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1.
阿留申病细小病毒的分离及VP2基因遗传衍生分析   总被引:2,自引:0,他引:2  
水貂阿留申病(Aleutian disease of mink,AD)是水貂的一种慢性传染病,病原为阿留申病细小病毒(Aleutian mink disease parvovirus,AMDV),属细小病毒科、细小病毒属。AD自1940年发现以来至今60年里,已经普遍存在于世界各地人工养殖的水貂种群中。对水貂养殖业造成了不可估量的经济损失。  相似文献   

2.
<正>水貂阿留申细小病毒(Aleutian mink disease parvo virus,AMDV)是感染水貂的自主复制型细小病毒,是引起水貂阿留申病的病原。AMDV感染水貂后会产生抗体依赖的病毒感染增强作用(Antibody-dependent enhancement,ADE),还没有效果较好的疫苗进行防控。本文主要  相似文献   

3.
正水貂阿留申病(Aleutian disease of mink,AD)是一种以水貂繁殖能力下降、冬季饮欲增强、食欲减退、逐渐消瘦死亡为主要临床症状的病毒性传染病,而且本病严重损害水貂的免疫系统,造成疫苗的免疫保护期缩短、抗体整齐度参差不齐,严重影响疫苗的免疫效果。本文针对国内水貂养殖及防控现状,提供了合理的检测净化方法以供广大养殖户参考,为国内种貂选育和商品貂的繁殖工作奠定基础。水貂阿留申病(ADM)又称浆细胞增多症(plas-  相似文献   

4.
阿留申病(Aleutian disease of mink)是水貂的一种慢性病毒性传染病,主要特征是全身性浆细胞增多,血清丙种球蛋白增高,肾小球肾炎以及纤维素性坏死性动脉炎,持续性病毒血症和母貂空怀显著增加。本病最初在"阿留申"品系  相似文献   

5.
<正>水貂阿留申病(Aleutian disease of mink),又称浆细胞增多症(Plasmacytosis),是由细小病毒科的阿留申病病毒(ADMV)引起的一种慢性传染病,导致自身免疫系统紊乱并逐渐衰竭,并发强烈的自身免疫。主要侵害网状内皮系统,其特征为浆细胞弥漫性增生、产生多量C-球蛋白和持续性的病毒血症。水貂阿留申病具有自身免疫  相似文献   

6.
水貂阿留申病(Aleutian disease of mink,AD),是以水貂繁殖能力下降、消痩、自身免疫病、高免疫球蛋白血症、肾衰竭死亡为基本特征的一种病毒性传染病。目前该病在我国呈现较高的感染率(60%~70%),严重影响我国养貂业的健康可持续发展。文中针对我国水貂阿留申病的流行及危害现状,提出合理的检测方法,为提升并稳定阳性貂的生产性能,逐步建立国内优良水貂育种群提供参考。  相似文献   

7.
为给抗水貂阿留申病(Aleutian disease of mink,ADM)的药物应用提供理论依据和进一步丰富水貂血液常规指标,试验研究了三种饲料添加剂对阿留申病水貂血液常规指标的影响,试验对常规饲养条件下的8~9月龄标准水貂母貂进行阿留申病毒(Aleutian disease virus,ADV)抗体检测,根据检测结果选取ADV阳性水貂(ADM水貂)238只、ADV阴性水貂(非ADM水貂)62只,分为抗申宝组、酵母多糖组、芪参散组和对照组,对照组只饲喂基础日粮。每组各随机选取3只(共24只)水貂分别在喂药前和喂药30 d后断趾采血,采用迈瑞BC-6600血细胞分析仪测定24项血液常规指标并比较。结果表明:饲喂三种饲料添加剂均可使ADM水貂的白细胞数(WBC)、血红蛋白含量(HGB)、血细胞比容(HCT)、血小板数(PLT)显著升高(P0.05)并达到正常水平,同时使红细胞数(RBC)和中性粒细胞数(NE)显著升高(P0.05);均可使非ADM水貂NE显著提高(P0.05);饲喂抗申宝还可使非ADM水貂的WBC、HGB、HCT、大血小板比率(P-LCR)、嗜酸细胞百分含量(EO%)和嗜碱细胞数(BA)显著升高(P0.05),饲喂芪参散后WBC、HGB、HCT、P-LCR、EO%显著升高(P0.05);未饲喂中草药的ADM水貂和非ADM水貂均出现淋巴细胞百分含量(LY%)显著下降(P0.05)。说明三种饲料添加剂均能增强水貂的生理机能,改善造血机能,均可调节ADM水貂的血常规指标,使其趋于正常;抗申宝对非ADM水貂血常规指标的改善相对最佳。  相似文献   

8.
正水貂阿留申病(Aleutian mink disease, AMD)是由AMD病毒(AMDV)感染水貂引起的自身免疫系统功能紊乱,并引发自身免疫的慢性、传染性疾病,在全球范围的水貂养殖国家造成了重大的经济损失~([1-2])。由于其特殊的致病机制和抗体依赖性增强作用(ADE)~([3-4]),尚无预防该病的商业疫苗。目前主要通过检疫淘汰病貂来净化貂厂,但  相似文献   

9.
水貂阿留申病(Aleutian mink disease, AMD)是由水貂阿留申病病毒(Aleutian mink disease virus, AMDV)引起的水貂的重要传染性疾病之一,深入开展对AMDV的研究对于该病的防控有重要意义。AMDV基因组全长约为4.8 kb,主要编码2种结构蛋白和3种非结构蛋白,它们在病毒复制、增殖及致病过程中发挥重要作用。AMDV的复制依赖于代谢活跃的细胞,对于幼貂,病毒感染肺泡Ⅱ型细胞会造成急性致死性肺炎,感染巨噬细胞则会引起成年水貂患高丙种球蛋白血症和免疫复合物介导的肾小球肾炎等慢性进行性疾病。笔者从AMDV侵入细胞的受体途径、诱导细胞凋亡途径及病毒复制等方面对其致病机理进行阐述。AMDV在全世界范围内广泛流行,现有的检测方法主要分为血清学诊断方法和分子生物学诊断方法。目前,尚未开发出安全有效的针对AMDV的商品化疫苗,随着生物学技术的快速发展,在灭活疫苗、DNA疫苗和亚单位疫苗的研制上有所进展;抗病毒的新方法,如筛选AMDV耐受貂,提高水貂免疫力和靶向适配体技术为AMD的防控提供了新思路。文章从AMDV编码蛋白功能、病毒细胞嗜性与复制、临床表现...  相似文献   

10.
水貂阿留申病毒(Aleutian mink disease virus,ADV)是一种主要侵染水貂的自主复制型细小病毒,是一种在水貂中广泛存在的重要病原体。病毒粒子的蛋白分为结构蛋白(VP1、VP2)和非结构蛋白(NS1、NS2)两类。VP1蛋白对病毒粒子产生感染性有重要作用;VP2蛋白是主要免疫功能区,能刺激机体产生中和抗体;NS1和NS2主要参与病毒的复制和基因的表达调节。文中对近年来国内外学者关于水貂阿留申病毒结构蛋白和非结构蛋白的研究情况进行归纳和总结。  相似文献   

11.
水貂阿留申病的历史回顾及最新研究概述   总被引:2,自引:1,他引:1  
水貂阿留申病是阻碍养貂业发展的世界性攻关病害。自人们发现该病至今已有50余年的历史,尽管国内外有关专家学者,从没间断过对该病的研究,但始终没能攻克该病的免疫防制问题;值得庆幸的是,在国家科委和农业部畜牧兽医司等部门的大力资助下,我们对阿留申病的免疫原性和免疫机制进行了较系统深入的研究,并研制出了阿留申病灭活疫苗,现已在多个大型貂场进行小试。该文对阿留申病的病史和危害,以及最新研究进展和重大技术突破进行了较全面系统的论述。  相似文献   

12.
In apparent or nonprogressive Aleutian disease virus infection was considered a subclinical but persistent viral infection in which infected mink did not develop tissue lesions, hypergammaglobulinemia, or high antibody titers. Transmission of Aleutian disease virus from mink with this type of infection was measured. Mink with inapparent Aleutian disease appeared healthy and had normal gamma-globulin values, but were capable of transmitting the disease by direct and indirect horizontal contact. The risk of direct or indirect horizontal transmission from mink with inapparent infection was less than from mink with progressive Aleutian disease. Infection also was directly transmitted from the dam to the kits, but again the risk of infection from dams with inapparent infection was less than from dams with progressive Aleutian disease. Mink infected from their dams before weaning developed the disease more slowly than mink which became infected after weaning.  相似文献   

13.
Aleutian Disease of Mink: I. Evidence of its Viral Etiology *   总被引:16,自引:8,他引:8       下载免费PDF全文
A suspension of tissues from field cases of Aleutian disease was used successfully to reproduce the disease in Aleutian mink. Similarly, suspensions of diseased tissues from the experimentally infected mink were used to transmit the agent of Aleutian disease to both Aleutian mink and standard dark mink. Seitz and millipore filtrates prepared from these tissue suspensions were also infective; a suggestion that the etiologic agent is a virus. Genetic factors and hypersensitivity are discussed as possibly contributing to development of the disease.  相似文献   

14.
Inapparent of nonprogressive Aleutian disease virus (ADV) infection is a subclinical but persistent virus infection of mink. Mink with the inapparent type of ADV infection when subjected to stress did not develop the progessive form of the disease. However, when challenged with a large dose of the virus, these mink did develop progressive Aleutian disease indicating that they were not highly resistant to the virus. Sera of mink with either the progressive of the inapparent type of ADV infection did not neutralise the virus. The anti-ADV antibody activity in mink with inapparent type of ADV infection was in the IgG fraction of the serum the same as in mink with progressive Aleutian disease. These data indicate that the resistance of the mink with inapparent infection as compared to mink with progressive Aleutian disease was not due to a difference in the class of immunoglobulin response to the virus. However, mink with progressive Aleutian disease showed a greatly increased immunoglobulin response.  相似文献   

15.
从水貂阿留申病毒(ADV)基因组特点出发,就阿留申病毒的分子生物学研究进展作以简单综述。  相似文献   

16.
Experiments were undertaken to investigate the potential of the enzyme-linked immunosorbent assay (ELISA) as a screening test for the diagnosis of the 2 known naturally occurring forms of Aleutian disease of mink. Anti-Aleutian disease virus (ADV) antibody activity was not detectable in the sera of mink with nonprogressive Aleutian disease despite the demonstration of antibody by counterimmunoelectrophoresis (CIEP) in the same sera. Anti-ADV antibody was detectable in 93% of sera from mink at various stages of experimentally induced progressive Aleutian disease. False-negative reactions occurred in sera which demonstrated high anti-ADV antibody titers by CIEP. As a consequence of the high prevalence of false-negative reactions, the ELISA was not considered to be an effective screening test. However, using CIEP as an indicator of ADV infection, the ELISA may be useful in differentiating mink with nonprogressive Aleutian disease from mink with progressive Aleutian disease.  相似文献   

17.
近年来,随着水貂养殖行业的不断发展,一些疫病也成为了制约水貂养殖业发展的重要因素。水貂阿留申病作为毛皮动物的三大疫病之一(阿留申病、犬瘟热、病毒性肠炎),是导致母貂产仔率下降、公貂配种能力降低和毛皮质量下降的一种高度接触性传染病。至今为止,还没有商品化的疫苗来控制该病的传播及蔓延。控制水貂阿留申病最好的方法是通过检测淘汰所有抗体为阳性的水貂,进而达到净化貂群的目的。而在抗体检测过程中,诊断抗原的制备和纯化决定着检测方法的敏感性、特异性和准确性。论文对目前阿留申病毒细胞抗原及基因工程抗原研究进展做一综述,为今后该病病原检测工作提供参考。  相似文献   

18.
One hundred mink with experimental viral plasmacytosis were examined for fibrinoid vascular lesions. Abnormal hyalin deposits were found in glomeruli in all cases of advanced disease. Fibrinoid arteritis occurred only in Aleutian type mink in this study. Seven of 30 experimentally infected Aleutian mink were found to have fibrinoid arteritis, together with other lesions of advanced plasmacytosis. The type of inoculum seemed of no consequence in development of vascular lesions. Equally severe lesions developed after inoculation with cell-free filtrates as were found in mink inoculated with crude tissue suspensions. These observations strengthen the concept of a virus as the primary etiologic agent and confirm the view that Aleutian disease is a convenient experimental model for studies on the collagen diseases.  相似文献   

19.
水貂阿留申病概述   总被引:3,自引:1,他引:3  
主要对水貂阿留申病的病原学、流行病学、致病机理、临床症状、病理变化、诊断和防制等方面进行了概述,以便对该病诊断和防制提供参考。  相似文献   

20.
Gross and microscopic lesions of Aleutian disease (AD) in mink and hypergammaglobulinemia in ferrets were compared. Both conditions were characterized by widespread proliferation of plasma cells, but proliferation was more prominent in mink infected with AD. Arteritis did not occur in hypergammaglobulinemic ferrets. Minimal or no glomerular alterations occurred in infected ferrets, but were severe in mink infected with AD. Bile duct proliferation was more prominent in diseased mink. Tissue alterations suggested that AD in Aleutian genotype mink is more rapidly progressive than is AD in ferrets, causing overt clinical disease and death. In contrast, hypergammaglobulinemia in ferrets appeared to progress more slowly, with little clinical evidence of disease. This is probably the result of a paucity of glomerular lesions in ferrets. Possible mechanisms to explain the differences in the development of lesions are discussed.  相似文献   

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