法氏囊在鸡淋巴细胞性白血病发生发展中的作用

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     

鸡淋巴细胞性自血病病毒和群特异性抗原（P27）在体内的分布与消长

应用生物素－亲和素法和电镜技术对接种鸡淋巴细胞性白血病病毒的实验鸡作了研究。结果：接种后１５ｄ的两只发病鸡雏骨髓中含有大量病毒抗原和群特异性抗原，ＢＡ阳性细胞主要是成髓细胞。接种后１个月一只实验鸡骨髓中形成成髓细胞性肿瘤结节，结节中成髓细胞ＢＡ弱阳性。接种两个月以后骨髓结构正常，各细胞群ＢＡ弱阳性。接种后１５ｄ法氏囊中即有病毒抗原和群特异性抗原，但主要是成髓细胞阳性。接种后２－５个月，法氏囊淋巴滤泡中一直存有病毒抗原和群特异性抗原，但以接毒后３－４个月时含量最高。接毒后６个月，法氏囊萎缩，结缔组织和成淋巴细胞ＢＡ弱阳性。电镜观察，在接毒后１－４个月的实验鸡法氏囊滤泡髓质巨噬细胞胞浆内和胞膜表面、网状细胞胞浆内和淋巴细胞之间观察到大量ＬＬ病毒粒子。根据ＢＡ法染色在法氏囊检出ＢＡ阳性细胞，或电镜在法氏囊检出大量ＬＬ病毒粒子。均可与ＭＤ相区别而建立ＬＬ病理学诊断。     

鸡实验性淋巴细胞性白血病的病理学研究

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。     

鸡实验性淋巴细胞性白血的病理学研究

给３５只１日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７批次的实验鸡做了病理学研究。结果：接毒后１５ｄ和１个月，部分实验鸡发生性细胞性白血病，主要表现为骨髓在髓细胞大量增生，或形成成髓细胞性肿瘤瘤结节，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淋巴细胞发生     

传染性法氏囊病病毒对法氏囊生长发育的影响

本试验运用传染性法氏囊病病毒变异 Ｅ 株，通过泄殖腔和鼻腔接种 １，８，１５，３０ 日龄雏鸡，通过尿囊腔接种８， １３，１８ 日龄鸡胚，全面而系统地观察了接毒后不同时间法氏囊的组织形态学变化，探讨了传染性法氏囊病病毒对胚胎发育时期和雏鸡发育时期法氏囊生长发育的影响。结果表明， Ｉ Ｂ Ｄ Ｖ 感染后１２～４８ ｈ，雏鸡法氏囊粘膜上皮细胞肿胀，坏死脱落，淋巴滤泡髓质部及皮质部淋巴细胞不同程度变性、坏死、排空，形成腺管样结构或囊状空泡： 接毒后７２～１４４ ｈ，法氏囊淋巴滤泡淋巴细胞坏死排空，淋巴滤泡萎缩，网状结缔组织大量增生，而胚胎发育时期，法氏囊粘膜上皮肿胀变性，法氏囊淋巴滤泡形成延迟或不完整，淋巴滤泡内淋巴细胞缺乏或空虚，说明传染性法氏囊病病毒变异 Ｅ 株对法氏囊造成严重的组织学危害，从而导致法氏囊生长发育阻滞，组织学形态和结构严重受损。     

传染性法氏囊病病毒（IBDV）人工感染SPF鸡的病理学观察

取３２０只３０～４０Ｈ龄ＳＰＦ鸡，经滴鼻和点眼接种传染性法氏囊病病毒（ＩＢＤＶ），接种后２４～７２ｈ出现死亡，病死率５１．２５％，死亡鸡剖检变化主要为法氏囊肿胀、出血，甚至呈紫葡萄样，脾脏肿大、出血，骨骼肌出血，腺胃肌胃交界处出血。病理组织学变化，呈现以法氏囊淋巴滤泡内髓质淋巴细胞坏死为主的特征性病变，并可在巨噬细胞浆内发现病毒包涵体。电镜观察，在法氏囊内淋巴细胞、异染性细胞、巨噬细胞浆内，见大量晶格状排列的病毒粒子和包涵体，表明ＩＢＤＶ首先损害法氏囊淋巴滤泡髓质内未成熟的Ｂ淋巴细胞，病毒在淋巴细胞内以包涵体方式增殖。     

应用生物素-亲和素法检测实验性传染性法氏囊病病鸡体内的病毒分布与消长

应用生物素—亲和素(BA)法检测实验性传染性法氏囊病(IBD)鸡,在法氏囊、脾脏、盲肠扁桃体、胸腺、肝脏、肺脏、肾脏和心脏均检出了阳性细胞,并证明鸡传染性法氏囊病病毒(IBDV)最早定位于法氏囊滤泡髓质区的淋巴细胞胞浆内并进行复制,法氏囊滤泡的淋巴细胞是IBDV的主要靶细胞.接毒后ld,法氏囊滤泡就见有许多病毒;2～3d.病毒数量激增并达到高峰;4～5d,病毒数量维持较高水平;6～7d,病毒数量显著减少.本实验结果表明,BA法可以作为IBD的特异诊断方法,法氏囊可作为检测本病的首选器官,在法氏囊滤泡的髓质检出阳性淋巴细胞、阳性异染性白细胞和阳性巨噬细胞,或主要检出阳性巨噬细胞,均可作为本病的特异性诊断指标.     

鸡实验性成髓细胞性白血病的细胞化学及超微结构

用鸡成髓细胞性白血病病毒（ＡＭＶ）ＢＡＪ－Ａ株鸡传代血浆毒感染１日龄伊莎鸡雏２０只，在接毒后１９￣２５ｄ于濒死期扑杀、采样，进行细胞化学和电镜检查。结果表明，肝、肾、法氏囊、胸腺及血液的成髓细胞来源于骨髓；其成髓细胞胞浆、胞膜及细胞间隙存在带有囊膜的含核心的病毒粒子。     

鸡淋巴细胞性白血病病毒和群特异性抗原（P^27）在体内的分布与消长

应用生物素－亲和素法和电镜技术对接种鸡淋巴细胞性白血病病毒的实验鸡作了研究。结果：接种后１５ｄ的两只发病鸡雏骨髓中含有大量病毒抗原和群特异性抗原，ＢＡ阳性细胞主要是成髓细胞。接种后１个月一只实验鸡骨髓中形成成髓细胞性肿瘤结节，结节中成髓细胞ＢＡ弱性。接种两个月以后骨髓结构正常，各细胞群ＢＡ弱阳性。接种后１５ｄ法氏囊中即有病毒抗原和群特异性抗原，但主要是成髓细胞阳性，接种后２￣５个月，法氏囊淋巴滤泡     

实验性新城疫雏鸡免疫器官的病理学研究

给２８日龄伊莎雏鸡人工接种新城疫病毒后，应用常规病理学检验、细胞化学和免疫组化技术对免疫器官的病理学变化作了研究。接毒１２ｈ，法氏囊滤泡的髓质、胸腺小叶的髓质、脾白髓、盲肠扁桃体的淋巴小结及弥散淋巴组织的部分淋巴细胞和网状细胞首先出现核浓缩、胞浆固缩等坏死变化。接毒１～３ｄ（潜伏期），骨髓、法氏囊滤泡、胸腺小叶、脾白髓和红髓、盲肠扁桃体粘膜层及弥散淋巴组织的淋巴细胞、巨噬细胞和网状细胞发生核浓缩、碎裂、胞浆固缩，强嗜酸性等坏死变化。接毒４～６ｄ死亡病例，这些免疫器官的淋巴组织散在呈蜂窝状空泡结构坏死灶（法氏囊为滤泡坏死），进一步崩解成无结构嗜酸性颗粒状物质。这些坏死变化可作为雏鸡新城疫诊断的根据。     

Importance of the medullary macrophage in the replication of lymphoid leukosis virus in the bursa of Fabricius of chickens

Electron microscopy and immunocytochemistry were used to study the development of lymphoid leukosis virus infection in the bursa of Fabricius of experimentally infected chicken embryos and chickens. In embryos infected at 7 days of incubation and killed 10 days later, virus particles and group-specific viral antigen were confined mainly to the connective tissue of the lamina propria of the bursal mucosal folds; a few developing follicles had discrete virions and group-specific antigen between cells. In chickens infected at 1 day of age, infection (as determined by use of electron microscopy and immunocytochemistry) was maximal in 1- to 4-month-old birds, and the greatest concentration of virus and group-specific viral antigen was in the medulla of the follicles. Although lymphoid leukosis virus was released from lymphocytes, epithelial cells, and macrophages, virus replication in the medullary macrophages was more active than that in the other cells. Normal medullary macrophages had cell membrane vesicles (50 to 80 nm in diameter) that covered part of all of the cell membrane surface. In infected chickens, virus particles frequently developed within these vesicles. Comparable vesicles were not found on cortical macrophages. Results of the present study indicated that the medullary macrophage was the principal host cell for replication of lymphoid leukosis virus in the bursa of Fabricius of the chicken.     

人工感染IBDV鸡法氏囊的电镜研究

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     

Prevention of avian lymphoid leukosis by induction of bursal atrophy with infectious bursal disease viruses.

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.     

Pathogenesis of duck plague in the bursa of Fabricius, thymus, and spleen.

White Pekin ducks were inoculated orally with duck plague virus and killed at 24-hour intervals after inoculation. Spleen, thymus, and bursa of Fabricius were collected and examined by light, fluorescent, and electron microscopy. Necrosis of lymphocytes occurred in the bursa of Fabricius, thymus, splenic periarteriolar lymphoid sheath (T lymphocytes), and splenic germinal centers (B lymphocytes). Viral nucleocapsids were present in the karyoplasm of lymphocytes, but these cells necrotized before virions were formed. Periarteriolar reticular sheath cells and sinusoidal lining cells in the spleen, epithelial cells in Hassall's corpuscle of the thymus, epithelial cells between the cortex and medulla of the follicles in the bursa of Fabricius, and macrophages in all 3 tissues contained nucleocapsids in the nuclei and virions in cytoplasmic vacuoles before necrosis occurred.     

雏鸡感染IBDV后法氏囊显微和超微结构的观察

运用光镜、电镜技术，观察了雏鸡实验感染传染性法氏囊病病毒（ＩＢＤＶ）后，其法氏囊显微和超微结构的动态变化。光镜观察表明，在感染早期，淋巴滤泡髓质部的淋巴细胞发生坏死，间质轻度水肿。感染后４ｄ，淋巴滤泡皮质内的毛细血管呈一典型的出血带环绕髓质，髓质部的淋巴细胞多已坏死、崩解。继之，整个淋巴滤泡呈网络状或囊状空泡。感染６ｄ以后，固有膜内的网状细胞和毛细血管大量增生，新的淋巴滤泡形成。电镜观察证明，在感染早期，淋巴细胞质内的内质网与核膜扩张，线粒体嵴紊乱或空泡化。继之，淋巴细胞核液化，细胞坏死、崩解。巨噬细胞和多核巨细胞大量出现，其胞浆内含有大量吞噬体和吞噬泡。     

Semen traits and fertility of White Leghorn males shown to be positive or negative for lymphoid leukosis virus in semen and feather pulp

1. Males from strains selected for high egg production (and other economic traits) and from unselected control strains were used to determine the frequency of shedding of lymphoid leukosis virus (LLV) into semen. The effect of the male's LLV status on semen production, fertility and hatchability was also examined in males of the unselected control strains. 2. The frequency of detection of exogenous LLV in semen by the phenotypic mixing test, and high concentrations of the viral group specific antigen in feather pulp by the complement fixation test, were both higher in control strains than in strains selected for high egg production. 3. Semen production was not reduced in LLV-shedding males. 4. Significant associations of LLV shedding with higher incidence of abnormal spermatozoa and reduced fertility were found in some populations but not in others. No significant effect of LLV shedding on hatchability was detected. 5. Tests for group specific antigen in feather pulp proved useful in identifying males that shed LLV in semen.     

鸡传染性法氏囊病超强毒感染后SPF鸡免疫器官病理学观察

IBDV超强毒株LX株接种2周龄SPF雏鸡后，其致病性不同于经典强毒株CJ801株，它主要引起接种鸡全身性炎症反应，法氏囊、脾脏、盲肠扁桃体等免疫器官中大量异嗜性白细胞、巨噬细胞浸润，淋巴细胞严重坏死崩解，胸腺皮质严重萎缩、坏死，骨髓中造血细胞减少、巨噬细胞和脂肪细胞增生。在接种后14d法氏囊淋巴滤泡严重萎缩、淋巴细胞排空形成囊腺样结构，未见恢复正常，其它免疫器官形态基本恢复正常。电镜观察，接种后2和4d可见胸腺淋巴细胞胞浆浓集、染色质周边化形成新月形，表现细胞凋亡特征；在法氏囊坏死淋巴细胞胞浆中可见60nm大小呈晶格排列或散在的病毒粒子。研究初步探明了鸡传染性法氏囊病病毒超强毒的致病机理。