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1.
用疑似猪冠状病毒性脑脊髓炎自然病例脑组织,脑内或脑内兼滴鼻接种于4头4日龄同窝仔猪结果4头实验仔猪都出现和自然病例相似的神经症状及非化脓性脑脊髓炎病变。病变以脑脊髓的软膜、小脑、嗅脑和颈部脊髓的实质比较明显。  相似文献   

2.
猪血凝性脑脊髓炎(PHE)是由血凝性脑脊髓炎病毒(HEV)感染引起猪的一种急性传染病,主要侵害1周龄~3周龄的哺乳仔猪。感染仔猪以呕吐、衰竭和神经症状为特征,病死率很高。血凝性脑脊髓炎病毒具有嗜神经性,主要从感染部位经外周神经向中枢神经系统传播,引起中枢神经系统损伤,从而造成非化脓性脑炎的病变。论文主要对猪血凝性脑脊髓炎的病原、临床症状和病理变化、致病机制、潜在危害及防治等方面进行综述。  相似文献   

3.
仔猪伪狂犬病的病理学研究   总被引:5,自引:0,他引:5  
实验用三周龄健康哺乳仔猪18头,随机分为三组,以三种接种途径(脑内注射、滴鼻和肌肉注射)、不同剂量感染三株伪狂犬病毒株(PrV-S、Pry-闽A和PrV-Shope)。发病仔猪于体温升高至41~12℃后反复出现神经症状。尸体剖检除脑膜充血水肿外,一些病例肺和肝出现小的坏死灶。病理组织学变化主要为淋巴细胞性脑膜脑脊髓炎和神经节的神经元广泛变性坏死。在大脑、神经节、扁桃体、肺和淋巴结发现核内包涵体。  相似文献   

4.
猪血凝性脑脊髓炎的研究现状   总被引:1,自引:0,他引:1  
猪血凝性脑脊髓炎是由血凝性脑脊髓炎病毒(HEV)感染引起猪的一种急性传染病,主要侵害乳猪。以呕吐、衰竭和脑脊髓炎为特征,死亡率很高。血清学检测证明猪感染HEV很普遍,可能是世界性的。作者对猪血凝性脑脊髓炎的病原、发病机理、临床症状、病理变化及常用的诊断技术和防制措施等几个方面的研究现状作了简要综述。  相似文献   

5.
猪血凝性脑脊髓炎是由红细胞凝集性脑脊髓炎病毒(HEV)引起的猪的急性传染病。以主要引起仔猪呕吐、食欲废绝、便秘、进行性消瘦及中枢神经系统功能障碍为特征,临诊上又称仔猪呕吐一消瘦病。初发病地区,病死率高。疫区的新生仔猪通常从初乳中获得被动保护,随后建立了日龄相关的抵抗力。  相似文献   

6.
鸡脑脊髓炎病由脑脊髓炎病毒感染所引起,雏鸡和成年鸡都能感染,通过消化道途径进行水平传播,也能经种蛋垂直传播;雏鸡发病后以神经症状表现为主,传播较快,病死率高,成年鸡感染后基本无症状,进入产蛋期的鸡群可出现产蛋减少,蛋品质下降;本病目前没有特效药物能够治疗,临床可通过疫苗免疫、加强环境消毒和提升管理水平等措施进行防控。  相似文献   

7.
禽脑脊髓炎免疫细胞类别和数量变化的分析   总被引:3,自引:0,他引:3  
本研究用AEV-NH937株分别给1日龄雏鸡口服感染和脑内接种,并在感染后的不同阶段采血、剖检,进行琼扩试验和病理组织学观察(H.E.染色、胶质细胞染色、RNA显色、ANAE显色),结果表明:AEV经不同途径感染均引起了典型的非化脓性脑脊髓炎,血清琼扩反应阳性,各免疫器官和中枢神经小血管周围均见RNA阳性细胞(主要是前浆细胞和浆细胞)明显增多。感染后机体出现了活跃而持续的体液免疫应答;同时也见ANAE阳性细胞(主要是巨噬细胞)增多。  相似文献   

8.
伪狂犬病是由伪狂犬病病毒引起猪和多种哺乳动物共患的急性传染病.其特征为奇痒(猪的症状不明显或无此症状),发热与脑脊髓炎.讷河市讷南镇一猪场发生猪流产、死胎及呼吸症状,仔猪出现脑脊髓炎、败血症,部分病猪还出现擦痒症状等.经用兔子接种试验诊断为猪伪狂犬病.  相似文献   

9.
AEV-NH937引起禽脑脊髓炎的病理学观察   总被引:1,自引:0,他引:1  
用禽脑脊髓炎病毒NH937毒株脑内接种1日龄SPF雏鸡,分别在攻毒后3,5,10,14,20,25和30d分别宰杀对照组两只和攻毒组4只,取大脑和小脑、固定、HE染色。结果临床发病在第6天出现,第9天普遍发病并开始死亡,到第14天死亡停止。在第3天时,软脑膜充血出血、神经元再现少量变性坏死,第10天和14天损伤性变化最重,后管套现象和小胶质细胞增生等占主导地位。  相似文献   

10.
对辽宁省某规模化猪场发病的哺乳仔猪,通过临床症状、血清学、病理学、动物试验和反转录多聚酶链式反应(PCR)方法进行综合诊断,确诊为猪繁殖与呼吸综合征(porcine reproductive and respiratory syndrone virus,PRRSV)与猪血凝性脑脊髓炎病毒(HEV)混合感染。RT-PCR检测结果证明,所感染的PRRSV为美洲型毒株,猪血凝性脑脊髓炎病毒多呈隐性感染,本猪场哺乳仔猪发生二者混合感染,可能与PRRSV感染猪免疫力降低,容易感染HEV而混合发病有关。  相似文献   

11.
为研究血凝性脑脊髓炎病毒(HEY)在人工感染仔猪体内的侵袭过程和分布规律,本实验采用滴鼻的方式感染5头1日龄未食初乳仔猪,并在感染后每隔24 h迫杀1头仔猪,采集鼻黏膜、气管、口腔黏膜、舌、食管、胃、肠、心肌、肝、脾、肺、肾、各段脊髓和脑等组织脏器制作切片,通过间接免疫组织化学方法检测HEV在仔猪体内的动态侵袭过程.此外,采用SYBR Green Ⅰ实时荧光定量PCR(Real-time PCR)方法检测病毒在各组织脏器中的分布情况.结果显示:感染病毒后2 d~3 d,仔猪出现精神沉郁、全身震颤等中枢神经系统症状,免疫组织化学检测可见病毒抗原首先出现于脑桥,并进一步蔓延至延髓和各段脊髓,最后进入小脑浦肯野氏细胞和大脑皮层锥体细胞中;Real-time PCR检测结果显示病毒广泛分布于大脑皮层、脑桥、延髓、脊髓和小脑等中枢神经系统的组织中,其中大脑皮层的检出率最高.  相似文献   

12.
本实验室2012年从江苏省太仓市某发病猪场分离到1株变异的伪狂犬病毒,命名为JS-2012。为了研究该分离株对仔猪的致病性,将12头15日龄的伪狂犬病毒阴性仔猪随机分为3组,其中2组(每组5头猪)分别通过肌肉注射和滴鼻接种JS-2012毒,第3组2头猪做空白对照。接种病毒的仔猪在攻毒后24 h体温均开始升高,4 d后开始死亡,死亡率为100%。临床观察发现,滴鼻组仔猪发病死亡明显快于肌肉注射组。对病死猪进行剖解,均可见大脑血管扩张并出血等典型的伪狂犬病病理变化。病理切片显示猪的脑蛛网膜下腔严重出血,其他各脏器也均有严重病理变化。结果表明该变异株JS-2012为伪狂犬强毒毒株。  相似文献   

13.
Twenty colostrum-fed piglets from three sows were separated from the sows 24 hours after birth and were randomly divided into five groups of four piglets each. Every piglet in each of four test groups was orally inoculated with about 10(10) colony forming units of Salmonella typhimurium, Salmonella choleraesuis var Kunzendorf or one of two isolates of Klebsiella pneumoniae. One group served as uninoculated controls. Piglets infected with K. pneumoniae developed severe diarrhea beginning about 12 hours after inoculation. They became dehydrated and weak but continued to drink. There were no morphological alterations in intestinal mucosa when piglets were killed and necropsied 48 or 72 hours after inoculation. Klebseilla pneumoniae was isolated from intestine and feces but not from liver or spleen. Piglets inoculated with S. choleraesuis became lethargic and disinterested in food by 24 hours after inoculation. Diarrhea developed by 48 hours after inoculation. Lesions at necropsy 60 or 72 hours postinoculation were subcutaneous edema, mesenteric lymphadenitis, diffuse intestinal superficial mucosal necrosis with villous atrophy, and focal deep ulceration in the ileum. Salmonella choleraesuis was isolated from all segments of intestine and from feces, liver and spleen. Piglets inoculated with S. typhimurium developed a relatively mild diarrheal disease with lesions similar to those with S. choleraesuis infection but less severe. The inoculated organism was recovered from all areas of intestine and from feces, liver and spleen. Serum from infected and control piglets had high (greater than 1:256) agglutinating titres against S. typhimurium but low titres (0 to 1:8) against S. choleraesuis. The agglutinins were assumed to originate from colostral antibodies.  相似文献   

14.
Five colostrum deprived hysterectomy-derived piglets were inoculated by the intratracheal route with a Porcine Respiratory Coronavirus (PRCV). The clinical effects and growth performances were compared with those in 5 similar piglets which were inoculated with Minimum Eagle Medium only. A transient hyperthermia, mild to severe dyspnoea, polypnoea and an obvious cessation of growth were recorded on infected pigs only whereas the control group did not show any adverse reaction after inoculation. The reasons for the variability of effects of experimental infection observed in previous trials, are discussed.  相似文献   

15.
An experimental model for subclinical edema disease was developed in weanling pigs. In multiple experiments, 3-week-old pigs were weaned, then inoculated intragastrically with 10(10) colony-forming units of an SLT-IIv-positive strain of Escherichia coli originally isolated from a pig with edema disease (principals). Control pigs were inoculated with a nonpathogenic E coli strain. Of 39 principals, 8 developed clinical edema disease within 14 days after inoculation. However, 20 of 21 principals that did not develop clinical signs of edema disease, but were submitted for necropsy examination at 14 days after inoculation, had characteristic vascular lesions of edema disease. Vascular lesions, found principally in ileum and brain, consisted of segmental necrosis of myocytes in the tunica media of small arteries and arterioles. None of the pigs inoculated with a nonpathogenic strain of E coli developed edema disease or vascular lesions. None of the principals necropsied at 2 days after inoculation had vascular lesions. Development of vascular lesions by 14 days after inoculation was used as the end point for detecting subclinical edema disease in the model.  相似文献   

16.
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.  相似文献   

17.
Five sows were inoculated with a cell-cultured, cytopathic strain of the virus of transmissible gastroenteritis (TGE). Two sows were inoculated intramuscularly, and three by the intramammary route. The response was measured by the neutralizing antibody titers in the serum and the milk, and by the protection against experimental challenge of piglets nursing the sows. There were no marked differences in the serum or milk antibody titers resulting after the two methods of inoculation, although milk titers at the time of challenge were higher after intramammary inoculation. Piglets nursing sows inoculated by the intramammary route were protected to a greater extent than those nursing sows inoculated intramuscularly.  相似文献   

18.
The virulence of a NAD-independent Actinobacillus pleuropneumoniae serotype 2 strain and NAD-dependent serotype 2, 3 and 9 strains was compared under experimental conditions. Hysterectomy-derived piglets were inoculated endobronchially with 50-500 cfu of these strains. All 23 piglets inoculated with the NAD-dependent strains developed acute disease within 12 hours post inoculation. Twenty-two of these piglets died within 24 hours after the first clinical signs. Three of nine piglets inoculated with the NAD-independent strain did not develop clinical disease. In the other six piglets, disease signs were similar as in the piglets inoculated with the NAD-dependent strains. No differences in clinical disease were observed between colostrum deprived piglets and piglets that obtained colostrum from a SPF sow.  相似文献   

19.
鸭黄病毒病为近年来新发的鸭病,给养鸭业带来了极大的经济损失。为了深入研究本病的防制,本试验对鸭黄病毒(duck flavivirus,DFV)进行了分离鉴定。取疑似感染DFV的病鸭病料,经细菌分离初步排除细菌感染后,应用RT-PCR检测呈现DFV阳性,处理后将其接种到鸭胚成纤维细胞(DEF)和健康鸭胚上进行病毒分离传代。结果显示,在DEF细胞上第1代48 h就开始出现CPE,随着时间的延长CPE更加明显,通常在72~96 h产生典型CPE;接种鸭胚每一代均出现死亡,且死亡时间多集中于接种后60~72 h,死亡鸭胚胚体水肿、出血、发育不良、胚肝严重出血、肿胀或斑驳样坏死等病变。将病毒DEF细胞和鸭胚分离物应用血凝试验、毒价测定、病毒中和试验、RT-PCR及人工感染试验进行检测鉴定,证明所分离到的病毒为DFV,并将其命名为DFV SDbz株。  相似文献   

20.
Subcutaneous injections of modified-live pseudorabies virus (PRV) vaccine into lambs caused clinical signs and death within 1 week after injection in 4 of 5 inoculated lambs. The clinical signs included depression, high fever, muscle fasciculations and convulsions, occasionally followed by death within 48 hours of the initial clinical signs. Histologic examinations and virus isolation procedures demonstrated PRV in the CNS of infected lambs. Sera from sick lambs remained negative for PRV antibodies. Two subsequent serial passages of the vaccine virus in lambs resulted in similar clinical signs and death in 6 of 10 inoculated lambs. Again, PRV was isolated from tissues of sick lambs, and the histopathologic findings were characteristic of the disease. Affected lambs remained seronegative to PRV, as did lambs that remained clinically normal after inoculation. There was no evidence of PRV transmission to uninoculated lambs and pigs housed with the infected lambs.  相似文献   

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