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1.
Nine bred gilts were vaccinated with 2 doses of a Clostridium perfringens type C toxoid at a 5-week interval. Time of vaccination during gestation differed among the gilts. Clostridium perfringens beta antitoxin in colostral samples and in serum samples was titrated in mice. Blood was collected from 2 to 5 neonatal pigs from each dam (total = 32 pigs) when the pigs were 36 to 48 hours old. Antitoxin titers in colostrum were 123 to 4.5 IU/ml, indicating considerable variation in individual responses of the gilts to toxoid. Serum titers of neonatal pigs reflected colostrum titers of their dams. This colostrum-to-serum titer correlation was essentially a straight-line fit by least-squares linear regression analysis, establishing a direct proportional relationship between colostrum titers and serum titers of neonatal pigs. In the dams, a correlation was not found between colostral titers and serum titers of blood samples collected 2 weeks after collection of colostrum.  相似文献   

2.
Weaned lambs, having a detectable level of maternal antibodies (1-2 units/ml) against C. perfringens type D, showed protective antitoxin levels lasting for 29 days after receiving a single parenteral dose of 200 units/kg hyperimmune serum. Lambs, having no maternal antibodies (less than 0,07 units/ml) to C. perfringens type D but receiving the same dose of hyperimmune serum, maintained protective antibody levels for only 21 days. Three weeks after the titres fell below the minimum protective level of 0,15 units/ml, both these groups were treated again in the same manner. The passive immunity conferred in both groups now lasted for 42 days. When the hyperimmune serum was administered to lambs already immunized by vaccination, a slight increase was noted in the antibody titre.  相似文献   

3.
Twenty-eight pups from a general pet population were vaccinated for canine parvovirus (CPV) with a combination vaccine every 3 weeks until the pups were 11 to 16 weeks old. Canine parvovirus antibody titers were measured by serum neutralization before each vaccination and greater than or equal to 2 weeks after the final vaccination. Eighteen pups that initially were seronegative for CPV seroconverted after 1 to 3 doses of modified-live virus CPV vaccine administered when the pups were between 8 and 16 weeks old; 16 of 18 seroconverted after the 1st dose. Of 10 pups that were seropositive for CPV at initial examination, 7 did not develop protective titers after 3 doses of vaccine, with the last dose given when the pups were 14 to 16 weeks old. Maternally derived antibody was the primary cause of vaccination failure.  相似文献   

4.
Swine serologically negative for anti-Leptospira antibodies were given 2 doses of a pentavalent vaccine (3 weeks between doses) prepared from Leptospira serovars canicola, icterohaemorrhagiae, hardjo, pomona, and grip-potyphosa (0.2 mg/serovar/dose). Leptospires used for vaccinal production were cultivated in a protein-free medium or in a bovine albumin-containing medium. All vaccinated swine had demonstrable antibody titers within 1 week of the initial vaccination. Peak microscopic agglutination titers were between 256 and 1,024 after the 2nd vaccinal dose was given. After challenge exposure with serovar canicola, control swine had titers of at least 13,653 and the vaccinated swine had titers of 3,403 to 8,192, depending on the vaccine. Leptospiremia and kidney infections were not detected in any canicola Moulton immunized swine, but did appear in control swine. The Al(OH)3 adjuvant had no obvious influence of any of the vaccinal titers.  相似文献   

5.
Avian botulism is a paralytic disease caused by a toxin produced by Clostridium botulinum type C. Since type C isolates from cases of avian botulism produced a neurotoxin consisting of a mosaic form of parts of type C and D neurotoxins, we examined the antitoxin titers in the convalescent sera of botulism-affected birds which belonged to family Anatidae. ELISA using the C/D mosaic neurotoxin as an antigen revealed that the antibody was detected in the sera at 2 weeks, but not at 5 weeks after the onset, suggesting that the antibody only appeared for a short period in the convalescent phase. However, we failed to detect the antibody titers with anti-chicken IgG instead of anti-duck IgG. We therefore examine the immunological properties of IgG among different families and species. The results revealed that different species of IgG in the same family exhibited strong cross-reactivity. Ducks immunized once with the toxoid together with a commercial oil-adjuvanted vaccine were found to develop sufficient antibody to protect against a challenge with a lethal toxin dose. The ELISA titers did not correspond to the neutralization titers in the sera of immunized ducks at the early stage during immunization. These findings suggest that the neutralizing titer was more useful than the ELISA titer for evaluating the protection against the toxin, but the ELISA technique may be applicable for detecting the occurrence of botulism.  相似文献   

6.
Clostridium perfringens type A live cultures or sonicated sporulating cells, all containing enterotoxin, were repeatedly inoculated into sheep and calves by the intraduodenal route over periods of 30 to 35 days. Serum antibody to C. perfringens enterotoxin, tested by ELISA, developed in four of seven sheep and in two of four calves. The titers ranged from 400 to 1600. The live organism introduced into the duodenum did not become established in the bacterial flora of the intestinal tract.  相似文献   

7.
Clostridium perfringens type A enterotoxin seroneutralization was carried out on sera from 50 horses recovered from grass sickness and from 100 other horses with no record of having had the disease. Of the affected horses, 70% had seroneutralizating titers higher than 1:64, half of these being equal or higher than 1:128. More than 88% of the horses with no record of grass sickness had titers lower than 1:64. These data support the theory of association between C perfringens type A toxins and grass sickness.  相似文献   

8.
A randomized study was conducted to determine if inoculation of the abomasum or jejunum with Clostridium perfringens Type A would induce jejunal hemorrhage syndrome in healthy cows. Twelve adult nonlactating dairy cows were inoculated with 10 mL of pure culture broth of C. perfringens type A (beta2 toxin positive) into the abomasum (n = 6) or jejunum (n = 6). On day 6, the cows were euthanized and samples for culture were taken from the abomasum, jejunum, and feces. No cows developed clinical signs of jejunal hemorrhage syndrome during the course of the study. Five of 6 abomasal samples and 1 of 6 jejunal samples were positive for C. perfringens Type A (beta2 negative) prior to inoculation. Eight of 12 abomasal samples, 11 of 12 fecal samples, and 10 of 12 jejunal samples were positive for C. perfringens Type A (beta2 negative) after inoculation. Intraluminal inoculation of C. perfringens Type A alone at this dose and under these conditions did not induce clinical signs of jejunal hemorrhage syndrome in adult dairy cows. The multifactorial nature of the disease likely contributed to our inability to reproduce the disease in this study.  相似文献   

9.
Clostridium perfringens has been shown to be widespread in the broiler chicken hatchery, grow-out, and processing operations. In a previous study, ribotypes of certain strains of C. perfringens isolated from processed chicken carcasses were shown to match ribotypes isolated from paper pad lining trays used to transport commercial chicks from the hatchery to the grow-out facility on the farm. These results suggest that C. perfringens contaminating the processed product could originate from facilities in the integrated poultry operation prior to grow out. In this study, samples were collected from the breeder farm, hatchery, previous grow-out flock, during grow out and after processing. In the first trial, C. perfringens was recovered from the breeder farms, the hatchery, previous grow-out flock, grow-out flock at 3 weeks of age, grow-out flock at 5 weeks of age, from processed carcasses, and from the breeder farm after processing in 4%, 30%, 4%, 0%, 2% and 16%, and 4% of the samples, respectively. In the second trial, the incidence of C. perfringens in samples collected from breeder farms, the hatchery, previous grow-out flock, grow-out flock at 3 weeks of age, grow-out flock at 5 weeks of age, and fromprocessed carcasses was 38%, 30%, 32%, 8%, 4%, and 8%, respectively. The genetic relatedness of the isolated strains as determined by ribotyping suggests that C. perfringens may be transmitted between facilities within the integrated broiler chicken operation.  相似文献   

10.
Clostridium perfringens type C is an important cause of enteritis and/or enterocolitis in several animal species, including pigs, sheep, goats, horses and humans. The disease is a classic enterotoxemia and the enteric lesions and associated systemic effects are thought to be caused primarily by beta toxin (CPB), one of two typing toxins produced by C. perfringens type C. This has been demonstrated recently by fulfilling molecular Koch's postulates in rabbits and mice. We present here an experimental study to fulfill these postulates in goats, a natural host of C. perfringens type C disease. Nine healthy male or female Anglo Nubian goat kids were inoculated with the virulent C. perfringens type C wild-type strain CN3685, an isogenic CPB null mutant or a strain where the cpb null mutation had been reversed. Three goats inoculated with the wild-type strain presented abdominal pain, hemorrhagic diarrhea, necrotizing enterocolitis, pulmonary edema, hydropericardium and death within 24h of inoculation. Two goats inoculated with the CPB null mutant and two goats inoculated with sterile culture media (negative controls) remained clinically healthy during 24h after inoculation and no gross or histological abnormalities were observed in the tissues of any of them. Reversal of the null mutation to partially restore CPB production also increased virulence; 2 goats inoculated with this reversed mutant presented clinical and pathological changes similar to those observed in goats inoculated with the wild-type strain, except that spontaneous death was not observed. These results indicate that CPB is required for C. perfringens type C to induce disease in goats, supporting a key role for this toxin in natural C. perfringens type C disease pathogenesis.  相似文献   

11.
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.  相似文献   

12.
根据GenBank中已发布的产气荚膜梭菌α、β、ε、τ毒素基因序列,分别设计并合成针对4种毒素基因的特异引物,通过优化多重PCR反应条件,建立1种简单的产气荚膜梭菌定型菌落多重PCR方法。结果显示：A、B、C、D、E5型产气荚膜梭菌参考菌株均扩增出了相应的预期目的条带,而大肠杆菌、巴氏杆菌和芽孢杆菌则均未能扩增出相应条带;将单个菌落稀释100倍,仍能扩增出相应的目的片段,该方法对B型和E型参考菌株最低检测量分别为2．6×10^4cfu／mL、1．2×10^4cfu／mL。应用该多重PCR方法从106份样品中检测到30株产气荚膜梭菌且均为A型,其中病死鸡的盲肠内容物分离率为36．5％（19／52）,健康鸡群新鲜粪便样品分离率为20．4％（11／54）。本研究建立的多重PCR方法特异性强,敏感度高,重复性好,可以有效进行产气荚膜梭菌的快速检测及5种血清型的鉴别,对产气荚膜梭菌的感染及食品安全问题的研究均具有重要意义。  相似文献   

13.
OBJECTIVE: To determine the percentage of broodmares and foals that shed Clostridium perfringens in their feces and classify the genotypes of those isolates. DESIGN: Prospective cross-sectional study. ANIMALS: 128 broodmares and their foals on 6 equine premises. PROCEDURES: Anaerobic and aerobic bacteriologic cultures were performed on feces collected 3 times from broodmares and foals. All isolates of C. perfringens were genotyped. RESULTS: Clostridium perfringens was isolated from the feces of 90% of 3-day-old foals and 64% of foals at 8 to 12 hours of age. A lower percentage of broodmares and 1- to 2-month-old foals shed C. perfringens in their feces, compared with neonatal foals. Among samples with positive results, C. perfringens type A was the most common genotype identified (85%); C. perfringens type A with the beta2 toxin gene was identified in 12% of samples, C. perfringens type A with the enterotoxin gene was identified in 2.1% of samples, and C. perfringens type C was identified in < 1% of samples. CONCLUSIONS AND CLINICAL RELEVANCE: Clostridium perfringens was identified from the feces of all but 6 foals by 3 days of age and is likely part of the normal microflora of neonatal foals. Most isolates from broodmares and foals are C. perfringens type A; thus, the clinical relevance of culture results alone is questionable. Clostridium perfringens type C, which has been associated with neonatal enterocolitis, is rarely found in the feces of horses.  相似文献   

14.
A study was carried out in the South of Italy to assess the role of clostridia in neonatal diseases of lambs and kids. Eighty-seven lambs and 15 kids belonging to 25 flocks were examined and Clostridium perfringens was the microorganism most commonly identified. C. perfringens isolates were analysed by polymerase chain reaction (PCR), in order to determine the prevalence of the genes cpa, cpb, cpb2, etx, iap and cpe. The most prevalent toxin-type of C. perfringens was found to be type A found in 84% of the cases with clostridial enterotoxaemia. No C. perfringens type B, C or E were found. C. perfringens type D was isolated in 16% of the cases. About 24% of the isolates were cpb2 positive. The prevalence of cpb2 across the different C. perfringens types varied. The beta(2)-toxin gene cpb2 was detected in 4/21 (19%) type A isolates, in 1/2 type D isolates, and in 1/2 type DE (cpe-carrying type D) isolates. The high rate of positivity to cpb2 among the isolates suggests that a vaccine based on the beta(2)-toxin, should be included in the vaccination schedule of the animals to confer adequate protection and to prevent the disease.  相似文献   

15.
Clostridium perfringens isolated from lambs with dysentery (n=117) were analysed by a DNA amplification technique, the polymerase chain reaction (PCR), in order to determine the prevalence of the alpha-, beta-, beta 2-, epsilon-, iota- and enterotoxin genes. The most prevalent toxin type of C. perfringens found was type B, containing the alpha-, beta-, and epsilon-toxin genes, representing 46% of the cases with clostridial dysentery. C. perfringens type C containing the alpha-, and beta-toxin genes was isolated in 20% and type D, which is characterized by the alpha- and epsilon-toxin genes, was isolated in 28% of all isolates. The recently discovered, not yet assigned beta 2-toxigenic type of C. perfringens was represented in 6% of all isolates. No C. perfringens type A containing the alpha-toxin alone and no type E, which harbours the ADP-ribosylating iota-toxin, were found in the diseased animals. None of the samples contained the enterotoxin gene. Only one type of C. perfringens was found in a given herd, revealing the epidemiological use of PCR toxin gene typing of C. perfringens. The animals originated from 79 different herds with sizes ranging from 30 to 250 animals, bred in the area of northern Greece.  相似文献   

16.
Clostridium perfringens type D-producing epsilon toxin is a common cause of death in sheep and goats worldwide. Although anti-epsilon toxin serum antibodies have been detected in healthy non-vaccinated sheep, the information regarding naturally acquired antibodies in ruminants is scanty. The objective of the present report was to characterize the development of naturally acquired antibodies against C. perfringens epsilon toxin in goats. The levels of anti-epsilon toxin antibodies in blood serum of goat kids from two different herds were examined continuously for 14 months. Goats were not vaccinated against any clostridial disease and received heterologous colostrums from cows that were not vaccinated against any clostridial disease. During the survey one of these flocks suffered an unexpectedly severe C. perfringens type D enterotoxemia outbreak. The results showed that natural acquired antibodies against C. perfringens epsilon toxin can appear as early as 6 weeks in young goats and increase with the age without evidence of clinical disease. The enterotoxemia outbreak was coincident with a significant increase in the level of anti-epsilon toxin antibodies.  相似文献   

17.
Currently, the factors/toxins responsible for Clostridium perfringens-associated avian enteritis are not well understood. To assess whether specific C. perfringens' toxinotypes are associated with avian enteritis, the isolates of C. perfringens from 31 cases of avian necrotic or ulcerative enteritis submitted between 1997 and 2005 were selected for retrospective analysis using multiplex PCR. C. perfringens was isolated from chickens, turkeys, quail, and psittacines. The toxinotypes of isolates from diseased birds were compared against the toxinotype of 19 C. perfringens isolates from avian cases with no evidence of clostridial enteritis. All C. perfringens isolates were classified as type A regardless of species or disease history. Although many isolates (from all avian groups) had the gene encoding the C. perfirngens beta2 toxin, only 54% produced the toxin in vitro when measured using Western blot analysis. Surprisingly, a large number of healthy birds (90%) carried CPB2-producing isolates, whereas over half of the cpb2-positive isolates from diseased birds failed to produce CPB2. These data from this investigation do not suggest a causal relationship between beta2 toxin and necrotic enteritis in birds.  相似文献   

18.
Pregnant gilts were vaccinated with two doses of alhydrogel adsorbed fimbrial antigens of Escherichia coli (K88ab, K88ac, K99 and 987P) supplemented with beta toxoid of Clostridium perfringens type C. Their piglets, and piglets of nonvaccinated gilts, were subsequently orogastrically challenged with one or other of the four fimbrial types of enteropathogenic E coli. Some of the vaccinated animals were reinjected with a single dose of the vaccine during second gestation and their piglets, and piglets of non-vaccinated sows, were challenged the same way as were litters of gilts. Blood serum and colostra were examined for antibodies to the four fimbrial antigens of E coli and for antitoxin to beta toxin of C perfringens type C. It was found that: (1) a highly significant reduction in mortality and morbidity was achieved in vaccinated litters against all four challenge strains of E coli; (2) excretion of K88ab and K88ac but not of K99 and 987P challenge strains was significantly reduced; (3) revaccination of sows by a single dose of the vaccine during second gestation conferred complete protection against mortality and highly significant protection against morbidity; (4) no correlation was noted between colostral or seroagglutinins to fimbrial antigens of E coli and mortality rates in litters challenged with homologous fimbrial types of E coli, but good correlation was found between colostral precipitins to K88 antigens and mortality rates in litters; (5) antitoxin value in 97 per cent of colostrum of vaccinated sows was 10 iu equivalent of C perfringens type C toxin or more per ml of colostrum.  相似文献   

19.
Very little is known about the occurrence of Clostridium perfringens and of diseases caused by this anaerobic bacterium in marine mammals, especially those that are free-living. During a scientific expedition to the Greenland Sea (West Ice) in spring 1999, faeces samples from 70 hooded seals (Cystophora cristata) were taken to isolate C. perfiringens. Subsequently, PCR analysis of the isolates was performed with oligonucleotide primers of the genes encoding the four major lethal toxins (alpha, beta, epsilon and iota) for classification of toxin type and of the genes encoding C. perfringens beta2-toxin and enterotoxin for further subclassification. In addition, a commercial ELISA kit for detection of C. perfringens alpha, beta- and epsilon-toxin was used. C. perfingens was isolated in samples from 38 (54.3%) hooded seals. All isolates were C. perfringens toxin type A (alpha-toxin positive). This is the first report on the occurrence of C. perfringens in this arctic marine mammal species. Myositis and enterotoxemia caused by C. perfrigens were described in other marine mammals and it may be assumed that the pathogenesis of an outbreak of disease is similar to that encountered in terrestrial animals. Although there is some controversy surrounding the enteropathogenicity and virulence of alpha-toxin (concerning enterotoxemia), this study suggests that a possible outbreak of enterotoxemia caused by C. perfringens type A in hooded seals may, however, not be excluded.  相似文献   

20.
The etiologic role of Clostridum perfringens type A in the acute abdominal syndrome characterized by abomasal and rumen tympany, abomasitis, and abomasal ulceration was investigated in neonatal calves. Eight calves, 4 to 12 days old, were inoculated intraruminally with toxigenic C perfringens type A. Before and after C perfringens inoculation, blood samples were collected from all calves for blood gas and serum biochemical analysis and for determination of serum copper concentration; ruminal fluid was obtained for isolation of C perfringens. Calves were monitored daily for clinical signs of the syndrome and, depending on the severity of clinical signs, they were either euthanatized or redosed within 4 to 7 days. After necropsy, specimens obtained from the abomasum and rumen for macroscopic and microscopic examination and for anaerobic bacteriologic culture were processed in routine manner. Intraruminal inoculation of C perfringens type A into healthy calves induced anorexia, depression, bloat, diarrhea, and in some calves, death. Serum copper concentration was within normal range. Necropsy revealed variable degrees of abomasitis, petechial and ecchymotic hemorrhages, and ulcers (ranging from pinpoint to nearly perforate) in the abomasum. Seven of those calves also had multiple trichobezoars in the rumen. These necropsy findings were not seen in calves (controls) given distilled H2O only. In affected calves, acute abdominal syndrome was unrelated to copper deficiency, and C perfringens type A given intraruminally was able to induce clinical signs similar to those of the naturally acquired disease.  相似文献   

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