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。     

鹅源新城疫病毒感染鸡的临诊症状及病理变化

用鹅源新城疫病毒BY株人工感染25日龄雏鸡，同时用鸡新城疫病毒标准强毒F48E8株作为攻毒对照，观察2株病毒感染鸡的临诊症状、病理变化，并加以比较。结果，2株病毒都可致试验鸡100％发病和死亡。BY组鸡于感染后51h出现症状，发病后48h全部死亡，主要大体病变为喉头严重出血、腺胃乳头或腺胃与肌胃交界处轻微出血、肠道黏膜局灶性出血坏死，病理组织学变化主要为消化器官和免疫器官内的细胞显著变性、坏死及出血等；F48E8组鸡于感染后72h出现症状，发病后36h感染鸡全部死亡，所表现的病理变化与BY组鸡相似，但腺胃和肠道的出血病变比BY组鸡显著。     

鸡传染性法氏囊病对鸡法氏囊和腺胃组织结构的影响

为了阐明鸡传染性法氏囊病对鸡法氏囊和腺胃组织结构的影响,以感染传染性法氏囊病的鸡的法氏囊和腺胃为供试材料,采用常规石蜡切片法制片,HE染色,显微镜下观察、拍照,对其进行病理组织学研究.主要病理组织学变化为:法氏囊上皮细胞变性、坏死;淋巴滤泡的结构尚存在,但大部分淋巴细胞已经消失,周围由增生的网状细胞排列成栅栏状的反应带.滤泡间的间质增宽;被膜下、滤泡之间见有大量红细胞,滤泡中心也发生坏死;上皮细胞增生,由单层变成多层,滤泡体积缩小,滤泡间结缔组织增生,有时滤泡中心也发生坏死,有大量异嗜性白细胞浸润;腺胃黏膜出血,上皮坏死脱落,腺胃结缔组织出血,腺小管间结缔组织出血.鸡感染法氏囊病病毒(IBDV)后严重损害了法氏囊的结构和免疫功能,并在一定程度上影响了腺胃的结构和功能.     

山东分离株鸡腺胃型传染性支气管炎的病理组织学和电镜观察

为探讨鸡腺胃型传染性支气管炎病毒(腺胃型IBV)引起鸡的病理组织变化和病毒超微结构特征,采用常规临床剖检、病理组织学显微观察技术及电子显微镜观察技术,对山东省3株病毒分离株(QX、DY、FC)引起的病理组织学变化和病毒的超微结构进行观察。结果表明,分离毒株可引起明显的腺胃组织炎症,主要表现腺胃黏膜内炎性细胞浸润,腺胃腺体上皮细胞增生,腺腔中有黏液、有多量坏死、脱落、崩解的腺细胞,以及单核细胞浸润,上皮细胞有多量空泡化等特点。在病理组织中观察到了大小为80~120m的病毒颗粒;通过鸡胚分离的病毒大小为80~150nm,该病毒略呈球形或梨形,有囊膜,囊膜表面覆有长12~25 nm的呈典型冠状的突起(团集的病毒则较少有冠状突起),为冠状病毒。该结果为进一步研究和有效防治腺胃型传染性支气管炎提供了科学参考。     

鸡传染性腺胃炎的人工复制试验

试验采用疑似鸡传染性腺胃炎病鸡的腺胃组织匀浆,经除菌处理后人工接种健康雏鸡,并进行了系统的动态病理学观察。结果表明：人工感染病例和自然病例的病理变化基本相同,其主要眼观病理变化为腺胃显著肿大、出血,小肠充血、出血;主要组织学变化为腺胃黏膜充血、出血、炎性水肿和浅层坏死,小肠黏膜急性炎症变化,肝脏、肾脏等实质细胞变性以致局灶性坏死,胸腺及法氏囊等淋巴组织萎缩。从自然病例和人工感染病例腺胃中均可分离到传染性支气管炎病毒。因此,可以认为传染性支气管炎病毒是鸡传染性腺胃炎的一种病原。     

疑似鸡传染性腺胃炎的病理学观察

本观察对北京某鸡场６ 例以腺胃肿大为主要特征的病鸡进行了系统的病理学观察,并对其中２ 例的腺胃及心肌进行了透射电镜观察,结果如下：６ 只鸡剖检均见有腺胃肿大,外观呈球状,腺胃壁明显增厚;心肌极度柔软,横经变宽;胸腺、脾脏、腔上囊发育不良或不发育。病理组织学观察可见各个病例的器官组织病变基本一致,主要特征是腺胃发生以淋巴细胞、巨噬细胞浸润为主的炎症变化,同时腺上皮增生或肥大、腺管扩张,有的呈现明显的非化 脓性坏死性炎症变化。肠道也具有非化脓性坏死性炎的变化,淋巴细胞弥漫浸润,粘膜上皮内淋巴细胞密集分布。心肌实质变性,节段性溶解坏死,间质水肿;全身淋巴器官发育不良,普遍呈“星空样变”。肝脏主要变化是肝细胞脂肪变性。个别见有溶解性坏死灶。气管粘膜上皮及杯状细胞增生,淋巴细胞局部性浸润。透射镜观察发现在腺上皮细胞及心肌细胞核内很易找见病毒样粒子,其直径为５０～７０ ｎｍ 。     

鸡传染性法氏囊病与其他疾病的鉴别诊断

肺脑型新城疫感染的发病鸡可见法氏囊的出血、坏死以及有干酪样物，腺胃及盲肠扁桃体出血；更主要的是肠道黏膜的出血性变化，尤其小肠中后段的出血。但法氏囊不见黄色胶冻样水肿，耐过的鸡也不见法氏囊的萎缩及蜡黄色。鸡新城疫多有呼吸道症状、神经症状，     

网状内皮组织增生病病毒、鸡贫血病毒、大肠杆菌混合感染诱导肉鸡腺胃炎

为诊断2019年11月山东某规模化养鸡场商品肉鸡暴发腺胃炎的病因，本试验对病鸡进行临床、大体病变、组织病理和血涂片观察以及病原学检测。结果显示，发病鸡主要表现为生长停滞(矮小),精神沉郁，消瘦，消化不良等；大体病变表现为胸肌苍白，腺胃肿大，腺胃乳头消失，脾脏和法氏囊萎缩；组织病变表现为腺胃炎性细胞浸润，腺管上皮细胞增生，腺胃和十二指肠均有淋巴细胞浸润，可见核分裂象；血涂片中发现大量幼稚红细胞和异形性红细胞，并且异嗜性粒细胞增多；血琼脂培养基长出大小均匀一致的灰白色单一菌落；聚合酶链式反应(PCR)检测显示为大肠杆菌(E.coli);病毒PCR检测显示为网状内皮组织增生病病毒(REV)、鸡贫血病毒(CAV)。最终该病例诊断为REV、CAV、E.coli混合感染引起肉鸡腺胃炎。     

番鸭呼肠孤病毒B3分离株的致病性研究

用番鸭呼肠孤病毒B3分离株接种番鸭胚，半番鸭胚和鸡胚，导致接种胚死亡，并产生基本一致的病理变化，死亡胚周身出血，肝，脾有灰白色坏死点，感染番鸭肝细胞出现颗粒变性，随后崩解，该 病毒具有经胚蛋，滴鼻，饮水，肌肉和爪垫注射与同居感染的能力，潜伏期3－11天，不同途径接种1日龄敏感番鸭死亡率达100％，接种1日龄番鸭，半番鸭和雏鸡爪垫可引起注射部位炎性反应，爪垫和肌肉注射1日龄半番鸭和雏鸡不引起死亡。感染番鸭主要可见肝，脾，心肌，肾，法氏囊，腺胃，肠粘膜下层等组织局灶性坏死，其中以肝，脾尤为显著，肝组织和脾白髓结构遭到严重破坏；肝，脑血管周围和肾间质，肺间质，心肌间有淋巴样细胞或／和吞噬细胞聚集，法氏囊淋巴细胞变性和坏死，电镜观察感染胚肝细胞和脾淋巴细胞胞浆内有大量病毒样颗粒及近核包涵 体，感染细胞多核化，空泡化及颗粒化，可见含有病毒样颗粒的凋亡细胞，吞噬细胞胞浆内和凋亡小体内有病毒样颗粒。     

SPF鸡人工感染鸡败血霉形体后呼吸系统的病理变化

10日龄SPF鸡气囊接种鸡败血霉形体（MG）R株，3－5天后出现的典型的MG感染症状，呼吸系统发生一系列典型的病理组织学变化。感染鸡和对照鸡的气管经固定、脱水、临界点干燥、镀金后置于扫描电镜下观察，感染鸡气管粘膜明显水肿，部分纤毛脱落或全部脱落。电镜下可见感染鸡的气管粘膜水肿增厚近2倍，粘膜下层单核细胞积聚，其间有数量不等的淋巴细胞聚集，粘液细胞显著减少或消失；气囊粘膜水肿增厚；肺组织中有淋巴细胞增生形成的结节，对照鸡呼吸系统的组织切片无变化。     

Epidemiology, pathology, and immunohistochemistry of layer hens naturally affected with H5N1 highly pathogenic avian influenza in Japan

Epidemiology, pathology, and immunohistochemistry were investigated in layer hens affected with H5N1 highly pathogenic avian influenza, which occurred for the first time in 79 years in Japan. The farm, which had a total of 34,640 chickens, experienced up to 43.3% mortality before the chickens were depopulated. Clinically, the affected chickens exhibited mortality without apparent clinical signs. Histologically, hepatocytic necrosis; necrosis of ellipsoids and follicles with fibrin in the spleen; necrosis with glial nodules in the brain stem, cerebrum, and cerebellum; necrosis of acinar cells in the pancreas; and necrosis of lymphoid tissues in intestinal lamina propria were seen. Occasionally, mild bronchiolitis, degeneration of smooth muscle fibers in the cecum, and mild tubulonephrosis were noted. Immunohistochemically, influenza virus antigens were detected often in the liver and spleen, heart, intestine, gizzard, proventriculus, and oviduct. In addition, antigens were seen also in the brain, kidney, pancreas, and ovary, but seldom in the lung and trachea. Virus antigen was mainly detected in the capillary endothelium and parenchymal cells. This suggests that virus excretion from the respiratory tract was not as prevalent as that from the digestive tract in the present cases.     

Response of Chickens to Infection with Newcastle Disease Virus Isolated from a Guinea Fowl

An isolate of Newcastle disease virus obtained from a guinea fowl was characterized as a viscerotropic velogenic strain based upon pathogenicity index studies. Following inoculation of the viral isolate oronasally into 3-week-old chickens, clinical signs appeared after an incubation period of 4–5 days and included dullness, depression, dyspnoea, diarrhoea and leg paralysis. The virus caused a mortality of 56% with haemorrhages at the tip of the glands of the proventriculus and caecal tonsil. Histopathological changes were prominent in the lymphoid organs, being characterized by depletion, degeneration and necrosis of the lymphoid tissues. The brain was the first organ affected, with changes being noticed 3 days after infection. Isolation of virus from various organs was more frequent from 5 to 10 days after infection, but the virus persisted in some of the organs until 21 days after infection. In spite of the high mortality, a good immune response was elicited by the isolate, as was evident from the antibody titre.     

Histologic features of transplantable lymphoid tumor (Olson) during growth and regression induced by serum therapy

Susceptible 3-week-old chicks were inoculated with cells of an avian transplantable lymphoid tumor (TLT) and then treated with serum from immune chickens, serum from control chickens, or balanced salt solution. Progressive tumor growth was observed in chickens of all 3 treatment groups. Tumor growth was followed by regression only in chicks treated with immune serum. Regression was characterized by necrosis of tumor cells, muscle regeneration, and lymphocyte and plasma cell infiltration.     

Pathology of specific-pathogen-free chickens inoculated with H5N1 avian influenza viruses isolated in Japan in 2004

Specific-pathogen-free chickens inoculated with H5N1 highly pathogenic avian influenza (HPAI) viruses isolated in Japan in 2004 were investigated pathologically. The chickens inoculated intravenously with the viruses died within 26 hr after inoculation. Macroscopically, minimal necrosis of the tip of the comb, and hemorrhages of the palpebral conjunctiva, liver, cerebellum, and muscles were rarely observed. Histologically, dead chickens had minimal focal necrosis of hepatocytes with fibrinous thrombi in sinusoids, mild necrosis of splenic ellipsoids with fibrinous exudation, minimal necrosis of the brain, mild necrosis of epidermal cells of the comb with congestion of the lamina propria, and hemorrhages and edema of the lamina propria of the conjunctiva. Virus antigens were seen in the sinusoidal endothelial cells and hepatocytes in the liver, the capillary endothelial cells of the spleen, the capillary endothelial cells and cardiac myocytes in the heart, the capillary endothelial cells and necrotic nerve cells in the brain, the capillary endothelial cells in the lamina propria of the comb, the renal tubular epithelial cells, and the pancreatic acinar cells. The chickens inoculated by natural infectious routes died within 1-4 days after inoculation. Macroscopically, some chickens had hemorrhages in the conjunctiva, edematous swelling of the face and wattles, hydropericardium, hemorrhages of the proventriculus and bursa of Fabricius, increased secretion of tracheal mucus, and congestion and edema of lungs. Histologic lesions by natural infectious routes were similar to those by intravenous inoculation, except for the pancreatic necrosis. This study suggests H5N1 HPAI viruses isolated in Japan in 2004 cause pathologic conditions similar to natural cases.     

免疫鸡群自然发生马立克氏病病理学观察

2013年3月,甘肃省某鸡场50日龄鸡发生疑似马立克氏病（MD）,导致大批死亡。为进行进一步确诊和病理学研究,分别采集样品进行琼脂扩散试验和病理组织学观察。结果显示,琼脂扩散试验呈马立克氏病病毒（MDV）抗原阳性。病理学观察显示,病鸡肝、脾、肾、心等实质器官程度不等肿大,色泽变淡,甚至形成大小不等和数量不一的灰白色结节;部分病鸡坐骨神经呈单侧性不规则肿粗,弹性降低或丧失;病鸡实质器官及坐骨神经组织中均出现大量多形态的类似淋巴细胞、成淋巴细胞、浆细胞、巨噬细胞及网状细胞聚集或散在,并可见典型的MD细胞,尤其在血管周围和淋巴管周围;各型肿瘤细胞和MD细胞异型性明显,肿瘤细胞周围实质程度不等变性、坏死,间质水肿。研究证明,该鸡场鸡病为MDV感染引起的马立克氏病（MD）,病理变化主要为高异型性的淋巴样肿瘤细胞的广泛浸润,肿瘤细胞恶性程度高、增生活跃。     

鸡腺胃病变型传染性支气管炎病毒感染试验

本文采用腺胃病变型传染性支气管炎患病鸡的腺胃病料和H95株分离株尿囊液毒,对不同品种、不同日龄的易感鸡,采用不同的感染途径进行感染,对其增重、死亡等数据进行统计分析,结果表明:供试不同品种的鸡在不同的感染途径下,采用腺胃病料和鸡胚尿囊液毒分别感染,均可引起不同程度的感染发病,并出现和自然病例相同的症状和典型的病理变化。随日龄的增长,其易感率和死亡率呈下降趋势。从感染死亡鸡中可重新回收到相应的病毒,发病耐过的鸡可产生特异性抗体。     

Pathological and immunohistochemical studies of subclinical infection of chicken anemia virus in 4-week-old chickens

Subclinical infection of chicken anemia virus (CAV) at 4 to 6 weeks of age, after maternal antibodies have waned, is implicated in several field problems in broiler flocks. In order to understand the pathogenesis of subclinical infection with CAV, an immunopathological study of CAV-inoculated 4-week-old SPF chickens was performed. Sixty 4-week-old SPF chickens were equally divided into CAV and control groups. The CAV group was inoculated intramuscularly with the MSB1-TK5803 strain of CAV. Neither mortality nor anemia was detected in the CAV and control groups. In the CAV group, no signs were observed, except that some chickens were grossly smaller compared with the control group. Sporadic thymus lobes appeared to be reddening and atrophied. Within the first two weeks p.i. of CAV, there was a mild to moderate depletion of lymphocytes in the thymus cortex and spleen in some chickens. Moreover, lymphoid depletion of the bursa of Fabricius, proventriculus and cecal tonsils was observed. Hyperplastic lymphoid foci were observed in the liver, lungs, kidneys and heart at the 4th week p.i. of CAV. Immunohistochemically, a moderate lymphoid depletion of CD4(+)and CD8(+) T cells in the thymus cortex and spleen was observed in some chickens within two weeks p.i. of CAV. CAV inclusions and antigens were detected infrequently in the thymus cortex and spleen. It could be concluded that the immunosuppression in subclinical infection with CAV occurs as a result of reduction of cellular immunity.     

Pathology of spontaneous colibacillosis in a broiler flock

Forty-eight of 134 chickens collected from a flock on a broiler farm were diagnosed pathologically and microbiologically to have colibacillosis. Both acute septicemia (seven birds, 1 to 36 days old) and subacute serositis (41 birds, 5 to 57 days old) were found. The former consisted of necrosis with fibrinous exudates in the ellipsoids and lymphoid follicles of the spleen, and fibrinous thrombi in sinusoids of the liver with occasional necrosis of hepatic cells. The latter had fibrinopurulent inflammation with granulomatous changes in the serosal tissues--including the epicardium, pericardium, and hepatic peritoneal sac--accompanied by septicemic lesions in the spleen and liver. Respiratory lesions (airsacculitis, pneumonia, and tracheitis) were noted in most chickens affected with acute septicemia and subacute serositis. Degenerative changes also were observed in the bursa of Fabricius.     

雏鹅实验性副粘病毒病的临诊症状及病理变化研究

用鹅副粘病毒BY株人工感染5日龄雏鹅，观察试验鹅的临诊症状和病理学变化。试验鹅最早于2d出现症状，3d开始死亡，死亡高峰期在3－5d,7d后停止死亡，总计试验鹅发病率为89.19%，死亡率为64.86%。主要临诊症状为精神不振，食欲降低或废绝，拉稀，流泪，流鼻液。主要大体病变为消化道粘膜的水肿、出血、坏死以及胰腺、脾脏组织的严重坏死。主要组织学变化为腺胃、肠道粘膜上皮细胞和胰腺腺泡上皮细胞严重变性、坏死、胸腺、脾脏、法氏囊等器官内淋巴细胞坏死、崩解，数量显著减少。     

Immunohistochemical localization of avian leukosis virus subgroup J in tissues from naturally infected chickens.

The tissue tropism of avian leukosis virus (ALV) subgroup J (ALV-J) was investigated in congenitally infected broiler chickens by an immunohistochemistry technique detecting gp85 viral glycoprotein. All organs examined contained detectable antigen. The most intense staining was in the adrenal gland, heart, kidney, and proventriculus. Intense staining for viral antigen in the heart may explain the ability of ALVs to cause cardiomyopathy. Although recent investigations failed to demonstrate specific viral staining in bone marrow from infected chickens, we were able to show moderate staining in myelocytic precursor cells in bone marrow. This finding agrees with previous work showing cell cultures of bone marrow are susceptible to ALV-J infection and the tendency of subgroup J to predominantly induce myeloid rather than lymphoid neoplasms.