Influence of bacteria on Clostridium perfringens infections in young chickens

When monoflora chickens with Lactobacillus acidophilus or Streptococcus faecalis were inoculated with Clostridium perfringens either in broth culture or resuspended in Gifu anaerobic medium broth or supernatant fluid, few or no chickens died. Approximately 50% of germ-free chickens died after inoculation of C. perfringens culture, whereas no conventional birds died after inoculation of broth culture. C. perfringens in the contents of duodenum from germ-free chickens numbered about 10(4) colony-forming units (CFU)/g after inoculation 10(8) CFU broth culture per bird, but in gnotobiotic and conventional chickens this organism decreased or was not detected. When C. perfringens was cultured in intestinal contents collected from germ-free chickens, C. perfringens proliferated but alpha toxin was not detected. These findings indicate that the pathogenicity of C. perfringens was suppressed by L. acidophilus or S. faecalis administered previously or inhibited by normal intestinal flora.     

Influence of Clostridium perfringens and its toxin in germ-free chickens

Twenty-one of 56 germ-free chickens died after receiving an oral inoculation of a broth culture of Clostridium perfringens. At necropsy there was detachment and disruption of the epithelial layer at the tips of villi and sloughed epithelial cells in the duodenum. These are characteristic lesions of necrotic enteritis. Germ-free chickens receiving either purified alpha-toxin or the supernatant of broth cultures of C perfringens died, but no bird died after receiving supernatant of broth cultures neutralised by anti-alpha-toxin serum. It was concluded that alpha-toxin of C perfringens was the cause of death in young germ-free chickens.     

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.     

产气荚膜梭菌α毒素的研究进展

产气荚膜梭菌 (Clostridiumperfringens)的致病作用一般由它所产生的胞外酶或毒素诱导。主要有α -毒素、β -毒素、θ -毒素及其他的一些胞外酶。本文针对产气荚膜梭菌α毒素的组成、结构、理化性质、作用机理及分子遗传等方面的研究进展作了简要综述。     

禽产气荚膜梭菌研究进展

产气荚膜梭菌（Clostridium perfringens,CP）是重要的食源性病原体之一,可对人类和动物健康造成严重威胁。CP在家禽中主要引起禽坏死性肠炎,严重影响了全球肉鸡贸易与生产。关于禽CP的研究当前主要集中于检测及分型方法、疫苗和耐药性方面。目前禽CP疫苗多处于实验室研发阶段,因此禽CP感染的防治主要依靠抗生素,而抗生素的频繁使用又导致了菌株耐药性问题,防治效果有限。因此,CP耐药性研究以及临床诊断技术完善及疫苗研发推进迫在眉睫。本文简述了CP的病原特点、致病机理及禽间的优势流行分型,梳理了禽CP不同检测方法的优点及分型方法,阐述了禽CP耐药现状以及疫苗研发方向及进展,提出了禽CP感染辅助防治措施,以期为CP感染防控提供参考。     

产气荚膜梭状芽孢杆菌病的流行与致病机制

产气荚膜梭状芽孢杆菌是人和动物肠道的正常菌群，亦是条件性致病菌，该菌感染主要由毒素导致的毒血症致病，因此，有针对地选用类毒素预防接种，才能防止本病流行。     

Endocrine and metabolic changes during altered growth rates in beef cattle

Eight steers from a group of 14 were fed ad libitum from 240 to 510 kg live weight, gaining at 1.4 +/- .2 kg/d. The six other steers were diet-restricted and grew at .37 +/- .09 kg/d from 240 to 307 kg, prior to ad libitum realimentation on the same diet to a final weight of 510 kg. Blood samples taken during the growth phases from both treatments were analyzed for insulin-like growth factor-I (IGF-I), triiodothyronine (T3), thyroxine (T4), glucose (GLU), nonesterified fatty acids (NEFA), and blood urea nitrogen (BUN) and (or) growth hormone (GH). During restricted growth, mean serum concentrations of GH were elevated (45.6 vs 23.4 ng/ml; P less than .05), serum concentrations of IGF-I decreased (108 vs 167 ng/ml; P less than .05) compared with control steers with ad libitum access to feed. Levels of T4 and GLU also were lower (P less than .05) during restricted than during normal growth. During early realimentation, levels of GLU (P less than .05), IGF-I (P less than .01), T4 and BUN (P less than .01) increased. Levels of T3 remained unchanged, whereas concentration of NEFA declined (P less than .001). Blood urea nitrogen decreased during early realimentation despite a large increase in diet protein intake and in protein storage, suggesting an increased efficiency of nitrogen use for protein synthesis. During realimentation, IGF-I levels rose above those of control steers and remained higher at the final weight of 510 kg (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)     

The roles of Clostridium difficile and enterotoxigenic Clostridium perfringens in diarrhea in dogs

In this prospective study, feces of dogs with diarrhea were compared with feces of normal dogs for the presence of Clostridium difficile, C difficile toxins A and B, C perfringens, and C perfingens enterotoxin (CPE). C difficile toxins A, B, or both were present in feces of 18 of 87 (21%) dogs with diarrhea and 4 of 55 (7%) normal dogs (P = 0.03), whereas CPE was present in the feces of 24 of 87 (28%) dogs with diarrhea and 3 of 55 (5%) normal dogs (P = 0.01). C difficile was isolated from 2 of 87 (2%) dogs with diarrhea but was not isolated from the feces of 55 normal dogs, possibly because of poor survival of the organism in fecal samples. C perfringens was isolated from the feces of 23 of 24 (96%) CPE-positive dogs with diarrhea, 52 of 63 (83%) CPE-negative dogs with diarrhea, and 39 of 55 (71%) CPE-negative dogs with normal feces. No correlation was found between C perfringens spore number and the presence of CPE.     

产气荚膜梭菌ε毒素及其疫苗研究进展

产气荚膜梭菌病是由产气荚膜梭菌引起的一种重要的人兽共患传染病,可导致山羊、绵羊等动物的肠毒血症或坏死性肠炎,并且可引起动物脑、心、肺和肾组织的水肿.B型和D 型产气荚膜梭菌所产生的ε毒素是引起动物上述病理变化和死亡的重要因素之一.虽然甲醛灭活的毒素疫苗能对动物产生保护性抗体,但是,灭活苗潜在的安全性原因使其在应用上受到限制.因此,基于ε毒素基因的重组疫苗和弱毒疫苗就成为人们研究的目标.     

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.     

Effect of a Probiotic on Prevention of Diarrhea and Clostridium difficile and Clostridium perfringens Shedding in Foals

Background

Up to 60% of foals develop diarrhea within 6 months after birth. Preventive measures are limited but potentially probiotics could be used.

Objective

To evaluate the effect of a newly designed probiotic on the incidence of foal diarrhea in a randomized field trial.

Animals

Seventy‐two healthy neonatal foals.

Methods

Randomized, placebo‐controlled field trial. Foals were administered a placebo or probiotic for 3 weeks and monitored for an additional week. A total of 3 fecal samples were taken from each foal at biweekly intervals. Statistical modeling was applied for comparison of incidence and duration of diarrhea and fecal shedding of Clostridium perfringens and Clostridium difficile between treatment and age groups.

Results

The overall incidence of diarrhea was 41 of 72 (59%) and did not differ (P = 0.37) between treatment groups. Foals treated with probiotics were more likely to develop diarrhea requiring veterinary intervention (P = 0.007). Age had a significant effect on incidence of diarrhea (P < 0.001); foals 8–15 days old having the highest probability of developing diarrhea. Duration of diarrhea and soft feces were not significantly different between groups. The prevalence of C. perfringens shedding was 55% with no difference between treatment groups (P = 0.23). The prevalence of C. difficile shedding was 11%.

Conclusion and Clinical Importance

There was no benefit of administering a 3‐week course of probiotics, but potential adverse effects were noted. Whether the probiotics lacked a clinical effect, or the choice of strains or dose was inadequate, is unknown. Clostridial shedding was not influenced by probiotics despite in vitro activity of probiotics.     

Effects of Lactobacillus acidophilus on the growth performance and intestinal health of broilers challenged with Clostridium perfringens

Background: Clostridium perfringens is the main etiological agent of necrotic enteritis. Lactobacil i show beneficial effects on intestinal health in infectious disease, but the protective functions of lactobacil i in C. perfringens-infected chickens are scarcely described. This study examined the effects of Lactobacil us acidophilus(L. acidophilus) on the growth performance and intestinal health of broiler chickens chal enged with Clostridium perfringens(C. perfringens) over a 28-day period. Using a 2 × 2 factorial arrangement of treatments, a total of 308 1-day-old male Arbor Acres broiler chicks were included to investigate the effects of Lactobacil us acidophilus(L. acidophilus) on the growth performance and intestinal health of broiler chickens chal enged with Clostridium perfringens(C. perfringens) during a 28-day trial.Results: During infection(d 14–21), C. perfringens challenge decreased the average daily gain(P 0.05), and increased feed conversion ratio and the mortality rate(P 0.05). However, dietary supplementation with L. acidophilus increased the body weight of C. perfringens-infected broilers on d 21(P 0.05), and tended to decrease the mortality(P = 0.061).C. perfringens challenge decreased the villus height(P 0.05), the ratio of villus height to crypt depth(P 0.05) and OCLN(occludin) m RNA expression(P 0.05), and increased the pro-inflammatory cytokine expression in the spleen and jejunum, the intestinal populations of C. perfringens and Escherichia(P 0.05), and the serum content of endotoxin(P 0.05), regardless of L. acidophilus supplementation. In contrast, dietary L. acidophilus reducedthe intestinal lesion score of challenged broilers(P 0.05), the m RNA expression of pro-inflammatory cytokines, ileal populations of Escherichia and serum endotoxin content(P 0.05), but increased the intestinal Lactobacillus populations(P 0.05),irrespective of C. perfringens challenge.Conclusion: Dietary addition of L. acidophilus could improve the intestinal health and reduce the mortality of broilers suffering from necrotic enteritis.     

家兔产气荚膜梭菌的分离、鉴定及致病性分析

为对疑似家兔产气荚膜梭菌病感染死亡的肉兔病例进行病原菌的分离鉴定,并分析其对家兔的致病性,试验采集死亡病例的肠道内容物,划线接种于兔鲜血平板和TSC选择鉴别培养基中,对病原菌进行分离纯化,利用细菌16SrDNA通用引物进行分子鉴定,分析其同源性,构建系统进化发育树,同时,对病原菌进行生化鉴定,并将病原菌腹腔接种30日龄肉兔,分析其致病性。结果表明,从病料中分离纯化到1株革兰氏阳性菌;通过对细菌16S rDNA基因测序分析及生化鉴定确定为产气荚膜梭菌,且在系统进化树中也与其聚为一簇;致病性分析发现,该菌对家兔具有较强的致死性,可使试验组肉兔在攻毒16h后全部死亡。综上所述,本研究成功获得1株具有较强毒性的兔源产气荚膜梭菌,为产气荚膜梭菌致病机制的研究奠定了基础,同时也为疫病诊断和防控提供了理论依据。     

产气荚膜梭菌肠毒素的分子生物学研究进展

产气英膜梭菌(Clostridium perfringens)是一种重要的人兽共患病的病原体,它是一类革兰氏阳性产芽孢的厌氧梭菌,可引起人的食物中毒和肠毒素相关腹泻.近年来,研究人员发现由产气英膜梭菌导致腹泻的主要原因与该菌在芽孢形成过程中产生的一种肠毒素有关.文章重点针对产气英膜梭菌肠毒素的生物学特性和致病机制等方面的研究做一综述.