鸡包涵体肝炎诊断报告

1988年春,某县一些专业户饲养的雏鸡发生一种以衰弱,肝脏大出血、边缘有散在性小坏死灶为特征的疫病。经调查和实验室检查初步诊断为鸡包涵体肝炎(IBH),现报告如下。     

鸡包涵体肝炎

鸡◇包◇涵◇体◇肝◇炎胡维华刘聚祥（河北农业大学动物科技学院，保定０７１００１）包涵体肝炎（ＩｎｃｌｕｓｉｏｎＢｏｄｙＨｅｐａｔｉｔｉｓ，ＩＢＨ）是由禽腺病毒（Ｆｏｗｌａｄｅｎｏｖｉｒｕｓ）引起的以肝脏受害为主，并在肝细胞中形成核内包涵体为特征的传染...     

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。     

某鸡场暴发鸡包涵体肝炎的诊断

1992年2月间,沈阳市某鸡场雏鸡暴发贫血病,发病率为15.4%(185/1200),死亡率为5%(60/1200)。剖检贫血病鸡可见骨髓呈黄白色,胸腺出血但萎缩不明显。以后又在6个鸡场暴发了相似的贫血病。但根据流行病学、临床症状、病理变化、细胞培养、人工感染发病试验和血清学试验诊断为鸡包涵体肝炎(IBH)。报道如下。     

鸡包涵体肝炎的临床诊断与防治

鸡包涵体肝炎是由腺病毒感染所引起的以肝脏脂肪变性与灶性坏死及肝细胞内出现包涵体为主要特征,再生障碍性贫血,呼吸道感染,出血性肠炎和产蛋量减少。给生产带来一定损失。     

鸽包涵体肝炎的病理组织学观察

鸽包涵体肝炎的病理组织学观察周接水编译吴辛校鸽包涵体肝炎由疱疹病毒和腺病毒感染引起，我国报道的鸽包涵体肝炎全部由腺病毒感染所致。本文对１９９３～１９９４年关东地区鸽的包涵体肝炎，进行了病理学检查和电子显微镜检查，并用鸟腺病毒抗原进行了免疫组织化学检查...     

鸡包涵体肝炎病毒CELOV 株的鉴定研究

采用鸡胚有限稀释法将鸡包涵体肝炎病毒（CELOV）纯化。将纯化的CELOV在SPF鸡胚上连续传10代,对各代次的毒种均进行毒价测定,并选择不同代次进行外源病毒、抗原性等方面的系统鉴定。结果表明,不同代次的病毒毒价稳定,病毒纯净、特异,无外源病毒感染。采用不同代次病毒鸡胚尿囊液制备3批琼脂扩散试验抗原敏感、特异,用原倍、2倍稀释的抗原可以与32倍稀释的阳性血清反应,出现清晰的沉淀线。抗原不与其它病原体的阳性血清反应。用CELOV制备的琼扩抗原可用于鸡包涵体肝炎病毒感染的血清学检测。     

主动脉弓狭窄小鼠心脏的病理形态学观察

利用B超观察主动脉弓狭窄(transverse aortic constriction,TAC)小鼠心脏随着手术时间的延长所发生的动态变化,探索如何利用病理学方法判断心脏肥厚性改变。以微创手术小鼠TAC模型为研究对象,同步采集不同时间点动物心脏进行B超和组织切片观察,通过心脏B超找出针对该模型动物心脏肥厚的病理学诊断方法。结果显示:病理切片采集的室间隔、左心室厚度与B超采集的相应指标,不具有相关性;而室间隔/右室壁厚度比与B超采集的室间隔、左心室厚度具有明确的相关性,随着手术后时间的延长,心肌细胞也逐渐增大。结果表明:小鼠在接受微创主动脉狭窄手术后,单独B超检查就可以准确地发现心肌肥厚性的改变,而从病理组织学观察来看,单纯的左心室厚度不能作为心肌肥厚的标准,而通过室间隔/右室壁厚度比,以及心肌细胞的大小,可以更准确的反应心肌的肥厚性改变。     

病毒性包涵体肝炎

IBH是一种由腺病毒引起的传染疾病,其特征为病鸡的肝脏和肾脏出血,出现营养不良性渐进性坏死,并伴有核内包涵体。特征性肉眼病变是肝脏肿大、营养不良,呈黄色,质地易碎（图1）。     

鸡包涵体肝炎病毒DNA探针的制备及其原位杂交的应用

用限制酶HirdⅢ和Ecorl双切鸡包涵体肝炎六邻体蛋白基因片段重组质粒，得到大小636bp的基因片段，用地高辛标记制备DNA探针，其灵敏度为0．1～0．3ng／μL。用该探针对感染鸡包涵体肝炎病毒的雏鸡肝组织进行原位杂交，结果表明病毒经口感染后12h肝细胞内出现病毒的复制，3～7d时病毒复制明显，9～16d病毒复制减弱。原位杂交表明鸡包涵体肝炎病毒主要定位于核内，同时也可进入胞浆中。地高辛标记鸡包涵体肝炎病毒DNA探针对检测该病毒DNA的灵敏度高，特异性强，操作方便，该探针可用于本病的分子病理学研究和特异性诊断。     

Vertical induction of the inclusion body hepatitis/hydropericardium syndrome with fowl adenovirus and chicken anemia virus

The hypothesis that fowl adenovirus (FAV) and chicken anemia virus (CAV), transmitted vertically and simultaneously, induce the inclusion body hepatitis (IBH)/hydropericardium (HP) syndrome in progeny chickens was tested. Thus, 35-wk-old light brown layer breeders, showing absence of antibodies against FAV and variable titers against CAV, were intramuscularly singly infected with the FAV serotype 4 isolate 341 or dually infected with CAV (isolate 10343) and FAV. All hens (groups A [FAV alone], B [FAV + CAV], and C [noninfected]) were clinically healthy throughout the experimental period. Both infectious viruses FAV and CAV were isolated from progenies obtained as early as 5 days after infection of their breeders. Hematocrit, serum proteins, and aspartate-aminotransferase values showed a few statistical differences between the progeny groups. Most of these differences were detected in the progeny chickens of group B. However, almost all values met reference values for the species. The pathologic findings showed that progeny chickens obtained from both singly and dually infected breeders developed macroscopic and histopathologic changes of IBH/HP. The pathologic findings shown by progeny chickens of group A (FAV) were not expected because neither synergism nor prior immunodepression by CAV was concurrent. Chickens of group B (CAV + FAV) also developed IBH/HP. Although not many differences in the evaluated parameters between groups A and B were statistically significant, most pathologic findings of group B indicated a more severe manifestation of the disease. However, because FAV alone did reproduce the syndrome, the results shown by group B would not allow a definitive confirmation of the hypothesis that the association of FAV and CAV is necessary for the successful induction of the IBH/HP syndrome in chickens when transmitted vertically.     

鸡包涵体肝炎肿瘤坏死因子α的动态变化与病变相关性的研究

应用FAV-Hb株试验感染1日龄SPF雏鸡,感染后分别于第1、2、3、4、5、7、10、13、16、21、26、31、36、41、46、51、56d扑杀,采外周血和脾脏,通过微量细胞病变法经L929细胞测定其TNFα活性,并对肝脏、脾脏、胸腺、法氏囊和盲肠扁桃体做病理学检查.结果表明FAV-Hb感染后第3 d在外周血开始测出TNFα活性,以后逐渐上升,第4 d达到小的峰值,随后下降,第13 d基本消失,并持续到第16 d,从21 dTNFα活性又开始回升,第46 d时达到最高峰,以后缓慢下降.感染鸡脾脏TNFα活性的变化规律与外周血基本一致,感染后第2 d起在脾脏测出少量TNFα,第7 d出现小峰值,以后下降到基本消失,从第21 d起重新测出TNFα,并逐渐上升,在36 d到56 d持续在较高的水平.病理组织学观察证实,FAV-Hb感染后,除肝脏和淋巴组织的损伤性变化外,从第1 d到第56 d,感染雏鸡肝脏的窦壁细胞,脾脏、胸腺、法氏囊和盲肠扁桃体的网状细胞表现出不同程度的活化增生,其增生程度与外周血和脾脏TNFα活性基本一致.鸡包涵体肝炎肿瘤坏死因子α动态变化的研究表明,FAV-Hb感染后,雏鸡体内TNFα的消长规律与病变的发生发展有较明显的相关性.     

鸡包涵体肝炎病毒荧光定量PCR滴度测定方法的建立及与不同滴定方法间的比较

本试验根据Gen Bank中I群禽腺病毒(FAV-Ⅰ)代表株AAU46933(CELO株)的Hexon基因序列设计一对通用引物,摸索了合适的扩增条件,建立了SYBR Green I荧光定量PCR方法,并对9株鸡包涵体肝炎毒株的病毒滴度进行了测定,并与OD260法、鸡胚病变法以及细胞病变法测定的结果进行比较。试验结果表明,本方法的检测下限为0.98×102拷贝/μL。以细胞病变法为标准测定方法,经统计学分析发现,鸡胚病变法与细胞病变法之间无统计学差异(P=0.591);荧光定量PCR法与细胞病变法测得结果之间存在线性相关性(相关系数r=0.965,P0.05);OD260法与细胞病变法测得的结果间无相关性(P0.05)。以上结果说明,荧光定量PCR法测定结果能够间接反映病毒感染力,与传统方法相比,该方法操作简单、耗时短、成本低,具有较高的应用价值。     

Psittacine inclusion body hepatitis in an aviary

Psittacine inclusion body hepatitis (also known as Pacheco's parrot disease) was believed to be responsible for fatal necrotizing hepatitis and splenitis in a variety of psittacine birds from a private aviary. Splenic cells and degenerative hepatocytes around the outer zone of necrotic areas had margination of nuclear material and large intranuclear inclusion bodies. Clinical signs consisted of weakness, anorexia, vomiting, loose feces, and slight ruffling of feathers. The source of the infection was undetermined, but could have been associated with 3 Patagonian conures within the aviary. Patagonian conures are well-recognized as clinically normal carriers. The outbreak was limited by strict quarantine and disinfection of the aviary for 14 days.     

Prevention of inclusion body hepatitis/hydropericardium syndrome in progeny chickens by vaccination of breeders with fowl adenovirus and chicken anemia virus

The hypothesis that an effective protection of progeny chickens against inclusion body hepatitis/hydropericardium syndrome (IBH/HP) can be achieved by dual vaccination of breeders with fowl adenovirus (FAV) serotype 4 and chicken anemia virus (CAV) was tested. Thus, 17-wk-old brown leghorn pullet groups were vaccinated by different schemes including single FAV (inactivated), single CAV (attenuated), FAV and CAV dually, or were not vaccinated (controls). Subsequent progenies of these breeders were challenged with the virulent strains FAV-341 and CAV-10343 following three strategies: 1) FAV-341 intramuscularly (i.m.) at day 10 of age (only FAV-vaccinated and control progenies); 2) FAV + CAV i.m. simultaneously at day 10 of age (all progenies); 3) CAV i.m. at day 1 and FAV orally at day 10 of age (all progenies). The induction of IBH/HP in these progenies was evaluated throughout a 10-day period. Both breeder groups vaccinated against FAV and those vaccinated against CAV increased virus neutralizing specific antibodies. Challenge strategy 1 showed 26.6% mortality in control progeny chickens and 13.3% in the progeny of FAV-vaccinated breeders. Presence of lesions in the liver of these groups showed no significant differences (P > 0.05), suggesting a discreet protective effect of the vaccine. Challenge strategy 2 showed 29.4% mortality in controls and 94% of chickens showed hepatic inclusion bodies (HIB). Single CAV vaccination of breeders did not demonstrate a beneficial effect, with both mortality and liver lesions resembling the nonvaccinated controls. FAV vaccination of breeders significantly reduced both mortality (7.4%) and liver lesions (26% HIB) (P < 0.05), providing protection against this challenge strategy. Dual vaccination of breeders with FAV and CAV proved to be necessary to achieve maximum protection of the progeny (no mortality and 7% HIB). Challenge strategy 3 produced no mortality but consistent liver damage in controls (96% HIB). In this case, both CAV and FAV + CAV-vaccinated breeders showed best protection results in terms of liver histopathology (8% and 0% HIB, respectively). FAV vaccination alone produced 24% HIB, similar to challenge strategy 2, demonstrating a lower protective effect.     

A primary epidemic of inclusion body hepatitis in broilers

Inclusion body hepatitis (IBH) was diagnosed in 15 broiler flocks supplied by one breeder in the South Island of New Zealand. The affected flocks suffered mortality up to 30%. Malaise and slightly increased mortality were noticed by growers from about day 12 post-hatch; mortality peaked in the fourth week, and, in most flocks, declined to normally accepted levels from day 33 on. Gross signs seen at necropsy usually included bone-marrow aplasia, atrophy of the bursa of Fabricius and the thymus, and swollen hemorrhagic livers with focal necrosis. Jaundice was seen in many surviving birds. In some flocks, there was also proventricular hemorrhage, mild tracheitis, and airsacculitis. Downgrading and condemnation rates were increased in all flocks. Eosinophilic intranuclear inclusion bodies were seen in hepatocytes of some affected birds. An adenovirus was isolated from a number of cases investigated. The disease in broilers was preceded by production drops associated with feed refusal and increased mortality in the breeder stock.