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1.
Kuldeep Dhama Naveen Kumar Mani Saminathan Ruchi Tiwari Kumaragurubaran Karthik M. Asok Kumar 《The Veterinary quarterly》2017,37(1):57-80
Duck virus enteritis (DVE), also called duck plague, is one of the major contagious and fatal diseases of ducks, geese and swan. It is caused by duck enteritis virus (DEV)/Anatid herpesvirus-1 of the genus Mardivirus, family Herpesviridae, and subfamily Alpha-herpesvirinae. Of note, DVE has worldwide distribution, wherein migratory waterfowl plays a crucial role in its transmission within and between continents. Furthermore, horizontal and/ or vertical transmission plays a significant role in disease spread through oral-fecal discharges. Either of sexes from varying age groups of ducks is vulnerable to DVE. The disease is characterized by sudden death, vascular damage and subsequent internal hemorrhage, lesions in lymphoid organs, digestive mucosal eruptions, severe diarrhea and degenerative lesions in parenchymatous organs. Huge economic losses are connected with acute nature of the disease, increased morbidity and mortality (5%–100%), condemnations of carcasses, decreased egg production and hatchability. Although clinical manifestations and histopathology can provide preliminary diagnosis, the confirmatory diagnosis involves virus isolation and detection using serological and molecular tests. For prophylaxis, both live-attenuated and killed vaccines are being used in broiler and breeder ducks above 2 weeks of age. Since DEV is capable of becoming latent as well as shed intermittently, recombinant subunit and DNA vaccines either alone or in combination (polyvalent) are being targeted for its benign prevention. This review describes DEV, epidemiology, transmission, the disease (DVE), pathogenesis, and advances in diagnosis, vaccination and antiviral agents/therapies along with appropriate prevention and control strategies. 相似文献
2.
Xuefeng Qi Xiaoyan Yang Anchun Cheng Mingshu Wang Dekang Zhu Renyong Jia Qihui Luo Xiaoyue Chen 《Research in veterinary science》2009,87(2):218-225
Duck virus enteritis (DVE) is an acute and contagious herpes virus infection of duck, geese and swans with high morbidity and mortality. The development of specific mucosal immune system against duck enteritis virus (DEV) infection for ducks has been hindered by a lack of knowledge concerning the purification of immunoglobulin A (IgA) of duck. In the present work, the method for purification of duck immunoglobulin A was developed, and the induction of intestinal mucosal immune responses against DEV was studied by orally infected ducklings with virulent DEV. The results showed that a continuous increased DEV DNA levels were observed in blood and various organs examined of orally infected ducklings throughout the infection, which was accompanied by the development of infection in ducklings from mild progressed to severe pathological lesions. Furthermore, a marked increased level of DEV-specific IgA and IgG antibodies in bile, serum and the intestinal tract, as well as the density of IgA+ cells in intestine were detected between 1 and 12 days p.i., followed by a drastic reduction of the antibody levels and the density of IgA+ cells at 15 days p.i. The results indicate that the DVE infection can stimulate both IgA-dominated antibody immune responses in the intestinal tract, and IgG-dominated antibody systemic immunity in the serum of ducklings orally inoculated with virulent DEV. The severe lesions of the villus epithelial cells and the lymphoid organs can suppress the intestinal mucosal immune responses. 相似文献
3.
Isolation of an apathogenic immunogenic strain of duck enteritis virus from waterfowl in California 总被引：2，自引：0，他引：2
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
4.
Quantitative analysis of virulent duck enteritis virus loads in experimentally infected ducklings 总被引：7，自引：0，他引：7
To better understand the pathogenesis of duck virus enteritis (DVE), the levels of viral DNA in various tissues of ducklings during acute stage of virulent duck enteritis virus (DEV) infection were investigated by using quantitative real-time polymerase chain reaction. The results show that the viral levels of DEV in systemic organs have a close correlation with the progression of disease. The rapid dissemination and active replication of virulent DEV in multiple systemic organs at the early phase of acute infection accelerate the progression of disease. The levels of viral DNA increase sharply soon after developed clinical signs of disease, and the extent of increase and the magnitude of DEV DNA load in various tissues of ducklings after the exhibition of clinical signs may be a critical determinant of the outcome of DEV infection. The relatively high levels of DEV in bursa and small intestine tissues of dead ducklings most likely reflect the abundance of target epithelial and lymphoid cells in these tissues, which therefore play a key role in the pathogenesis of acute DVE and manifest as severe tissue lesions on the bursa and small intestine. 相似文献
5.
Duck viral enteritis (DVE) was diagnosed in an outbreak of the disease in a resident population of Muscovy ducks (Cairina moschata domesticus) on a privately owned multispecies game bird production facility in Illinois, where it claimed 625 ducks. This disease condition had not been reported previously in domestic ducks in Illinois. Although other varieties and age groups of domestic waterfowl (i.e., black ducks, rhumen ducks, Pekin ducks, ducklings, and geese) were present on the game bird farm, the morbidity and mortality (100%) in this epornitic was solely limited to adult ducks of the Muscovy lineage. The clinical signs in the affected ducks were lethargy, diarrhea, dehydration, and death within 2-3 hr of onset of symptoms. Gross pathologic changes were nonspecific and included ecchymotic hemorrhage, effusion of fluid and blood within body cavities reflective of an acute systemic infectious disease. Light microscopic findings were necrosis of primarily digestive lining epithelium and variable lymphohistiocytic infiltration within mucosal and serosal connective tissues. Intranuclear inclusions resembling characteristic herpetic (i.e., Cowdry type A) inclusions were observed primarily in the digestive, respiratory, and reproductive tracts; liver; and spleen. Esophageal candidiasis, bacteriosis, and systemic Pasteurella anatipestifer infections, thought to be concurrent or opportunistic infections, were present in several ducks. DVE virus was demonstrated in infected Muscovy duck embryo fibroblast cells by direct DVE virus-specific fluorescent antibody staining. 相似文献
6.
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
7.
Development of a polymerase chain reaction to detect Vietnamese isolates of duck virus enteritis. 总被引：16，自引：0，他引：16
L I Pritchard C Morrissy K Van Phuc P W Daniels H A Westbury 《Veterinary microbiology》1999,68(1-2):149-156
A polymerase chain reaction (PCR) method for the detection of duck virus enteritis (DVE) virus in tissues of infected and affected ducks, and in cell culture was developed. This required us to obtain specific nucleotide sequence information as we could not find any specific data about the genome of the virus. We found the assay to be highly effective in detecting the virus under experimental conditions and to be easily transferred to laboratories in Vietnam where it is being used in studies on the epidemiology of the disease. We have applied this simple and rapid diagnostic method to the detection of DVE isolates grown in cell culture and tissues from infected birds. The assay was also able to differentiate DVE from other avian herpesviruses, such as Marek's disease, infectious laryngotracheitis virus and goose herpesvirus. 相似文献
8.
Pathogenicity of a low-virulence duck virus enteritis isolate with apparent immunosuppressive ability 总被引：9，自引：0，他引：9
Duck enteritis virus (DEV) was isolated from commercial 2-to-6-wk-old white Pekin ducks experiencing 25%-30% mortality and high morbidity. Secondary infections with Pasteurella multocida, Riemerella anatipestifer, and Escherichia coli were frequently seen in affected ducks. The isolated virus was identical to the prototype DEV by virus neutralization test but differed from the classic DEV by causing lymphoid organ atrophy and inconsistent hemorrhagic lesions in the intestinal annular bands. Attempts to reproduce the disease in white Pekin ducks were unsuccessful until the virulence of the virus was increased by three passages in Muscovy ducklings. Significant thymic atrophy (P < or = 0.001) was detected during the first 10 days postinfection (DPI), but thymus size returned to normal by 17-24 DPI. However, bursal atrophy increased significantly (P < or = 0.001) from 4 DPI until the end of the experiment (39 DPI). Reduction in body weight was significant (P < or = 0.05) between 4 and 6 DPI. There was massive depletion of thymic and bursal lymphocytes with lymphoid necrosis in the thymus, bursa, spleen, and Harderian gland. Eosinophilic intranuclear inclusions were observed in thymus, bursa, spleen, esophagus, cloaca, liver, conjunctiva, and Harderian gland. Occasional intracytoplasmic inclusions were also found scattered in the epithelial cells of conjunctiva, esophagus, bursa of Fabricius, and cloaca. Virus was recovered from experimentally infected ducks from thymus, bursa, spleen, liver, kidneys, trigeminal ganglion, and cloaca during the first 10 days of infection. These findings suggest that a low-virulent DEV can cause a massive lymphoid atrophy and can sustain immunosuppression as noted by the secondary bacterial infection. 相似文献
9.
为研究鸭瘟病毒的组织细胞嗜性及其潜伏部位,采用real-timePCR技术对人工感染后病毒的组织器官分布进行了动态定量分析。结果表明,鸭瘟病毒在肝、脾、外周血淋巴细胞、法氏囊、三叉神经节、肾、肺和心脏等均能增殖;动态定量分析发现,随疾病发展各器官病毒荷载量不断上升,至死亡时达到顶峰;肝、脾中病毒载量高,出现时间早,持续时间长;耐过鸭多数组织器官中病毒逐渐消失,但三叉神经节及外周血淋巴细胞在感染后38d仍能检测到低拷贝病毒DNA,表明除三叉神经节外,外周血淋巴细胞也很可能是潜伏部位。 相似文献
10.
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
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12.
应用单克隆抗体的免疫组织化学法研究雏鸭体内鸭瘟病毒的分布 总被引：3，自引：1，他引：3
本实验应用了免疫组织化学的单克隆抗体间接酶标染色法，对人工感染鸭瘟病毒雏鸭的组织切片进行染色观察。旨在研究病毒在鸭体内分布，对其进行定位。研究结果显示，鸭的心脏、肝脏、脾、胸腺、肠、法氏囊、胰、肺、肾等组织的细胞浆内均出现了染色的特异阳性反应物。结果表明，鸭瘟病毒广泛分布于感染雏鸭的各种组织器官，并造成一定的组织病理变化。 相似文献
13.
Duck enteritis virus (DEV) is a herpesvirus that causes an acute, contagious, and fatal disease. In the present article, we introduce a quantitative real-time polymerase chain reaction (PCR) assay for DEV DNA using TaqMan technology and a two-step protocol. It was confirmed to be rapid, sensitive, and specific for DEV detection. The primers and probe were designed and directed to the DNA polymerase gene of DEV. The method will provide a valuable tool for rapid laboratory diagnosis of DEV infection. By virtue of its high-throughput format and its ability to accurately quantify the viral DNA, the method may be useful for large epidemiological surveys and clarification of pathogenesis, such as latency and reactivation of the virus. 相似文献
14.
A chicken embryo-adapted duck enteritis virus (DEV) strain is the most widely used vaccine against duck virus enteritis (DVE) infection. The kinetics of attenuated DEV vaccine was examined in tissues of ducklings vaccinated by the mucosal or systemic route at 20 days of age and sampled regularly up to 60 days post-vaccination (p.v.). Significant numbers of virus genomes in the lymphoid and other parenchymatous organs were first detected at 60 min p.v., and subsequently rose to peak levels during 90 min to 1 day p.v. independent of the route of vaccine administration. The peak level of vaccine virus in the individual parenchymatous organs of subcutaneously immunized ducklings was significantly higher than that of orally or nasally immunized ducklings. The route of vaccine administration had significant effect on the initial tissue distribution of vaccine virus in respiratory and digestive tracts. Vaccine viruses spread to digestive tract and trachea tissues by mucosal route, i.e. oral and nasal administration, early than that by subcutaneous route. The rapid early increase of vaccine virus levels in all samples examined followed by a steady decline from 90 min to 6 days p.v. The real-time PCR analysis of a variety of tissues is significant for further investigation of the mechanism of vaccinal protection, and the optimization of vaccination regimes. 相似文献
15.
The biology of latent infection by bovine herpesvirus 2 (BoHV-2), the agent of mammillitis in cows, remains largely unknown. We herein report attempts to reactivate the latent infection and investigated the sites of BoHV-2 latency in experimentally infected sheep. Ewes inoculated with BoHV-2 in the udder’s skin shed virus for up to five days, developed mammillitis and seroconverted. However, attempts to reactivate latent infection by dexamethasone administration at day 40 pi failed. Nevertheless, viral DNA - and not infectious virus - was detected by PCR in several nerve ganglia and/or regional lymph nodes (LNs) of all animals at day 40 post-reactivation. Likewise, lambs previously inoculated with BoHV-2 in the nose harbored latent viral DNA in trigeminal ganglia, tonsils and regional LNs. These results demonstrate that BoHV-2 establishes latent infection in nerve ganglia and in regional lymphoid tissues, yet virus reactivation is not easily achieved by standard protocols used. 相似文献
16.
Following primary infection of the eye, oral cavity, and/or nasal cavity, bovine herpesvirus 1 (BHV-1) establishes latency in trigeminal ganglionic (TG) neurons. Virus reactivation and spread to other susceptible animals occur after natural or corticosteroid-induced stress. Infection of calves with BHV-1 leads to infiltration of lymphocytes in TG and expression of IFN-gamma (interferon-gamma), even in latently infected calves. During latency, virus antigen and nucleic acid positive non-neural cells were occasionally detected in TG suggesting there is a low level of spontaneous reactivation. Since we could not detect virus in ocular or nasal swabs, these rare cells do not support high levels of productive infection and virus release or they do not support virus production at all. Dexamethasone (DEX) was used to initiate reactivation in latently infected calves. Foci of mononuclear or satellite cells undergoing apoptosis were detected 6h after DEX treatment, as judged by the appearance of TUNEL+ cells (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling). BHV-1 antigen expression was initially detected in lymphocytes and other non-neural cells in latently infected calves following DEX treatment. At 24h after DEX treatment, viral antigen expression and nucleic acid were readily detected in neurons. Our data suggest that persistent lymphocyte infiltration and cytokine expression occur during latency because a low number of cells in TG express BHV-1 proteins. Induction of apoptosis and changes in cytokine expression following DEX treatment correlates with reactivation from latency. We hypothesize that inflammatory infiltration of lymphoid cells in TG plays a role in regulating latency. 相似文献
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18.
商品肉鸭鸭瘟病毒的分离与鉴定 总被引：1，自引：0，他引：1
采用鸭胚成纤维细胞培养从山东和北京两地暴发的鸭瘟临床病例中分离到两株鸭肠炎病毒（DEV），分别命名为SD和BJ。以单抗介导的间接免疫荧光（IFA）检测方法，对两个分离株感染细胞滴片进行间接IFA检测，可见感染细胞内有明显的蓝绿色荧光。试验感染7日龄北京鸭可引起鸭瘟的典型临床症状．死亡率为100％（3／3），取试验感染死亡鸭肝脏、法氏囊和脑组织等制备石蜡包埋切片，利用单抗进行免疫组化检验，除脑组织外均检测到病毒抗原。根据在GenBank上已发表的DEV两段序列设计两对引物，采用聚合酶链式反应（PCR）对野毒sD株人工感染鸭肝脏和BJ珠自然发病鸭肝脏病科提取核酸为模板进行扩增，得到预期大小为765bp和1954bp的目的片段，对长片段进行测序，与发表序列进行比较，毒株间的碱基序列同源性达到99．73％。 相似文献
19.
R E Gough 《The Veterinary record》1984,114(11):262-265
From 1977 to 1983 the Central Veterinary Laboratory, Weybridge confirmed 19 outbreaks of duck virus enteritis in the United Kingdom. All the outbreaks involved collections of captive waterfowl and there were no reported cases in commercial ducks. In many instances the disease was associated with contact with migrating waterfowl, particularly male mallards (Anas platyrhynchos). Muscovy ducks (Cairina moschata) and related species appeared to be particularly susceptible. The most sensitive system for isolating the virus was muscovy duck embryo tissue cultures. The duckling inoculation test was found to be the most reliable method of confirming the disease. 相似文献
20.
W L Mengeling K M Lager D M Volz S L Brockmeier 《American journal of veterinary research》1992,53(11):2164-2173
Various procedures of vaccination for pseudorabies were compared for their effects on shedding, latency, and reactivation of attenuated and virulent pseudorabies virus. The study included 6 groups: group 1 (10 swine neither vaccinated nor challenge-exposed), group 2 (20 swine not vaccinated, but challenge-exposed), and groups 3 through 6 (10 swine/group, all vaccinated and challenge-exposed). Swine were vaccinated with killed virus IM (group 3) or intranasally (group 4), or with live virus IM (group 5) or intranasally (group 6). The chronologic order of treatments was as follows: vaccination (week 0), challenge of immunity by oronasal exposure to virulent virus (week 4), biopsy of tonsillar tissue (week 12), treatment with dexamethasone in an attempt to reactivate latent virus (week 15), and necropsy (week 21). Vaccination IM with killed or live virus and vaccination intranasally with live virus mitigated clinical signs and markedly reduced the magnitude and duration of virus shedding after challenge exposure. Abatement of signs and shedding was most pronounced for swine that had been vaccinated intranasally with live virus. All swine, except 4 from group 2 and 1 from group 4, survived challenge exposure. Only vaccination intranasally with live virus was effective in reducing the magnitude and duration of virus shedding after virus reactivation. Vaccination intranasally with killed virus was without measurable effect on immunity. Of the 55 swine that survived challenge exposure, 54 were shown subsequently to have latent infections by use of dexamethasone-induced virus reactivation, and 53 were shown to have latent infections by use of polymerase chain reaction (PCR) with trigeminal ganglia specimens collected at necropsy. Fewer swine were identified by PCR as having latent infections when other tissues were examined; 20 were identified by testing specimens of olfactory bulbs, 4 by testing tonsil specimens collected at necropsy, and 4 by testing tonsillar biopsy specimens. Eighteen of the 20 specimens of olfactory bulbs and 3 of the 4 tonsil specimens collected at necropsy in which virus was detected by PCR were from swine without detectable virus-neutralizing antibody at the time of challenge exposure. One pig that had been vaccinated intranasally with live virus shed vaccine virus from the nose and virulent virus from the pharynx concurrently after dexamethasone treatment. Evaluation of both viral populations for unique strain characteristics failed to provide evidence of virus recombination. 相似文献