鸡包涵体肝炎鸡胚肝细胞包涵体特性的研究

应用鸡包涵体肝炎病毒 FAV- Hb株试验感染 SPF鸡胚 ,通过透射电镜对感染鸡胚肝脏的观察 ,表明 FAV- Hb株可引起鸡胚肝细胞内形成三种类型的包涵体 ,即非病毒性中等电子密度包涵体 ,病毒性包涵体和非病毒性高电子密度包涵体 ,各型包涵体均可见于胞核或胞浆内 ,但胞核是包涵体首先形成的部位 ,核内包涵体通过核膜进入胞浆。各型包涵体在其形成过程中有较密切的关系。     

鸡包涵体肝炎及防治措施

<正>鸡包涵体肝炎是由禽腺病毒引起的鸡的一种急性传染病,主要特征是突然发病,迅速死亡,死亡率急升,肝脏肿胀、出血及肝细胞内出现核内包涵体,再生障碍性贫血。1963年美国学者首次报道了本病,目前本病已呈世界性分布。1病原本病的病毒为一种禽腺病毒,为双股DNA病毒,病毒粒子直径为70～90nm,无囊膜,二十面体对称结构,在核内复制可以产生嗜酸性和嗜碱性包涵体。病毒的血清型众多,已经被认定了的血清型有12种。     

血液B淋巴细胞在鸡包涵体肝炎病中变化规律的研究

包涵体肝炎(Inclusion B0dy Hepatitis，IBH)，又称贫血综合症(Anemia Syndrome)，是由禽腺病毒引起的鸡的一种急性传染病，主要侵害雏鸡，是危害养禽业发展的一种急性病毒性传染病。其特征为：病鸡死亡突然增多，严重贫血、黄疸，肝肿大有出血和坏死灶，肝细胞见有核内包涵体。其病理学特征勾坏死性肝炎，肝细胞核内出现嗜酸性或嗜碱性核内包涵体，临床表现为贫血、白色水样下痢。     

鸡包涵体肝炎的症状及其诊治措施

鸡包涵体肝炎是由禽腺病毒引起的一种急性传染病,病鸡死亡突然增多,严重贫血、黄疸、肝脏肿大出血和坏死灶,可见肝细胞核内有包涵体.该病又称贫血综合征.     

鸡包涵体肝炎的治疗

鸡包涵体肝炎是有禽腺病毒引起的鸡的一种急性传染病。以鸡群死亡突然增多,肝脏肿大出血、坏死灶,肝细胞核内包涵体为特征。今年夏季发病有上升趋势。     

肉鸡包涵体肝炎的诊断及防制

鸡包涵体肝炎是禽腺病毒引起鸡的一种急性传染病,禽腺病毒广泛存在于自然界,在许多国家都有鸡场污染或发病的报道。其特征为病鸡死亡突然增多,严重贫血、黄疸、肝肿大有出血和坏砸灶,肝细胞见有核内包涵体。     

鸡包涵体肝炎

鸡包涵体肝炎(IBH),又称传染性贫血、出血综合症。是由禽腺病毒属中的鸡腺病毒引起的一种急性传染病。其特征是幼鸡群死亡率突然增高,病鸡严重贫血,并迅速出现黄疸。剖检可见肝脏肿大、脂肪变性和出血等,肝细胞内出现核内包涵体。 一、历史分布及其危害 鸡包涵体肝炎,首次被Helmbolde和Fyaziex     

鸡包涵体肝炎的诊断与防治

鸡包涵体肝炎是由禽腺病毒引起鸡的急性传染病,以病鸡死亡突然增多,严重贫血、黄疸、肝脏重大出血和坏死灶,可见肝细胞核内有包涵体为特征。该病又称贫血综合征。1流行特点本病可发生水平和垂直传播,在自然感染时,病毒可通过消化道、呼吸道、眼结膜感染发病。     

鸡包涵体肝炎及其诊治

鸡包涵体肝炎是由禽腺病毒引起的鸡的一种急性传染病，以病鸡死亡突然增多，严重贫血、黄疸、肝脏重大出血和坏死灶，可见肝细胞核内有包涵体。1984年以后，我国通过血清学检查确定东北、华北、华南各地均有该病存在，山东省也不例外。有人从内蒙古某地分离到一株IBH病毒，经鉴定为禽腺病毒8型。     

吕梁地区肉鸡 包涵体肝炎的流行情况

鸡包涵体肝炎由腺病毒引起，以肝脏出血、严重贫血、黄疸、肌肉出血和死亡率突然增高，并在肝细胞中形成核内包涵体为特征，该病又称贫血综合征。最近，在吕梁地区肉鸡养殖场零星出现一种黄肝病，经诊断分析认为，目前流行的黄肝病中以包涵体肝炎多见。虽然主要是零星发病，但有的鸡群发病严重，现结合实践把本病的情况做个简介。     

Inclusion body hepatitis in broiler chickens in Iraq

Eighteen outbreaks of inclusion body hepatitis (IBH) were identified in broiler chickens in Baghdad in 1977 and 1978. The disease was seen mainly in 4-to-6-week-old broiler chickens. The mortality rate did not exceed 1% in any outbreak investigated. The most common gross findings were stellate or punctiform hemorrhagic areas in markedly fatty livers. Noticed in many cases were enlarged and pale kidneys, hemorrhagic lesions in the skeletal muscles, and pale fattened bone marrow. Histological examination of tissues revealed fat droplets and intranuclear inclusion bodies in degenerated liver cells. Eosinophilic inclusion bodies were seen in all cases. Only five cases had basophilic inclusions along with the eosinophilic ones. The etiologic agent was isolated on chorioallantoic membrane (CAM) of 12-day-old embryonated chicken eggs. The disease was produced experimentally in 4-week-old chicks using infected CAM suspension.     

Experimental induction of the cutaneous form of Marek's disease in broilers

Straight-run chickens of the Ross broiler hybrid were experimentally infected with the skin homogenates of sound broilers, broilers conditionally edible, and broilers confiscated for alternations in skin. The chickens infected with the homogenates of healthy skin were negative in the Marek's disease test. In 17% of the chickens infected with the skin from the conditionally edible broilers, macroscopically observable cutaneous lesions were induced and 60% of the infected chickens had microscopic changes in the skin; visceral organs were always affected by the infection. In the chickens infected with the skin of a confiscated bird, the long storage exerted its unfavourable effect and the infected birds were negative in the Marek's disease test. Our results indicate that the active form of Marek's disease was induced.     

H9亚型禽流感病毒感染鸡生理指标的分析

通过测定H9亚型禽流感发病鸡群及健康鸡群的某些生化指标,发现H9亚型禽流感疾病状态下皮质醇激素、甲状腺激素和血清钙的水平均与健康鸡群差异显著,而生长激素和血清磷无明显差异.这些变化是由于机体对疾病的抵抗或代谢紊乱产生的,可以作为疾病诊断的依据.     

Lesions in chickens with spontaneous or experimental infectious hepato-myelopoietic disease (inclusion body hepatitis) in Germany.

A group of 83 two-to-eighteen-week-old chickens with acute infectious hepato-myelopoietic disease (a German form of inclusion-body-hepatitis) were observed to have the following histologic lesions: panmyelophthisis, small foci of liver necrosis, often with intranuclear inclusion bodies in hepatocytes (15 to 20% of chickens), involution-like atrophy of the bursa of Fabricius and thymus, loss of lymphatic tissue in spleen and cecal tonsils, and nonpurulent myocarditis. In 18 survivors 6 to 8 weeks after clinical signs of disease, nonpurulent myocarditis but normal lymphatic organs and bone marrow were present. A group of 75 chickens were infected after hatching with the field isolant "1942." Between the 3rd and 9th weeks postinoculation the same histologic changes-though mostly milder-were demonstrated. This syndrome differs somewhat from the syndrome described as inclusion body hepatitis in America and Europe.     

Humoral and cell-mediated immune responses in chickens with infectious bursal disease

Primary and secondary immune responses to Newcastle disease virus (NDV) was evaluated in chickens infected with infectious bursal disease virus (IBDV) at one and 28 days of age. The geometric mean primary hemagglutination-inhibition antibody titers (GMT) of chickens infected with IBDV at one day of age was significantly lower (P less than or equal to 0.01) than those infected at 28 days of age. Infection with IBDV had no influence on secondary immune response to NDV. The effect of IBDV infection at one day of age on the cell-mediated immunity of chickens was evaluated by skin allograft acceptance or survival time. There was no significant difference between the percentage of grafts accepted in IBDV infected and noninfected control chickens. However, the mean graft survival time in the IBDV infected chickens was significantly longer (P less than or equal to 0.05) than those in the control group. This suggested a suppression of cell-mediated immunity due to IBDV infection.     

Comparison of disease susceptibility and subclass-specific antibody response in SC and FP chickens experimentally inoculated with Eimeria tenella, E. acervulina, or E. maxima

Susceptibility to disease and the subclass-specific antibody response to Eimeria tenella, E. acervulina, and E. maxima were compared in two inbred strains of chickens, FP (B15B21) and SC (B2B2). FP strain was more susceptible to coccidiosis than SC chickens based on oocyst production, lesion score, and clinical signs. FP chickens infected with E. tenella had more severe cecal lesions and a significantly lower hematocrit level than SC chickens. FP chickens infected with E. acervulina excreted five times as many oocysts at 6 days postinfection as SC and showed a 71% reduction in plasma carotenoid level compared with controls (56% reduction in SC chickens). Body-weight change did not correlate with other signs of disease. Both SC and FP chickens produced high levels of serum IgM and IgG and biliary IgA. Although SC chickens had a slightly higher antibody response than FP chickens at 7 days postinoculation, both strains maintained high levels of IgM, IgG, and IgA for a prolonged period post primary inoculation. Although SC and FP chickens show different disease susceptibility to coccidiosis, they demonstrate similar antibody response.     

Persistence of velogenic viscerotropic Newcastle disease virus in litter.

Litter in a room which had housed chickens and turkeys actively infected with velogenic viscerotropic Newcastle disease was no longer infectious for susceptible chickens placed there 10 to 14 days later.     

INTERACTION BETWEEN INFECTIOUS BURSAL DISEASE VIRUS AND NEWCASTLE DISEASE VIRUS IN CHICKENS

The Australian strain of infectious bursal disease virus (IBDV), 002/73, affected the response of chickens to Newcastle disease virus (NDV). The titre of serum antibodies to NDV in chickens infected with IBDV was significantly lower than that of birds infected with NDV alone. It also appeared that IBDV affected NDV excretion from chickens as NDV was more frequently isolated from chickens infected with IBDV, IBDV infection did not alter the pathogenicity of NDV in chickens. This Australian strain of IBDV therefore appeared to be immunodepressive in one-day-old chickens.     

Lack of interaction between avian leukosis virus subgroup J and fowl adenovirus (FAV) in FAV-antibody-positive chickens

Unfounded field speculation has suggested that avian leukosis virus subgroup J (ALV-J) predisposes young meat-type chickens to inclusion body hepatitis caused by fowl adenovirus (FAV). To address this hypothesis, we infected 1-day-old grandparent meat-type chickens carrying maternal antibodies against FAV with a field isolate of FAV associated with inclusion body hepatitis in broilers, ALV-J, or both FAV and ALV-J. We examined the effects of FAV alone or in combination with ALV-J on the basis of clinical signs, overall mortality, growth rate, and gross and microscopic lesions. With such criteria for evaluating possible interactions, we found no significant differences in the dually infected birds in comparison with chickens that received a monovalent challenge with either FAV or ALV-J.     

母鸡输卵管畸形发生原因的分析

某种鸡场一群艾维茵父母代种鸡中出现“假性母鸡”,剖检发现输卵管畸形。这批种鸡在17日龄时发生过某传染病。进行发病情况调查、对病死雏鸡的剖检和开产期病死母鸡的剖检、病料鸡胚感染和传代试验及新城疫病毒干扰试验。结果,鸡胚感染中第3代出现侏儒胚,干扰组的新城疫血凝价均低于20,对照组新城疫血凝价高于40。综合分析,可以判定该雏鸡在3周龄发生的疾病是鸡传染性支气管炎,以及可以确定该鸡群中不少鸡只出现输卵管畸形是由鸡传染性支气管炎病毒早期感染而引起的。