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一.鸡马立克氏病、马立克其人和匈牙利的骄傲 在禽病界,没有人不知道马立克氏病的,但为什么叫马立克氏病,却未见得人人知道其历史。马立克(Marek)是匈牙利历史上著名的兽医病理学家。他于1907年发现并报道了鸡的一种以四肢麻痹为特症的疾病,当时称之为多发性神经炎。后来发现,这类病鸡在发生单核淋巴细胞     

鸡抗马立克氏病育种的挑战和机遇

马立克氏病是威胁养禽业健康发展的严重疾病之一.作者从遗传角度综述了控制鸡马立克氏病的研究进展,并提出了以全基因组扫描和侯选基因法相结合的策略寻找马立克氏病遗传抗病分子标记.     

鸡马立克氏病的诊断方法与防控建议

马立克氏病是鸡最常见的淋巴组织增生性疾病,其特征是形成外周神经及其他器官中的单核细胞浸润和肿瘤。鸡马立克氏病是由疱疹病毒引起的,具有高度传染性,其致病性与其他鸡淋巴肿瘤疾病不同。鸡马立克病的发病率和死亡率高,危害大,常继发鸡病原体,是一种急性传染病,马立克氏病破坏法氏囊、胸腺、脾脏等免疫器官,引起强烈的免疫抑制,并影响各种疫苗的预防效果。病鸡是鸡马立克氏病主要传染源,一旦感染可迅速在鸡群中散播,造成严重的经济损失,因此可以通过实施合理的马立克病诊断和监测方法,积极推广有效的综合防治措施,进一步降低马立克病对鸡造成的经济损失。本文就鸡马立克病给养禽业造成的损失,对鸡马立克病的病因、流行特点、诊断方法以及防控措施等进行了详细论述,以期为防治鸡马立克氏病提供积极有效的方案。     

马立克氏病免疫失败的原因及防制

马立克氏病是马立克氏病毒引起的鸡表现神经症状或内脏发生大量肿瘤为特征的传染病.该病无特效药物,通常在雏鸡出壳后24小时内进行预防接种.但近几年来陆续发生经马立克火鸡疱疹病毒(HVT)冻干疫苗防疫的鸡群仍有马立克氏病发生,死亡率达20%～30%,鸡群的生产水平不高,给养鸡单位和个人带来了巨大的经济损失.分析这些鸡群的发病情况,发现引起马立克氏病免疫失败的原因主要与疫苗的保护率、毒株和接种方法等有关,应采取综合性防制措施,强化免疫效果,控制马立克氏病的发生.     

马立克氏病的防治和肿瘤病

一、前言 马立克氏病是由马立克氏病病毒引起的可造成严重经济损失的世界性家禽流行病.造成高感染率和死亡率的原因是由于马立克氏病病毒不断地在体内各内脏器官形成肿瘤(Tumor)以及神经系统被淋巴球浸润后造成麻痹(Paralysis)所导致的结果.     

鸡马立克氏病疫苗研究进展及病毒毒力进化态势

鸡马立克氏病是一种常见的以淋巴组织增生为主要特征的高度接触性传染病.本文分析了马立克氏病毒毒株进化情况,以及引起病毒毒力进化的原因,对马立克氏病疫苗研制进展进行了概述.提出应从免疫方法、免疫佐剂、遗传抵抗等方面入手,缓解病毒毒力增强的态势,进而减少马立克氏病的发生和传播,降低该病给养禽业带来的经济损失.     

生产高质量小母鸡的免疫程序和步骤 续完

马立克氏病为了便于讨论这个问题,让我们假设在孵化厂就正确进行了马立克氏病免疫。然而,雏鸡即使接受过正确的免疫接种,仍然有可能爆发马立克氏病。预防马立克氏病爆发的诀窍是防止雏鸡在早期接触马立克氏病病毒。为此,第一步是要在雏鸡到来前对雏鸡舍进行清洗和消毒,特别重要的是要确保所有尘埃和皮屑都被清除干净,因为马立克氏病病毒可在这些东西里存活数年。在育雏场或联合体内实行单一年龄育雏和严格的生物安全措施对马立克氏病的预防具有很大的帮助。一般而言,在鸡群中早期实行严格的卫生措施和精心的管理,可以减少感染马立克氏病的机会。     

鸡马立克氏病的诊断和防治中易混淆的几个问题

1马立克氏病 由疱疹病毒属中的马立克氏病毒（MDV）引起的,以神经麻痹或肝瘤形成为特征的T淋巴细胞浸润和增生的疾病为马立克氏病。这3个要素中如果其中一个不符,就不能诊断为马立克氏病。有些人把凡是出现坐骨神经麻痹者症状都认为是马立克氏病,也有人把所有内脏肿瘤都认为是马立克氏病，都是不正确的。     

马立克氏病疫苗:过去、现在和未来——Richard L. Witter在纪念Bart Rispense会上的演讲(节选)

Dr. Witter是美国兽医界两位院士之一以及 HVT Fc126疫苗株的发现者，曾任美国农业部地区禽病和肿瘤研究所所长、世界禽病大会和国际马立克氏病会议主席。在马立克氏病、网状内皮增生病、禽白血病等禽的病毒性肿瘤病研究方面做出了重大贡献，是世界著名学者，曾两度访问中国， 1999年在中国召开的世界禽病大会作为特邀代表出席。本文是 Dr. Witter于 2000年 8月在加拿大蒙特利尔召开的第六届世界马立克氏病和家禽会议上作的特邀发言。该文总结了马立克氏病过去研究的历史，阐述了今后马立克氏病防制的主要观点。     

鸡马立克病的防控

马立克病是鸡的一种淋巴组织增生性肿瘤病,其特征为外周神经淋巴样细胞浸润和增大,引起肢(翅)麻痹,以及性腺、虹膜、各种脏器、肌肉和皮肤肿瘤病灶.介绍了鸡马立克病的发病情况、临床症状、病理变化、实验室诊断,提出对马立克病的防控原则为加强预防措施与免疫接种,特别要尽早免疫.     

A comparative evaluation of the protective efficacy of rMd5deltaMeq and CVI988/ Rispens against a vv+ strain of Marek's disease virus infection in a series of recombinant congenic strains of White Leghorn chickens

Marek's disease (MD) is a lymphoproliferative disease of domestic chickens caused by a highly infectious, oncogenic alpha-herpesvirus known as Marek's disease virus (MDV). MD is presently controlled by vaccination. Current MD vaccines include attenuated serotype 1 strains (e.g., CVI988/Rispens), avirulent serotype 2 (SB-1), and serotype 3 (HVT) MDV strains. In addition, recombinant MDV strains have been developed as potential new and more efficient vaccines to sustain the success of MD control in poultry. One of the candidate recombinant MDV strains, named rMd5deltaMeq, was derived from Md5, a very virulent strain of MDV lacking the MDV oncogene Meq. Our earlier reports suggest that rMd5deltaMeq provided protection equally well or better than commonly used MD vaccines in experimental and commercial lines of chickens challenged with very virulent plus (vv+) strains of MDV. In this study, maternal antibody-positive (trial 1) and negative (trial 2) chickens from a series of relatively MD resistant lines were either vaccinated with the rMd5deltaMeq or CVI988/Rispens followed by infection of a vv+ strain of MDV, 648A, passage 10. This report presents experimental evidence that the rMd5deltaMeq protected significantly better than the CVI988/Rispens (P < 0.01) in the relatively resistant experimental lines of chickens challenged with the vv+ strain of MDV. Together with early reports, the rMd5deltaMeq appeared to provide better protection, comparing with the most efficacious commercially available vaccine, CVI988/Rispens, for control of MD in lines of chickens regardless of their genetic background.     

Mortality of one-week-old chickens during naturally occurring Marek's disease virus infection

Marek's disease (MD) is a disease of chickens that occurs worldwide and has serious economic consequences. MD can present as one of several forms, with the most commonly occurring forms being the lymphoproliferative diseases. Under experimental conditions, an early mortality syndrome has been recognized following infection by some but not all strains of MD virus (MDV). This is the first report of a confirmed case of mortality due to naturally occurring MDV infection in 1-week-old, nonvaccinated, chickens. Necrotizing lesions were observed in the bursa of Fabricius, lung, duodenum, jejunum, and proventriculus, and large intranuclear inclusion bodies were a striking feature in tissues with lesions in all birds. Immunohistochemical staining for the pp38 protein of MDV revealed abundant pp38 antigen in the affected tissues, confirming the presence of MDV within the lesions. PCR yielded an amplicon with 97% homology to the meq gene of MDV. No evidence of co-infection by either of the immunosuppressive agents chicken anemia virus and infectious bursal disease virus was detected.     

Evolution of Marek's disease -- a paradigm for incessant race between the pathogen and the host

Marek's disease (MD) is a highly contagious lymphoproliferative disease of poultry caused by the oncogenic herpesvirus designated Marek's disease virus (MDV). MD has a worldwide distribution and is thought to cause an annual loss over 1 bn US dollars to the poultry industry. Originally described as a paralytic disease, today MD is mostly manifested as an acute disease with tumours in multiple visceral organs. MD is controlled essentially by the widespread use of live vaccines administered either in ovo into 18-day-old embryos or into chicks immediately after they hatch. In spite of the success of the vaccines in reducing the losses from the disease in the last 30 years, MDV strains have shown continuous evolution in virulence acquiring the ability to overcome the immune responses induced by the vaccines. During this period, different generations of MD vaccines have been introduced to protect birds from the increasingly virulent MDV strains. However, the virus has countered each new vaccine with ever more virulent strains. This continuous race between the virus and the host is making the control of this poultry health problem a major challenge for the future.     

Marek's disease in turkeys. I. A seven-year survey of commercial flocks and experimental infection using two field isolates

Marek's disease virus (MDV) causes immunosuppression and tumors in chickens, but the turkey is an unusual host for the virus, and tumors caused by MDV in turkeys are unique. We describe the prevalence of turkey tumors in Israel between 1993 and 2000, their molecular diagnosis by polymerase chain reaction (PCR), and the natural distribution of herpesvirus of turkeys (HVT). Most clinical cases with tumors in commercial turkeys were diagnosed as MDV. The reproduction of Marek's disease (MD) in turkeys by two turkey MDV strains, Ar and La, was analyzed, and it was shown that these strains can induce tumors in experimental trials. The severity of experimental disease differed from those features of the original outbreak, since a less severe disease was recorded.     

Comparative analysis of Marek's disease virus (MDV) glycoprotein-, lytic antigen pp38- and transformation antigen Meq-encoding genes: association of meq mutations with MDVs of high virulence

Marek's disease (MD) is a highly contagious lymphoproliferative and demyelinating disorder of chickens. MD is caused by Marek's disease virus (MDV), a cell-associated, acute-transforming alphaherpesvirus. For three decades, losses to the poultry industry due to MD have been greatly limited through the use of live vaccines. MDV vaccine strains are comprised of antigenically related, apathogenic MDVs originally isolated from chickens (MDV-2), turkeys (herpesvirus of turkeys, HVT) or attenuated-oncogenic strains of MDV-1 (CVI-988). Since the inception of high-density poultry production and MD vaccination, there have been two discernible increases in the virulence of MDV field strains. Our objectives were to determine if common mutations in the major glycoprotein genes, a major lytic antigen phosphoprotein 38 (pp38) or a major latency/transformation antigen Meq (Marek's EcoRI-Q-encoded protein) were associated with enhanced MDV virulence. To address this, we cloned and sequenced the major surface glycoprotein genes (gB, gC, gD, gE, gH, gI, and gL) of five MDV strains that were representative of the virulent (v), very virulent (vv) and very virulent plus (vv+) pathotypes of MDV. We found no consistent mutations in these genes that correlated strictly with virulence level. The glycoprotein genes most similar among MDV-1, MDV-2 and HVT (gB and gC, approximately 81 and 75%, respectively) were among the most conserved across pathotype. We found mutations mapping to the putative signal cleavage site in the gL genes in four out of eleven vv+MDVs, but this mutation was also identified in one vvMDV (643P) indicating that it did not correlate with enhanced virulence. In further analysis of an additional 12 MDV strains, we found no gross polymorphism in any of the glycoprotein genes. Likewise, by PCR and RFLP analysis, we found no polymorphism at the locus encoding the pp38 gene, an early lytic-phase gene associated with MDV replication. In contrast, we found distinct mutations in the latency and transformation-associated Marek's EcoRI-Q-encoded protein, Meq. In examination of the DNA and deduced amino acid sequence of meq genes from 26 MDV strains (9 m/vMDV, 5 vvMDV and 12 vv+MDVs), we found distinct polymorphism and point mutations that appeared to correlate with virulence. Although a complex trait like MDV virulence is likely to be multigenic, these data describe the first sets of mutations that appear to correlate with MDV virulence. Our conclusion is that since Meq is expressed primarily in the latent/transforming phase of MDV infection, and is not encoded by MDV-2 or HVT vaccine viruses, the evolution of MDV virulence may be due to selection on MDV-host cell interactions during latency and may not be mediated by the immune selection against virus lytic antigens such as the surface glycoproteins.     

马立克氏病病毒感染鸡羽髓上皮细胞差异蛋白质组学研究

为鉴定鸡羽髓上皮细胞感染马立克氏病病毒(MDV)前后差异表达的蛋白,本研究以MDV强毒GA株人工感染SPF鸡,并通过双向电泳技术进行分析.结果显示:在病毒感染后4 d、7 d、14 d和21 d显著差异表达的蛋白点分别有2个、8个、25个和9个;而通过质谱技术鉴定出29种蛋白质,其中包括能量代谢相关蛋白、增殖和凋亡相关蛋白、细胞骨架蛋白、信号传导蛋白、转录相关蛋白、免疫相关蛋白和其他功能蛋白质.本实验首次对鸡羽髓上皮细胞感染MDV后各时期蛋白表达水平的变化进行研究,鉴定了多种差异表达蛋白质,为进一步揭示MDV与宿主的相互关系、感染性病毒粒子的成熟和致病机制提供了依据.     

Immune responses against Marek's disease virus

It is more than a century since Marek's disease (MD) was first reported in chickens and since then there have been concerted efforts to better understand this disease, its causative agent and various approaches for control of this disease. Recently, there have been several outbreaks of the disease in various regions, due to the evolving nature of MD virus (MDV), which necessitates the implementation of improved prophylactic approaches. It is therefore essential to better understand the interactions between chickens and the virus. The chicken immune system is directly involved in controlling the entry and the spread of the virus. It employs two distinct but interrelated mechanisms to tackle viral invasion. Innate defense mechanisms comprise secretion of soluble factors as well as cells such as macrophages and natural killer cells as the first line of defense. These innate responses provide the adaptive arm of the immune system including antibody- and cell-mediated immune responses to be tailored more specifically against MDV. In addition to the immune system, genetic and epigenetic mechanisms contribute to the outcome of MDV infection in chickens. This review discusses our current understanding of immune responses elicited against MDV and genetic factors that contribute to the nature of the response.     

Rapid detection of Marek's disease virus in feather follicles by loop-mediated amplification

Marek's disease (MD) remains a serious problem in the production of poultry. The disease is caused by Marek's disease virus (MDV), and despite the ubiquitous use of vaccination to control losses, MD still affects poultry farming worldwide. The aim of this study was to develop a loop-mediated isothermal amplification (LAMP) method for the simple and inexpensive detection of MDV in feather tips of chickens. Two pairs of specific primers complementary to the meq oncogene of MDV were designed, targeting the sequence of the very virulent MDV strain, RB1B. Bst polymerase was used for the isothermal amplification of viral DNA at 65 C for 90 min in a water bath. The fluorescence signal was identified in MDV-positive samples after the addition of SYBR Green and ultraviolet (UV) illumination. The sensitivity of LAMP was 2 log 10 plaque-forming units (PFU)/ml of HPRS16 and 10(3) copies/il of plasmid containing the target gene (meq) and was equal in sensitivity to PCR amplification. Due to the use of three sets of primers, LAMP was highly specific for MDV-1 DNA. The developed LAMP technique is a rapid and simple tool for the specific detection of MDV in samples of feathers taken from live chickens. Since the use of thermocyclers is not necessary for LAMP assay, it can be conducted by small laboratories and even field veterinarians.     

Comparison of blood and feather pulp samples for the diagnosis of Marek's disease and for monitoring Marek's disease vaccination by real time-PCR

Comparison of blood and feather pulp (FP) samples for the diagnosis of Marek's disease (MD) and for monitoring Marek's diseases vaccination in chickens (serotypes 2 and 3 vaccines) by real time-PCR was evaluated. For diagnosis of MD, quantification of serotype 1 Marek's disease virus (MDV) DNA load was evaluated in 21 chickens suffering from MD. For each chicken, samples of blood and FP were collected and MDV DNA load was quantified. Solid tumors are the sample of choice for MD diagnosis by real time-PCR and, hence, 14 solid tumors were included in the study as positive controls. Load of MDV DNA in FP was equivalent to that detected in solid tumors (threshold cycle [Ct] ratio above 1.7). MDV DNA load in blood samples was lower than in solid tumors and FP samples. Nonetheless, there was a statistically significant correlation of the results obtained from FP and blood (r = 0.92). Results of the Pearson correlation test showed that Ct ratio values of 1.7 in FP correspond to Ct ratio values of 1.2 in peripheral blood. For monitoring vaccines, serotypes 2 and 3 MDV DNA load was evaluated in blood and FP samples of vaccinated chickens. Serotype 2 MDV DNA load was evaluated in samples of blood and FP from 34 chickens vaccinated with SB-1 strain. Serotype 3 MDV DNA load was evaluated in blood and FP samples from 53 chickens vaccinated with HVT strain. For both serotypes, frequency of positive samples and load of vaccine DNA was higher in FP than in blood samples. There was not a statistically significant correlation between the load of SB-1 DNA (r = 0.17) or HVT DNA (r = -0.04) in FP and blood. Our results show that the load of serotypes 1, 2, and 3 DNA is higher in FP than in blood. Diagnosis of MD could be done using both FP and blood samples. Monitoring of MD vaccination by real time-PCR required the use of FP samples. There were a high percentage of false negative samples when using blood to detect serotypes 2 and 3 MDV by real time-PCR.