Hemorrhagic enteritis associated with Clostridium perfringens type A in a dog

A female Shetland sheep dog died suddenly with hemorrhagic diarrhea and vomitting, and was examined pathologically and microbiologically. Gross pathological change was restricted to the intestinal tract. The intestine contained watery, blood-stained fluid. Histopathologically, the principal intestinal lesion was superficial mucosal hemorrhagic necrosis at the jejunoileum. Many Gram-positive bacilli were found adhering to the necrotic mucosal surface in parts of the intestinal tract. Clostridium perfringens in pure culture were isolated from jejunal contents by anaerobic culture. These results suggested that the typical lesion of this case coincided with canine hemorrhagic enteritis and enterotoxemia due to C. perfringens infection could be the cause of sudden death.     

Hemorrhagic diathesis caused by multiple myeloma in a three-month-old foal

Multiple myeloma was diagnosed in a 3-month-old Quarter Horse foal with chronic weight loss, chronic bronchopneumonia, and epistaxis. The foal had pancytopenia, thrombocytopenia, and monoclonal beta-globulinemia. Bone marrow aspirates contained between 80 and 90% plasma cells.     

The necrotizing enteritis by Clostridium perfringens type C in piglets: practical observations,control and epidemiology

Necrotizing enteritis in piglets is caused by the spore-forming anaerobe Clostridium perfringens type C. The pathology is believed to be due to the production of beta-toxin by the agent and the infection tends to persist in affected herds despite appropriate hygiene measures. During the period 1989 to 2001, 35 outbreaks were observed in 15 herds in a limited geographic region in northwestern Switzerland in the canton of Fribourg. Initial outbreaks of acute disease were followed by chronic manifestations of necrotizing enteritis in eleven herds. Since clinical symptoms in case of chronic necrotizing enteritis and of mixed infections were rather non-specific, diagnosis in all herds was confirmed by gross pathological analysis, intestinal histology and bacteriological culture. After initial evaluation in 135 litters (1500 piglets), metaphylaxis consisted of penicillin for outbreaks of acute disease or of amoxycillin-clavulanic acid pending results of laboratory confirmation. Vaccination with a C. perfringens toxoid vaccine (Gletvax 6, also containing E. coli pilus antigens) together with penicillin chemoprophylaxis was used in 2400 litters (27,000 piglets). In 12 to 17% of litters disease recurred during this combined prophylaxis. Necrotizing enteritis persisted in all affected herds throughout the follow-up period.     

Clostridium perfringens type C and Clostridium difficile co-infection in foals

Clostridium perfringens type C is one of the most important agents of enteric disease in newborn foals. Clostridium difficile is now recognized as an important cause of enterocolitis in horses of all ages. While infections by C. perfringens type C or C. difficile are frequently seen, we are not aware of any report describing combined infection by these two microorganisms in foals. We present here five cases of foal enterocolitis associated with C. difficile and C. perfringens type C infection. Five foals between one and seven days of age were submitted for necropsy examination to the California Animal Health and Food Safety Laboratory. The five animals had a clinical history of acute hemorrhagic diarrhea followed by death and none had received antimicrobials or been hospitalized. Postmortem examination revealed hemorrhagic and necrotizing entero-typhlo-colitis. Histologically, the mucosa of the small intestine and colon presented diffuse necrosis and hemorrhage and it was often covered by a pseudomembrane. Thrombosis was observed in submucosal and/or mucosal vessels. Immunohistochemistry of intestinal sections of all foals showed that many large bacilli in the sections were C. perfringens. C. perfringens beta toxin was detected by ELISA in intestinal content of all animals and C. difficile toxin A/B was detected in intestinal content of three animals. C. perfringens (identified as type C by PCR) was isolated from the intestinal content of three foals. C. difficile (typed as A(+)/B(+) by PCR) was isolated from the intestinal content in 3 out of the 5 cases. This report suggests a possible synergism of C. perfringens type C and C. difficile in foal enterocolitis. Because none of the foals had received antibiotic therapy, the predisposing factor, if any, for the C. difficile infection remains undetermined; it is possible that the C. perfringens infection acted as a predisposing factor for C. difficile and/or vice versa. This report also stresses the need to perform a complete diagnostic workup in all cases of foal digestive disease.     

Subcutaneous abscess caused by Clostridium perfringens and osteomyelitis in a dog

A case of a subcutaneous abscess caused by Clostridium perfringens infection in a five-month-old dog is reported in this study. Clinical examination, radiological findings and cytological analysis of abscess fluid were consistent with Clostridium induced disease. Treatment including drainage of the abscess and antibiotic therapy led to rapid clinical improvement. However, despite aggressive medical therapy and proper wound care, the deep soft tissue infection led to osteomyelitis with premature closure of the growth plates of the tibia and secondary bone shortening. Prolonged treatment with metronidazole and amoxicillin-clavulanic acid resulted in an excellent outcome with normal weight bearing.     

Haemorrhagic necrotising enteritis in foals associated with Clostridium perfringens

Two foals aged 35 and 48 h from 2 Thoroughbred studs died several hours after developing clinical signs of depression, severe haemorrhagic diarrhoea and dehydration. Both foals had an acute haemorrhagic enteritis extending from the anterior jejunum to the terminal ileum which was characterised histologically by villus necrosis. Necrotic villi were surrounded by large numbers of rod-shaped Gram positive bacteria. Clostridium perfringens was recovered from the intestines of both foals and the isolates were considered to be C. perfringens type C. Other cases of diarrhoea were also observed in foals of the same age on these 2 studs, but the aetiology of these was not determined.     

A型产气荚膜梭菌致奶牛腹泻的诊断与防制

20 0 1年 8～ 9月 ,江苏某奶牛场奶牛陆续发生腹泻 ,采用氟哌酸治疗一段时间之后 ,收效甚微 ,因而怀疑为由产气荚膜梭菌所致的腹泻 ,遂对其进行了实验室诊断和药敏试验 ,并采取了相应的措施 ,取得了较好的效果。现将内容报告如下。1　病料采集与细菌分离从发病奶牛群中随机采集病牛新鲜排粪 1 2份 ,用灭菌生理盐水做 1∶ 1稀释后 ,用酪蛋白 -硫酸亚铁 -环丝氨酸琼脂 ( TSC,购自德国 Merck公司 )平板划线分离 ,置厌氧培养罐 (购自 Merck公司 ) 37℃培养 2 4 h,TSC琼脂平板上长出多量疑似菌落 ,菌落形态为圆形、突起、边缘整齐、表面湿润…     

The successful experimental induction of necrotic enteritis in chickens by Clostridium perfringens: a critical review

Necrotic enteritis (NE) is one of the most important enteric diseases in poultry and is a high cost to the industry worldwide. It is caused by avian-specific, Necrotic Enteritis Beta toxin (NetB)-producing, strains of Clostridium perfringens that also possess in common other virulence-associated genes. In Europe the disease incidence has increased since the ban on in-feed “growth promoting” antibiotics. Because of this, many recent studies of NE have focused on finding different ways to control the disease, and on understanding its pathogenesis. Frustratingly, reproduction of the disease has proven impossible for some researchers. This review describes and discusses factors known to be important in reproducing the disease experimentally, as well as other considerations in reproducing the disease. The critical bacterial factor is the use of virulent, netB-positive, strains; virulence can be enhanced by using tpeL- positive strains and by the use of young rather than old broth cultures to increase toxin expression. Intestinal damaging factors, notably the use of concurrent or preceding coccidial infection, or administration of coccidial vaccines, combined with netB-positive C. perfringens administration, can also be used to induce NE. Nutritional factors, particularly feeding high percentage of cereals containing non-starch polysaccharides (NSP) (wheat, rye, and barley) enhance disease by increasing digesta viscosity, mucus production and bacterial growth. Animal proteins, especially fish meal, enhance C. perfringens proliferation and toxin production. Other factors are discussed that may affect outcome but for which evidence of their importance is lacking. The review compares the different challenge approaches; depending on the aim of particular studies, the different critical factors can be adjusted to affect the severity of the lesions induced. A standardized scoring system is proposed for international adoption based on gross rather than histopathological lesions; if universally adopted this will allow better comparison between studies done by different researchers. Also a scoring system is provided to assist decisions on humane euthanasia of sick birds.     

Coccidia-induced mucogenesis promotes the onset of necrotic enteritis by supporting Clostridium perfringens growth

This study tested the hypothesis that a host mucogenic response to an intestinal coccidial infection promotes the onset of necrotic enteritis (NE). A chick NE model was used in which birds were inoculated with Eimeria acervulina and E. maxima and subsequently with Clostridium perfringens (EAM/CP). A second group of EAM/CP-infected birds was treated with the ionophore narasin (NAR/EAM/CP). These groups were compared to birds that were either non-infected (NIF), or infected only with E. acervulina and E. maxima (EAM), or C. perfringens (CP). The impact of intestinal coccidial infection and anti-coccidial treatment on host immune responses and microbial community structure were evaluated with histochemical-, cultivation- and molecular-based techniques. Barrier function was compromised in EAM/CP-infected birds as indicated by elevated CFUs for anaerobic bacteria and C. perfringens in the spleen when compared to NIF controls at day 20, with a subsequent increase in intestinal NE lesions and mortality at day 22. These results correlate positively with a host inflammatory response as evidenced by increased ileal interleukin (IL)-4, IL-10 and IFN-gamma RNA expression. Concurrent increases in chicken intestinal mucin RNA expression, and goblet cell number and theca size indicate that EAM/CP induced an intestinal mucogenic response. Correspondingly, the growth of mucolytic bacteria and C. perfringens as well as alpha toxin production was greatest in EAM/CP-infected birds. The ionophore narasin, which directly eliminates coccidia, reduced goblet cell theca size, IL-10 and IFN-gamma expression, the growth of mucolytic bacteria including C. perfringens, coccidial and NE lesions and mortality in birds that were co-infected with coccidia and C. perfringens. Collectively the data support the hypothesis that coccidial infection induces a host mucogenic response providing a growth advantage to C. perfringens, the causative agent of NE.     

Necrotic enteritis potential in a model system using Clostridium perfringens isolated from field outbreaks

Necrotic enteritis is an enteric disease of avian species caused by the anaerobic bacterium Clostridium perfringens. The disease is regularly controlled in the broiler chicken industry with antimicrobials in feed but is reemerging in areas such as Europe where there is a ban on antimicrobials as growth promoters. To study prospective therapies, researchers must be able to reproduce this disease in a controlled environment, but this is not always possible because of differences in the pathogenicity of C. perfringens strains. Our objective was to test the potential of five isolates (SNECP43, 44, 47, 49, and 50), taken from field cases of necrotic enteritis, at recreating the disease in a controlled challenge experiment. SNECP43 and 50 were derived from a common clone, with SNECP50 passed in vivo and SNECP43 subcultured in vitro. Four hundred birds were divided into 16 pens, with three pens each receiving one of five treatments, with one control pen. Day-old birds were raised on a high wheat-based diet to promote necrotic enteritis development and were challenged with between 3.4 x 10(9) and 3.2 x 10(11) colony-forming units (cfu) of C. perfringens in feed for a period of 24 hr starting on day 13 of the challenge experiment. Lesion scores were assessed on two birds per pen sacrificed on day 17 and on any dead birds during the 25-day study. Growth performance was assessed up to 25 days, and mortality recorded throughout. Only SNECP50 produced necrotic enteritis mortalities significantly different (P < or = 0.05) from the control. The five isolates were also typed using pulsed-field gel electrophoresis to assess their genetic relatedness. All epidemiologically unrelated isolates were deemed genetically unrelated, whereas SNECP43 and 50 differed by only a single minor band. Toxin type was assessed using polymerase chain reaction (PCR), which was also used for the detection of the gene encoding the beta2-toxin.     

Clostridium perfringens type A myonecrosis in a horse in Korea

Acute hemorrhagic myonecrosis accompanied by severe inter- and intrafascicular edema and hemorrhage of the right gluteal area was diagnosed in a 13-year-old male thoroughbred horse. Once the muscular and fascicular changes were subsided, the horse then developed acute respiratory problem. Histologically, the lung had diffuse severe hemorrhage with mild neutrophilic infiltration. The cause of death was acute respiratory failure that is believed to occur secondary to toxaemic event. Alpha and beta2 toxin secreting Clostiridum perfringens type A was isolated from the muscle and lung. The diagnosis was based on the light microscopic examination, bacterial toxinotyping and toxin genotyping from the muscular and pulmonary lesion. Also, susceptibility of the isolates to antimicrobial agents was determined.     

Predisposing factors in enterotoxemias of camels (Camelus dromedarius) caused by Clostridium perfringens type A.

C. perfringens type A was isolated from different organs and intestines from breeding and racing camels which died from peracute and acute enterotoxemias in two separate outbreaks. Pathological changes in the digestive tract were mild in breeding camels, and severe in racing camels. A polyvalent clostridial antiserum of bovine origin given intravenously had a life-saving effect on breeding camels, but not on racing camels. In the two outbreaks, fifty percent of the breeding camels were suffering from an acute Trypanosoma evansi infection, and 25% of the racing camels had developed a salmonellosis. It is suggested that both infections played an important role as predisposing factors for the outbreak of C. perfringens enterotoxemias.     

亚急性型仔猪红痢的诊断和防制

由C型产气荚膜梭菌引起的仔猪红痢是造成哺乳仔猪死亡的重要传染病之一 ,最急性型和急性型病例因有明显的便血症状而易确诊[1] ,但亚急性型病例往往出现非出血性腹泻 ,粪便呈黄色水样 ,易与仔猪黄痢相混淆 ,给临床诊断和预防控制带来许多困难。笔者在实践中遇到一起由C型产气荚     

A型产气荚膜梭菌α-毒素生产发酵工艺

利用全自动机械搅拌发酵罐对A型产气荚膜梭菌α-毒素的生产发酵工艺进行研究。设立温度、pH值和发酵时间3个因素,采用L9(34)正交优化设计方法,确定各因素对A型产气荚膜梭菌α-毒素产毒量的影响程度,并绘制发酵过程细菌生长曲线和产毒曲线。结果显示,pH对细菌的产毒量影响显著(0.01P0.05),发酵时间、温度对细菌产毒量影响不显著(P0.05)。结果表明,pH7.0、发酵温度43℃、发酵时间6 h为A型产气荚膜梭菌α-毒素生产发酵工艺条件。     

Toxigenic characteristics of Clostridium perfringens type C in enterotoxemia of domestic animals.

Eleven Clostridium perfringens type C strains isolated from fatal cases of hemorrhagic enterotoxemia of Canadian calves, a piglet, and a foal were studied for the production of soluble antigens. All the isolates from calves and a foal failed to produce delta toxin, but were capable of producing large amounts of lethal beta toxin. A strain isolated from a piglet produced delta, but very little beta toxin. Other differences were relatively minor. The results indicated that young domestic animals may be susceptible to all subtypes of C. perfringens type C. A simple method of using blood agar plates coated with type A antiserum for demonstration of hemolytic patterns was found advantageous in differentiation of C. perfringens strains.     

仔猪产气荚膜梭菌肠毒血症病原诊断及疫苗研究Ⅲ.7株A型产气荚膜梭菌菌株的产毒素试验

本试验对7株A型产气荚膜梭菌菌株在不同培养基、不同培养温度和不同培养时间的产毒力进行了试验。结果表明，培养基的种类和培养时间对菌株的产毒素能力影响较大，而培养温度则影响较小。所试菌株中C57-1菌株的产毒素能力最强，是制备疫苗的最佳菌株。