麻鹿和梅花鹿肠毒血症的诊治

鹿肠毒血症是由魏氏梭菌引起的一种急性肠毒血症。该病是由于魏氏梭菌在肠道内大量繁殖,产生毒素所致魏氏梭菌根据毒素-抗毒素中和试验分为A、B、C、D、E五型。每型产生一种主要毒素,一种或数种次要毒素,肠毒血症是由D型魏氏梭菌引起的一种疾病1 流行情况 宁夏中卫某鹿场原有32只麻鹿和     

麻鹿和梅花鹿肠毒血症的诊断与防治

鹿肠毒血症是由D型魏氏梭菌引起的一种急性肠毒血症 ,病的发生是由于魏氏梭菌在肠道内大量繁殖 ,产生毒素所引起。魏氏梭菌根据毒素 -抗毒素中和试验分为A、B、C、D、E五型。每型产生一种主要毒素 ,一种或数种次要毒素。肠毒血症是由D型魏氏梭菌引起的一种疾病。1　流行情况宁夏中卫某鹿场原有 32头麻鹿和梅花鹿。 2 0 0 1年 6月 ,从甘肃某鹿场调入 4 5头两种鹿 ,8月中旬 ,又从该鹿场调入 79头两种鹿 ,使该鹿场鹿群数达 15 6头。从 6月份鹿场调入鹿群后不久 ,在鹿群中有不同年龄的鹿发生症状相似的病 ,最急性无任何症状突然发病 ,多在 4…     

鹿巴氏杆菌病和肠毒血症混合感染的诊断与防治

鹿巴氏杆菌病是由多杀性巴氏杆菌引起的鹿的一种急性传染病 ,广泛流行于世界各地 ,严重影响养鹿业的发展。巴氏杆菌有许多血清型 ,鹿巴氏杆菌属于多杀性巴氏杆菌。肠毒血症是D由型魏氏梭菌引起的一种急性肠毒血症 ,是由于魏氏梭菌在肠道内大量繁殖 ,产生毒素所引起。魏氏梭菌根据毒素—抗毒素中和试验分为A、B、C、D、E五型 ,每型产生一种主要毒素 ,一种或数种次要毒素。肠毒血症是由D型魏氏梭菌引起的一种疾病。1　流行情况宁夏中卫某鹿场原有 32只麻鹿和梅花鹿 ,2 0 0 1年 6月 ,从甘肃省某鹿场调入麻鹿和梅花鹿共 45只 ,8月中旬 ,又从…     

D型产气荚膜梭菌ε毒素研究进展

D型产气荚膜梭菌常引起新生羔羊痢疾和山羊、牛等家畜的肠毒血症,致死性强,对畜牧业造成很大的危害.ε毒素是D型产气荚膜梭菌的主要致死性毒力因子和保护性抗原,从分子生物学的角度对该毒素的研究具有重要实际意义.论文主要对国内外关于D型产气荚膜梭菌ε毒素分子生物学结构与性质,ε毒素引起的家畜肠毒血症以及对其作用靶器官肾脏和脑组织破坏的致病机理进行了介绍,对国内外D型产气荚膜梭菌ε毒素预防措施进行了综述,为研究D型产气荚膜梭菌ε毒素结构与功能的关系以及预防治疗动物肠毒血症提供参考.     

一起兔魏氏梭菌病的诊治

兔魏氏梭菌病又称兔魏氏梭菌性肠炎,是由A型魏氏梭菌所产毒素引起的肠毒血症。以急性腹泻、排黑色水样粪便、盲肠浆膜出血斑和胃黏膜出血、溃疡为主要特征。     

春夏之交改换饲料不要太快 青草和青储饲料配比要适量——小牛肠毒血症的诊断与防治

肠毒血症主要是绵羊的一种急性毒血症,是由D型魏氏梭菌（Cl．Welehii）在肠道中大量繁殖,产生毒素所引起的。病畜死后其肾易软化,因此又称为“软肾病”。这种病发生于小牛较少见。2007年6～7月间,河北省某奶牛场12～16月龄的小牛群先后有7头发病,死亡5头,经临床和实验室诊断是由魏氏梭菌引起的小牛肠毒血症。     

兔的魏氏梭菌病

兔魏氏梭菌病(又称兔魏氏梭菌性肠炎或兔肠毒血症)。是由魏氏梭菌所引起的以急性下痢为特征的家兔消化道疾病。 魏氏梭菌有6个菌型,可分泌12种毒素。家兔魏氏梭菌病是由A型(我国1979年才发现)或E型及其所产生的外毒毒所引起的。该致病菌广泛存在于动物的肠道、粪便及土壤中,在正常情况下,增殖缓慢,产毒量少。当气候和饲料突变,动物胃肠道环     

麻鹿和梅花鹿肠毒血症的诊断

鹿肠毒血症是由魏氏梭菌引起的一种急性肠毒血症。该病是由于魏氏梭菌在肠道内大量繁殖,产生毒素所引起的。魏氏梭菌根据毒素———抗毒素中和试验分为A、B、C、D、E五型。每型产生一种主要毒素,一种或数种次要毒素。肠毒血症是由D型魏氏梭菌引起的一种疾病。1流行情况宁夏中卫某鹿场原有32只麻鹿和梅花鹿。2001年6月,从外地某鹿场调入45只麻鹿和梅花鹿,8月中旬,又从该鹿场调入79只两种鹿,使该鹿场鹿数达156只。从6月份鹿场调入鹿后不久,鹿群中不同年龄的鹿相继发病。最急性无任何症状突然发病,多在4～5h后倒毙,病程稍长的表现精神沉郁,…     

宠物兔肠毒血症防治探讨

正宠物兔肠毒血症是肠道内致病菌快速增殖产生大量毒素,并被肠壁吸收进入血液循环,造成毒血症和重要组织脏器损伤与衰竭的一种疾病。1病原特性目前国内外报道与兔肠毒血症有关的致病菌主要有A型魏氏梭菌和致病性大肠杆菌。A型魏氏梭菌属梭状芽胞杆菌,广泛存在于土壤、河水和空气中。该菌不能在健康动物肠粘膜上沾附或侵袭,但在适宜环境因素及条件下,能高速增殖,引起梭菌性肠毒血症。例如喂食高淀粉日粮或     

成年奶牛产气荚膜梭菌肠毒血症的防治

奶牛产气荚膜梭菌肠毒血症是由产气荚膜梭菌(魏氏梭菌)在肠道中大量繁殖产生毒素而引起奶牛的毒血症,多见于犊牛,成年奶牛发生此病少见。2006年黑龙江省农垦857农场发生成年奶牛产气荚膜梭菌(D型)肠毒血症,东北农业大学专家专门为     

Genotyping of Clostridium perfringens isolated from domestic and exotic ruminants and swine

Clostridium perfringens types A, B, C, D and E are known to cause severe enteritis/enterotoxaemia and diseases (especially caused by type A) belonging to the gas oedema complex in many species. Samples from the small intestine as well as faeces of domestic and exotic animals suffering from enterotoxaemic signs or having died within days after first occurance of toxaemia were submitted for typing C. perfringens toxovars by multiplex PCR. The following species have been investigated: domestic sheep (Ovis ammon; n = 10), domestic goat (Capra aegagrus hircus; n = 26), Japanese serow (Capricornis sumatraensis; n = 4), lechwe waterbuck (Hydrotragus leche; n = 1), blackbuck (Antilope cervicapra; n = 1), European reindeer (Rangifer tarandus tarandus; n = 4), domestic swine (Sus scrofa; n = 52), and collared peccary (Tayassu albirostris; n = 1). Interestingly, the predominant C. perfringens toxovar in domestic sheep was type A. This toxovar could also be diagnosed in all reindeer, in three Japanese serows, one lechwe waterbuck and most pigs (n = 47), the majority of those being at suckling age. Type D was the most prevalent toxovar (n = 18) in domestic goats, but also types A and E could be identified as pathogens in this species. Type C could only be found in domestic swine (n = 5) and in one case of clostridiosis in a Japanese serow. Two cases of enterotoxaemia in goats, one case in reindeer, and a single case in blackbuck and collared peccary were caused by C. perfringens type E. Genotyping of C. perfringens is recommended before starting vaccination programmes as it could be shown, that the importance of specific toxovars has been underestimated in specific species and/or age groups.     

Enterotoxaemia in goats

Enterotoxaemia of sheep and goats occurs worldwide, but the condition in goats is poorly understood. The disease in goats is mostly caused by Clostridium perfringens type D, although the role of the toxins of this microorganism in the pathogenesis of the disease is not fully understood. The disease occurs in three forms, peracute, acute and chronic, the cardinal clinical sign of the acute and chronic forms being diarrhoea. The main biochemical alterations are hyperglycaemia and glycosuria, while at necropsy the disease is often characterized by haemorrhagic colitis. The typical histological changes observed in the brain of sheep with enterotoxaemia are not considered to be a common feature of enterotoxaemia in goats. Although the pathogenesis of caprine enterotoxaemia has not yet been properly defined, it is usually accepted that the presence of C. perfringens type D in the small bowel, together with a sudden change to a diet rich in carbohydrates, is the main predisposing factor for the disease. Vaccination seems to be poorly effective in preventing caprine enterotoxaemia, which might be due to the fact that the enteric form of the disease is partially independent of circulating C. perfringens toxin. More studies are needed on caprine enterotoxaemia, especially of its pathogenesis and immunity, in order to develop more efficient control measures for this disease.     

山东疫区魏氏梭菌血清型的多重PCR检测

采用多重PCR对从流行过魏氏梭菌病的牧场粪便样品中分离魏氏梭菌的α、β、ε、ι 毒素基因进行了检测,确定了血清型。电泳成像显示,仅魏氏梭菌扩增出了特异性条带,其他对 照菌株无,说明该方法具有很高的特异性。通过对山东德州、枣庄、泰安、临沂、青岛等地养殖场 的418个样品分离的62个菌株的检测,检出率为14．8％,均为A型。研究确认,多重PCR是 魏氏梭菌血清型鉴别的一种快速、简便的研究方法,山东省流行型别与国外报道不完全一致。     

Detection of Clostridium perfringens epsilon toxin by ELISA

An enzyme-linked immunosorbent assay (ELISA) has been developed as an alternative to neutralisation tests in mice to detect Clostridium perfringens type D epsilon toxin in the intestinal contents of animals which have died from suspected enterotoxaemia. The test was sensitive and quantitative and gave excellent agreement with the mouse protection test.     

The Early Effects of Clostridium perfringens Type D Epsilon Toxin in Ligated Intestinal Loops of Goats and Sheep

Clostridium perfringens type D produces enterotoxaemia in goats, sheep and other animals. The disease is caused by C. perfringens epsilon toxin and, while enterotoxaemia in goats is usually characterized by enterocolitis, the disease in sheep is characterized by systemic lesions (such as lung and brain oedema) with minor and inconsistent changes observed in the intestine. A possible explanation for these differences is that epsilon toxin is more promptly absorbed by the ovine than by the caprine intestine. In an attempt to clarify this, we examined the early effects of epsilon toxin on caprine and ovine intestine. Intestinal loop assays were performed to analyse the physiological and morphological changes induced by epsilon toxin in the intestine of these species. Fluid accumulation was observed in caprine and ovine ileum and colon treated with epsilon toxin. Ileal loops from goats treated with epsilon toxin retained sodium and water earlier than ovine ileal loops treated with the same toxin. Histological analysis showed morphological alterations in the colon of both species as early as 2 h after the commencement of epsilon toxin treatment; these changes were more marked in goats than in sheep. No morphological changes were observed in the ileum of either species after 4 h incubation with epsilon toxin. These results suggest that epsilon toxin modifies ion and water transport in the small and the large intestine of goats and sheep through different mechanisms.     

Causes of death in sheep exported live by sea

Post-mortem examinations were conducted on 950 dead and terminally ill sheep during assembly for export and during transport by sea from Fremantle, Western Australia to various Middle East ports. Causes of death were grouped into 5 major categories; inanition (deaths associated with reduced feed intake, including hypocalcaemia and hypomagnesaemia), salmonellosis (enteric and septicaemic), trauma, diseases associated with excessive feed intake (lactic acidosis and enterotoxaemia) and miscellaneous diseases (mostly of farm origin). During assembly the causes of death were salmonellosis 53.4%, miscellaneous diseases 23.8%, trauma 12.6%, inanition 10.2%, acidosis 3.9%, enterotoxaemia 3.4% and no diagnosis was made in 3.4%. During shipping the causes of death in defined populations of sheep in 5 voyages were; inanition 43.4%, salmonellosis 20.2%, trauma 10.6%, miscellaneous diseases 5.9%, enterotoxaemia 1.0% and no diagnosis was made in 19.0%. The range of mortality rates per 10,000 sheep at risk for the first 11 days at sea in 5 voyages were inanition 52.6 to 76.7, salmonellosis 7.8 to 109.8, trauma 2.1 to 17.1, miscellaneous diseases 5.9 to 17.1 and enterotoxaemia nil to 10.3.     

The effect of passive immunization on active immunity against Clostridium perfringens type D in lambs

Lambs in different stages of development of active immunity against Clostridium perfringens type D were treated with partially purified immunoglobulin in an attempt to superimpose a passive immunity on an existing or developing active immunity. Three different studies were undertaken to determine the impact of partial purified immunoglobulins on these vaccinated animals. In 2 of the 3 studies, active immunity was induced by administering the normal routine enterotoxaemia vaccinations and allowing the basic immunity to become established, for a period ranging from 2 weeks for the animals in study 1 and 4 months for those in study 2, before passive immunization with the partially purified immunoglobulins took place. An increase in the epsilon antibody titre occurred in each of the 2 studies after the animals were passively immunized with immunoglobulin, though this increase was not statistically significant (P greater than 0.05). In the 3rd study, when the animals were given the initial vaccination of the Onderstepoort enterotoxaemia oil adjuvant vaccine together with the immunoglobulin, an immediate increase in the epsilon antitoxin titre occurred that was statistically significant (P less than 0.05) 2-14 days after administration. No negative effects were noted on the development of an initial active immunity or an existing active immunity against Clostridium perfringens type D when they were passively immunized with partially purified immunoglobulin.     

A role for the Clostridium perfringens beta2 toxin in bovine enterotoxaemia?

Non-enterotoxigenic type A Clostridium perfringens are associated with bovine enterotoxaemia, but the alpha toxin is not regarded as responsible for the production of typical lesions of necrotic and haemorrhagic enteritis. The purpose of this study was to investigate the putative role of the more recently described beta2 toxin. Seven hundred and fourteen non-enterotoxigenic type A C. perfringens isolated from 133 calves with lesions of enterotoxaemia and high clostridial cell counts (study population) and 386 isolated from a control population of 87 calves were tested by a colony hybridisation assay for the beta2 toxin. Two hundred and eighteen (31%) C. perfringens isolated from 83 calves (62%) of the study population and 113 (29%) C. perfringens isolated from 51 calves (59%) of the control population tested positive with the beta2 probe. Pure and mixed cultures of four C. perfringens (one alpha+beta2+, one alpha+enterotoxin+ and two alpha+) were tested in the ligated loop assay in one calf. Macroscopic haemorrhages of the intestinal wall, necrosis and haemorrhages of the intestinal content, and microscopic lesions of necrosis and polymorphonuclear and mononuclear cell infiltration of the intestinal villi were more pronounced in loops inoculated with the alpha and beta2-toxigenic C. perfringens isolate. These results suggest in vivo synergistic role of the alpha and beta2 toxins in the production of necrotic and haemorrhagic lesions of the small intestine in cases of bovine enterotoxaemia. However, isolation of beta2-toxigenic C. perfringens does not confirm the clinical diagnosis of bovine enterotoxaemia and a clostridial cell counts must still be performed.     

Effect of avilamycin, tylosin and ionophore anticoccidials on Clostridium perfringens enterotoxaemia in chickens

In order to study the prophylactic and metaphylactic effect of antomicrobial growth promoters and ionophorous anticoccidials on the incidence of Cl. perfringens enterotoxaemia in chickens, experimental attempts were performed with 675 chickens in 27 trials. The birds were intraduodenally infected with Cl. perfringens type A (ATCC 3624). The following antimicrobial growth promoters and ionophore anticoccidials were used either on their own or in combination: avilamycin, narasin, monensin and tylosin. While infected and non-medicated trials showed an average incubation period of 1 week, clinical symptoms occurred 2-4 days later in infected and medicated birds. Avilamycin medicated birds had the longest incubation period. In the infected and non-medicated trials, a mortality rate of 16%-36% was noted within 3 weeks post infection. The avilamycin trials showed a mortality rate of 0-8% (0-2 birds died) and the narasin and monensin a mortality rate of 0-8%, respectively. In the combination groups (monensin + avilamycin or narasin + avilamycin), the mortality rate ranged from 0 to 4%. Tylosin showed a very good metaphylactic/therapeutic effect against Cl. perfringens enterotoxaemia. Following infection, medicated birds showed a significantly better bodyweight gain than the chickens, whose feeds had not been supplemented. From epidemiological point of view, the systematic prevention of coccidiosis is a key in the control of Cl. perfringens enterotoxaemia in chickens.     

Obituary - Dudley Arthur Gill

Extract

D. A. Gill died in Sydney on May 1, 1973, at the age of 72. He received his training at the Royal Veterinary College, London, where he qualified in 1922. He then did a Diploma of Veterinary State Medicine at Edinburgh. He joined the New Zealand Department of Agriculture as a Veterinary Officer and from 1928 he was second in charge at the Wallaceville Veterinary Laboratory. While he was at Wallaceville he did some first-class research on the problems of listeriosis and enterotoxaemia. The house that he built at Wallaceville he later sold to his friend Dr I. J. Cunningham.