鸡溃疡性肠炎的病理学观察

对自然发病和人工感染发病的溃疡性肠炎病鸡进行了病理学观察，该病的特征性剖检变化为肝脏肿大，在肝脏表面有大小不一的黄白色坏死斑点，肝脏边缘有大片坏死区，小肠粘膜或盲肠粘膜有豆粒大，圆形的溃疡灶，其组织学变化以肝细胞和肠道上皮细胞的坏死为特征。     

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。     

鸡腺胃型传染性支气管炎的病理变化

对１９９５年以来在江苏一些县市养鸡场和养鸡专业户蛋鸡群发生的鸡腺胃型传染性支气管炎的自然病例和人工感染病例进行了系统的病理学观察。自然病例和人工感染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,小肠充血、出血和炎症;主要组织学变化为腺胃粘膜充血、出血、炎性水肿和浅层坏死,小肠粘膜急性炎症变化,肝、心、肾等实质细胞变性以至局灶性坏死,脾、胸腺及法氏囊的淋巴组织萎缩。     

鸡奇异变形杆菌病病理学研究

本研究运用组织学，组织化学等方法对鸡奇异变形杆菌病自然和实验病例进行了比较病理学研究，结果表明，雏鸡感染本病后体内受侵器官比较广泛，但主要脾脏，法氏囊，胸腺和盲肠扁桃体等淋巴器官的淋巴细胞变性，坏死，其中脾脏损伤最严重，法氏囊和盲肠扁桃体次之，胸腺受损害轻微，这些免疫器官和外周血液中的各类免疫活性细胞数无题出现不同程度的下降；中枢神经系统主要表现为非化脓性脑膜炎和脑软化，腿部肿骼肌变性，坏死，坐骨     

雏鹅人工感染沙门菌的病理组织学观察

为了研究沙门菌感染雏鹅的主要病理组织学变化。采取腹腔注射沙门菌人工感染7日龄健康雏鹅,对发病雏鹅进行病理剖检,并采取肺脏、肝脏、脾脏和肠道病料制作病理切片,光学显微镜下进行病理组织学观察。受感染雏鹅剖检病变可见皮下、心肌、肺脏、脾脏、肠道、脑膜等多处出血,肝脏坏死,胆囊、脾脏肿大;显微病理组织学变化为肝、脾、肺、肠道等器官出血、细胞变性、坏死,有炎性细胞浸润。结果表明,感染沙门菌雏鹅出现了广泛性的组织损伤,同时伴随着机体各器官明显的炎症反应。     

鸡奇异变形杆菌病病理学研究

本研究运用组织学、组织化学等方法对鸡奇异变形杆菌病自然和实验病例进行了比较病理学研究。结果表明，雏鸡感染本病后体内受侵器官比较广泛，但主要是脾脏、法氏囊、胸腺和盲肠扁桃体等淋巴器官中的淋巴细胞变性、坏死，其中脾脏损伤最严重，法氏囊和盲肠扁桃体次之，胸腺受损害较轻微，这些免疫器官和外周血液中的各类免疫活性细胞数均出现不同程度的下降；中枢神经系统主要表现为非化脓性脑膜炎和脑软化，腿部骨骼肌变性、坏死，坐骨神经束间有少量炎性细胞浸润，胃肠发生卡他性炎症，心、肝、肾实质器官淤血、变性；奇异变形杆菌对鸡的致病作用主要为内毒素所致，且内毒素的致病作用较活菌液的致病作用强。     

鸭瘟病理组织学动态观察

鸭瘟病毒（DPV）强毒经人工感染和同居感染成年鸭后，采用聚合酶链反应（PCR）检测为鸭瘟后，在不同时间段对各给织器官的病理组织损伤进行了观察．表现为：人工接种后24h被检器官组织显现出病理变化．机体中枢免疫器官法氏囊、胸腺表现为淋巴细胞数量降低，组织间隙加大；脾脏组织病变较为严重，其余器官组织均出现程度较轻的组织损伤。接种后48h，中枢免疫器官的淋巴细胞极度减少、网状细胞增生、器官组织结构模糊不清，充血、出血严重；一些生命重要器官则出现明显细胞肿胀，肠道等器官组织也有细胞变性、出血等不可逆病理变化。居感染组织损伤与人工接种组织相似，只是发生时间偏后约50h。提示：接种DPV强毒的感染鸭和同居鸭的免疫器官严重受损，甚至引超免疫抑制。此外，两组实验鸭的肝细胞、肾小管上皮细胞及脾脏、法氏囊、胸腺的网关细胞中的核内包涵体结构，可在病理组织学上为鸭瘟诊提供依据。     

鸽实验性感染鹅副黏病毒的病理学研究

对人工感染鹅副黏病毒病鸽的病理变化进行了观察研究。结果表明,病鸽各种组织器官均有明显的组织损伤,但较集中于消化系统、神经系统和免疫系统。主要肉眼病变为肺瘀血、水肿,胰腺、脾脏局灶性坏死,肠黏膜水肿、增厚或有出血、坏死,脑充血、出血;主要组织学变化为腺胃、肠道黏膜上皮坏死、脱落或伴有严重出血,肝、肾、心脏等器官实质细胞变性、坏死,胸腺、脾脏、法氏囊等免疫器官淋巴细胞坏死,淋巴组织萎缩。     

吉林省黄牛“猝死症”的病理学研究——实验病例的病理形态学观察

本实验用牛源性Ａ型魏氏梭菌，绿脓杆菌，弗氏柠檬酸杆菌，普通变形杆菌的培养物和冠状病毒、粘膜病毒的细胞培养物人工接种黄牛，死后进行病理检查，结果证明：接种细菌的病例，其实质器官的主质细胞发生变性和局灶性凝固性坏死等退行性病变，全身组织广泛性出血，尤以心内膜为甚，肠粘膜有局灶性坏死灶，并能从肝脏和脾脏检出魏氏梭菌。而细菌与病毒先后接种的病例，除见上述病变之外，还在实质器官及胃肠道粘膜中见有较多的淋巴细     

雏鸡人工感染传染性腔上囊病毒时淋巴器官的组织病理学观察

本研究观察了人工感染传染性腔上囊病毒(IBDV)的雏鸡的腔上囊、胸腺,脾脏、盲肠扁桃体、Harder′s腺等淋巴器官的组织病理学变化。结果显示全部感染鸡腔上囊都有特异性病理变化:表现淋巴小结髓质坏死,髓质、皮质同时坏死,淋巴细胞数量明显减少;未分化上皮细胞立方化;间质充血、水肿增宽或成纤维细胞增生;粘膜水肿、上皮细胞变性;脾脏、盲肠扁桃体、胸腺和Harder′s腺亦有不同程度的组织学改变。     

Acute toxicological experiment of T-2 toxin in rabbits

Rabbits were treated with a single oral dose (1, 2, 4, 6, 8, 10 or 15 mg/kg body mass) of T-2 fusariotoxin. Doses of 4 mg or higher killed the animals in 24 to 48 h. As opposed to the controls, in the treated rabbits gross pathological and histopathological examinations revealed acute catarrhal gastroenteritis, necrosis of lymphoid cells of the gastrointestinal mucosa, centrolobular dystrophy of the liver, necrosis of cells of the mononuclear phagocyte system (MPS) in the liver, tubulonephrosis, focal dystrophy of the adrenal cortex, lymphocyte depletion involving both T- and B-cell-dependent zones of the lymphoid organs (spleen, lymph, ampulla ilei), and depletion and necrosis of the myelopoietic cell colonies of the bone marrow. Similar but milder changes were observed in surviving rabbits exsanguinated 48 h after treatment. In addition to the direct damage done to the digestive tract mucosa and liver, the toxin severely damaged the cells participating in humoral and cell-mediated immunity and in the local defence of the intestinal mucosa, and markedly impaired phagocytosis and granulocytopoiesis. In another experiment rabbits were given oral doses of 2 mg/kg body mass T-2 toxin daily for several days. One rabbit was killed by bleeding every day. In rabbits killed beyond day 7 there was subacute catarrhal gastritis, emaciation, and hypertrophy of the adrenal cortex.     

Pathological and immunohistochemical study of experimental peste des petits ruminants virus infection in goats

Peste des petits ruminants (PPR) is an emerging, economically important viral disease of goats and sheep in the Indian subcontinent. In the present investigation, 15 hill goats were experimentally infected with 2 ml of 10% splenic suspension of a virulent isolate of PPR virus (PPR/Izatnagar/94) that had caused heavy mortality (>75%) in goats during 1994 outbreaks in northern India. More than 86% (13 of 15) animals died between 9 and 13 days post inoculation at the height of temperature or when temperatures were declining. Necropsy findings included congestion of gastrointestinal tract (GIT), nasal sinuses, consolidation of antero-ventral lobes of lungs, engorged spleen, and occasionally oedematous lymph nodes. Histopathological examination of major organs of GIT revealed degeneration and necrosis of labial mucosa, severe mucosal and submucosal congestion, degeneration and necrosis of intestinal epithelium and lymphoid cell depletion from Peyer's patches along with presence of syncytia at times. Lungs showed broncho-interstitial changes and presence of intracytoplasmic and intranuclear eosinophilic inclusions in alveolar macrophages and syncytial cells. These changes in lungs were frequently complicated with serofibrinous pneumonia (57%, eight of 14). Lymphocytolysis and occasional syncytia formation were evident in the lymphoid tissues. Immunohistochemical (IHC) findings included presence of PPR virus antigen in the labial, intestinal, and bronchiolar epithelial cells, pneumocytes, macrophages and syncytial cells in lungs, and lymphoid (intact and necrotic) and reticular cells in lymphoid organs. The findings of the study indicated the highly virulent nature of the PPR virus isolate (PPR/Izatnagar/94), causing 100% mortality and characteristic pathological changes in the target organs such as lungs, intestines and lymphoid tissues. The results of the IHC study suggested that indirect immunoperoxidase could be an alternative method in the absence of more sophisticated methods of laboratory diagnosis of PPR virus infection in goats.     

Preliminary study on duck enteritis virus-induced lymphocyte apoptosis in vivo

We studied apoptosis induced by duck enteritis virus (DEV) in vivo, focusing on the lymphoid organs that constitute the main targets for infection: thymus, bursa of Fabricius (BF), and spleen. Fifty Pekin ducks were inoculated subcutaneously with a virulent strain of DEV. The morphology of lymphoid organs of these infected ducks was observed by light microscopy and transmission electron microscopy. Cell death by classical necrosis was observed in lymphocytes of the DEV-infected thymus, BF, and spleen. Lymphocyte apoptosis also was observed at the same time, and it was further confirmed by in situ terminal deoxynucleotidyl transferase dUTP nick-end labeling and agarose gel electrophoresis. We conclude that apoptosis and necrosis of lymphocytes induced by DEV infection resulted in the depletion of lymphocytes and that apoptosis of lymphocytes may play an important role in the pathogenesis of duck viral enteritis.     

鸵鸟新城疫的病理形态学观察

通过病理剖检、病理组织学及电镜负染观察等方法对来自山东、河南等地的15只表现典型新城疫症状的发病鸵鸟的死亡原因进行系统研究分析。病理剖检可见发病鸵鸟全身广泛性出血,其中以消化道黏膜出血为主;病理组织学观察可见其病理特征以消化道黏膜出血,细胞变性、坏死、脱落为主,同时伴发心肌纤维和肾小管上皮细胞的颗粒变性,脾脏和肺脏充血、出血以及其头颈部的水肿,淋巴组织的坏死等病理变化。电镜负染观察可见圆形、椭圆形或纺锤形,直径200~500 nm,具有明显纤突的典型副黏病毒粒子。以上试验结果证实鸵鸟的死亡原因为新城疫病毒感染所致。     

雏鸡免疫器官与消化器官发育中肥大细胞的观察

本试验通过Carony's液固定,阿尔新蓝-藏红O复染(AB/SO)法,对1~7日龄雏鸡免疫器官和消化器官中肥大细胞(mast cells,MC)的形态、分布及数量变化进行观察分析.结果表明,免疫器官中MC集中分布在胸腺髓质内、脾脏红白髓交界处、法氏囊的淋巴小结周围组织内;消化器官中MC密集分布于腺胃固有层和胃腺周围、肠的固有层及黏膜下层、肝脏窦状隙和中央静脉周围.雏鸡主要免疫器官与消化器官MC数量随日龄增长均呈上升趋势.     

The formation process of button ulcers in pigs experimentally infected with a subgenotype 2.1 isolate of classical swine fever virus

We evaluated the role of classical swine fever virus (CSFV) in the formation of button ulcers in the mucosa of the gastrointestinal tract. Histopathological and immunohistochemical analyses of pigs experimentally infected with a subgenotype 2.1 isolate of CSFV, which was isolated in Japan in 2019, revealed follicular necrosis in the submucosal mucosa-associated lymphoid tissue and herniation of crypts as factors that contribute to the development of button ulcers during CSFV infection. These findings indicate that CSFV induces follicular necrosis and is one of the causative agents of button ulcers in pigs.     

Study on Mast Cells Development in Immune Organ and Digestive Organ of Chick

For observing and analyzing the motpha,distribution and quantity of mast cells (MC),the differentiation time and degree of immune organs and digestive organs in different ages of chicken were fixed by Carnoy's,stained by AB/SO.The results showed that MC concentrated in the thymus medulla;In spleen,MC distributed in the junction of red pulp and white pulp;MC were seen in the tissue around the lymphoid nodules in bursa of fabricicus tissue. MC distributed with the lamina propria and compound tubular gland in stomach;MC distributed in the lamina propria,sub mucosa of intestine;More MC in liver concentrated around sinusoids and the central vein.The number of MC in the main immune organs and digestive organs of 1 to 7 day old chicks showed an increasing trend.     

Characterization of NCR1+ cells residing in lymphoid tissues in the gut of lambs indicates that the majority are NK cells

Natural killer (NK) cells are important for immune protection of the gut mucosa. Previous studies have shown that under pathologic conditions NK cells, T cells and dendritic cells are found co-localised in secondary lymphoid organs where their interaction coordinates immune responses. However, in the gut-associated lymphoid tissues (GALTs), there are few detailed reports on the distribution of NK cells. Sheep harbour several types of organised lymphoid tissues in the gut that have different functions. The ileal Peyer’s patch (IPP) functions as a primary lymphoid tissue for B cell generation, while the jejunal Peyer’s patches (JPPs) and colon patches (CPs) are considered secondary lymphoid tissues. In the present study, we analysed tissues from healthy lambs by flow cytometry and in situ multicolour immunofluorescence, using recently described NCR1 antibodies to identify ovine NK cells. Most NCR1+ cells isolated from all tissues were negative for the pan T cell marker CD3, and thus comply with the general definition of NK cells. The majority of NCR1+ cells in blood as well as secondary lymphoid organs expressed CD16, but in the GALT around half of the NCR1+ cells were negative for CD16. A semi-quantitative morphometric study on tissue sections was used to compare the density of NK cells in four compartments of the IPPs, JPP and CPs. NCR1+ cells were found in all gut segments. Statistical analysis revealed significant differences between compartments of the primary lymphoid organ IPP and the secondary lymphoid organs of the JPPs and CP. NK cells co-localised and made close contact with T cells, dendritic cells and other NK cells, but did not show signs of proliferation. We conclude that NK cells are present in all investigated segments of the sheep gut, but that presence of other innate lymphoid cells expressing NCR1 cannot be excluded.     

Pathogenesis of 'sheep-associated' malignant catarrhal fever in rabbits

Pathogenesis studies of experimentally produced sheep-associated malignant catarrhal fever (MCF) in laboratory rabbits are described. Animals were examined at intervals after inoculation. The principal change was a proliferation of lymphoid cells which began as soon as three days and became quite pronounced by 13 days after inoculation. The appendix, mesenteric lymph node and spleen were most obviously affected. The reason for this was a progressive increase in T-lymphocytes, which appeared to be a hyperplasia rather than neoplasia in T-dependent areas of these organs. Lymphoid cells also accumulated in interstitial spaces of non-lymphoid organs. The use of cyclosporin-A suppressed the lymphoid proliferation but rabbits still developed clinical MCF after a similar incubation period. It is suggested that the agent of MCF might produce its effect by infecting and causing a dysfunction of lymphoregulatory cells, resulting in benign polyclonal T-lymphocyte proliferation. Terminal necrosis could be due to natural killer cell activity.