鸭H5N1型高致病性禽流感的病理组织学观察

对发生H5N1型高致病性禽流感鸭场的鸭进行了病理组织学观察。结果显示，该养鸭场患鸭禽流感病鸭的剖检变化以眼结膜潮红出血，心肌白色条纹状坏死、条带样出血，胰腺有白色或透明坏死点，胃肠出血等为特征。组织学以非化脓性脑炎、胰腺坏死、心肌坏死、坏死性脾炎的病理变化为主。     

雉鸡自然感染高致病性禽流感的病理组织学观察

本研究对已经确诊为自然感染发生高致病性禽流感的病死雉鸡的各组织器官进行病理学观察。结果发现,该养殖场的病、死雉鸡出现明显和广泛的出血和组织损伤,腹部、腿部皮下肌肉、肺、脾出血,心肌条索状坏死,胰腺、脾、肾、肝脏等器官灶状坏死。组织病理学变化以典型的病毒性心肌炎、淋巴细胞性脑炎、间质性肺炎、间质性肾炎,急性出血性肠炎,以及胰腺、肝脏、脾脏的变质性炎症等为主要特征。     

鹅鸡共发副粘病毒病的诊疗

扬州市某养鹅专业户放养45日龄鹅200只，30日龄和15日龄草鸡各20余只，未防疫。鹅于40日龄左右有少部分发病，精神萎顿、不食、拉黄白色稀粪；在鹅发病后，鸡也有类似症状而先后发病死亡。发病后1周内，第1批鸡已全部死亡，发病后10d，第2批鸡也开始出现同样症状，并死亡2只。鹅、鸡曾服用土霉素等抗菌素治疗无效。1病理变化　　鹅的主要病理变化为全身皮下出血，胸骨出血；肝脏肿大，有白色坏死点；脾脏肿大，表面呈白色花斑状坏死，大小不等；心冠脂肪出血；嗉囊与腺胃连接处有严重出血斑块，腺胃呈条纹状出血；胰腺出血或有坏死灶；整个…     

鹅副粘病毒病的病理变化

对国内最近报道的一种新的传染病－鹅副粘病毒病的自然病例和人工感染病进行了系统的病理学观察。结果表明，自然病例和人工感染病例的病理变化基本一致。主要肉眼病变为肠道粘膜广泛出血，坏死、溃疡；脾脏、胰腺出现粟粒样白色坏死点；胸腺、法氏事体积缩小；脑水肿、充血。主要组织学变化为肠道粘膜上皮细胞严重坏死、脱落；肝、心、肾等器官实质细胞变性、坏死；胸腺、脾脏、法氏囊的淋巴细胞坏死，淋巴组织萎缩。     

鸡肝炎-心包积液综合征的病理学诊断

2015年8月-11月对45例山东省近期流行的鸡肝炎-心包积液综合征剖检病变及组织病理学变化进行观察分析,并对肝组织进行透射电镜观察。剖检病变以心包积液、出血性坏死性肝炎、肺淤血水肿、肾变性肿胀、脾淤血肿胀、胰腺点状坏死及脑膜充血为特征。病理组织学观察主要表现为肝细胞灶状坏死并伴有核内嗜碱性或嗜酸性包涵体,心肌纤维变性,心间质充血、水肿及巨噬细胞浸润,胰腺上皮细胞变性、坏死,偶尔见核内嗜碱性包涵体,肾小管上皮细胞变性、间质淤血出血,肺淤血、水肿,免疫器官淋巴细胞坏死,肠黏膜发生出血性卡他性炎症。电镜观察肝细胞核内晶格状排列直径70nm左右的病毒粒子,本研究为该病的发病机制研究提供了试验基础。     

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。     

朗德鹅疑似白血病的病理组织学观察

对某种鹅场疑似白血病的朗德鹅进行了病理组织学观察。剖检可见病鹅极度消瘦，肝、肾、脾、胆囊和卵巢等组织器官呈不同程度肿瘤样病理变化。其中肝病变尤为明显，稍肿胀，表面有颗粒状弥漫性结节，切面有斑驳状异变；肾苍白，质硬，正常结构消失，形成肿瘤结节；胆囊变硬，胆囊壁增厚。组织切片观察可见肝细胞大量坏死，结缔组织增生，淋巴细胞浸润，肿瘤细胞增生；肾小管上皮脱落，肾间质与肾小球有不同程度的坏死，血管球结构模糊；脾淋巴细胞显著减少，异嗜性粒细胞增多，有多量肿瘤细胞浸润；胰腺、卵巢、胆囊等则有纤维化、淋巴细胞浸润和凝固性坏死等病理变化。     

雏鹅曲霉菌性肺炎的诊断

2005年1月，河北某养殖公司饲养的商品鹅出现以呼吸困难、肺炎为主要特征的疑似病例。病鹅主要表现为肺部长满粟粒大小结节，小肠黏膜及胰腺坏死，经病理学诊断为雏鹅曲霉菌性肺炎，该病例从症状到病理变化均比较典型，现将情况报道如下。     

西藏鸡新细菌病病理学研究

对自然发病死亡的２０只鸡进行系统的剖检及病理学观察。结果发现，该病的病理学特征主要表现为：肝肿大，质脆，表面出血，肝细胞变性及坏死；肠道（以十二指肠及空肠）病变明显，肠道淤血、出血，肠粘膜上皮细胞坏死脱落，固有层充血、出血、水肿；心脏淤血、出血，心肌坏死，肺、肾、脾均有不同程度的淤血、出血。研究结果表明，在心、肝、脾性组织切片中可见有多量的圆形（０．４μｍ左右）、具有抗酸梁色特性的和种细菌故定为新     

鹅Ⅰ型副粘病毒病的鉴定与防治初探

从广东省花都市、清远市的病死鹅中分离到２株病毒。发病鹅群为１５天龄至２月龄，死亡率超过４０％；临诊表现以拉白色、绿色粪便，阴茎及肛门外翻，眼潮红为主要特征；剖检见喉头出血，气管潮红，肝肿大，胰腺有坏死斑，个别病例在腺胃肌胃交界处有出血，胸部皮下有出血...     

Pathology of Murine Cytomegalovirus Infection in Newborn Mice. Muscle, Heart and Brown Fat Lesions

Newborn mice were inoculated intracerebrally with murine cytomegalovirus and studies were made of the pathological changes in the striate and cardiac muscle and brown fat. Widespread necrosis was seen in muscle and brown fat in the early stages of the infection. Necrotic lesions became calcified. By 56 days lesions were not resolved in the heart and brown fat but were completely resolved in skeletal muscle.     

犬细小病毒病的病理学观察

文章对一例吉娃娃幼犬细小病毒病肠炎综合征病例进行了病理学诊断和检查,发现肠道广泛坏死,有充血出血现象,心脏心肌柔软,凝血不良,心房扩张,且伴有慢性出血性肺炎.光镜下见肠绒毛上皮细胞广泛变性、坏死、脱落,肠腔中有大量脱落的绒毛上皮细胞和炎性渗出物,固有层有多少不等的炎性细胞浸润,肠腺和肠绒毛上皮均可见特征性的核内包涵体;心肌纤维也有程度不等的变性、坏死,炎症细胞浸润.     

Pathobiology of A/chicken/Hong Kong/220/97 (H5N1) avian influenza virus in seven gallinaceous species

Direct bird-to-human transmission, with the production of severe respiratory disease and human mortality, is unique to the Hong Kong-origin H5N1 highly pathogenic avian influenza (HPAI) virus, which was originally isolated from a disease outbreak in chickens. The pathobiology of the A/chicken/Hong Kong/220/97 (H5N1) (HK/220) HPAI virus was investigated in chickens, turkeys, Japanese and Bobwhite quail, guinea fowl, pheasants, and partridges, where it produced 75-100% mortality within 10 days. Depression, mucoid diarrhea, and neurologic dysfunction were common clinical manifestations of disease. Grossly, the most severe and consistent lesions included splenomegaly, pulmonary edema and congestion, and hemorrhages in enteric lymphoid areas, on serosal surfaces, and in skeletal muscle. Histologic lesions were observed in multiple organs and were characterized by exudation, hemorrhage, necrosis, inflammation, or a combination of these features. The lung, heart, brain, spleen, and adrenal glands were the most consistently affected, and viral antigen was most often detected by immunohistochemistry in the parenchyma of these organs. The pathogenesis of infection with the HK/220 HPAI virus in these species was twofold. Early mortality occurring at 1-2 days postinoculation (DPI) corresponded to severe pulmonary edema and congestion and virus localization within the vascular endothelium. Mortality occurring after 2 DPI was related to systemic biochemical imbalance, multiorgan failure, or a combination of these factors. The pathobiologic features were analogous to those experimentally induced with other HPAI viruses in domestic poultry.     

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.     

Galenia africana L. poisoning in sheep and goats: hepatic and cardiac changes.

Lesions in 4 field cases (3 sheep and 1 goat) of 'waterpens' or water belly, caused by the plant Galenia africana, are described. The clinical pathological and pathological findings in 7 sheep which were drenched with toxic plant material are also reported. Inappetence, ruminal stasis and apathy as well as tachycardia were noticed in some of the sheep towards the end of the dosing period. The most prominent clinical pathological change in the experimental animals was an increase in the activity of gamma-glutamyltransferase which in some animals occurred within days after commencement of dosing. This indicates liver involvement in the early stages of the intoxication, and at this stage no heart abnormalities were detected clinically, clinical pathologically or with cardiac function tests. Decrease in cardiac function were recorded in 2 sheep towards the end of the dosing period. Liver and heart lesions were present in all the animals. In some cases hepatic changes were mild and characterized by dilation of central veins and sinusoids and, less commonly, centrilobular fibrosis. More advanced lesions included centrilobular fibrosis and bridging between neighbouring lobules with adjacent areas of coagulative necrosis, lysis and ballooning degeneration of hepatocytes. Myocardial changes occurred in the free ventricular walls and interventricular septum and comprised hypertrophy of myocytes with consequent degeneration and necrosis and fibrosis. In cases of longer duration myocytes were diffusely atrophic with scattered groups of remaining hypertrophic fibres. The clinical pathological and pathological features suggest that G. africana is primarily hepatotoxic with myocardial involvement occurring only in the terminal stages of the intoxication.     

Comparative pathological studies on domestic geese (Anser anser domestica) and Muscovy ducks (Cairina moschata) experimentally infected with parvovirus strains of goose and Muscovy duck origin

Parvovirus infection of Muscovy ducks caused by a genetically and antigenically distinct virus has been reported from Germany, France, Israel, Hungary, some Asian countries and the USA. The pathological changes include those of degenerative skeletal muscle myopathy and myocarditis, hepatitis, sciatic neuritis and polioencephalomyelitis. In the study presented here, day-old and 3-week-old goslings and Muscovy ducks were infected experimentally with three different parvovirus strains (isolates of D-216/4 from the classical form of Derzsy's disease, D-190/3 from the enteric form of Derzsy's disease, and strain FM from the parvovirus disease of Muscovy ducks). All three parvovirus strains caused severe disease in both day-old and 3-week-old Muscovy ducks but in the goslings only the two strains of goose origin (D-216/4 and D-190/3) caused disease with high (90-100%) mortality when infection was performed at day old. Strain FM (of Muscovy duck origin) did not cause any clinical signs or pathological lesions in the goslings. In the day-old goslings and Muscovy ducks the principal pathological lesions were severe enteritis with necrosis of the epithelial cells (enterocytes) of the mucous membrane and the crypts of Lieberkühn, and the formation of intranuclear inclusion bodies. Other prominent lesions included hepatitis and atrophy (lymphocyte depletion) of the lymphoid organs (bursa of Fabricius, thymus, spleen). In goslings infected with the strain originating from the classical form of Derzsy's disease mild myocarditis was also detected. After infection at three weeks of age, growth retardation, feathering disorders, myocardial lesions (degeneration of cardiac muscle cells, lympho-histiocytic infiltration) and hepatitis were the most prominent lesions in both geese and Muscovy ducks. In addition to the lesions observed in the geese, muscle fibre degeneration, mild sciatic neuritis and polioencephalomyelitis were also observed in the Muscovy ducks infected with any of the three parvovirus strains.     

Evaluation of ultrastructural changes associated with encephalomyocarditis virus in the myocardium of experimentally infected piglets

OBJECTIVE: To evaluate the ultrastructural changes and localization of encephalomyocarditis virus (EMCV) and viral pathogenesis in the myocardium of experimentally infected piglets. ANIMALS: Eight 20-day-old piglets. PROCEDURE: Six piglets were inoculated oronasally with 5 ml (10(6) median tissue culture infective dose/ml) of EMCV suspension, and 2 were used as uninfected controls. Piglets were euthanatized or died between postinoculation days 1 and 3. Samples of heart tissue from all piglets were evaluated histologically, by virus isolation, and by use of immunohistochemistry and electron microscopy. RESULTS: All infected piglets had gross or microscopic lesions of interstitial myocarditis. immunohistochemically, EMCV antigen was detected in the cytoplasm of cardiac muscle cells, Purkinje fibers, and endothelial cells and in the nucleus of cardiac muscle cells and Purkinje fibers. Ultrastructural lesions were characterized by degeneration and necrosis of cardiac muscle cells and Purkinje fibers. Virus was present intracytoplasmically in cardiac muscle cells, Purkinje fibers, and endothelial cells of capillaries and intranuclearly in cardiac muscle cells. The cell membranes of the Purkinje fibers and endothelial cells had distinct protrusions that contained virus particles. In control piglets, no lesions were found, and no EMCV antigen was detected. CONCLUSIONS: Localization of EMCV intracytoplasmically or intranuclearly in various myocardial cells may well reflect the sites of viral proliferation. The presence of virus particles in cell membrane protrusions and in vacuoles within the lumen of capillaries indicates that virus is released not only by disintegration of the host cell but also via exocytosis.     

A neonatal calf with concurrent meningoencephalitis by Enterobacter cloacae and enteritis by attaching and effacing Escherichia coli (O128)

A neonatal calf developed nervous symptoms followed by diarrhea. The principal pathological changes were fibrinopurulent meningitis with necrosis of the cerebral parenchyma, and attaching and effacing lesions in the intestine. Cerebral necrosis was frequently associated with vascular changes. Enterobacter cloacae was isolated from the brain and Escherichia coli (O128) from the intestinal content. These suggest that cerebral and intestinal lesions were caused by the isolated organisms, and that most necrosis of the cerebral parenchyma might be infarctive.     

一起群发性奶牛尿素中毒的临床研究

2004年南京某奶牛公寓由于饲养户在奶牛饲料中添加尿素方法不当,引起群发性尿素中毒。该牛群共有奶牛87头,发病64头,药物治疗56头,治愈54头,死亡10头,均为成母牛。作者调查了发病牛群的病史、临床症状、病理变化、治疗情况,对中毒奶牛的血液进行生化分析,并与正常奶牛比较,结果血清谷草转氨酶(AST)、γ-谷氨酰转移酶(GGT)、碱性磷酸酶(ALP)、磷酸肌酸激酶(CK)、磷酸肌酸激酶同工酶(CK-MB)、肌酐(CRE)、尿素氮(UN)、葡萄糖(GLU)、乳酸脱氢酶(LDH-L)等差异极显著(P<0·01),尿素(UREA)、血清K等差异显著(P<0·05),这些指标活性升高说明病牛心肌、胃肠平滑肌、肝肾等存在与病死牛的病理变化相一致的损伤。