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1.
An indirect immunoperoxidase method was employed in the detection of the group specific antigen of avian leukosis virus in the oviduct, spleen, myocardium and bursae of Fabricius of chickens. In the magnum of the oviduct the group specific antigen was detected at the base and in the lumina of glands. In the spleen the group specific antigen was found in and around the arterioles, sheathed capillaries, and in the capsular tissue. In the myocardium the group specific antigen was present in the intercellular spaces and also in some myocardial cells. The bursa of Fabricius had concentrations of the group specific antigen in the medullary parts of follicles over the surface of large lymphoid cells. Absolute ethyl alcohol with acetone and modified Bouin's fluid were suitable as fixatives for preserving the group specific antigen in specimens embedded into low melting point paraffin.  相似文献   

2.
鸡实验性淋巴细胞性白血病的病理学研究   总被引:1,自引:0,他引:1  
给35只1日龄伊莎褐蛋母鸡雏腹腔接种淋巴细胞性白血病病毒RAV-1株,应用常规病理技术,对接毒后第15天、1、2、3、4、5、6个月7个批次的实验鸡做了病理学研究。结果:接毒后15d和1个月,部分实验鸡发生了成髓细胞性白血病,主要表现为骨髓成髓细胞大量增生,或形成成髓细胞性肿瘤结节,肝、心、肾、法氏囊等内脏器官出现成髓细胞聚集;接毒后2~6个月,实验鸡发生了淋巴细胞性白血病,主要表现为法氏囊髓质淋巴细胞发生转化,成淋巴细胞克隆增殖形成成淋巴细胞克隆增殖灶,在肝、心、肾、脾、腺胃等器官中形成成淋巴细胞性肿瘤结节。据此,可对鸡淋巴细胞性白血病做出病理组织学诊断。  相似文献   

3.
人工感染IBDV鸡法氏囊的电镜研究   总被引:7,自引:0,他引:7  
通过透射电镜系统观察了人工感染传染性法氏囊病病毒(IBDV)后鸡法氏囊各类细胞的病理变化。感染后12 ̄24h,病毒粒子主要见于髓质淋巴细胞中,细胞中可见到大量纤维样病毒发生基质及无囊膜包围的大型病毒晶格,细胞核染色质浓缩,核中出现纤维样结构。感染后36h,淋巴细胞开始大量裂解死亡。无囊膜包围的病毒晶格也出现于髓质网状细胞中,被感染的网状细胞并不裂解,而表现出细胞凋亡的特征:染色质固缩呈颗粒块状,胞  相似文献   

4.
Chicken embryos and healthy adult chickens naturally infected with lymphoid leukosis virus were used to investigate viral inclusion bodies in myocardial cells by light and electron microscopies and by immunocytochemical technique. Intracytoplasmic viral matrix inclusion bodies frequently appeared in the myocardium of adult chickens, but not in that of embryos. In light microscopic preparations, inclusions were irregularly distributed, were basophilic, and contained ribonucleic acid. Ultrastructurally, inclusions in myocardial cells were in areas containing numerous interstitial C-type particles. Early inclusions were composed of clusters of ribosomes associated with sarcoplasmic tubules; spherical bodies developed among these ribosomes. Mature inclusions were composed of numerous spherical bodies (50 to 75 nm) with interspersed ribosomes and of ribosomes clustered at the periphery. Inclusions were not membrane-enclosed. Occasionally, spherical bodies were in paracrystalline arrays. Multiple budding occurred on cell membranes adjacent to matrix inclusions. The viral group-specific protein, p27, was demonstrated by the peroxidase-antiperoxidase method and by the protein A-gold method in the spherical bodies, in nucleoids of mature virus particles, and among ribosomes of inclusions. The results indicate that the matrix inclusions were the result of lymphoid leukosis virus infection and were the product of viral protein synthesis on ribosomes.  相似文献   

5.
Ten-day-old chicken embryos were inoculated with isolates of myeloblastosis-associated virus that induced osteopetrosis of slow or rapid onset. Bursa of Fabricius, thymus, spleen, bone marrow, kidney, liver, and lung were examined at 15, 17, and 19 days in ovo and at 7 and 25 days after hatching by histologic and immunoperoxidase techniques. Tissues from 19-day-old in ovo embryos also were examined by electron microscopy. The lymphoid organs of embryos inoculated with all isolates manifested changes suggesting inhibited development. Virus was most often associated with macrophages, heterophils, and nonlymphoid stromal cells in these organs. Viral particles and antigen were abundant in tissues from embryos inoculated with slow-onset isolates, but cell necrosis was infrequent. The kidney and bursa had especially abundant viral particles and antigen. Conversely, viral particles and antigen were minimal in tissues from embryos inoculated with the rapid-onset isolate, yet intravascular cellular thrombi, substantial cell necrosis, and increased heterophils and hemocytoblasts were found.  相似文献   

6.
用鸡淋巴细胞性白血病病毒RAV-1株接种35只1日龄伊莎鸡雏,于接毒后不同批次扑杀,采取法氏囊做组织学、免疫细胞化学、透射电镜观察。结果:接毒后1个月,法氏囊滤泡髓质淋巴细胞开始转化,接毒后2~5个月更明显,在法氏囊滤泡髓质区形成淋巴细胞克隆增殖灶。接毒后6个月,法氏囊萎缩。BA法染色表明法氏囊一直存有病毒和群特异性抗原,以接毒后3~4个月含量最高。电镜观察,在接毒后1~4个月的实验鸡法氏囊滤泡髓质淋巴细胞、巨噬细胞和网状细胞中观察到LL病毒粒子。组织学、免疫细胞化学和电镜观察都表明法氏囊是该病毒的主要靶器官,法氏囊决定鸡淋巴细胞性白血病的发生发展。  相似文献   

7.
Intravenous inoculation of chickens with a waterfowl-origin type A influenza virus resulted in high titers of virus in kidney tissues and viral nucleoprotein in renal tubular epithelial cells and in intestinal mucosal epithelial cells. Virus titers in kidneys of four of eight clinically normal chickens sampled on days 3 and 5 postinoculation (PI), one dead chicken on day 3 PI, and one dead chicken on day 7 PI exceeded 10(6) mean embryo infectious dose per gram of tissue. Using immunofluorescent and immunoperoxidase staining, viral nucleoprotein was identified in the cytoplasm and nucleus of tubular epithelial cells in kidneys and in nucleus of mucosal epithelial cells lining villi in the lower small intestine. Based on the low intravenous pathogenicity index for this virus (0.3) along with the high virus titers in kidney tissues and localization of viral antigen in kidney important site for replication of avian influenza (AI) virus of low pathogenicity. Recovery of type A influenza viruses from cloacal swabs could result from viral replication in kidneys as well as in the lower intestine and/or the bursa of Fabricius.  相似文献   

8.
Five groups of genetically susceptible chickens were inoculated at hatching with lymphoid leukosis virus; four of these were given infectious bursal viruses of varying virulence at 14 days of age and one group was not inoculated (control). All chickens in the control group developed evidence of lymphoid leukosis by 180 days. Two groups given relatively virulent bursal disease viruses, which destroyed bursal lymphoid cells, did not develop lymphoid leukosis. Treatment with avirulent vaccines had no visible effect on bursal morphology and did not significantly alter the incidence of lymphoid leukosis in two other groups, although the time of development was delayed. Results of our study show that viral-induced destruction of the bursa of Fabricius eliminates the development of lymphoid leukosis but that infection without bursal destruction has little effect on lymphoid leukosis.  相似文献   

9.
Studies of reticuloendotheliosis virus-induced lymphomagenesis in chickens   总被引:1,自引:0,他引:1  
Seventy-three percent of chickens inoculated with the chick syncytial strain of reticuloendotheliosis virus (REV) at hatching developed lymphomas by 39 weeks of age. Neonatal treatment with cyclophosphamide or surgical bursectomy at 2, 4, 8, or 12 weeks of age significantly (P less than 0.01) reduced lymphoma development. In a further experiment, surgical bursectomy of REV-infected chickens followed by intravenous inoculation of the chickens with a single cell suspension of their own bursa cells at 2, 4, 9, or 13 weeks of age resulted in lymphoid tumors in chickens treated at 9 or 13 weeks but not in chickens treated at 2 or 4 weeks of age. Furthermore, this treatment did not shorten the incubation period for lymphoma development. These findings argue very strongly that transforming target cells are primarily in the bursa of Fabricius. The data also suggest that a minimum residency of 4 weeks in the bursa is required for infected bursa cells to become transformed. Therefore, lymphomagenesis induced by REV in chickens appears similar to that induced by the avian leukosis virus group.  相似文献   

10.
The aim of the present study was to evaluate the presence of lymphocytes and granulocytes in different stages of embryonic development and on the first posthatching day. The lymphocytes present in the bursa of Fabricius and thymus were evaluated by histological analysis of the yolk sac, bursa of Fabricius, thymus, liver and bone marrow of 100 chicken embryos divided into groups and treated with: (I) Marek's disease vaccine as viral antigen, (II) Marek's disease vaccine plus lymphokines, (III) lymphokines, and (IV) vaccine diluent. Group V was not treated. Samples were taken on days 14, 17 and 20 of incubation and on the first posthatching day. An increase in the number of epithelial matrix as precursors of lymphoid follicles was observed in the bursa of Fabricius of embryos inoculated with lymphokines compared to embryos in all the other groups (p < 0.05). In addition, a higher amount of granulocytes was found in the yolk sac and liver of embryos inoculated with lymphokines than in the embryos of all other groups (p < 0.05). In the bone marrow, no significant difference was observed among the treated groups concerning the amount of granulocytes. The results suggest that administration of antigens or protein molecules at an early stage of embryonic development increases the presence of granulocytes in the liver and granulopoiesis in the yolk sac, and also increases the number of epithelial matrixs in the bursa of Fabricius.  相似文献   

11.
应用组织病理学和电子显微镜技术对以传染性法氏囊病病毒不同毒株人工感染后不同感染时间鸡的法氏囊、肾脏、脾脏进行了检查。结果显示:法氏囊淋巴滤泡髓质首先被破坏,滤泡之间水肿,整个淋巴滤泡前B淋巴细胞崩解、坏死,网状细胞和巨噬细胞增生。72小时后,几乎见不到前B淋巴细胞。168小时法氏囊萎缩,上皮增生。脾脏和肾脏仅出现轻微变化。超微结构变化特征是淋巴样组织坏死,法氏囊组织中的前B淋巴细胞、巨噬细胞和网状细胞内有大量约60nm的病毒颗粒,呈结晶状排列,有的细胞中可见到多个病毒结晶体。  相似文献   

12.
法氏囊在鸡淋巴细胞性白血病发生发展中的作用   总被引:3,自引:1,他引:2  
用鸡淋巴细胞性白血病病毒RAV-1株接种35只1日龄伊莎鸡雏,于接毒后不同批次扑杀,采取法氏囊做组织学、免疫细胞化学、透射电镜观察。结果:接毒后1个月,法氏囊滤泡髓质淋巴细胞开始转化,接毒后2~5个月更明显,在法氏囊滤泡髓质区形成成淋巴细胞克隆增殖灶。接毒后6个月,法氏囊萎缩。生物素-亲和素(BA)法染色表明法氏囊一直存有病毒和群特异性抗原,以接毒后3~4个月含量最高。电镜观察,在接毒后1~4个月的实验鸡法氏囊滤泡髓质淋巴细胞、巨噬细胞和网状细胞中观察到淋巴细胞性白血病(LL)病毒粒子。组织学、免疫细胞化学和电镜观察都表明法氏囊是该病的主要靶器官之一,法氏囊在鸡淋巴细胞性白血病的发生发展中起一定的作用  相似文献   

13.
试验旨在探讨不同来源的传染性支气管炎病毒(Infectious bronchitis virus,IBV)诱导SPF鸡发病的免疫机制。选用140只1日龄SPF白来航鸡,随机分为4组,3组攻毒组通过滴鼻点眼途径分别接种鸡源IBV强毒株、鸡源IBV弱毒株和野鸡源IBV毒株3个毒株,对照组以同种方式接种等量灭菌的磷酸盐缓冲液。在感染后12 h、36 h、72 h、7 d和14 d,每组随机选取5只进行剖检,并分别采集法氏囊、肾脏和气管组织,剩余鸡用于观察临床症状、发病及死亡情况。应用实时荧光定量PCR检测攻毒后不同时间点采集的各组织中IBV的病毒载量、Toll样受体(Toll-like receptors,TLRs)及部分细胞因子(白细胞介素(interleukin,IL)和干扰素(interferon,IFN))表达量的变化。结果显示,感染不同来源IBV毒株之后仅鸡源IBV强毒株感染组SPF鸡出现抑郁、翅膀下垂、甩头等典型的临床症状,且在感染后5~10 d共有7只死亡,死亡率为20%。病理剖检发现,感染鸡源IBV强毒株的鸡肾脏肿大、尿酸盐沉积和有花斑样病变,而感染野鸡源IBV毒株、鸡源IBV弱毒株和对照组的鸡无明显的眼观病变。实时荧光定量PCR结果显示,在鸡源IBV强毒株组的法氏囊、肾脏和气管3个组织中均检测到病毒。对照组和野鸡源IBV毒株组中均未检测到病毒,鸡源IBV弱毒株组只在部分组织中检测到病毒。在感染后72 h,鸡源IBV强毒株组与其他各组相比,TLR1、TLR2、TLR3、TLR5、TLR7和TLR15基因在法氏囊中的表达量均显著升高(P<0.05),IL-6和IFN-β参与更强烈的抗病毒免疫反应;在感染后7 d,鸡源IBV弱毒株组与其他各组相比,肾脏中TLR2、TLR3、TLR15、TLR21、IL-6和IL-18基因表达量均显著升高(P<0.05)。野鸡源IBV感染后36 h法氏囊组织中IFN-γ基因表达量显著上调(P<0.05)。综上所述,3个IBV毒株中仅鸡源IBV强毒感染引起SPF鸡典型临床发病症状与可视组织病变,且可提高SPF鸡组织中免疫相关因子的基因表达量。本研究结果揭示,不同来源的IBV对SPF鸡的不同致病性与其感染诱导的免疫反应不同有关。  相似文献   

14.
Specific-pathogen-free white leghorn chickens were inoculated at 1 day of age with avian leukosis virus (ALV, RAV-1). All chickens in Expt. 1, killed 33 or 64 days postinoculation, had focal chronic lymphocytic or lymphoplasmacytic myocarditis. Among those held beyond 33 days, eight of 22 developed lesions in the myocardium that resulted in a chronic circulatory syndrome (CCS) typical of right-sided heart failure. Chickens in Expt. 2 were held for 210 days, and 21% of 125 developed CCS. In Expt. 2, ALV particles were found by electron microscopy in myocardium of 100%, 72%, and 89% of inoculated chickens that developed CCS, lymphoid leukosis, or that had no gross lesions, respectively. These findings were in accord with the immunoperoxidase staining of tissue sections for group-specific antigen of ALV. In areas of extensive virus replication, there were often abnormal virus particles and also round bodies, which may have been remnants of host-cell membranes formed in the budding process. In contrast to findings in hearts, the spleens were usually negative for virus and viral antigen.  相似文献   

15.
The pathogenesis of 4 isolates of turkey-origin reovirus (NC/SEP-R44/03, NC/98, TX/98, and NC/85) and 1 chicken-origin reovirus (1733) was examined by infecting specific pathogen free (SPF) poults. These turkey-origin reovirus (TRV) isolates were collected from turkey flocks experiencing poult enteritis and are genetically distinct from previously reported avian reoviruses. Microscopic examination of the tissues collected from the TRV-infected poults revealed different degrees of bursal atrophy characterized by lymphoid depletion and increased fibroplasia between the bursal follicles. To understand the relationship between virus spread and replication, and the induction of lesions, immunohistochemical staining (IHC) for viral antigen, in situ hybridization (ISH) for the detection of viral RNA, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay for the detection of apoptosis in affected tissues was performed. Both IHC and ISH revealed viral antigen and RNA in the surface epithelial cells of the bursa, in macrophages in the interstitium of the bursa and, to lesser degree, in splenic red pulp macrophages and intestinal epithelial cells. Increased apoptosis of bursal lymphocytes and macrophages was observed at 2 and 5 days postinoculation. No lesions were found in tissues from poults inoculated with the virulent chicken-origin strain, however viral antigen was detected in the bursa and the intestine. Although all TRVs studied displayed similar tissue tropism, there were substantial differences in the severity of the lesions produced. Poults inoculated with NC/SEP-R44/03 or NC/98 had moderate to severe bursal atrophy, whereas poults inoculated with TX/98 or NC/85 presented a mild to moderate bursal lymphoid depletion. The lymphoid depletion observed in the bursa appears to be the effect of an indirectly induced apoptosis and would most likely result in immune dysfunction in poults infected with TRV.  相似文献   

16.
On tissues from naturally infected non-Aleutian mink an immunohistological study was performed using monoclonal antibodies and the immunoperoxidase method. Structural proteins of ADV were demonstrated in cryosections and in ethanol-fixed and paraffin-embedded material which provide antigen detection in a similar amount together with good histological structure. In lymphoid organs viral antigen was restricted to B-cell areas, particularly lymphoid follicles. The pattern of antigen distribution was typical for follicular dendritic cells which are capable to retain immune complexes. Beside macrophages in the interior of lymphoid follicles most likely proliferating B-lymphoblasts reveal nuclear and cytoplasmatic presence of structural proteins indicating viral replication. Cells of the mononuclear phagocyte system such as cells of lymphatic sinuses and hepatic Kupffer cells harbor viral protein in the cytoplasm, probably resulting from phagocytosis of immune complexes. Renal glomeruli were consistently negative for virus antigen whereas in interstitial infiltrates cells resembling macrophages stained positive for ADV structural proteins.  相似文献   

17.
Abdel-Alim GA  Saif YM 《Avian diseases》2002,46(4):1001-1006
The pathogenicity of serotype 2 OH strain of infectious bursal disease virus (IBDV) to specific-pathogen-free (SPF) chicken embryos and 2-wk-old SPF chickens and turkey poults was investigated. The virus was pathogenic for chicken embryos after five passages as evidenced by pathologic changes in inoculated embryos. The embryo-adapted virus was not pathogenic for 2-wk-old SPF chickens and turkey poults as indicated by lack of clinical signs, gross or microscopic lesions in the bursa of Fabricius of inoculated birds. Bursa-to-body-weight ratios of the inoculated chickens and turkey poults were not significantly different from those of uninoculated controls. Virus-neutralizing antibodies to serotype 2 IBDV were detected in inoculated chickens and turkeys. Results of this study indicated that the embryo-adapted serotype 2 OH IBDV isolate that is pathogenic for chicken embryos is infectious but not pathogenic in chickens and turkeys.  相似文献   

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20.
传染性法氏囊病病毒(IBDV)为dsRNA病毒,可造成雏鸡法氏囊损伤进而发生免疫抑制;MDA5是能够特异性识别dsRNA病毒的模式识别受体。为研究鸡MDA5(chMDA5)信号通路在IBDV致雏鸡法氏囊病理损伤中的作用,试验选取50只14日龄SPF雏鸡随机分为IBDV感染组和空白对照组,每组25只,IBDV感染组雏鸡通过点眼、滴鼻感染IBDV JIC7株病毒液,0.6 mL·只-1,空白对照组雏鸡经相同途径给予相同剂量无菌PBS,感染IBDV后第1、4、7、21及35天采集雏鸡法氏囊。采用qRT-PCR方法检测法氏囊中IBDV载量,chMDA5及chMDA5信号通路衔接蛋白(chIPS-1)、转录因子(chIRF3和chNF-κB)、下游产物细胞因子(chIFN-βchTNF-αchIL-1βchIL-6) mRNA水平变化;间接免疫荧光法检测chMDA5蛋白表达变化,传统病理学方法检查法氏囊病理组织学变化。结果发现,雏鸡感染IBDV后,其法氏囊中chMDA5、chIPS-1、chIRF3、chNF-κBchIFN-βchTNF-αchIL-1βchIL-6的表达量均显著高于对照组,且法氏囊组织发生形态损伤,上述变化趋势与IBDV载量变化基本一致。结果表明,雏鸡法氏囊chMDA5及其信号转导通路可被IBDV激活,参与到IBDV感染雏鸡法氏囊损伤与抗损伤过程中。  相似文献   

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