Responses of broiler chickens orally challenged with Clostridium perfringens isolated from field cases of necrotic enteritis

The present study examines the responses of broiler chickens to oral administration of Clostridium perfringens freshly isolated from field cases of necrotic enteritis (NE). The challenge studies included long-term exposure and short-term exposure, factored in with dietary and management variables including high levels of dietary components such as fish meal, meat meal, abrupt change of feed, and fasting. In the long-term exposure trials, the birds were orally inoculated daily, with 1 ml (1.0 or 2 x 10(8) CFU/ml) of an overnight culture of C. perfringens for 7 days. Short-term exposure trials involved challenge with 1 ml (3 x 10(10) CFU/ml) administered as a single dose. The responses of broilers to orally administered C. perfingens under laboratory controlled conditions are presented and discussed in the context of authentic field cases of necrotic enteritis. None of the challenge trials produced overt clinical signs of NE and there were no mortalities associated with oral exposure to high doses of C. perfringens. However, many of the challenged birds showed distinctly pronounced pathological changes in the intestinal tissue. On gross examination the responses in birds challenged orally with C. perfringens could be placed into two categories: (1) no apparent pathological changes in the intestinal tissue and (2) sub-clinical inflammatory responses with focal, multi-focal, locally extensive, or disseminated distribution throughout various sections of duodenum, jejunum, ileum, and ceca. In birds that responded with intestinal lesions, hyperemia and occasional hemorrhages were the main gross changes. In some birds, the mucosa was covered with a brownish material, but typically, the mucosa was lined by yellow or greenish, loosely adherent material. Mild gross changes were seen in some control birds, but both qualitatively and quantitatively, the lesions were distinctly more pronounced in the challenged birds. Upon histological examination, none of the experimentally exposed birds showed overt mucosal necrosis typical of field cases of NE, but typically the lamina propria was hyperemic and infiltrated with numerous inflammatory cells. Most significant changes were seen at the interface of the basal domain of enterocytes and lamina propria. Multifocally, these areas were extensively edematous, allowing for the substantial disturbance of the structural integrity between the lamina propria and the enterocytes. The lesions observed in the present study were consistently reproduced in all of our challenge trials, hence these responses may signify newly emerging patterns of sub-clinical enteric disorders in contemporary strains of poultry. The pathological changes observed in broilers challenged orally with C. perfringens in the present study, differ significantly from those reported previously, and must be clearly differentiated from those described in cases of NE or ulcerative enteritis. Although no overt necrosis of the intestinal mucosa typical of field cases of NE were observed in the present study, the birds challenged with C. perfringens showed strong inflammatory reaction to the introduced pathogens. The distinct features of the microscopic lesions were changes involving apparently normal enterocytes at the interface of the basal domain of villar epithelia and lamina propria. Although the pathological changes in the intestinal tissues observed in our trials appear to be rather subtle when compared to field cases of NE, the nature of these lesions suggest a significant negative effect on the digestive physiology of intestinal mucosa.     

猪增生性肠炎的诊断及防治措施

猪增生性炎是一种常见的接触性肠道传染病,对猪增生性肠炎的诊断及防治措施进行了阐述。     

鸭病毒性肠炎病毒致鸭胚成纤维细胞发生凋亡作用的研究

研究通过HE染色镜检发现,鸭病毒性肠炎病毒CH强毒株(DEV-CHv)可致鸭胚成纤维细胞(DEF)出现染色质颗粒化、细胞核变形等显著凋亡特征;TUNEL试验显示,接毒组细胞核内有多量棕黄色DAB显色颗粒,表明细胞出现了凋亡现象;DNA Ladder检测表明,接毒组细胞具有分子量分别为180～200bp及其整数倍的凋亡梯带电泳图谱特征;电镜观察发现,接毒组细胞具有染色质浓缩、边移,胞浆严重空泡化,细胞核严重变形,形成凋亡小体等典型凋亡特征.上述研究结果表明鸭病毒性肠炎病毒具有显著的致鸭胚成纤维细胞发生凋亡的作用.     

Enteritis associated with Yersinia pseudotuberculosis infection in a buffalo

SUMMARY: A week after transport a 4 month old buffalo calf developed diarrhoea. Its condition gradually deteriorated and it died. Necropsy revealed acute haemorrhagic enteritis and enlarged mesenteric lymph nodes. Haemorrhages and numerous microabscesses were detected in the lamina propria of the small intestine associated with colonies of Gram negative bacteria. Yersinia pseudotuberculosis was isolated from the small intestine and from mesenteric lymph node. Enteritis caused by Y pseudotuberculosis does not appear to have been reported previously in buffalo in Australia.     

ULTRASONOGRAPHIC APPEARANCE AND ETIOLOGY OF CORRUGATED SMALL INTESTINE

An ultrasound pattern of corrugated, and sometimes thickened, bowel wall has been associated with pancreatitis and small intestinal lymphangiectasia. In a retrospective study, records of dogs and cats with an ultrasound diagnosis of corrugated bowel were examined for age, breed, gender, presenting complaint, abdominal radiographic results, and final diagnosis. Eighteen dogs and six cats had an ultrasound diagnosis of corrugated bowel. The final diagnosis was pancreatitis (12 of 24), peritonitis (4 of 24), enteritis (2 of 24), pancreatic neoplasia (2 of 24), diffuse abdominal neoplasia (1 of 24), lymphocytic-plasmacytic enteritis (1 of 24), thrombosis/infarction (1 of 24), and protein-losing enteropathy and acute renal failure (1 of 24). The presence of bowel wall corrugation, although a nonspecific finding, should alert one-to the possibility of pancreatitis, enteritis, peritonitis, neoplasia, or bowel wall ischemia.     

鸭病毒性肠炎病毒基因组异构体的研究

为研究鸭病毒性肠炎病毒(DEV)基因组异构体的存在形式,本研究在已建立的以pCC1FOS为载体的DEV疫苗株基因文库基础上对DEV全序列进行了测定,并进一步对DEV基因组的异构体进行了研究。对261个重组fosmid中的DEV基因组片段的末端序列进行测序及序列分析,初步证明了DEV基因组有3种异构体,即P型、IS型和ILS型,未发现IL型的存在。并且,以上3种异构体在基因组中所占比例分别为77.1%、8.6%和14.3%。通过对11个重组fosmid的全序列测定,进一步确认了以上3种异构体的存在。该结果为DEV的分类提供了重要实验依据。     

猪增生性肠炎研究进展及防控措施

胞内劳森菌为严格细胞内寄生的无芽孢细菌,革兰氏染色阴性,抗酸染色阳性。主要感染3~20周龄猪而引起"猪增生性肠炎",临床表现慢性间歇性下痢或急性出血性下痢,排焦油样黑色粪便或血便。病理变化为小肠后段和结肠前段肠黏膜层增厚隆起,形成特征性分枝状皱折,肠腺上皮剧烈增生,形成畸形排列的分枝状肠腺。本病可进行流行病学、临床特征、病原学、病理学、血清学、分子生物学诊断,并需要与猪痢疾、猪梭菌性肠炎、仔猪副伤寒等病进行临床鉴别。本病的防控,应从猪群管理、引种、消毒、药物预防等方面考虑,接种疫苗是行之有效的措施。     

麝鼠肠炎沙门氏菌灭活苗的制作及应用

通过临床上分离鉴定的麝鼠肠炎沙门氏菌自制灭活苗，经过保护性试验、安全性试验、田间试验等表明，肠炎沙门氏菌灭活苗对防制麝鼠肠炎沙门氏菌病有较好的效果．     

Stanniocalcin-1 protects bovine intestinal epithelial cells from oxidative stress-induced damage

Chronic enteritis can produce an excess of reactive oxygen species resulting in cellular damage. Stanniocalcin-1(STC-1) reportedly possesses anti-oxidative activity, the aim of this study was to define more clearly the direct contribution of STC-1 to anti-oxidative stress in cattle. In this study, primary intestinal epithelial cells (IECs) were exposed to hydrogen peroxide (H₂O₂) for different time intervals to mimic chronic enteritis-induced cellular damage. Prior to treatment with 200 µM H₂O₂, the cells were transfected with a recombinant plasmid for 48 h to over-express STC-1. Acridine orange/ethidium bromide (AO/EB) double staining and trypan blue exclusion assays were then performed to measure cell viability and apoptosis of the cells, respectively. The expression of STC-1 and apoptosis-related proteins in the cells was monitored by real-time PCR and Western blotting. The results indicated that both STC-1 mRNA and protein expression levels positively correlated with the duration of H₂O₂ treatment. H₂O₂ damaged the bovine IECs in a time-dependent manner, and this effect was attenuated by STC-1 over-expression. Furthermore, over-expression of STC-1 up-regulated Bcl-2 protein expression and slightly down-regulated caspase-3 production in the damaged cells. Findings from this study suggested that STC-1 plays a protective role in intestinal cells through an antioxidant mechanism.     

含LacZ表达盒的鸭瘟病毒TK基因缺失转移载体的构建

根据GenBank已发表的鸭瘟病毒活疫苗C-KCE株基因组序列设计一对引物,扩增出含TK基因完整ORF的2.7 kb的片段,克隆至pMD18T simple载体。利用该片段内的两个酶切位点Xho I和EcoR V,切除TK基因内的244 bp,用T4 DNA聚合酶补平末端;pVAX1-LacZ用Nru I和Nar I双酶切,回收含LacZ表达盒的4.1 kb片段,通过平末端连接将LacZ表达盒插入到TK基因中,从而获得了转移载体pTK-LacZ,为构建重组鸭瘟病毒奠定了基础。