Effect of Herbanoplex CP on broiler chicken's performance following a nondefined challenge or intestinal lesion score using a necrotic enteritis challenge model     

《The Journal of Applied Poultry Research》2021,30(2):100161

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Death of a neonatal lamb due to Clostridium perfringens type B in New Zealand     

JS Munday  H Bentall  D Aberdein  M Navarro  FA Uzal  S Brown 《New Zealand veterinary journal》2020,68(4):242-246

ABSTRACT

Case history and clinical findings: A flock of 20 sheep was kept within three paddocks on a single property. None of the animals in the flock had been vaccinated against any disease for at least three years. Abdominal bloating and haemorrhagic diarrhoea were observed in Lamb 1 at 24 hours-of-age. The lamb subsequently died within an hour of the onset of clinical signs. Lamb 2 was 3-days-old when observed to be recumbent with opisthotonus. The lamb was treated with dextrose, vitamins B1 and B12, and penicillin G, but died 4 hours later.

Pathological findings: Examination of Lamb 1 revealed markedly increased gas within the peritoneum and within dilated loops of intestine. The intestines were dark red and contained large quantities of haemorrhagic fluid. Histology of the intestines revealed peracute mucosal necrosis with minimal accompanying inflammation. The intestinal lumen contained cell debris, haemorrhage, and myriad large Gram-positive bacilli. The intestines of Lamb 2 did not appear bloated or reddened. However, multiple fibrin clots were visible within the pericardial sac. Histopathological examination revealed small foci of necrosis within the mucosa of the distal intestine. The necrotic foci were often associated with large numbers of large Gram-positive bacilli.

Immunohistochemsitry and molecular biology: Intestinal samples from Lamb 1 were processed for Clostridium perfringens immunohistochemistry, which revealed large numbers of intralesional, positively immunostained rods. Fragments corresponding to the expected sizes for genes encoding alpha, beta, and epsilon C. perfringens typing toxins were amplified by PCR from DNA extracted from formalin-fixed sections of intestine.

Diagnosis: Lamb dysentery due to C. perfringens type B.

Clinical relevance: C. perfringens bacteria have a worldwide distribution, but disease due to C. perfringens type B has only been diagnosed in a small number of countries and has never been reported in New Zealand or Australia. C. perfringens type B produce both beta toxin and epsilon toxins, therefore both haemorrhagic enteritis and systemic vascular damage can develop. As many animals are exposed to C. perfringens without developing disease, there must be additional unknown factors that resulted in disease in these particular sheep. Vaccines that specifically protect against C. perfringens type B are available and may be recommended for use in smaller non-commercial flocks, as in the present case.  相似文献   

Necrotic enteritis challenge regulates peroxisome proliferator-1 activated receptors signaling and β-oxidation pathways in broiler chickens     

Kosar Gharib-Naseri  Sara de Las Heras-Saldana  Sarbast Kheravii  Lihong Qin  Jingxue Wang  Shu-Biao Wu 《动物营养（英文）》2021,7(1):239

Necrotic enteritis (NE) is an important enteric disease in poultry and has become a major concern in poultry production in the post-antibiotic era. The infection with NE can damage the intestinal mucosa of the birds leading to impaired health and, thus, productivity. To gain a better understanding of how NE impacts the gut function of infected broilers, global mRNA sequencing (RNA-seq) was performed in the jejunum tissue of NE challenged and non-challenged broilers to identify the pathways and genes affected by this disease. Briefly, to induce NE, birds in the challenge group were inoculated with 1 mL of Eimeria species on day 9 followed by 1 mL of approximately 10⁸ CFU/mL of a NetB producing Clostridium perfringens on days 14 and 15. On day 16, 2 birds in each treatment were randomly selected and euthanized and the whole intestinal tract was evaluated for lesion scores. Duodenum tissue samples from one of the euthanized birds of each replicate (n = 4) was used for histology, and the jejunum tissue for RNA extraction. RNA-seq analysis was performed with an Illumina RNA HiSeq 2000 sequencer. The differentially expressed genes (DEG) were identified and functional analysis was performed in DAVID to find protein–protein interactions (PPI). At a false discovery rate threshold <0.05, a total of 377 DEG (207 upregulated and 170 downregulated) DEG were identified. Pathway enrichment analysis revealed that DEG were considerably enriched in peroxisome proliferator-activated receptors (PPAR) signaling (P < 0.01) and β-oxidation pathways (P < 0.05). The DEG were mostly related to fatty acid metabolism and degradation (cluster of differentiation 36 [CD36], acyl-CoA synthetase bubblegum family member-1 [ACSBG1], fatty acid-binding protein-1 and -2 [FABP1] and [FABP2]; and acyl-coenzyme A synthetase-1 [ACSL1]), bile acid production and transportation (acyl-CoA oxidase-2 [ACOX2], apical sodium–bile acid transporter [ASBT]) and essential genes in the immune system (interferon-, [IFN-γ], LCK proto-oncogene, Src family tyrosine kinase [LCK], zeta chain of T cell receptor associated protein kinase 70 kDa [ZAP70], and aconitate decarboxylase 1 [ACOD1]). Our data revealed that pathways related to fatty acid digestion were significantly compromised which thereby could have affected metabolic and immune responses in NE infected birds.  相似文献   

毛皮动物犬瘟热、细小病毒性肠炎和脑炎防治技术指南   总被引：1，自引：0，他引：1  

程世鹏  易立  陈立志  司方方  王建科 《特产研究》2010,32(2):66-69

为了预防、控制和消灭毛皮动物犬瘟热、细小病毒性肠炎和脑炎,依据《中华人民共和国动物防疫法》及有关法律法规,制定毛皮动物犬瘟热、细小病毒性肠炎和脑炎防治技术指南,指导毛皮动物犬瘟热、细小病毒性肠炎和脑炎防控。  相似文献   

人工感染雏鹅新型病毒性肠炎的病理形态学发展规律的研究   总被引：5，自引：0，他引：5  

程安春 《畜牧兽医学报》2001,32(4):362-370

40只2日龄四川白鹅口服感染雏鹅新型病毒性肠炎病毒，在不同阶段解剖发病和死亡雏鹅，电镜观察组织器官的病理变化发展规律，接种后第2天，十二指肠绒毛顶部上皮细胞发生坏死、脱落。随着感染时间延长，上皮细胞的坏死、脱落迅速向绒毛基部发展，并伴随固有膜炎性细胞浸润和坏死，病变向着空肠段发展，进一步发展为纤维素性坏死性肠炎，于小肠中后段形成假膜包裹肠内容物的栓塞物或直接由纤维素性渗出物与地不死肠粘膜混合凝固形成栓塞物阻塞肠腔，使外观膨大，肺充血和出血，肾充血、出血及肾小管上皮细胞变性。部分病例肝颗粒变性、脂肪变性，后期部分病例气管、腺胃上皮细胞脱落，早期部分病例心充血和出血，食道、胰腺及脑正常，电镜下可观察到小肠上皮细胞核畸形、固缩、核仁消失、核膜模糊和胞核崩解；胞浆严重空化，形成含有很多病毒粒子的“封入体”；粗面内质网扩张呈囊状，其上的核蛋白体严重脱落；线粒体外膜破裂或嵴断裂及空化，部分受到损害的线凿全充满大量的病毒粒子；形成肠道栓子的外层假膜有大量的病毒粒子、细菌以及坏死的肠上皮细胞，肝脏细胞粗面内质网严重扩张及部分线粒体肿胀、脊断裂；而心肌细胞粗面内质网的轻度扩张及胞核畸形。本文还对雏鹅新型病毒性肠炎与小鹅瘟的病理变化进行了比较分析。  相似文献   

应用单克隆抗体的免疫组织化学法研究雏鸭体内鸭瘟病毒的分布   总被引：3，自引：1，他引：3  

胡薛英  谷长勤  程国富  周诗其  苏敬良  杨健 《中国预防兽医学报》2006,28(3):320-322

本实验应用了免疫组织化学的单克隆抗体间接酶标染色法，对人工感染鸭瘟病毒雏鸭的组织切片进行染色观察。旨在研究病毒在鸭体内分布，对其进行定位。研究结果显示，鸭的心脏、肝脏、脾、胸腺、肠、法氏囊、胰、肺、肾等组织的细胞浆内均出现了染色的特异阳性反应物。结果表明，鸭瘟病毒广泛分布于感染雏鸭的各种组织器官，并造成一定的组织病理变化。  相似文献   

用间接免疫荧光染色法检测鸭病毒性肠炎病毒在人工感染鸭体内的侵染过程和分布规律     

程安春  韩晓英  汪铭书  袁桂萍  徐超  廖永洪 《畜牧兽医学报》2007,38(9):942-946

用鸭病毒性肠炎病毒（DEV）CHv强毒株感染成年鸭复制鸭病毒性肠炎急性病例,分别于接种后不同时间,取心、肝、脾、肺、肾、胸腺、食道、十二指肠、胰腺、法氏囊和脑组织,制作切片,应用间接免疫荧光染色法（IFA）检测DEV在鸭体内的侵染过程和分布规律。结果显示：感染后4 h可在脾脏、胸腺和法氏囊中检测到DEV抗原;感染后6 h可在肝脏、食道、十二指肠、直肠及肺脏检测到DEV抗原;IFA对各组织器官中DEV的平均检出率为肝脏46/50、脾脏48/50、肺脏46/50、肾脏0/50、肠道46/50、法氏囊46/50、胸腺47/50、胰腺0/50、大脑0/50、食道44/50、心脏0/50。研究表明：在急性病例中,脾脏、法氏囊、胸腺、食道、肠道、肝脏和肺脏为DEV的主要靶器官;接种后,病毒首先在脾脏、胸腺、法氏囊中出现,然后病毒迅速传播到肝脏、消化道和肺脏中;IFA检测石蜡切片中DEV的方法具有直观、特异性强的优点,是对DEV进行检测和抗原定位的较好方法。  相似文献   

我国狐貂貉犬瘟热与细小病毒肠炎的免疫预防现状与问题   总被引：1，自引：0，他引：1  

张振兴 《经济动物学报》1998,2(1):56-59

长期以来,我国狐貂貉饲养经历了多次大起大落,其原因除体制、生产及销售无序混乱外,品种退化、饲养管理粗放、技术低下和主要传染病屡有发生、流行也是重要因素。其中犬瘟热与细小病毒肠炎疫苗质量不稳定、免疫程序不合理是免疫失败而招致疫病发生、流行的关键因素。  相似文献   

水貂细小病毒性肠炎灭活疫苗保存期试验     

柴秀丽  闫喜军  吴威  罗国良  赵传芳 《经济动物学报》2008,12(3)

对2~8℃条件下保存90,120,150,180,210,240,300,360 d的水貂细小病毒性肠炎灭活疫苗接种水貂进行免疫试验,结果表明:保存300 d的疫苗接种水貂30 d后血清中水貂肠炎细小病毒(MEV)HI抗体均在1∶32以上,免疫水貂强毒攻击均获得100%保护,确定水貂细小病毒细胞灭活疫苗保存期为300 d。该结果为水貂细小病毒细胞灭活疫苗运输和保存提供了理论依据。  相似文献   

北极狐出血性肠炎病原分离鉴定   总被引：1，自引：1，他引：0  

闫新华  闫喜军 《中国预防兽医学报》1999,21(5):331-332

从排血便为主要临床特征的濒死期育成北极狐肠内容物中分离到 ５ 株革兰氏阳性大杆菌，各株菌的 ３７℃ ８ 小时厌气肉肝汤纯培养上清液 ０２ｍ ｌ小鼠尾静脉注射，１２ 小时内 １００％ 死亡。生理生化鉴定证实分离菌为产气荚膜杆菌（ Ｂ．ａｅｒｏｇｅｎｅｓｃａｐｓｕｌａｔｕｓ）。血清定型结果表明，分离的 ５ 株菌均为 Ａ 型产气荚膜杆菌。以饲喂狐的变质鱼浸出液静脉注射小鼠引起死亡，并从该浸出液中也分离到 Ａ 型魏氏梭菌，证实该病的发生是饲料传播。  相似文献