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1.
给8头3日龄同窝仔猪经口感染猪流行性腹泻病毒“吉”毒株的猪胎肠单层细胞培养物,于感染后在第18、30、45、96h扑杀,进行病理组织学和病理组织化学研究。病理组织化学(硷性磷酸酶、ATP酶、琥珀酸脱氢酶、单胺氧化酶)的变化早于病理组织学变化。组织学变化以小肠绒毛上皮细胞脱落、绒毛短缩为特征,其中以空肠中,后部的肠绒毛变化最严重;临床症状与病理变化呈正相关,感染后24~36h,实验仔猪呕吐、腹泻最明显,而感染30h扑杀的实验仔猪,小肠绒毛短缩,上皮细胞脱落最严重。作者认为,初期腹泻主要是小肠绒毛柱状上皮能量生成不足,吸收和运输障碍所致;而后期则是肠绒毛柱状上皮能量生成不足,吸收表面积严重减少,绒毛柱状上皮严重变性导致的消化不良共同作用的结果。  相似文献   

2.
《畜牧与兽医》2015,(12):134-136
为了对引起北京地区仔猪腹泻的轮状病毒进行致病性研究,购买未采食母乳的初生仔猪6头,分成2组,试验组3头仔猪口服并皮下注射三代细胞病毒1 m L,观察其临床症状;分别在感染前及感染后24、48、72、96 h等采集肛门拭子,RT-PCR检测病毒抗原,观察排毒情况;取感染5 d后的小肠、肝、脾等组织,观察病理学变化。结果显示:试验仔猪感染12 h,肛门拭子即可检测到轮状病毒,一直持续到第5天。组织切片观察发现,仔猪小肠上皮细胞及周围绒毛发生变性,上皮细胞变圆、肿胀、核肿大,细胞边缘不规则。变性细胞从基质脱落至管腔,萎缩绒毛被扁平上皮细胞覆盖,固有层有少量细胞碎片。  相似文献   

3.
猪流行性腹泻流行病学研究进展   总被引:2,自引:0,他引:2  
<正>猪流行性腹泻(PED)是由猪流行性腹泻病毒(PEDV)感染引起的一种以急性腹泻、呕吐、严重脱水为主要临床症状的急性、高度传染性、高致死性病毒性肠道传染病。PEDV可感染各年龄段的猪,以哺乳仔猪最易感,经口鼻感染后病毒直接进入小肠,在肠绒毛上皮细胞增殖进而对细胞器造成损伤,导致的细胞功能障碍引起肠黏膜细胞坏死、肠绒毛脱落,从而引起腹泻,脱水,小肠臌气、扩张、积液等临床症状,严重者可导致仔猪死  相似文献   

4.
为了加深对猪流行性腹泻病理学损害的认识,试验采用常规石蜡切片及免疫组织化学方法对确诊为变异猪流行性腹泻病毒(Porcine epidemic diarrhea virus,PEDV)引起的患病仔猪主要脏器的病理变化及抗原定位进行了研究。结果表明:猪流行性腹泻患病仔猪胃黏膜脱落,肠系膜肿胀充血、乳糜管消失;小肠绒毛上皮细胞坏死、脱落,肠绒毛缩短,肠壁变薄;肠系膜淋巴结髓质区瘀血出血;小肠绒毛上皮细胞、肠腺细胞、隐窝部位、小肠绒毛固有层和肠系膜淋巴结出现PEDV强阳性表达。说明PEDV的主要靶器官是胃肠黏膜上皮、腺体及相应的淋巴结,而胃、肠等器官的损伤是该病的主要病理变化特征。  相似文献   

5.
正仔猪流行性腹泻多由病毒引起,以腹泻仔猪的高死亡率为主要特征,多发于寒冷季节。如果饲养场(户)不提前预防,一旦爆发,将难以控制,可给养猪场(户)带来巨大的经济损失。1发病特点近年来该病流行范围很广,1周龄内患猪发病治愈率很低,死亡率可高达85%~100%。剖检病死仔猪,可见肾脏出血,肾盂有黄色微粒损伤,眼观变化仅限于小肠扩张,充满黄色液体,肠系膜充血,淋巴结水肿,肠绒毛萎缩。组织学变化,可见空肠段上皮细胞形成空泡和表皮脱落,肠绒毛  相似文献   

6.
《山东饲料》2007,(1):27-27
症状猪流行性腹泻是由病毒引起的一种猪的肠道传染病,多发于寒冷季节。主要症状为呕吐、腹泻和脱水。眼观小肠扩张,肠内充满黄色液体,肠系膜充血,肠系膜淋巴结水肿,小肠绒毛缩短。各种年龄的猪都能感染发病。哺乳仔猪发病率最高,母猪发病率变动很大,一般为15%-90%。  相似文献   

7.
云南省香格里拉市某藏猪场育肥猪出栏屠宰时,陆续发现部分个体小肠肠系膜浆膜下有大量葡萄串状透明无味气泡,病因不明,但病猪在仔猪阶段有腹泻病史。为调查发病原因和致病机理,以便提出防控措施,采集该养猪场4头患病猪和1头正常猪的抗凝全血、小肠组织和肠系膜淋巴结,进行病毒核酸PCR扩增、细菌分离培养和组织病理显微观察。在患病猪中,未检出与腹泻有关的猪瘟病毒、猪流行性腹泻病毒、传染性胃肠炎病毒和轮状病毒核酸;血琼脂有氧和厌氧培养均只分离到大肠杆菌,并排除常见致病血清型及常见毒力基因;组织病理检查发现,肠黏膜下层有大量空泡,肠腺及其杯状细胞体积明显增大,组织间隙扩大,肠系膜及其淋巴结分别见嗜酸性粒细胞和巨噬细胞增多,病变肠系膜淤血。分析认为,该病病因应考虑养殖区域海拔较高,猪肠内大肠杆菌异常发酵产气的可能,但如何防治需进一步研究。  相似文献   

8.
【目的】 在从腹泻仔猪粪便中分离鉴定猪A群轮状病毒(Rotavirus group A, RVA)并了解其致病性。【方法】 应用MA-104细胞从仔猪腹泻粪便中分离鉴定RVA, 将其经口感染健康初生仔猪, 观察其临床症状, 并利用实时荧光定量PCR检测排毒、HE染色观察病理变化、免疫组织化学(immunohistochemistry, IHC)试验了解病毒分布。【结果】 分离到1株可引起MA-104细胞明显细胞病变的G9P[23] RVA, 命名为RVA/Pig-tc/CHN/SCJY-13/2017/G9P[23](简称SCJY-13株), 病毒滴度为105.5 TCID50/100 μL。经口感染SCJY-13株的仔猪在感染后11 h出现腹泻, 持续到感染后165 h完全恢复, 其发病率为100%(7/7), 病死率为28.57%(2/7)。感染后8 h可从仔猪肛拭子检测到病毒核酸, 直至感染后192 h, 峰值出现在感染后24 h。感染后54 h各段小肠病毒载量达到最高, 其中回肠中病毒载量最高, 显著高于十二指肠、空肠(P<0.05);HE染色和IHC检测结果显示, SCJY-13在感染仔猪小肠的绒毛及隐窝中大量聚集, 尤其是回肠段; SCJY-13株感染引起十二指肠、空肠和回肠绒毛固有层大量淋巴细胞浸润、黏膜上皮细胞和肠绒毛尖端空泡变性、柱状细胞增多、绒毛断裂脱落等, 以回肠段较严重。【结论】 SCJY-13株能引起新生仔猪100%发病, 其主要靶位区在回肠, 感染后排毒时间长。本试验结果为猪RVA的致病性研究提供了一定的参考依据。  相似文献   

9.
本研究对泰安某规模化猪场12日龄病死仔猪进行剖检观察、病理组织学观察和病原学检测.结果发现,感染猪以呕吐、腹泻为主要临床特征,剖检病死猪可见肠壁变薄透明并在肠腔内聚集大量黄色液体,肠系膜血管充血,且肠系膜淋巴结水肿;结肠绒毛萎缩变性、充血出血.PCR检测显示猪流行性腹泻病毒阳性,对其S基因测序并进化分析显示,该猪场感染...  相似文献   

10.
旨在研究猪δ冠状病毒(porcine deltacoronavirus, PDCoV)感染对仔猪免疫系统的影响。选取10头5日龄健康仔猪随机分为空白对照组和PDCoV感染组(n=5),PDCoV感染72 h后剖解仔猪,采集仔猪的胸腺、扁桃体、脾脏和淋巴结(颈浅淋巴结、腹股沟淋巴结、髂下淋巴结、下颌淋巴结和肠系膜淋巴结),4%(g/L)的多聚甲醛溶液固定,苏木精-伊红染色观察免疫系统病理变化,免疫组织化学检测病毒分布。苏木精-伊红染色结果显示,PDCoV感染仔猪后脾和淋巴结都出现了明显的病理损伤。脾小梁增生;红髓增多,红髓和白髓界线不清、分布铁黄素颗粒;白髓萎缩,脾小结减少,淋巴细胞减少。淋巴结局部组织出现毛细血管充血或轻微出血,皮质和髓质界线不清,淋巴小结体积增大,数量增多,生发中心明显变大。免疫组织化学结果显示,仔猪肠系膜淋巴结有大量病毒分布,下颌淋巴结存在少量病毒,其余免疫组织无病毒分布。上述结果说明,PDCoV感染后可引起仔猪免疫器官产生病理损伤,降低仔猪的免疫功能,这为深入了解PDCoV致病机制和临床防控提供了理论依据。  相似文献   

11.
Maedi visna virus (MVV) vertical transmission in sheep via infected colostrums is a very important route of infection in lambs. To verify colostral transmission and to study early viral entry in lambs, colostrum samples, and small intestine and mesenteric lymph nodes of lambs born from experimentally infected ewes were examined by histopathology, immunohistochemistry (IHC) and in situ hybridisation (ISH) studies. In particular, newborn lambs were naturally fed maternal colostrum and humanely killed at 10, 24, 48, 72, 96 h and 7 and 10 days after birth; two caesarian-derived lambs served as uninfected controls. No lesions suggestive of MVV infection were found, but marked immunoreactions for MVV capsid antigen (CA, p28) were detected in lambs fed maternal colostrum and in macrophages cultured from colostrum. IHC results in lambs suggest an initial viral absorption by intestinal epithelial cells at the tip of the villi, passage to mononuclear cells in the lamina propria and involvement of ileum Peyers' patches and mesenteric lymph nodes, with different staining patterns depending on infection times. ISH on intestinal sections of the 72 h lamb revealed the presence of proviral DNA in epithelial cells at the tip of the villi, suggesting a role for these cells in early MVV replication. The results contribute to knowledge about the pathogenesis of ovine lentivirus infection suggesting that the small intestine and mesenteric nodes are the sites of entry and propagation of MVV in lambs fed colostrums from infected ewes.  相似文献   

12.
The effects of hyperimmune cow colostrum (HCC) on experimentally induced porcine epidemic diarrhea (PED) were investigated in piglets. In experiment 1, four 2-day-old piglets fed HCC containing an antibody titer of 1:512 and another four piglets fed unimmune cow colostrum (UCC) were orally inoculated with 10LD50 of PED virus. The piglets were given colostrum three times a day at 4 hr intervals. Half of the piglets fed HCC showed diarrhea and recovered, and all piglets survived. In contrast, all piglets fed UCC developed diarrhea and three of them died. In experiment 2, 2-day-old piglets fed HCC containing antibody titers of 1:512, 1:128 and 1:32, and UCC were inoculated with PED virus, and survival rates after challenge were 100, 75, 50 and 0 %, respectively. In experiment 3, 1-day-old piglets fed HCC with 1:512 antibody titer or UCC were inoculated and necropsied at 24, 48 and 72 hr after the inoculation for pathological examination. Piglets fed HCC remained healthy and PED virus antigen was not detected in the epithelial cells of the small intestine, and the length of the villi in small intestine was normal. On the other hand, in piglets fed UCC, villous atrophy and PED virus antigen were observed in epithelial cells of the jejunum and ileum from 24 hr. It was concluded that oral administration of HCC to piglets was effective in preventing PED virus infection and reduced their mortality.  相似文献   

13.
A porcine respiratory coronavirus (PRCV) was inoculated by aerosol into nine hysterectomy-derived and colostrum-deprived pigs at the age of one week. They were killed at different times after inoculation and tissues were sampled for virus isolation and immunofluorescence. Results indicate that virus replicated to high titres in the respiratory tract. Replication mainly occurred in alveolar cells but also in epithelial cells of nasal mucosa, trachea, bronchi, bronchioli, in alveolar macrophages and in tonsils. After primary replication in the respiratory tract, viraemia occurred. Virus also reached the gastrointestinal tract after swallowing. Subsequently, PRCV was observed to replicate in the ileum. The infection spread within a few days from the ileum to the duodenum. Replication in the small intestine remained limited to a few cells located in or underneath the epithelial layer of villi and, or, crypts. The cell type could not be identified. Virus was isolated from mesenteric lymph nodes in all pigs, but immunofluorescence was not observed. Results show that small changes in molecular structure between transmissible gastroenteritis virus and PRCV resulted in important changes in host cell tropism.  相似文献   

14.
Transmissible gastroenteritis virus (TGEV) infection of piglets results in a very rapid and massive release of IFN-alpha in serum and secretions. The objective of this work was to characterize the IFN-alpha-producing cells (IPC) in tissues of TGEV-infected piglets. Caesarean-derived colostrum-deprived piglets were infected orally with the TGEV virulent Miller strain and IPC were characterized in situ by immunohistochemistry, using a rabbit anti-pig IFN-alpha antiserum. IPC were almost exclusively detected in intestinal tissues and mesenteric lymph nodes (MLN), as early as 6 h post inoculation (p.i.), with a peak at 12-18 h. They disappeared by 24 h. IPC were localized between enterocytes in the small intestine epithelial layer, in the lamina propria, around the Peyer's patches and, at highest frequency, in MLN. Very few IPC were present in the spleen and popliteal lymph nodes of infected piglets. Double immunohistochemical staining for IFN-alpha and leukocyte markers on MLN cryosections showed that IPC were mainly Swine Leukocyte Antigen (SLA) class II positive, and were not stained by an anti-macrophage (SWC3a) MAb. In addition, double staining with anti-TGEV and anti-IFN-alpha MAbs showed that viral antigens were present in MLN, close to IPC. These results show for the first time the presence of IPC in gut mucosa and gut-associated lymphoid tissues in response to an enteropathogenic virus. Moreover, this work shows that IFN-alpha released in serum is likely to originate almost exclusively from gut IPC triggered locally by viral antigens to produce IFN-alpha, since there were very few IPC in spleen or peripheral lymph nodes. MHC class II molecule expression by gut-associated IPC suggests that these cells may be the in vivo mucosal counterparts of the dendritic cells recently shown to produce IFN-alpha after in vitro viral induction.  相似文献   

15.
Gross and histologic lesions of paratuberculosis were studied in water buffaloes. Small intestines and associated mesenteric lymph nodes of 405 water buffaloes were examined. Of these, 20 animals having visible changes of intestinal thickening, mucosal corrugations, and enlargement of mesenteric lymph nodes exhibited histologic alteration characteristics of mild to moderate granulomatous inflammation. The histologic lesions observed in these animals were classified into 3 grades on the basis of type of cellular infiltration, granuloma formation, and presence of acid-fast bacilli. Grade-1 lesions observed in 8 animals were marked by the presence of scattered epithelioid macrophages amid large number of lymphocytes in the intestinal villi and in the paracortical regions of the associated mesenteric lymph nodes. Another 8 animals classified under grade-2 revealed microgranulomas, infiltration with a larger number of epithelioid macrophages besides lymphocytes in the intestinal villi, and granulomas in the mesenteric lymph nodes. Grade-3 lesions observed in 4 animals were characterized by the presence of epithelioid granulomas and giant cells in the intestines and the mesenteric lymph nodes. The Ziehl-Neelsen's stained tissue sections revealed acid-fast bacilli in grade-3 and -2 animals and acid-fast granular debris in grade-1 animals. Among these 20 buffaloes, 14 (70%) were positive in the IS900 specific polymerase chain reaction and 6 (30%) were positive in the bacterial culture.  相似文献   

16.
The distribution and diameter of the pores of epithelial basement membrane in the intestinal villi and the lymph nodules of ileal Peyer's patches were investigated in the rat small intestine by scanning electron microscopy after the removal of the overlying epithelial cells with OsO(4) maceration. In the duodenum, jejunum and ileum, the pores were mainly distributed at the upper three fourths of the villi, but were scarce around the top of the villi. The diameter of some of the pores in the upper three fourths of the villi was larger than that of those in the lower portion. The protrusion of lymphocytes and the cytoplasmic processes of macrophages were also seen at the orifices of the pores. In ileal Peyer's patches, in contrast, pores were densely distributed in the lower one third of the follicle-associated epithelium (FAE) where M cells were mainly seen. Furthermore, these pores were larger than those found in the upper two thirds. Lymphocytes or cytoplasmic processes of macrophages were frequently seen in the lower one third of FAE. These results suggest that the pores at the basement membrane correspond to the passage of the immunocompetent cells which are in contact with M cells or villous columnar epithelial cells and that the abundance of pores is a sign of aggressive interaction between the particular epithelial cells and the immunocompetent cells at the upper three fourths of intestinal villi and the lower one third of FAE in the rat small intestine.  相似文献   

17.
Histochemical studies were performed on tissues from piglets of different ages treated orally with iron dextran soon after birth. The mucosal cells in the distal region of the small intestine were heavily laden with stainable iron granules during the first three days after the iron administration. The absorptive epithelial cells are desquamated within seven to ten days after birth. Consequently, the number of iron granules gradually diminishes during the first seven days after treatment and no iron granules are demonstrated 12 days after the administration of iron. The iron dextran complex is pinocytosed in newborn piglets and then transported via the lymphatic system. Thus the sinusoidal lining cells of the body and mesenteric lymph nodes are already heavily laden with iron granules 24 hours after oral treatment. This iron store is released only slowing during the first weeks of life. Great amounts of iron granules are demonstrated in the liver and spleen macrophages during the first week after the administration of iron. Due to the rapid utilization of iron in growing piglets these iron stores diminish sharply during the weeks following birth. The distribution of stainable iron in the lymph nodes, liver and spleen seven days after intramuscular injection of iron dextran in newborn piglets was comparable to that for oral administration at that stage of the experiment.  相似文献   

18.
The first aim of our study was to obtain information on the transmission of antigen-specific antibodies from colostrum to respiratory tract mucosa in piglets. The second aim was to confirm the biological relevance of the presence of lymphocytes in colostrum and the already described fact that these cells can penetrate the intestinal barrier and "colonize" peripheral blood and lymphatic tissues of piglets. Therefore, we performed an experiment in which sows were immunized with a model antigen Keyhole Limpet Hemocyanin and their piglets were euthanized at different intervals after birth and colostrum intake. Colostrum, bronchoalveolar lavage fluid and blood samples were collected for serological detection of antigen-specific antibodies. Lymphocytes isolated from peripheral blood and lymphatic tissues (mesenteric and tracheobronchial lymph nodes and spleen) of piglets were in vitro activated with the antigen. We found that colostrum-derived antibodies can cross into the respiratory tract mucosa. Furthermore, we found that antigen-specific lymphocytes were detectable in mesenteric lymph nodes and peripheral blood, but very rarely in spleen and tracheobronchial lymph nodes.  相似文献   

19.
Shiga-toxigenic E. coli (STEC) strains that produce Shiga toxin Stx2e cause oedema disease in weaned piglets. The purpose of the present study was to investigate the impact of Stx2e released in mesenteric lymph nodes on disease pathogenesis. Colistin and ampicillin were intramuscularly administered to piglets of the experimental group simultaneously challenged with STEC strain, type O139:F18ab, Stx2e+. Piglets of the control group were challenged with STEC only. The strain was naturally resistant to ampicillin and susceptible to colistin. After the challenge, colonisation of the intestines was observed in both antibiotic-treated piglets and control piglets without antibiotic treatment. Histochemistry and scanning electron microscopy revealed sporadic colonisation of the small intestine in the piglets. STEC was detected in the mesenteric lymph nodes of untreated piglets. The clinical manifestations of oedema disease were observed in both groups. In the antibiotic-treated group (11 piglets), oedema disease developed in 10 piglets, eight of which died or were euthanized ante finem. In the untreated group (11 piglets), oedema disease developed in five piglets, four of which died or were euthanized ante finem. We therefore propose that the STEC lysed by colistin suddenly released the toxin from bacterial cells immediately after their passage through the intestinal wall. That could explain a more severe course of oedema disease in the treated piglets. Even though high amounts of STEC were present in the lymph nodes of untreated piglets, the toxin was not released abruptly because the bacterial cells were not damaged.  相似文献   

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