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1.
人工感染鸭病毒性肠炎急性病例超微结构变化   总被引:1,自引:0,他引:1  
用鸭病毒性肠炎病毒(Duck enteritis virus,DEV)CH强毒株感染成年鸭复制鸭病毒性肠炎急性病例,分别于接种后不同时间,取心、肝、肾、脾、胸腺、十二指肠、法氏囊、脑和胰组织,制作超薄切片,电镜观察。结果表明:病变最早发生于肝和肾,而鸭死亡后以免疫器官和消化器官损伤最严重;各种细胞的变化主要表现为细胞肿胀,染色质或浓缩、碎裂或溶解,线粒体溶解成空泡样结构,其他细胞器破坏;脾、胸腺、法氏囊以及小肠固有层中的淋巴细胞在感染24h后,在出现细胞坏死的同时还出现较为明显的细胞凋亡变化;而鸭死亡后淋巴细胞主要表现为黑洞核样变化,整个细胞凝聚深染,染色质固缩,细胞浆均质深染,细胞膜模糊或不完整。  相似文献   

2.
为研究鸭病毒性肠炎病毒(DEV)CH强毒株在感染鸭体内的分布和形态学发生规律,应用透射电镜和超薄切片技术对人工感染DEV的成年鸭各组织器官进行观察。结果表明:感染后12h在脾脏和法氏囊首先观察到少量的DEV出现,24h后在脾、胸腺和法氏囊以及死亡鸭的肝、肠和胰中均观察到具有典型的疱疹病毒粒子及其核衣壳形态的DEV。DEV病毒核衣壳有空心型、致密核心型、双环型和内壁附有颗粒型4种形态,存在胞核和胞浆两种装配方式。病毒成熟有两种方式:一为细胞核内核衣壳在核内获得皮层,通过核内膜获得囊膜成为成熟病毒;二为核内核衣壳通过内外核膜进入胞浆,核内和胞浆内的核衣壳在细胞浆中获得皮层,然后在各种质膜上获得囊膜,最后成熟病毒通过细胞破裂或其他方式释放到细胞外。伴随着病毒的复制、装配和成熟,细胞中出现多种核内和胞浆包涵体、核内致密颗粒、核内微管和中空短管、胞浆电子致密小体等结构。  相似文献   

3.
研究通过HE染色镜检发现,鸭病毒性肠炎病毒CH强毒株(DEV-CHv)可致鸭胚成纤维细胞(DEF)出现染色质颗粒化、细胞核变形等显著凋亡特征;TUNEL试验显示,接毒组细胞核内有多量棕黄色DAB显色颗粒,表明细胞出现了凋亡现象;DNA Ladder检测表明,接毒组细胞具有分子量分别为180~200bp及其整数倍的凋亡梯带电泳图谱特征;电镜观察发现,接毒组细胞具有染色质浓缩、边移,胞浆严重空泡化,细胞核严重变形,形成凋亡小体等典型凋亡特征.上述研究结果表明鸭病毒性肠炎病毒具有显著的致鸭胚成纤维细胞发生凋亡的作用.  相似文献   

4.
用鸭病毒性肠炎病毒(DEV)CHv强毒株感染成年鸭复制鸭病毒性肠炎急性病例,分别于接种后不同时间,取心、肝、脾、肺、肾、胸腺、食道、十二指肠、胰腺、法氏囊和脑组织,制作切片,应用间接免疫荧光染色法(IFA)检测DEV在鸭体内的侵染过程和分布规律。结果显示:感染后4 h可在脾脏、胸腺和法氏囊中检测到DEV抗原;感染后6 h可在肝脏、食道、十二指肠、直肠及肺脏检测到DEV抗原;IFA对各组织器官中DEV的平均检出率为肝脏46/50、脾脏48/50、肺脏46/50、肾脏0/50、肠道46/50、法氏囊46/50、胸腺47/50、胰腺0/50、大脑0/50、食道44/50、心脏0/50。研究表明:在急性病例中,脾脏、法氏囊、胸腺、食道、肠道、肝脏和肺脏为DEV的主要靶器官;接种后,病毒首先在脾脏、胸腺、法氏囊中出现,然后病毒迅速传播到肝脏、消化道和肺脏中;IFA检测石蜡切片中DEV的方法具有直观、特异性强的优点,是对DEV进行检测和抗原定位的较好方法。  相似文献   

5.
鸭肠炎病毒单克隆抗体的制备   总被引:1,自引:0,他引:1  
采用差速离心和蔗糖密度梯度离心法提纯鸭肠炎病毒(DEV)鸭胚成纤维细胞适应毒,免疫BALB/c小鼠,取脾细胞与SP2/0骨髓瘤细胞融合,经间接ELISA筛选,有限稀释法3次克隆,获得了2株稳定分泌DEV单克隆抗体的杂交瘤细胞株1B8和2G8。经鉴定,2株单克隆抗体分别为IgM和IgG1亚类,腹水ELISA效价均达到1:10^7以上。以2G8单抗腹水为材料,采用间接免疫荧光抗体技术对DEV标准毒感染的鸭胚成纤维细胞进行检测,结果表明,用该抗体可特异性检出接毒后6h感染细胞中的DEV,且感染后48h免疫荧光强度最高,该单抗与细胞成分和鸭肝炎病毒无交叉反应。将杂交瘤细胞冻存3和6个月,复苏后仍能稳定分泌单克隆抗体。  相似文献   

6.
鸭病毒性肠炎(DVE),又称鸭瘟(DP),大头瘟,是由鸭病毒性肠炎病毒(DEV)引起的常见于鸭、鹅和其他雁形目禽类的一种急性、热性、败血性传染病。其特征是流行广泛、传播迅速、发病率和死亡率高,是目前危害水禽的常见疫病之一。  相似文献   

7.
正雏鸭养殖阶段的病毒性肠炎也称鸭瘟,是鸭感染鸭病毒性肠炎病毒引起的一种传染病,该病容易扩散、传感性强、死亡率非常高,雏鸭病毒性肠炎会引起较大的经济损失,因为雏鸭比成年鸭的抵抗力弱,所以雏鸭病毒性肠炎后会有较高的死亡率,必须采取有效的诊断和防治的方法,才能降低病毒性肠炎对雏鸭的危害。  相似文献   

8.
鸭病毒性肠炎(DVE),又名鸭瘟(DP),是鸭、鹅及多种雁形目禽类的一种急性、热性、败血性传染病.其病原为鸭肠炎病毒(DEV),属疱疹病毒科未分类病毒,具有疱疹病毒典型的形态和结构[1].  相似文献   

9.
传染性囊病病毒诱导细胞凋亡的初步观察   总被引:5,自引:0,他引:5  
用1株IBDV强毒株感染易感小鸡,对病鸡法氏囊进行电镜观察及DNA电泳分析,直接观察到病鸡法氏囊中B淋巴细胞凋亡的典型形态学特征和生化变化:染色质凝聚成团,集于核膜旁,胞膜与核膜出现凹陷,细胞拉长变形,最后细胞裂解成由膜包围着的小团,被网状细胞和巨噬细胞吞噬;感染IBDV24~48h的法氏囊细胞总DNA在电泳谱上呈梯状条带,而从正常的法氏囊提取的总DNA在电泳谱上只有1条带。结果表明,IBDV感染小鸡之后,导致了法氏囊中B淋巴细胞的凋亡。作者据此推断,细胞凋亡是造成B淋巴细胞数量减少,从而导致小鸡免疫抑制的原因  相似文献   

10.
为探究核衣壳蛋白(NP)对鸭肠炎病毒(DEV)增殖的影响,笔者根据GenBank上DEV-NP基因序列,设计并构建pSilencer-DEV-NP,采用三种不同方式处理转染鸭胚成纤维(DEF)细胞后,应用荧光显微镜法和FQ-PCR法分析pSilencer-DEV-NP对DEV增殖的影响,结果显示:经荧光显微镜法观察,pSilencer-DEV-NP-l~4在DEF细胞中均呈现绿色荧光;FQ-PCR法扩增并计算,pSilencer-DEV-NP-l~4对DEV增殖的沉默效率分别为81.10%、72.69%、77.35%和67.69%;采用三种方法处理,pSilencer-DEV-NP-1对DEF细胞中DEV的增殖均有沉默作用,但沉默效率不尽一致,其中先后转染后感染时pSilencer-DEV-NP-1的沉默效果最好,在处理60h时沉默效率高达69.20%;同时转染和感染时pSilencer-DEV-NP-1的沉默效果次之,在处理48h时沉默效率最好仅达63.79%;先感染后转染时pSilencer-DEV-NP-1的沉默效果较差,在处理60h时沉默效率最高仅为52.58%。上述研究结果提示,核衣壳蛋白对鸭肠炎病毒增殖具有一定的影响,为阐明核衣壳蛋白在鸭肠炎病毒复制与增殖的作用机制奠定了理论基础。  相似文献   

11.
We studied apoptosis induced by duck enteritis virus (DEV) in vivo, focusing on the lymphoid organs that constitute the main targets for infection: thymus, bursa of Fabricius (BF), and spleen. Fifty Pekin ducks were inoculated subcutaneously with a virulent strain of DEV. The morphology of lymphoid organs of these infected ducks was observed by light microscopy and transmission electron microscopy. Cell death by classical necrosis was observed in lymphocytes of the DEV-infected thymus, BF, and spleen. Lymphocyte apoptosis also was observed at the same time, and it was further confirmed by in situ terminal deoxynucleotidyl transferase dUTP nick-end labeling and agarose gel electrophoresis. We conclude that apoptosis and necrosis of lymphocytes induced by DEV infection resulted in the depletion of lymphocytes and that apoptosis of lymphocytes may play an important role in the pathogenesis of duck viral enteritis.  相似文献   

12.
Vaccination of ducks with an apathogenic strain of duck enteritis virus resulted in protection against challenge with the virulent Lake Andes strain of duck enteritis virus by intramuscular inoculation or contact exposure. Antisera produced in the vaccinated ducks were able to transfer resistance against the challenge strain to recipient ducks. Antisera against duck enteritis virus were cytotoxic for duck enteritis virus-infected duck embryo fibroblasts in the presence of guinea pig complement. These in vivo and in vitro data suggest that the humoral immune mechanism plays a role in protecting ducks from duck enteritis virus infection.  相似文献   

13.
番鸭呼肠孤病毒病雏番鸭实质器官的超微结构   总被引:2,自引:0,他引:2  
对人工感染番鸭呼肠孤病毒发病雏番鸭的心、肝、肺、肾、脾脏、胸腺、法氏囊等7种实质器官的超微结构进行了观察。电镜下发现:心、肝、肺、肾等实质器官出现不同程度的细胞变性、水肿以及局灶性溶解坏死;各器官血管内皮细胞脂滴增多、水肿以至坏死脱落.通透性增加;浆细胞、淋巴细胞和吞噬细胞呈散在或灶性浸润于坏死区和实质细胞间。免疫器官脾脏、胸腺和法氏囊中的部分淋巴细胞、浆细胞坏死和不同程度凋亡,且细胞溶解坏死形成大小不一的坏死灶并被大量增生的吞噬细胞所吞噬,淋巴细胞数量明显减少。上述结果提示,番鸭呼肠孤病毒能导致番鸭免疫抑制。  相似文献   

14.
The aim of this work was to investigate developmental changes in cell proliferation and apoptosis in normal duck bursa of Fabricius using flow cytometry and immunohistochemistry. Studies were carried out on Tianfu ducks on days 24 and 27 of embryogenesis (E24 and E27) along with days 20, 70, and 200 of postnatal development (P20, P70, and P200). Results showed that the percentage of G0/G1 bursa cells significantly increased between E24 and P200 while the percentage of cells in the S phase or G2 + M phase as well as the proliferating index obviously decreased during the same period. Proliferation cell nuclear antigen was detected in lymphocyte and interfollicular epithelium. The proliferative lymphocyte density tended to decrease from E24 to P200. Apoptotic bodies in macrophages, free apoptotic bodies, or nuclei with condensed chromatin in lymphocytes in follicles were identified by transferase-mediated dUTP nick-end labeling. Both flow cytometry and microscopic analysis reveal that the proportion of apoptotic cells and apoptotic lymphocyte density increased from E24 to P20, fell on P70, then rose again on P200. Our foundings demonstrate that cell proliferation decreases and apoptosis increases with age. These changes may account for duck bursa development and involution.  相似文献   

15.
W Lin  K M Lam  W E Clark 《Avian diseases》1984,28(3):641-650
A herpesvirus isolated from waterfowl dying of duck enteritis (DE) was tentatively designated the Sheridan-83. It was serologically related to the original Holland and Lake Andes (LA) strains of duck enteritis viruses (DEV). Other biological characteristics indicated that the Sheridan-83 was more closely related to the Holland strain than to the LA virus. The Sheridan-83 was nonpathogenic to ducks, and ducks inoculated with this virus developed resistance to challenge with the virulent strain LA.  相似文献   

16.
为探讨猴头菇多糖对呼肠孤病毒感染雏番鸭组织病变及细胞凋亡的影响。本实验通过建立呼肠孤病毒感染的肝脾组织病变的动物模型,应用猴头菇多糖对感染番鸭进行防治,给药组分别添加0.01%,0.02%,0.03%的猴头菇多糖,观察其对肝脾组织病变及其细胞凋亡的影响。实验结果发现给药组的番鸭发病时间延迟、死亡率下降,细胞病变坏死较少,用中剂量的猴头菇多糖的治疗呼肠孤病毒病效果最明显。实验数据还表明猴头菇多糖给药组在病毒感染的早期促进细胞凋亡,晚期抑制细胞凋亡,这可能是猴头菇多糖能对呼肠孤病毒感染产生积极影响的原因,它有助于防止病毒在细胞中的扩散甚至有利于病毒的清除。此项研究为国内首次报道。  相似文献   

17.
Cell proliferation and apoptosis in the normal duck thymus during embryonic and post-embryonic development were studied. The flow cytometry assay shows that the level of G(0)/G(1) thymic cell population and the proportion of apoptotic cells increased with age, while the levels of S phase, G(2) + M phase and the proliferating index decreased with age. Proliferation cell nuclear antigen (PCNA) was mainly detected in the nuclei of lymphocytes. The number of PCNA-positive cells in the cortex and medulla significantly decreased with age. Transferase-mediated dUTP nick-end labelling (TUNEL) reaction stained apoptotic bodies in the cytoplasm of macrophages and free apoptotic bodies or nuclei with condensed chromatin in lymphocytes. The number of TUNEL-positive cells in the cortex and medulla markedly increased with age. The amount of proliferation and apoptotic cells in the thymic cortex was higher than that in the medulla. The balance between proliferation and apoptosis in the duck thymus may account for the process of thymic development and involution.  相似文献   

18.
鸭坦布苏病毒(DTMUV)感染是引起蛋鸭产蛋下降的疾病,给禽类养殖业带来极大的经济损失。本研究对DTMUV感染病鸭卵巢的病毒定位及产生的病理损伤进行观察,以了解DTMUV对病鸭卵巢的病理损伤。主要运用病理剖检、常规石蜡切片及HE染色、免疫组织化学等技术对自然感染DTMUV的病鸭进行研究。结果显示:感染蛋鸭临床表现主要以产蛋量骤然下降为特征,严重病例站立不稳,倒地抽搐,最后衰竭而死。剖检眼观病变表现为卵泡充血、出血,破裂,组织病理学变化主要是生长卵泡和成熟卵泡的颗粒细胞增生、凋亡或坏死;卵泡周围有大量空泡状细胞和小动脉增生,增生的动脉平滑肌细胞坏死,大量炎性细胞浸润;免疫组织化学检测结果显示增生的空泡状细胞为上皮细胞,DTMUV主要位于卵泡的颗粒细胞内。综上表明,DTMUV主要分布在颗粒细胞内,颗粒细胞发生增生、凋亡或坏死,导致卵泡闭锁,进而引起蛋鸭产蛋量下降,为阐明DTMUV的感染机制提供理论基础。  相似文献   

19.
Pathogenesis of duck plague in the bursa of Fabricius, thymus, and spleen.   总被引:12,自引:0,他引:12  
White Pekin ducks were inoculated orally with duck plague virus and killed at 24-hour intervals after inoculation. Spleen, thymus, and bursa of Fabricius were collected and examined by light, fluorescent, and electron microscopy. Necrosis of lymphocytes occurred in the bursa of Fabricius, thymus, splenic periarteriolar lymphoid sheath (T lymphocytes), and splenic germinal centers (B lymphocytes). Viral nucleocapsids were present in the karyoplasm of lymphocytes, but these cells necrotized before virions were formed. Periarteriolar reticular sheath cells and sinusoidal lining cells in the spleen, epithelial cells in Hassall's corpuscle of the thymus, epithelial cells between the cortex and medulla of the follicles in the bursa of Fabricius, and macrophages in all 3 tissues contained nucleocapsids in the nuclei and virions in cytoplasmic vacuoles before necrosis occurred.  相似文献   

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