDHV) intramuscularly. Observations of clinic symptoms, pathological changes of optical microscope and transmissional electron microscope were carried out on the ducklings, also, the serum biochemical value was determined 12 h, 24 h, 48 h, 96 h, 168 h, 336 h, 504 h and 672 h post inoculation, lymphocyte
Acid- a -naphthyl-acetate esterase (ANAE) histo-chemical staining method, determination of
different leukocytes were used to study the pathological model.
The results showed mat: infected ducklings began to appear nerve symptoms such as inappetence, ataxia and kicking spasmodically with both legs 12-24 h post inoculation, and then died with their heads drawn back and their leg stretched The fastigium of death was the period 48-72 h post inoculation, and the mortality was 41%. The results of postmortem examinations showed that: swelling and hemorrhage appeared in liver, spleen had a change of swelling and appeared white and red in the surface; swelling and congestion in kidney, uric acid salt deposit in some ducklings; white focus in the surface of pancreas with the shape of pinpoint could be seen in some ducklings.
The results of H.E. staining showed mat the major lesions of liver appeared hemonhagic and necrotic changes, which changed from hydropic degeneration 24 h post inoculation, to fatty degeneration and focal hemorrhage 48 h later; men to severe ballooning degeneration after 96 h, lightly hydropic degeneration and bill canaliculi hyperplasia could be seen even 672 h (4 weeks) post inoculation; the pathological changes of spleen appeared majorly after inoculating for 48 h, which appeared that the number of lymphocyte surround the white pulp reduced sharply, and that the appearance of foam cell when the reticular cell phagocytized lipidic material; focal hemorrhage occurred in the renal tubular epithelium 48 h post inoculation, and then 96 h,karyopyknosis in the proximal tubule and different size vesicles in the cytoplasm could be found; the lesion of pancreas
appeared mostly after inoculating for 48-96 h, which appeared focal fatty degeneration; number of lymphocyte in the medulla of bursa of Fabricuis reduced sharply after inoculating for 48 h.
The results of TEM (Transmissional Electron Microscope) showed that: after inoculating for 12 h, we could find dissolvation of hepatin, karyo pyknosis, and disappearing of organelle in liver. The ultra-structure of the liver which ducklings occurred nerve symptoms and had been killed showed that, it had massive, severe hemorrhage and fatty degeneration, and organelles in the cytoplasm dissolved and even disappeared, fatty vesicles in different size could be seen in the cytoplasm; it could be found in the spleen that swelling of lymphocytes, organelles in the cytoplasm and nucleus dissolved and even disappeared; the lesions of cerebrum were karyo pyknosis or even karyolysis, empty and bright area could be seen around the vas; the lesions of pancreas were mitochondria swelling, vacuolar degeneration, endoplasmic reticulum exceedingly distending, and some fatty lipid-like material could be found in the cytoplasm.
The results of the serum biochemical value showed that: the level of serum GOT and GPT went up and rose to maximum 96 h post inoculation; the level of TP and ALB went down and decreased to minimum 96 h post inoculation; the level of UA increased a Iittlel68 h post inoculation. There were no significant changes of ChE and CRE.
Blood ANAE+-lymphocyte ratio constantly rose after 48 hpost inoculation then began to fall to normal level until 504 h post inoculation. The results of WBC classifying counting showed that: heterophil ratio decreased, lymphocyte and monocyte ratio.There were no significant changes of eosinophil and basophil.
So we could see that, there were certain differences between the DVH-I and
人工感染后其临床症状为：接种后12-24h，精神沉郁、缩颈弓背，出现划水样姿势，随后开始出现死亡，死后呈典型的角弓反张姿势。雏鸭死亡高峰为接种后48-72h，死亡率为41％。死亡鸭剖检可见：肝显著肿大、出血；脾肿大，表面呈红白相间的斑驳状；肾脏肿大，淤血，尿酸盐沉积；法氏囊肿大。其他脏器无明显眼观变化。
剖杀鸭组织学检查结果显示：肝脏：接种后24h，肝细胞发生肿胀，水泡变性，48h后出现脂肪变性及局灶性出血，96h后呈现严重的气球样变，直至672h仍有轻度空泡样变和小胆管增生；脾脏：接种后48h，脾小体外围淋巴细胞数目明显减少，网状细胞增生；肾脏：接种后24h至96h，近曲小管上皮细胞核固缩，胞浆内出现大小不一的空泡；胰脏：接种后48-96h，表现为局灶性脂肪变性；法氏囊：接种后48h，淋巴小结髓质部淋巴细胞数目明显减少。
透射电镜对肝、脑、肾、胰四种组织超微结构观察表明：肝脏接种12h后肝糖原溶解，胞浆内细胞器溶解至消失，细胞核固缩；发生神经症状后剖杀雏鸭表现在肝细胞广泛严重的脂肪变性及坏死，胞浆内细胞器溶解至消失；脾脏内淋巴细胞肿胀，坏死(核固缩、核溶解)，胞核和胞浆内细胞器溶解甚至消失；大脑主要表现为神经细胞核固缩或核溶解；胰脏主要表现在胰腺细胞胞浆内线粒体肿胀，空泡样变，内质网极度扩张，胞浆内脂质样物质聚集。
血清生化指标测定结果表明：雏鸭感染新型DHV后，GOT和GPT活性升高，并在接种后96h达到最高值；TP和ALB含量降低，并于接种后96h降至最低值；UA含量在接种后168h下降；ChE、CRE在感染后无明显变化。
华中农业大学硕士学位论文
试验组血液中ANAE十淋巴细胞比例(%)从接种后48h开始持续阳氏，直到接种后
504h恢复正常。白细胞分类计数结果表明:异嗜性白细胞比例降低，淋巴细胞和单核细
胞比例升高。嗜酸性和嗜碱性白细胞比例在感染后无明显变化。
由此作者认为，新型鸭病毒性肝炎在组织病理学变化上和I型鸭病毒幽干炎存在不同
之处，新型DHV引起的肝脏、脾脏、法氏囊及脑等组织的病变较I型DHV明显。病毒
对脑组织的直接损伤可能是使雏鸭出现神经症状的原因之一。
166,7-days old healthy ducklings were divided randomly into 2 groups, 100 for the tested group and 66 for the control group. The pathological model of New Duck Viral Hepatitis (NDVH) was duplicated through inoculating New Duck Hepatitis Vims (NDHV) intramuscularly. Observations of clinic symptoms, pathological changes of optical microscope and transmissional electron microscope were carried out on the ducklings, also, the serum biochemical value was determined 12 h, 24 h, 48 h, 96 h, 168 h, 336 h, 504 h and 672 h post inoculation, lymphocyte
Acid- a -naphthyl-acetate esterase (ANAE) histo-chemical staining method, determination of
different leukocytes were used to study the pathological model.
The results showed mat: infected ducklings began to appear nerve symptoms such as inappetence, ataxia and kicking spasmodically with both legs 12-24 h post inoculation, and then died with their heads drawn back and their leg stretched The fastigium of death was the period 48-72 h post inoculation, and the mortality was 41%. The results of postmortem examinations showed that: swelling and hemorrhage appeared in liver, spleen had a change of swelling and appeared white and red in the surface; swelling and congestion in kidney, uric acid salt deposit in some ducklings; white focus in the surface of pancreas with the shape of pinpoint could be seen in some ducklings.
The results of H.E. staining showed mat the major lesions of liver appeared hemonhagic and necrotic changes, which changed from hydropic degeneration 24 h post inoculation, to fatty degeneration and focal hemorrhage 48 h later; men to severe ballooning degeneration after 96 h, lightly hydropic degeneration and bill canaliculi hyperplasia could be seen even 672 h (4 weeks) post inoculation; the pathological changes of spleen appeared majorly after inoculating for 48 h, which appeared that the number of lymphocyte surround the white pulp reduced sharply, and that the appearance of foam cell when the reticular cell phagocytized lipidic material; focal hemorrhage occurred in the renal tubular epithelium 48 h post inoculation, and then 96 h,karyopyknosis in the proximal tubule and different size vesicles in the cytoplasm could be found; the lesion of pancreas
appeared mostly after inoculating for 48-96 h, which appeared focal fatty degeneration; number of lymphocyte in the medulla of bursa of Fabricuis reduced sharply after inoculating for 48 h.
The results of TEM (Transmissional Electron Microscope) showed that: after inoculating for 12 h, we could find dissolvation of hepatin, karyo pyknosis, and disappearing of organelle in liver. The ultra-structure of the liver which ducklings occurred nerve symptoms and had been killed showed that, it had massive, severe hemorrhage and fatty degeneration, and organelles in the cytoplasm dissolved and even disappeared, fatty vesicles in different size could be seen in the cytoplasm; it could be found in the spleen that swelling of lymphocytes, organelles in the cytoplasm and nucleus dissolved and even disappeared; the lesions of cerebrum were karyo pyknosis or even karyolysis, empty and bright area could be seen around the vas; the lesions of pancreas were mitochondria swelling, vacuolar degeneration, endoplasmic reticulum exceedingly distending, and some fatty lipid-like material could be found in the cytoplasm.
The results of the serum biochemical value showed that: the level of serum GOT and GPT went up and rose to maximum 96 h post inoculation; the level of TP and ALB went down and decreased to minimum 96 h post inoculation; the level of UA increased a Iittlel68 h post inoculation. There were no significant changes of ChE and CRE.
Blood ANAE+-lymphocyte ratio constantly rose after 48 hpost inoculation then began to fall to normal level until 504 h post inoculation. The results of WBC classifying counting showed that: heterophil ratio decreased, lymphocyte and monocyte ratio.There were no significant changes of eosinophil and basophil.
So we could see that, there were certain differences between the DVH-I and
引文
[1] 上海第一医学院主编．组织学．北京：人民卫生出版社，1981：580-590
[2] 中国人民解放军兽医大学编．兽医检验．北京：农业出版社，1979：14-16
[3] 王丙云，赵金全，冯军等．不同毒力鸭肝炎病毒对雏鸭肝脏抗氧化功能的影响．中国兽医学报，2002，22(5)：450-452
[4] 王永浩，唐玉心，王亚鸣．T淋巴细胞的酸性非特异性酯酶标记及其定位．江西农业大学学报，1984，1：1-10
[5] 邓家栋．临床血液学．上海：上海科学出版社，1985：554-555
[6] 刘兆宇，程安春．雏鸭病毒性肝炎的研究进展．中国家禽，2002，24(10)：6-9
[7] 阴天榜，刘兴友等著．家禽免疫学．北京：中国农业出版社，1999：51-59
[8] 吴题．ELISA法检测鸭病毒性肝炎抗体的方法研究及应用．[北京农业大学硕士研究生论文]．1990
[9] 张玉生，刘巨雄，刘娜．动物生理学．吉林：吉林人民出版社，2000：18-111
[10] 张宗明，裘法祖．肝性脑病发病机制的研究进展．普外临床．1993，8(5)：376-378
[11] 李勃，刘新莲．检测肝病患者血清胆碱酯酶的临床意义．中西医结合肝病杂志，2001，11(5)：281
[12] 汪铭书，程安春．鸭病毒性肝炎研究：强毒在雏鸭和成年鸭体内的分布和排泄．中国兽医学报，1997，17(3)：254-257
[13] 苏敬良，黄瑜，贺荣莲等．新型鸭肝炎病毒的分离及初步鉴定．中国兽医科技，2002，32(1)：15-16
[14] 陈大宇．内生肌酐清除率测定在肾脏疾病中的应用．华夏医学．2001，14(4)：454-455
[15] 陈建红等．鸭肝炎自然病例与鸭肝炎病毒人工发病病例组织病理学观察．中国预防兽医学报，2001，23(3)：203-205
[16] 娄强．危重病人低蛋白血症的研究进展．《国外医学》麻醉学与复苏分册，2001，22(6)：359-361
[17] 禹旺盛，赵振华．鸭病毒性肝炎的发生和病理形态学观察．内蒙古农牧学院学报，1991，12(1)：133-136
[18] 胡薛英，程国富，周诗其等．试验感染鸭病毒性肝炎的组织病理学研究．华中农业大学学报．2000，19(1)：48-50
[19] 胡薛英，苏敬良．程国富，周诗其．新型鸭肝炎病毒试验感染雏鸭的组织病理学．中国兽医学报，2002，22(6)：549—551
[20] 胡薛英，程国富，周诗其等．鸭病毒性肝炎发病机理的研究：实验感染雏鸭血清生化指标的测定．华中农业大学学报．1996，15(3)：254-256
[21] 胡薛英．鸭病毒性肝炎发病机理的初步研究．[华中农业大学硕士研究生论文]．1996
[22] 贺东生，刘福安，徐立群．鸭肝炎病毒的分子生物学基础及其研究现状．国外兽医学-畜禽传染病，1997，17(4)：19-21
[23] 徐福南，周芳．鸭病毒性肝炎的组织病理学研究．中国兽医科技，1990，2：6-7
[24] 徐福南，陈溥言，李劲松．用不同毒力株鸭肝炎病毒人工感染雏鸭的病理学研究．畜牧与兽医，1990，22(4)：154-155
[25] 徐福南，周芳．鸭病毒性肝炎的组织病理学研究．中国兽医科技．1990c，(2)：6-7
[26] 秦艳玲．血清胆碱酯酶在肝病诊疗中临床意义的探讨．广西医学．2001，23(4)：737-739
[27] 高桥贡，板垣博著[日]．家畜的临床检查．哈尔滨科技报社．哈尔滨，1989：13-15
[28] 彭南秀．雏鸭病毒性肝炎血清酶和血胆红素的动态研究．中国兽医科技．1998a，(28)3：24-25
[29] 彭南秀．雏鸭病毒性肝炎的动态病理学研究．中国兽医科技，1998b，28(8)：22-23
[30] 程国富，胡薛英，周诗其等．单克隆抗体PAP法对实验感染雏鸭体内鸭肝炎病毒的定位检测华．中农业大学学报．1996，15(6)：568-572
[31] 程国富．鸭病毒性肝炎的病理学研究进展．国外兽医学—畜禽疾病．1993，14(2)：10-13
[32] 潘静．血清尿酸浓度降低的临床意义．临床检验杂志．2000，18(6)：380-381
[33] Adamiker D. Electron.microscopy studies on viral hepatitis of ducklings: Ⅱ. Findings in spleen and muscle. Zentralbl Veterinarmed B. 1969,16(7):620-36
[34] Ahmed AA, El-Abdin YZ, Hamza S, Saad FE. Effect of experimental duck virus hepatitis infection on some biochemical constituents and enzymes in the serum of white Pekin ducklings. Avian Dis .1975, 19(2):305-10
[35] Akulov, A. V. , L. M. Kontrimavichus, and A. D. Maiboroda. Susceptibility of geese to duck hepatitis virus. Veterinarys. 1972, 3: 47
[36] Asplin, F. D. Examination of sera from wildfowl for antibodies against the viruses of duck plague, duck hepatitis and duck influenza. Vet Res. 1970, 87:182-183
[37] B．W．卡尔尼克主编．禽病学(第十版)．北京：中国农业出版社．1999，841-850
[38] Friend, M., and D. O. Trainer. Experimental duck hepatitis in the mallard. Avian Dis. 1972, 16: 692-699
[39] Hwang, J. and E. Doughherty of poultry to duck hepatitis viral infection. Am J
Vet Res. 1974, 35: 477-479
[40] Levine, P. P. and J. Fabricant. A hitherto-undescribed virus disease of ducks in North America. Cornell Vet. 40: 71-86
[41] Maiboeda, A. D. Formation of duck hepatitis virus in culture cells. Veterinariya. 1972, (8): 5-7
[42] Mennella G R and G mandella. Glutamic-oxaloacetic(GOT) and glutamicpyruvic(GPT) transaminases in the blood serum in experimental viral hepatitis of ducklings. Arch Vet Ital, 1977, 28: 187-190
[43] P 班克斯，W 巴特利，L N 伯特著．组织的生物化学．张世荣，冯北元译．北京：科学出版社，1984：194-241
[44] Rahn, D.P. Susceptibility of turkeys to duck hepatitis virus and turkey hepatitis virus. MS Thesis, University of Illinois. 1962
[45] Sandhu, T. S., B. W. Calnek, and L. Zeman. Pathologic and serologic characterization of a variant of duck hepatitis type Ⅰ virus. Avian Dis. 36: 932-936
[46] Syurin V N, I I Paniker. [Immuunogenesis and pathogensis of viral hepatitis of ducks]. Veterinariya. 1977, 8: 53-55
[47] Toth, T. E. Study of an agent causing mortality among ducklings immune to duck virus hepatitis. Avian Dis. 1969, 13: 834-846
[2] 中国人民解放军兽医大学编．兽医检验．北京：农业出版社，1979：14-16
[3] 王丙云，赵金全，冯军等．不同毒力鸭肝炎病毒对雏鸭肝脏抗氧化功能的影响．中国兽医学报，2002，22(5)：450-452
[4] 王永浩，唐玉心，王亚鸣．T淋巴细胞的酸性非特异性酯酶标记及其定位．江西农业大学学报，1984，1：1-10
[5] 邓家栋．临床血液学．上海：上海科学出版社，1985：554-555
[6] 刘兆宇，程安春．雏鸭病毒性肝炎的研究进展．中国家禽，2002，24(10)：6-9
[7] 阴天榜，刘兴友等著．家禽免疫学．北京：中国农业出版社，1999：51-59
[8] 吴题．ELISA法检测鸭病毒性肝炎抗体的方法研究及应用．[北京农业大学硕士研究生论文]．1990
[9] 张玉生，刘巨雄，刘娜．动物生理学．吉林：吉林人民出版社，2000：18-111
[10] 张宗明，裘法祖．肝性脑病发病机制的研究进展．普外临床．1993，8(5)：376-378
[11] 李勃，刘新莲．检测肝病患者血清胆碱酯酶的临床意义．中西医结合肝病杂志，2001，11(5)：281
[12] 汪铭书，程安春．鸭病毒性肝炎研究：强毒在雏鸭和成年鸭体内的分布和排泄．中国兽医学报，1997，17(3)：254-257
[13] 苏敬良，黄瑜，贺荣莲等．新型鸭肝炎病毒的分离及初步鉴定．中国兽医科技，2002，32(1)：15-16
[14] 陈大宇．内生肌酐清除率测定在肾脏疾病中的应用．华夏医学．2001，14(4)：454-455
[15] 陈建红等．鸭肝炎自然病例与鸭肝炎病毒人工发病病例组织病理学观察．中国预防兽医学报，2001，23(3)：203-205
[16] 娄强．危重病人低蛋白血症的研究进展．《国外医学》麻醉学与复苏分册，2001，22(6)：359-361
[17] 禹旺盛，赵振华．鸭病毒性肝炎的发生和病理形态学观察．内蒙古农牧学院学报，1991，12(1)：133-136
[18] 胡薛英，程国富，周诗其等．试验感染鸭病毒性肝炎的组织病理学研究．华中农业大学学报．2000，19(1)：48-50
[19] 胡薛英，苏敬良．程国富，周诗其．新型鸭肝炎病毒试验感染雏鸭的组织病理学．中国兽医学报，2002，22(6)：549—551
[20] 胡薛英，程国富，周诗其等．鸭病毒性肝炎发病机理的研究：实验感染雏鸭血清生化指标的测定．华中农业大学学报．1996，15(3)：254-256
[21] 胡薛英．鸭病毒性肝炎发病机理的初步研究．[华中农业大学硕士研究生论文]．1996
[22] 贺东生，刘福安，徐立群．鸭肝炎病毒的分子生物学基础及其研究现状．国外兽医学-畜禽传染病，1997，17(4)：19-21
[23] 徐福南，周芳．鸭病毒性肝炎的组织病理学研究．中国兽医科技，1990，2：6-7
[24] 徐福南，陈溥言，李劲松．用不同毒力株鸭肝炎病毒人工感染雏鸭的病理学研究．畜牧与兽医，1990，22(4)：154-155
[25] 徐福南，周芳．鸭病毒性肝炎的组织病理学研究．中国兽医科技．1990c，(2)：6-7
[26] 秦艳玲．血清胆碱酯酶在肝病诊疗中临床意义的探讨．广西医学．2001，23(4)：737-739
[27] 高桥贡，板垣博著[日]．家畜的临床检查．哈尔滨科技报社．哈尔滨，1989：13-15
[28] 彭南秀．雏鸭病毒性肝炎血清酶和血胆红素的动态研究．中国兽医科技．1998a，(28)3：24-25
[29] 彭南秀．雏鸭病毒性肝炎的动态病理学研究．中国兽医科技，1998b，28(8)：22-23
[30] 程国富，胡薛英，周诗其等．单克隆抗体PAP法对实验感染雏鸭体内鸭肝炎病毒的定位检测华．中农业大学学报．1996，15(6)：568-572
[31] 程国富．鸭病毒性肝炎的病理学研究进展．国外兽医学—畜禽疾病．1993，14(2)：10-13
[32] 潘静．血清尿酸浓度降低的临床意义．临床检验杂志．2000，18(6)：380-381
[33] Adamiker D. Electron.microscopy studies on viral hepatitis of ducklings: Ⅱ. Findings in spleen and muscle. Zentralbl Veterinarmed B. 1969,16(7):620-36
[34] Ahmed AA, El-Abdin YZ, Hamza S, Saad FE. Effect of experimental duck virus hepatitis infection on some biochemical constituents and enzymes in the serum of white Pekin ducklings. Avian Dis .1975, 19(2):305-10
[35] Akulov, A. V. , L. M. Kontrimavichus, and A. D. Maiboroda. Susceptibility of geese to duck hepatitis virus. Veterinarys. 1972, 3: 47
[36] Asplin, F. D. Examination of sera from wildfowl for antibodies against the viruses of duck plague, duck hepatitis and duck influenza. Vet Res. 1970, 87:182-183
[37] B．W．卡尔尼克主编．禽病学(第十版)．北京：中国农业出版社．1999，841-850
[38] Friend, M., and D. O. Trainer. Experimental duck hepatitis in the mallard. Avian Dis. 1972, 16: 692-699
[39] Hwang, J. and E. Doughherty of poultry to duck hepatitis viral infection. Am J
Vet Res. 1974, 35: 477-479
[40] Levine, P. P. and J. Fabricant. A hitherto-undescribed virus disease of ducks in North America. Cornell Vet. 40: 71-86
[41] Maiboeda, A. D. Formation of duck hepatitis virus in culture cells. Veterinariya. 1972, (8): 5-7
[42] Mennella G R and G mandella. Glutamic-oxaloacetic(GOT) and glutamicpyruvic(GPT) transaminases in the blood serum in experimental viral hepatitis of ducklings. Arch Vet Ital, 1977, 28: 187-190
[43] P 班克斯，W 巴特利，L N 伯特著．组织的生物化学．张世荣，冯北元译．北京：科学出版社，1984：194-241
[44] Rahn, D.P. Susceptibility of turkeys to duck hepatitis virus and turkey hepatitis virus. MS Thesis, University of Illinois. 1962
[45] Sandhu, T. S., B. W. Calnek, and L. Zeman. Pathologic and serologic characterization of a variant of duck hepatitis type Ⅰ virus. Avian Dis. 36: 932-936
[46] Syurin V N, I I Paniker. [Immuunogenesis and pathogensis of viral hepatitis of ducks]. Veterinariya. 1977, 8: 53-55
[47] Toth, T. E. Study of an agent causing mortality among ducklings immune to duck virus hepatitis. Avian Dis. 1969, 13: 834-846
© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号 地址：北京市海淀区学院路29号 邮编：100083 电话：办公室：(+86 10)66554848；文献借阅、咨询服务、科技查新：66554700 |