牛传染性鼻气管炎的诊断和预防研究进展

牛传染性鼻气管炎是一种由牛传染性鼻气管炎病毒感染引起的牛呼吸道接触性传染病,临床多表现为呼吸道症状,同时伴有多器官的炎症,还会引起妊娠母牛流产.该病毒可以感染任何年龄、品种的牛,对犊牛的危害最大.随着现代化牧场的规模不断扩大、集约化程度日益增高,该病的发病率也在逐年上升,阻滞了奶牛业以及肉牛养殖业的健康发展.从牛传染性鼻气管炎的诊断方法和预防措施方面阐述近年来该病的研究进度,以期为牛传染性鼻气管炎疾病的诊断和预防提供参考.     

牛疱疹病毒1型检测技术及疫苗研究进展

牛传染性鼻气管炎(Infectious bovine rhinotracheitis,IBR)是由牛疱疹病毒I型(Bovine herpes virus-1,BHV-1)引起的牛的一种急性、热性、接触性传染病.该病毒的危害性在于病毒侵入牛机体后,潜伏在一些特定的部位,致使病毒持续性感染,病牛长期甚至终身带毒,给控制和消灭本病带来很大困难,给全球养牛业造成了重大经济损失.文章就BHV-1分子生物学、诊断及各类疫苗进行阐述,旨在为该病的进一步研究提供理论参考.     

青海省牛传染性鼻气管炎血清学调查

从青海省互助、玛多、海晏、玉树、贵德、德令哈、共和等14个地区采集420份牛血清样品,应用间接酶联免疫吸附试验(ELISA)调查了青海省牛传染性鼻气管炎病毒的感染情况。结果在420份被检牛血清样品中,共检出阳性血清样品200份,平均阳性率为47.62%(200/420)。     

鸡传染性喉气管炎的病理组织学观察

目的:通过鸡传染性喉气管炎病理组织学实验观察,发现鸡传染性喉气管炎在组织学上的病理变化,为该病引起的组织学病理变化和发病过程提供研究资料.方法:从疑似感染鸡传染性喉气管炎的病鸡中选取5只,运用实验室方法进行确诊,对其气管和喉结进行采样,制作石蜡切片,使用H.E.染色方法进行染色,并观察病理组织学变化.同时,使用5只健康鸡的相同部位做对照.结果:鸡感染传染性喉气管炎病毒后,气管和喉结组织结构有明显的脱落、肿大、膨胀情况,并伴有炎性侵润.喉结粘膜上皮细胞间变得疏松,破坏了原有腺体结构.     

牛传染性鼻气管炎病的研究进展

牛传染性鼻气管炎(Infectious bovine rhinotracheitis,IBR)又名牛疱疹病毒Ⅰ型(Bovine herpesvirus-1,BHV-1)感染症,是一种急性、热性、接触性传染病,以高热、呼吸困难、鼻炎、鼻窦炎、上呼吸道炎症和潜伏感染为主要特征。该病目前在世界范围内流行,除南美部分国家之外,世界各国都已分离到该病毒,在我国部分省市该病有蔓延趋势。文章主要针对该病的病原学、流行病学、诊断与防控进行了阐述,为认识和研究该病提供一定的理论参考。     

牛病毒性腹泻病毒(BVDV)E0蛋白原核表达及间接ELISA方法的建立

牛病毒性腹泻病毒(BVDV)能够引起牛羊的持续感染,临床上很难对其根除,建立该病有效检测方法对净化畜群具有重要意义。本研究构建BVDV E0蛋白基因重组表达载体在大肠杆菌中诱导表达,用重组的E0蛋白为包被抗原,确定抗原最佳包被浓度为5μg/mL,最佳血清稀释比为1∶10,最佳封闭液为5%脱脂奶粉,最佳封闭条件为37℃封闭2 h,酶标二抗稀释度为1∶5000,作用时间为30 min,样品临界值X+2S为0.278。该方法与IDEXX的BVDV间接ELISA试剂盒比较总符合率为86%,与口蹄疫病毒、牛支原体、牛传染性鼻气管炎病毒、牛副结核、牛布鲁氏菌病阳性血清无交叉反应。该检测方法能够用于BVDV抗体水平的临床检测,可为感染病畜的合理淘汰提供实验依据。     

鸡呼吸系统疾病的临床分析及防治对策研究

呼吸系统疾病是养鸡过程遇到的最常见，也是危害最严重的疾病之一。尤其是鸡新城疫、鸡传染性支气管炎、鸡传染性鼻炎、鸡传染性喉气管炎等几种呼吸系统病更为常见。     

鸡六种病毒多重PCR检测方法的建立和应用

禽流感(Avian influenza,AI)、鸡新城疫(Newcastle disease,ND)、鸡传染性支气管炎(Infectious bronchitis,IB)、鸡传染性喉气管炎(Infectious laryngotracheitis,ILT)、鸡传染性法氏囊病(Infectious bursal disease,IBD)和鸡减蛋综合症(Egg drop syndrome 76,EDS-76)是6种常见的禽类病毒性传染病,给养鸡业造成重大经济损失。依据NCBI核酸数据库中禽流感病毒(Aiv)、新城疫病毒(Ndv)、鸡传染性支气管炎病毒(Ibv)、传染性法氏囊病(Ibdv)、鸡传染性喉气管炎病毒(Iltv)及减蛋综合征病毒(Edsv)基因序列,设计了6对特异性引物,建立并优化针对鸡Aiv、Ndv、Ibv、Ibdv、Iltv和Edsv的多重PCR鉴别诊断方法,同时进行现场检测应用。结果显示该多重PCR体系检测限为100fg,与其他常见病原体无交叉反应。研究表明鸡六种病毒多重PCR方法具有较高敏感性与特异性,在禽类常见病毒现场诊断方面具有广阔的应用前景。     

高致病性禽流感防治政策法律知识问答

1．一类动物疫病包括哪些？ 一类动物疫病包括：口蹄疫、猪水疱病、猪瘟、非洲猪瘟、非洲马瘟、牛瘟、牛传染性胸膜肺炎（牛肺疫）、牛海绵状脑病（疯牛病）、痒病、蓝舌病、小反刍兽疫、绵羊痘和山羊痘、禽流行性感冒（高致病性禽流感）、鸡新城疫。     

为塑膜日光温室种植、养殖、沼气的开发利用提供技术服务

春季气候干燥，温差大，也是畜禽各类疾病易发的季节。常见一些畜群的上呼吸道疾病以及一些传染病的流行。如猪瘟、猪丹毒、猪肺疫、羊痘、羊肠毒血症、羊快疫、鸡新城疫、禽流感、鸡传染性支气管炎、喉气管炎等病。因此作好畜禽各种病的预防是广大养殖户的当务之急，根据不同病的流行特点，应采取以下预防措施：     

奶牛乳房炎的病因分析

对引起奶牛乳房炎的病原微生物，包括接触传染性病原菌和环境性病原菌的种类及症状做了阐述与分析。     

Infectious foot-and-mouth disease virus derived from a cloned full-length cDNA of OH／CHA／99

The China foot-and-mouth virus (FMDV) isolate OH/CHA/99 was isolated from swine, which was unable to infect bovine thyroid cells in vitro or to cause typical disease in bovines following intradermal inoculation in the tongue. To enhance antigenicity, replication, maturation and pathogenicity studies of OH/CHA/99, an infectious fulllength cDNA clone, designated pBIFMDV, was prepared. The in vitro and in vivo biological properties of the virus derived from pBIFMDV were studied by analyzing antigenicity, plaque morphology and virulence in pigs. The results showed that the virus derived from pBIFMDV had the same biological properties as the parent strain OH/CHA/99; the fulllength infections cDNA clone, pBIFMDV, will be very useful in studies of the antigenicity, virulence, pathogenesis, maturation and replication of FMDV.     

Transmissible and genetic prion diseases share a common pathway of neurodegeneration

Prion diseases can be infectious, sporadic and genetic. The infectious forms of these diseases, including bovine spongiform encephalopathy and Creutzfeldt-Jakob disease, are usually characterized by the accumulation in the brain of the transmissible pathogen, an abnormally folded isoform of the prion protein (PrP) termed PrPSc. However, certain inherited PrP mutations appear to cause neurodegeneration in the absence of PrPSc, working instead by favoured synthesis of CtmPrP, a transmembrane form of PrP. The relationship between the neurodegeneration seen in transmissible prion diseases involving PrPSc and that associated with ctmPrP has remained unclear. Here we find that the effectiveness of accumulated PrPSc in causing neurodegenerative disease depends upon the predilection of host-encoded PrP to be made in the ctmPrP form. Furthermore, the time course of PrPSc accumulation in transmissible prion disease is followed closely by increased generation of CtmPrP. Thus, the accumulation of PrPSc appears to modulate in trans the events involved in generating or metabolising CtmPrP. Together, these data suggest that the events of CtmPrP-mediated neurodegeneration may represent a common step in the pathogenesis of genetic and infectious prion diseases.     

The abundance threshold for plague as a critical percolation phenomenon

Percolation theory is most commonly associated with the slow flow of liquid through a porous medium, with applications to the physical sciences. Epidemiological applications have been anticipated for disease systems where the host is a plant or volume of soil, and hence is fixed in space. However, no natural examples have been reported. The central question of interest in percolation theory, the possibility of an infinite connected cluster, corresponds in infectious disease to a positive probability of an epidemic. Archived records of plague (infection with Yersinia pestis) in populations of great gerbils (Rhombomys opimus) in Kazakhstan have been used to show that epizootics only occur when more than about 0.33 of the burrow systems built by the host are occupied by family groups. The underlying mechanism for this abundance threshold is unknown. Here we present evidence that it is a percolation threshold, which arises from the difference in scale between the movements that transport infectious fleas between family groups and the vast size of contiguous landscapes colonized by gerbils. Conventional theory predicts that abundance thresholds for the spread of infectious disease arise when transmission between hosts is density dependent such that the basic reproduction number (R(0)) increases with abundance, attaining 1 at the threshold. Percolation thresholds, however, are separate, spatially explicit thresholds that indicate long-range connectivity in a system and do not coincide with R(0) = 1. Abundance thresholds are the theoretical basis for attempts to manage infectious disease by reducing the abundance of susceptibles, including vaccination and the culling of wildlife. This first natural example of a percolation threshold in a disease system invites a re-appraisal of other invasion thresholds, such as those for epidemic viral infections in African lions (Panthera leo), and of other disease systems such as bovine tuberculosis (caused by Mycobacterium bovis) in badgers (Meles meles).     

“疯牛病”与“疯人病”——蛋白粒与蛋白粒疾病

蛋白粒是一个不含核苷酸的蛋白性粒子,能够传染动物和人．引起大脑损伤及死亡．蛋白粒疾病包括羊瘙痒病、牛海绵体脑炎、人的克氏-约氏病、杰氏-斯氏-斯氏病以及致命性家族失眠症．本文从蛋白粒与人类和动物疾病的关系,回顾了蛋白粒疾病发生及传染的过程．具有不同氨基酸组成的蛋白粒,存在着可溶性的ＰｒＰC型及不溶性ＰｒＰＳＣ型．只有ＰｒＰＳＣ是传染性的．通过对蛋白粒结构与功能的剖析,讨论了蛋白粒的基因、蛋白粒的产生以及可能的致病机理（Ｘ蛋白被发现与细胞内蛋白粒增生有关）．最后,对蛋白质、ＤＮＡ和ＲＮＡ之间的遗传信息流提出了一个新的假说．     

Homozygous prion protein genotype predisposes to sporadic Creutzfeldt-Jakob disease.

The human prion diseases, Creutzfeldt-Jakob disease (CJD) and Gerstmann-Str?ussler syndrome (GSS), are neurodegenerative diseases that are unique in being both infectious and genetic. Transmission of both diseases and the animal spongiform encephalopathies (for example, scrapie and bovine spongiform encephalopathy) to experimental animals by intracerebral inoculation with brain homogenates is well documented. Despite their experimental transmissibility, missense and insertional mutations in the prion protein gene are associated with both GSS and familial CJD, demonstrating that the human familial cases are autosomal dominant diseases. More than 80% of CJD cases occur sporadically, however, and are not known to be associated with mutations. Here we report that 21 of 22 sporadic CJD cases and a further 19 of 23 suspected sporadic CJD cases are homozygous at the polymorphic amino-acid residue 129; 51% of the normal population are heterozygous at this site. We argue that homozygosity predisposes towards sporadic CJD and that this directly supports the hypothesis that interaction between prion protein molecules underlies the disease process.     

Monoclonal antibodies inhibit prion replication and delay the development of prion disease

Prion diseases such as Creutzfeldt-Jakob disease (CJD) are fatal, neuro-degenerative disorders with no known therapy. A proportion of the UK population has been exposed to a bovine spongiform encephalopathy-like prion strain and are at risk of developing variant CJD. A hallmark of prion disease is the transformation of normal cellular prion protein (PrP(C)) into an infectious disease-associated isoform, PrP(Sc). Recent in vitro studies indicate that anti-PrP monoclonal antibodies with little or no affinity for PrP(Sc) can prevent the incorporation of PrP(C) into propagating prions. We therefore investigated in a murine scrapie model whether anti-PrP monoclonal antibodies show similar inhibitory effects on prion replication in vivo. We found that peripheral PrP(Sc) levels and prion infectivity were markedly reduced, even when the antibodies were first administered at the point of near maximal accumulation of PrP(Sc) in the spleen. Furthermore, animals in which the treatment was continued remained healthy for over 300 days after equivalent untreated animals had succumbed to the disease. These findings indicate that immunotherapeutic strategies for human prion diseases are worth pursuing.