家兔氟中毒的病理组织学观察

通过对家兔分别灌服 2mg/kg,5mg/kg,1 0mg/kg ,的氟化钠 ,成功复制出家兔亚急性氟中毒的模型。试验家兔于 6～ 1 0d内死亡。其剖检主要病变为心肌质地变软 ,心肌、肝脏表面有部分淤血和轻度出血 ;肾脏被膜易脱落 ,肿胀和部分出血 ;胃肠粘膜易脱落或出血 ;可视粘膜苍白等症状。其病理组织学变化为肝细胞空泡变性、颗粒变性 ,局部坏死 ,核溶解、消失 ,部分神经细胞变性坏死 ,肾小球肿胀出血等变化     

硝基苯染毒致小鼠脑的毒性作用

为探讨硝基苯染毒致小鼠脑的毒性作用,用灌胃的方法对试验小鼠进行了硝基苯染毒,染毒剂量分别为26、52、105mg／kg,每日染毒1次,共30d。于末次染毒后第2d将小鼠脱颈椎处死,立即取出脑,检测SOD和GSH—Px活性和．MDA含量,并对其显微及超微结构进行了观察。结果,硝基苯对小鼠脑有明显的毒性作用,主要表现为大脑血管间隙扩大,周围神经纤维疏松;小脑、海马区部分浦肯野氏细胞核固缩、核溶解,锥体细胞核固缩;神经细胞肿胀,线粒体明显肿胀,粗面内质网形态扩张;大部分胶质细胞电子密度增加,胞核变小、核固缩,胞质内细胞器明显减少;有些神经纤维脱髓鞘,神经微丝溶解;随着染毒剂量的加大,MDA含量逐渐升高,CAT和SOD活性不断显著降低。结果表明,硝基苯可以通过氧化应激和诱发细胞凋亡对小鼠脑组织造成损伤。     

绵羊变异黄芪中毒的治疗试验

将变异黄芪中毒绵羊１２只分三组 进行治疗试验。试验绵羊每日灌服芪草汤一剂，喂青干燕麦草和红豆草，自由饮水和活动。同时进行临床，实验室，心电图及病理学检查。结果显示，服药之次日，试验羊即食欲增加，第５天症状开始减轻，第８天症状基本消失。血液生化，免疫功能及心电图等各项指标，均趋向改善。     

多黏菌素对雏鸡不同组织中SOD活性及丙二醛含量的影响

以口服给药方式给雏鸡喂服不同剂量多黏菌素B，测定了不同组织中SOD活性和MDA的含量。结果表明，低剂量组雏鸡；肝脏和心脏在给药后第8天，肾脏在第4天，脾脏和大脑在第12天SOD活性显著升高；肝脏，脾脏和心脏于第8天，肾脏于第4天，大脑于第12天MDA含量显著降低。高剂量组雏鸡；肝脏，肾脏和心脏中SOD活性在给药后第1天极显著升高，脾脏和大脑在给药后第4天，胰腺和十二指肠于第12天SOD活性显著升高；肝脏于给药后第1天MDA含量显著降低，脾脏，肾脏和心脏于给药后第4天及胰腺和十二指肠子第12天MDA含量显著降低。SOD活性升高后随之下降而MDA含量下降后则随之升高，毒性反应主要表现为肝毒性，肾毒性，脾毒性，心脏毒性和神经毒性。     

仔猪实验性铅中毒的病理学研究

选择长白仔猪l2头．体质量8～12kg，随机分成试验组(8头)和对照组(4头)。试验组仔猪用醋酸铅溶液按日剂量60mg／kg体质量饮水．对照组仔猪正常饲喂．持续14周。结果试验仔猪临床表现消瘦、厌食或绝食，腹泻、惊厥及肌肉震颤等症状。血液学检查，试验仔猪呈小细胞性、低色素性贫血，其外周血中中、晚幼红细胞增多．且能见到嗜碱性点彩颗粒。病理眼观变化：心脏扩张．心包有积液；肝、肾肿大，呈土黄色；脾稍肿大，切面呈暗红色．结构模糊；肺膨大，质地脆弱；胃、肠黏膜潮红、肿胀．胃壁充血、出血；大脑膜血管充血。病理组织学检查：心肌纤维变性、坏死；肝细胞发生颗粒和脂肪变性,汇管区血管充血；脾小梁静脉扩张，脾窦有大量红细胞浸润；肺支气管黏膜上皮和肾小管上皮细胞变性、坏死；小肠、大肠黏膜上皮变性坏死、脱落．腺体杯状细胞增多；脑膜血管扩张充血．神经细胞水肿，胞浆溶解。组织超微结构观察：肝细胞核周间隙和核膜界限不清．线粒体扩张呈囊状；肾小管上皮细胞核及线粒体基质部分缺失，局部空泡化；大脑、小脑、脑干、脊髓神经细胞及其线粒体基质局部缺失，神经胶质细胞及神经纤维不同程度出现溶解斑。用原子吸收分光光度计法测定仔猪外周血、心、肝、肾、脑及股骨的铅含量．其血液铅平均质量浓度达2．64mg／L，被检组织中以股骨的铅含量为最高．达到24．6μg／g，依次为肾、肝、心，脑．其测定值分别是正常对照组仔猪的40、117、130、79、195和76倍。     

兔病毒性出血症的病理学观察

兔病毒性出血症又名“兔瘟”，是严重危害家兔的主要传染病，常呈毁灭性流行而给养兔生产带来极大的经济损失。一段时间来，在泰安市周边地区不断有本病发生，为了给本病的诊断和防制提供更进一步的理论依据，笔者对自然病例进行了系统的肉眼观察和组织病理学检查。１　材料和方法典型自然病例５例，取自泰安市郊区某养兔场，急性期自然死亡后立即进行剖检，详细记录肉眼病变，迅速取心、肝、脾、肺、肾、胃、肠、淋巴结、大脑、小脑等组织用１０％中性福尔马林固定后，常规石蜡切片，苏木素－伊红染色，镜检。２　结果２１　大体检查病尸…     

高浓度味精水治疗狗中毒效果观察

味精,学名谷氨酸钠,L-谷氨酸钠,在机体内可分解为谷氨酸,进而参加机体代谢,合成其它氨酸.我们在平时兽医临床诊疗中发现用味精和水混合成高浓度溶液后灌服误食中毒死的猫、狗疗效很好；今年11月份的一天傍晚，一条家养狗因误食中毒死鼠而发生中毒，病狗临订表现为精神沉郁、流涎、站立不稳，共济失调；当即用市售50g装的味精30g，开水500g溶化味精，待稍凉后分两次口腔灌服病狗（两间隔时间约15分钟），配合注射阿托品0.5毫长,至第二天上午基中毒症关已基本上消失,能够进食,吠叫。同时在临床工作中，我们用同样的方法治疗猫食毒鼠中毒也收…     

人工感染黄曲霉毒素雏鸭的病理学动态变化

给7日龄樱桃谷鸭饲喂含黄曲霉毒素AFB，的饲料，分别于采食AFB1后第12、24、48、72、96、120、144、168、192h各剖杀2只雏鸭，观察病理变化并采取组织病料，制作石蜡切片观察组织病理学变化和超薄切片观察超微结构变化。眼观病变为气囊有黄色纤维性物质渗出，肝、肾肿大，质地变脆。组织病理学变化为胆管增生，肝细胞空泡变性及后期极度肿胀；肾小管上皮细胞颗粒变性和散在凝固性坏死；脾红髓淤血，脾窦扩张；大脑膜水肿扩张，脑实质毛细血管扩张；心肌纤维、十二指肠腺上皮细胞、胰腺细胞颗粒变性。超微结构变化为肝细胞中空泡大量聚集导致细胞核变形，肾上皮细胞线粒体肿胀变形，大脑神经细胞髓鞘溶解及胰腺细胞酶原颗粒减少。表明，AFB，对雏鸭心、肝、脾、肺、肾、脑、十二指肠、胰腺等均有明显病理损害，以肝的病变最为严重和典型。     

米醋在家畜临床上的应用

1．治家畜支气管炎。牛、马用含醋酸5％的米醋250毫升，甘草15克，冰片0．5克，清水1000毫升，混合后用胃管投送，每日1次，连用5～7天，猪、羊按1／5量服用；或用含醋酸5％的米醋250毫升，枇杷叶(去毛)25克，加水1500毫升，煎至1000毫升，取汁灌服，每日1次，连服1周，猪、羊按1／5量服用；用含醋酸5％的醋250毫升，蜂蜜150毫升，加凉开水800～1000毫升，混匀灌服，连服2～4次，猪、羊按1／5量服用。     

自发性急性犬瘟热的原发性脱髓性脑病

为了进一步观察犬瘟热病毒引起的原发性脑损伤和包涵体形成的特点，调查脑组织的损伤与神经症状的关系，对10只急性犬瘟热病犬的脑组织进行了详细的病理学研究。为了仔细地观察病变，本试验按照解剖学关系将脑组织分成3个大部分和11个切面，即大脑(4个切面)，脑干(5个切面)和小脑(2个切面)。组织切片经HE、LFB和免疫组织化学染色后进行检查，结果表明：在大脑，脱髓呈弥漫性发生，程度较轻；脑干的周围或靠近第三脑室的白质脱髓较重；小脑在轻度或中度脱髓的基础上常出现严重的多发性脱髓灶。脱髓部呈空泡或海绵状，有少量胶质细胞存在，但无炎性反应。脱髓性病损是非时称性发生，对神经束没有特殊的亲和力。在脑室的室管膜细胞内发现有较多的嗜酸性胞浆或核内包涵体。用抗犬瘟热病毒抗体染色，带有包涵体的室管膜细胞呈现强阳性反应。部分锥体细胞，神经核细胞和漓氏细胞变性、溶解或胞浆深染。胞核浓缩。这种变化以小锥体神经细胞表现得最为明显。根据此研究结果，作者认为由犬瘟热病毒引起的原发性脑组织损伤是一种脱髓性脑病，而不是脑炎变化；位于室管膜细胞内的包涵体对于脑组织犬瘟热的确诊具有重要的作用；由于犬瘟热病毒引起神经细胞的损伤是非特异性的，对脑组织的侵害是非对称性的。对神经束的作用无特殊的亲和力，所以患犬瘟热的犬在临床上可出现不同的神经症状。     

铜缺乏奶牛神经递质酶的组化特征

为探讨铜缺乏对奶牛大脑、小脑及脊髓乙酰胆碱酯酶（ACHEase)组化特征（分布特点及活性）的影响，本实验选择铜缺乏症高发区自然发病的奶犊牛6头，剖杀后采集大脑、小脑、脊髓作冰冻切片及酶组化染色，以6头同年生健康奶犊牛为对照。实验结果表明，发病奶牛大脑、小脑及脊髓中ACHEase计数值均显著低于对照组奶牛（P＜0．05）；除大脑外，铜缺额奶牛脊髓上小脑中ACHEase的扫描值也显著低于对照组（P＜0．05）；发病奶牛脊髓小脑中ACHEase的扫描值也低于对照组（P＜0．05）；发病奶牛组织中ACHEase酶颗粒的分布也发生特征性的变化。结论：神经递质酶活性的改变是导致奶牛铜缺乏症病理过程的重要原因。     

The histopathogenesis of paralytic rabies in six-week-old C57BL/6J mice following inoculation of the CVS-11 strain into the right triceps surae muscle

A fatal encephalomyelitis was developed after intracerebral and hind limb inoculation of in 6-week-old C57BL/6J mice by the inoculation of fixed rabies virus (CVS-11 strain), intracerebrally and into hind. After the intracerebral inoculation, virus antigens were detected in the cerebral cortex and hippocampus at 2 days postinoculation (PI), and later spread centrifugally to thalamus, brain stem, cerebellum, spinal cord and spinal ganglia. At 4 days PI, severe apoptosis and DNA fragmentation were observed in the hippocampus and cerebral cortex. All mice infected intracerebrally were dead without limb paralysis at from 10 to 11 days PI. In contrast, mice infected with virus intramuscularly were persistently observed virus antigens in the myocytes at the site of inoculation from 2 days PI. At 4 days PI, the antigens were demonstrated in the spinal dorsal root ganglia, spinal cord and muscle spindles without their detection in the cerebrum and hippocampus. There were no apoptosis in the spinal cord and dorsal root ganglia, however hind limb paralysis was found in all infected mice. Hind limb paralysis was progressed to quadriparalysis, and mice were dead from 11 to 13 days PI. From 4 days PI, necrosis of neuron was observed in the the spinal and dorsal ganglia with infiltration of lymphocyte. This study suggested that the necrosis of spinal neurons was more important to cause the paralysis of hind limb rather than the severe cerebral infection and apoptosis in C57BL/6J mice infected with CVS-11 strain. The virus primarily replicated in the muscles was ascended the spinal cord via afferent fibers and retrogradely invaded the cerebrum, and with subsequent spread to muscle spindles.     

Gliomatosis cerebri in two dogs

A 3.5 yr old Saint Bernard was evaluated for nonambulatory tetraparesis and cranial nerve dysfunction, and a 7 yr old rottweiler was evaluated for progressive paraparesis. Clinical signs of left-sided vestibular and general proprioceptive ataxia and cranial nerve VII dysfunction in the Saint Bernard suggested a lesion affecting the brain stem. Signs in the rottweiler consisted of general proprioceptive/upper motor neuron paraparesis, suggesting a lesion involving the third thoracic (T3) to third lumbar (L3) spinal cord segments. MRI was normal in the Saint Bernard, but an intra-axial lesion involving the T13-L2 spinal cord segments was observed in the rottweiler. In both dogs, the central nervous system (CNS) contained neoplastic cells with features consistent with gliomatosis cerebri (GC). In the Saint Bernard, neoplastic cells were present in the medulla oblongata and cranial cervical spinal cord. In the rottweiler, neoplastic cells were only present in the spinal cord. Immunohistochemistry disclosed two distinct patterns of CD18, nestin, and vimentin staining. GC is a rarely reported tumor of the CNS. Although GC typically involves the cerebrum, clinical signs in these two dogs reflected caudal brainstem and spinal cord involvement.     

Hexachlorophene and cuprizone induce the spongy change of the developing rat brain by different mechanisms: the role of 2', 3'-cyclic nucleotide 3'-phosphodiesterase (CNPase)

The goal of this research was to identify mechanisms responsible for the spongy change induced in rats after repeated hexachlorophene (HCP) or cuprizone (CPZ) dosing. Rats were dosed with 35 mg/kg HCP for 5 days followed by drug withdrawal for 7 days suffered spongy changes to the white matter of the cerebrum, cerebellum, medulla oblongata, and spinal cord that were accompanied by degeneration of oligodendroglia. The severity of both lesions increased prominently on day 5; however, the spongy change decreased and degeneration of oligodendroglia reversed on day 12 (7 days after dosing ceased). On day 12, cerebral cortex oligodendroglia were stained strongly by anti-CNPase. Other rats were fed for 8 days with powdered chow containing 1% (w/w) CPZ, which was then withdrawn for 16 days. The rats exhibited the spongy change in the white matter of the cerebrum and cerebellum as well as oligodendroglial cell death from day 3. The severity of both lesions increased prominently on day 8. Cerebral cortex oligodendroglia were stained strongly by anti-CNPase on days 3 to 8 and decreased to the control levels by day 24 (16 days after dosing ceased). Electron microscopy revealed that oligodendroglia frequently displayed apoptotic morphology. These findings suggest that CNPase expression was induced in the course of restoration following HCP-induced insults to oligodendroglia and the myelin sheath, and in the course of demyelination by CPZ-induced damage to oligodendroglia. However, the role of CNPase on both courses is unclear.     

Comparative pathogenicity of avian encephalomyelitis viruses in chicken embryos.

Multiplications of wild, various embryo-adapting and completely embryo-adapted avian encephalomyelitis (AE) viruses in chicken embryos were compared by the fluorescent-antibody technique (FAT). With a wild AE virus, viral antigens were randomly seen in the central nervous system (CNS), appearing least often in the cerebellum. Other organs seldom became test positive, except for heart and kidney. Even with 4 chicken brain-passaged viruses in the process of embryo adaptation, there was little augmentation of antigens except in the alimentary tract. However, the 2 midpassage viruses showed a peculiar localization of antigens in the white matter of the lumbosacral cord, together with the appearance of test-positive spinal ganglion cells. With 2 strains of embryo-adapted AE virus, the antigens appeared first in the spinal ganglion cells and secondly in the lumbosacral cord and then spread to the cerebrum. Subsequently, clinical signs of AE were evident. This peculiar invasion order was a prominent feature.     

Nervous tissue lesions caused by elaphostrongylosis in wild Swedish moose

During the first 5 months of 1985, 35 moose were obtained for necropsy at the National Veterinary Institute, Uppsala, Sweden. 17 (49 %) of these cases were found to be infected with Elaphostrongylus sp. The nematodes were found in the epidural space of the spinal cord and brain, around and in the sciatic nerves and in muscle fasciae. Predilection sites appeared to be near cauda equina and the fasciae of the thoracic, gracilis and sartorius muscles.Most of the infected animals were calves. Both sexes were equally represented. Pathological changes found were characterized by focal haemorrhages and oedema. The changes were present in the muscle fasciae and in the leptomeninges of the brain and spinal cord. Beside infiltrates of mainly lymphocytes and plasma cells, adult nematodes, larvae and eggs were observed.Cases with mild gliosis in the cerebrum and degenerative changes of peripheral nerve roots affecting the epi- and perineurium were also found. In one case the inflammatory changes reached the endoneurium of a sciatic nerve bundle and in another case into a ganglion.Inflammatory reactions against the parasite were mainly directed towards eggs. In loose connective tissue close to nerve tissue in the central nervous system larvae were found close to eggs and remains of eggs indicating that eggs may hatch at this site.This investigation shows that natural infections with Elaphostrongylus sp. occur in wild moose and may produce pathological changes in large peripheral nerves and in the central nervous system.     

Progressive encephalomyelopathy and cerebellar degeneration in 10 captive-bred cheetahs

Progressive ataxia, with head tremor, developed in 10 captive-born cheetah cubs under six months of age. The condition was usually preceded by coryza and an ocular discharge. Initially the ataxia and weakness affected the hindquarters, then the forelegs, and head tremor developed later. Significant pathological changes were confined to the central nervous system. There was widespread Wallerian degeneration in the funiculi of the spinal cord (except those in the dorsal columns), in the medulla and in the cerebellum. In the cerebellum there was degeneration of Purkinje cells and of the molecular and granular cell layers. There was chromatolysis in the Purkinje cells, the ventral horn cells of the spinal cord and in the neurons of the lateral vestibular nucleus. The olivary nucleus was necrotic. There were foci of inflammatory cells in the molecular layer of the cerebellum and in the medulla. The cause of the disease remains unknown.     

Morphologic and immunoperoxidase study of neurologic lesions in naturally acquired rabies of raccoons.

Histopathologic (hematoxylin and eosin [HE]) and immunoperoxidase (streptavidin-biotin complex) methods were used for examination of formalin-fixed tissues of rabid raccoons from an enzootic area of Pennsylvania. Extensive morphologic lesions of rabies encephalitis were present in the cerebrum and the brain stem regions. Negri bodies were detected by both methods and were present in the brain (cerebral cortex, hippocampus, brain stem, cerebellum, and cervical spinal cord) and in the ganglia of the trigeminal nerves. The viral inclusions were also seen in ganglion cells in the tongue, parotid salivary glands, pancreas, intestines, and adrenal glands. These sites were not associated with any inflammatory cellular infiltrate. The immunoperoxidase method was superior to HE for the detection of Negri bodies. Because lesions of rabies encephalitis were consistently observed in the cerebrum, brain stem, and cervical spinal cord regions, these areas of the brain should be included when raccoons are examined by the fluorescent antibody test for rabies.     

Sur l'Involution de la Bourse de Fabricius chez le Canard

On the involution of the bursa of Fabricius of the duck
The morphological and structural aspects of the functional aspects of the involution were studied light- and electronmicroscopically in ducks 90 to 150 days old. The first involutionary changes were observed in the interfollicular connective tissue around day 100. Following this, cells left the periphery of the follicles; they were connected with collagen fibers and positioned themselves between the lymphocytes of the cortex that became thinner before it disappeared.
On day 135 the medulla lost its lymphocyte content through wide ducts which opened directly into the lumen of the bursa. On day 150 the bursa experienced a massive overgrowth; almost all follicles had disintegrated and only small groups of cells remained which consisted principally of reticuloepithelial cells and some lymphocytes.
Cysts were not observed during the involution of the bursa.