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1.
《中国工作犬业》2009,(8):F0003-F0003
犬瘟热感染机体后,病毒首先在上呼吸道巨噬细胞和淋巴细胞中复制,然后扩散到系统各淋巴结及多种淋巴器官包括脾、胸腺、骨髓和胃肠淋巴组织等,造成淋巴组织退行性病变从而引起免疫抑制。  相似文献   

2.
为了探明高致病性猪繁殖与呼吸综合征病毒(HP-PRRSV)JXA1分离株感染藏猪、藏梅猪和大约克夏猪后,病毒在猪体内的分布规律,本研究利用荧光定量RT-PCR技术检测3个品种猪感染4×105TCID50/m L的JXA1分离株后0、4、7和14 d体内的15个器官(心、肝、脾、肺、肾、大脑、小肠、颌下腺、颌下淋巴结、甲状腺、胸腺、支气管淋巴结、肠系膜淋巴结、腹股沟淋巴结和扁桃体)的病毒载量。结果表明,在整个感染期间,藏梅猪和大约克夏猪的15个器官中均检测到JXA1分离株,而藏猪的心、肝、脾、肾、小肠、颌下腺和甲状腺以及感染后14 d的脑中未检测到JXA1分离株;在JXA1分离株感染3个品种猪4、7和14 d,藏猪病毒载量最多的器官分别是扁桃体、腹股沟淋巴结和颌下淋巴结,藏梅猪分别是脾、脾和肺,大约克夏猪分别为胸腺、肺和颌下淋巴结。本研究证实了JXA1分离株在3个品种猪体内的分布规律和器官嗜性均存在明显差异。  相似文献   

3.
1流行特点病羊是本病的主要传染源,病毒存在于飞沫、唾液里,通过咳嗽和喘气将病毒排出体外,传染给易感羊。在患病妊娠母羊的胎盘里也存有病毒,可将病原传染给胎羊。患病羊只可通过飞沫传播病毒,尤其在气喘或咳嗽时,病毒随唾液或气流散播在空气和自然界中,邻近的羊只经呼吸道吸入这种感染性气溶胶而造成传染,也可通过胎盘垂直传播给羔羊。病毒一经侵入则发病率很高。绵羊最易感,其次为山羊。各种品种的绵羊都能感染本病,以美利奴绵羊最为易感,母羊的发病率较  相似文献   

4.
我们从免疫鸡卵卵黄提取免疫球蛋白制备 IBD荧光抗体,得到了特异性强、灵敏性高、基本上无非特异性反应的诊断制剂。用 CEF 细胞培养可直接(?)以 PBG98株1BDV 弱毒人工感染3日龄雏鸡的器官组织中分离到了病毒。本试验应用荧光抗体试验和 CEF 细胞培养检查和分离病毒的方法证明病毒在感染后的雏鸡体内分布和持续时间如下:强毒在被感染的3日龄雏鸡体内分布于法氏囊、胸腺、肾、直肠、肺、肝等器官。以法氏囊中的病毒浓度最高,扮续时间为8日。在感染有9周龄雏鸡体内分布于法氏囊、盲肠、盲肠扁桃体、十二指肠、胸腺、哈德氏腺、脾、肾、肝等器官;肺、心脏、脑、胰脏中未检出病毒。病毒浓度以法氏囊中最高,持续时间长达9日。弱毒在被感染的3日龄雏鸡体内分布于直肠、法氏囊、胸腺、肝、脾、肺。病毒在直肠中的浓度略高于法氏囊,持续时间亦较长,亦为8日。  相似文献   

5.
鹅副粘病毒的组织嗜性   总被引:2,自引:0,他引:2  
用单克隆抗体介导的免疫过氧化物酶(MC-IP)技术,对21只鹅副粘病毒病鹅体内的病毒抗原进行定位,结合组织病理学观察结果,探讨了鹅副粘病毒的组织嗜性。结果显示,除脑和心脏未检测到病毒外,在气管、肺、食道、肝脏、腺胃、胰腺、肠、哈氏腺、胸腺、脾脏、法氏囊、肾脏等器官都能检测到病毒,病毒抗原定位于上述器官的各种上皮细胞,淋巴细胞、网状细胞和巨噬细胞的胞浆内,其中以胃肠粘膜上皮细胞和法氏囊、胸腺、脾脏的淋巴细胞和网状细胞内检出率高,阳性反应强。这些结果提示,鹅副粘病毒是一种泛嗜性病毒,胃肠粘膜上皮和淋巴组织是其主要侵嗜部位。  相似文献   

6.
边界病(border disease,BD)是由边界病毒(BDV)引起绵羊和山羊的一种病毒性疾病,临床症状表现为母羊不孕、流产和死胎,以及羔羊体型异常,多毛,震颤,因此又称"多毛震颤病","茸毛症".该病的主要传播途径是垂直传播,持续性感染的羔羊是该疾病在绵羊中传播的潜在主要传染源.山羊相对绵羊感染症状相对较轻,主要表...  相似文献   

7.
本研究旨在揭示感染JSRV病羊体内检测不到循环抗体的免疫学机理。用地高辛(DIG)标记制备enJS-RV-env探针,原位杂交法检测妊娠70 d的绵羊胎儿(免疫器官初步形成期)、妊娠130 d胎儿(即将出生的)和出生7日龄羔羊的胸腺、脾脏、肠淋巴结和肺脏内enJSRVmRNA表达情况。并利用Real-Ti me PCR法,对enJSRVmRNA在以上组织中的表达进行定量分析。结果表明,在所检测组织内均有阳性信号出现,而阴性对照组均没有阳性信号;enJSRVmRNA在胎儿和初生羔羊各免疫器官高水平表达,特别是在妊娠130 d胎儿和初生7日龄羔羊的胸腺和脾脏中表达水平比较高,而在各时期的肺脏组织中都检测到低水平表达。本试验结果为机体对exJSRV的感染产生免疫耐受这一假说提供了有力的证据。  相似文献   

8.
探讨番鸭呼肠孤病毒强毒株和弱毒株在番鸭免疫器官中的分布和排毒的差异。结果显示强毒株在感染后1d就可在脾脏、法氏囊、胸腺检出病毒RNA,高峰期为攻毒后7~14d;直到感染后35d,在免疫器官中不能检测到病毒RNA。接种强毒株后7d开始向外界排毒,而14d后停止向外界排毒。雏鸭免疫弱毒疫苗后3d,即可在脾、胸腺、法氏囊中检出病毒RNA;高峰期为攻毒后7~14d,免疫后21d免疫器官中的检测逐渐降低,直到感染后28d,在免疫器官中不能检测到病毒RNA。表明番鸭接种活疫苗后7d开始向外界排毒,而11d后停止向外界排毒。  相似文献   

9.
为了澄清鸡传染性法氏囊病病毒(IBDV)的致病性与病毒抗原分布之间的关系,将强毒株(Ehime/91、DV86)与弱毒株(JI)比较,电镜观察法氏囊,胸腺,脾脏和骨髓中的病毒靶细胞,尽管所有毒株都引起相似的法氏囊萎缩,强毒株还引起胸腺重量指数的大幅度下降,以及盲肠扁桃体,胸腺,脾脏和骨髓的严重损伤,免疫组织化学法检测经Ehime/91或DV86株感染鸡的组织内抗原表明,骨髓和脾中出现大量的抗原阳性  相似文献   

10.
禽副粘病毒2型(PMV-2)致病性的研究   总被引:1,自引:0,他引:1  
7日龄SPF鸡经滴鼻、点眼感染PMV-2,可引起轻微的呼吸道症状,病理组织学观察可见气管粘液分泌亢进和少量的淋巴细胞浸润。PMV-2与传染性支气管炎(IBV)或鸡毒支原体(MG)协同感染比单纯感染这三种病原的任何一种均呈现更严重的呼吸道症状,病理组织变化呈气管纤毛部分或全部脱落,气管粘膜上皮细胞不同程度的变性、脱落。固有层和粘膜下层严重水肿,有大量淋巴细胞、巨噬细胞和异嗜细胞浸润。SPF雏鸡感染PMV-2后的不同时间检查病毒在鸡体内的分布规律,结果表明,PMV-2在法氏囊中大量分布;气管、肺、胸腺中有较多病毒;大脑、脾和肾脏只有少量病毒存在。上述实验结果揭示PMV-2感染SPF雏鸡致病性较弱,PMV-2在鸡呼吸道综合征中起一定作用。  相似文献   

11.
作者运用免疫组织化学技术,首次对我国一类保护物种宁夏滩羊各组织中朊蛋白(PrP)的分布进行定性、定位研究。结果显示,PrP在滩羊的大脑、脑干、小脑、心脏、肝脏、脾脏、肾脏及淋巴结均有表达,尤其在脾脏、肾脏、脑干、淋巴结中的表达量丰富,而肺脏检测结果为阴性。此研究确定了朊蛋白在滩羊各组织中的表达与分布状况,并优化了朊蛋白检测的技术条件,为羊痒病的诊断与检测提供技术支持。  相似文献   

12.
The c-Met proto-oncogene is the receptor for hepatocyte growth factor (HGF), which is a member of the tyrosine kinase family. Activation of the HGF/c-Met signal pathway leads to cell proliferation, motility, regeneration, and morphogenesis. In this study, the complete nucleotide sequence of complementary DNA (cDNA) of canine c-Met was cloned, and its distribution was determined in tissues. The canine c-Met cDNA clone had an open reading frame of 4419 bp that encoded a putative polypeptide of 1383 amino acids. The c-Met mRNA was expressed in a variety of canine tissues including peripheral blood mononuclear cells (PBMC), bone marrow, liver, kidney, lung, stomach, uterus, testis, thymus, lymph node, small intestine, colon, adrenal gland, thyroid gland, heart, muscle, skin, pancreas, ovary, prostate, spleen, fat, cerebrum, and cerebellum. In addition, the c-Met mRNA expression in normal and regenerated liver was examined. The levels of the mRNA increased 2-fold in regenerated liver compared to that found in normal liver, indicating that c-Met is involved in various functions including remodeling of canine hepatocytes.  相似文献   

13.
鸭瘟病毒弱毒株在免疫雏鸭体内的分布和排毒规律   总被引:9,自引:5,他引:9  
鸭瘟病毒(DPV)弱毒Cha株经皮下、口服和滴鼻3种途径免疫1日龄雏鸭,应用聚合酶链反应(PCR)检测了病毒在体内分布和排毒规律。Cha株免疫雏鸭后,对血液、心、肝、脾、肺、肾、十二指肠、直肠、法氏囊、胸腺、胰腺、延脑、大脑、小脑、舌、肌肉、骨髓、粪便和食道共19种组织PCR检测结果如下:(1)皮下接种雏鸭后4h,即可在心、肝、脾、肾、法氏囊、胸腺、胰腺、延脑、大脑和小脑共10种组织中检出DPV的DNA;8h后,所有采取的组织器官均可检测到DPV的DNA。(2)口服接种雏鸭后4h,可在舌和食道中检测到DPV的DNA;8h后,可在心、肝、脾、肾、胸腺、胰腺、延脑、大脑、小脑、舌、食道和血液共12种组织器官中检出DPV的DNA。(3)滴鼻接种雏鸭后4h,未能在各种组织中检出DPV的DNA;8h后,可在心、肝、脾、肾、胸腺、延脑、大脑、小脑、舌、食道和血液共11种组织中检测到DPV的DNA。(4)在3种免疫途径中,检出时间最早和检出率最高的组织器官为肝脏、脑(大脑、小脑和延脑);3种途径免疫的鸭,从免疫后12h至21d均能从所有采集的组织中检测出DPV DNA。  相似文献   

14.
用粪肠球菌人工感染羔羊,复制粪肠球菌病病理模型。病理组织学观察可见病羊大、小脑有微血栓形成;大脑有噬神经和卫星化现象;肝细胞、肾小管上皮细胞变性、坏死、肾间质出血;脾脏的动脉周围淋巴鞘出现有许多上皮样细胞组成的上皮样细胞结节。结果表明,粪肠球菌引起羔羊出现的神经症状是非化脓性脑炎引起的,同时还伴随败血症变化。  相似文献   

15.
The lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) isoenzyme distributions in tissues of the ICR mouse, Wistar rat, guinea pig and golden hamster were analyzed by histoelectrophoresis. Tissues obtained were as follows: liver, pancreas, stomach, small intestine, heart, femoral muscle, uterus, kidney, spleen, lymph node, cerebrum, spinal cord and erythrocyte. Histoelectrophoresis was for the direct analysis of LDH and CPK isoenzymes in the tissues and had high practical value compared with previous tissue-extraction methods. In tissues of the mouse, guinea pig and golden hamster, LDH isoenzymes showed five bands. In the rat, LDH isoenzyme was separated into four fractions. CPK isoenzyme showed three bands; BB, MB and MM. In some tissues, the MM band was separated into two sub fractions.  相似文献   

16.
All sheep older than 1 year of age from a flock of the Rygja breed in which clinical scrapie was detected for the first time in two animals (4%) were examined for accumulation of pathogenic prion protein (PrPSc) by immunohistochemistry in the obex, the cerebellum, and the medial retrophayngeal lymph node. In addition, six lambs, 2-3 months old, all offspring of PrPSc-positive dams, were examined for PrPSc in the ileal Peyers' patch (IPP), the distal jejunal lymph node, the spleen, and the medial retropharyngeal lymph node (RPLN). In this flock, 35% (17/48) of the adult sheep showed accumulation of PrPSc, an eightfold increase compared with clinical disease. All positives carried susceptible PrP genotypes. Three sheep had deposits of PrPSc in the RPLN and not in the brain, suggesting that this organ, easily accessible at slaughter, is suitable for screening purposes. Two 7-year-old clinically healthy homozygous V136Q171 ewes showed sparse immunostaining in the central nervous system and may have been infected as adults. Further, two littermates, 86-days-old, showed PrPSc in the IPP. Interestingly, one of these lambs had the intermediate susceptible PrP genotype, VA136QR171. In addition to early immunolabeling in the dorsal motor nucleus of the vagal nerve, a few of the sheep had early involvement of the cerebellum. In fact, a 2-year-old sheep had sparse deposits of PrPSc in the cerebellum only. Because experimental bovine spongiform encephalopathy (BSE) in sheep seems to behave in a similar manner as natural scrapie, these results, particularly regarding spread of infectivity, may have implications for the handling of BSE should it be diagnosed in sheep.  相似文献   

17.
Mycophenolic acid (MPA) is a mycotoxin commonly found as Penicillium genus secondary metabolite in feedstuffs and silages. Feeding with MPA contaminated silages may modulate the immune system in the farm animals and can cause appetite lost, ketosis, paralysis and abortion. The aim of the present study was to characterize the long-term MPA effect on both the inosine monophosphate dehydrogenase (IMPDH) isoforms I and II mRNA expression in white blood cells (WBC) and various tissue of healthy sheep. In treated animals 300 mg MPA/day/sheep was applied. In all investigated tissues the IMPDH I and II mRNA was abundant: WBC, spleen, thymus, ileum, jejunum, kidney, liver, pharyngeal and mesenterial lymph node. An efficiency-corrected relative quantification of the IMPDH types I and II isoforms mRNA were performed by normalizing with the constant reference gene expression of beta-actin. High IMPDH I mRNA expression levels were seen in kidney > mesenterial lymph node > jejunum > spleen > pharyngeal lymph node. Medium and low abundance was found in ileum > WBC > liver > thymus. Type II mRNA was highly expressed in liver > thymus > jejunum. In pharyngeal lymph node > spleen > ileum > mesenterial lymph node > kidney > WBC medium to low IMPDH II mRNA concentrations were detected. Under MPA treatment the IMPDH I mRNA expression was not significantly regulated in WBC, only trends of down- and upregulation were observed. Surprisingly in jejunum an upregulation could be observed (P < 0.05). In pharyngeal lymph node a tendency to downregulation was shown. This may be due to frequent ruminant activities and frequent exposition of MPA to the pharyngeal lymph nodes. In contrast to type I mRNA expression, IMPDH II mRNA was significantly downregulated in ileum (3.4-fold, P < 0.01) and tendencies in downregulation could be seen in jejunum (5.1-fold, P = 0.14). In addition, significant downregulation of IMPDH II gene expression over the entire feeding experiment could be shown in WBC of MPA-treated animals compared with untreated animals (P < 0.05). In conclusion, the recent study demonstrates that feeding sheep with MPA-contaminated silage did not induce IMPDH I mRNA expression in various tissues and blood, except in jejunum, but has suppressive effects on IMPDH II mRNA expression in WBC and ileum.  相似文献   

18.
Thrombomodulin (TM) is a glycoprotein localized mainly on endothelial cell surfaces, and is a major regulator of vascular thromboresistance. The entire open reading frame of canine TM cDNA comprises 1737 bp, encoding 578 amino acid residues. Comparison of the deduced amino acid sequence from canine TM with those of human, mouse, rat, rabbit and bovine (partial) TM sequences revealed 73.1%, 69.1%, 65.8%, 74.3% and 69.5% identity, respectively. Canine TM mRNA expression was confirmed by RT-PCR analysis in lung, liver, spleen, kidney, pancreas and lymph node, and was relatively low in heart, cerebrum, urinary bladder and uterus. The present results provide valuable data for research into canine coagulation disorders.  相似文献   

19.
20.
During the past several years, acute infections with bovine viral diarrhea virus (BVDV) have been causally linked to hemorrhagic and acute mucosal disease-like syndromes with high mortality. The majority of BVDVs isolated in such cases have been classified as type II on the basis of genetic and antigenic characteristics. It was our objective to examine clinical disease, lesions and potential sites of viral replication, following experimental BVDV type II infection in young calves. On approximately day 35 after birth, calves that had received BVDV-antibody-negative colostrum were infected by intranasal inoculation of 5 x 10(5) TCID50 of BVDV type II isolate 24,515 in 5 mL of tissue culture fluid (2.5 mL/nostril). Calves were monitored twice daily for signs of clinical disease. Approximately 48-72 h after infection, all calves developed transient pyrexia (39.4-40.5 degrees C) and leukopenia. Beginning on approximately day 7 after infection, all calves developed watery diarrhea, pyrexia (40.5-41.6 degrees C), marked leukopenia (> or = 75% drop from preinoculation values), variable thrombocytopenia, and moderate to severe depression. Calves were euthanized on days 10, 11, or 12 after infection due to severe disease. Gross and histological lesions consisted of multifocal bronchointerstitial pneumonia (involving 10%-25% of affected lungs), bone marrow hypoplasia and necrosis, and minimal erosive lesions in the alimentary tract. Immunohistochemical staining for BVDV revealed widespread viral antigen usually within epithelial cells, smooth muscle cells and mononuclear phagocytes in multiple organs, including lung, Peyer's patches, gastric mucosa, thymus, adrenal gland, spleen, lymph nodes, bone marrow, and skin. This BVDV type II isolate caused rapidly progressive, severe multisystemic disease in seronegative calves that was associated with widespread distribution of viral antigen and few gross or histological inflammatory lesions.  相似文献   

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