Endocytosis of Clostridium botulinum type B neurotoxin into rat brain synaptosomes

Clostridium botulinum type B neurotoxin cleaves VAMP (vesicle-associated membrane protein)/synaptobrevin into two fragments, which results in inhibition of neurotransmitter release. The induced fragment did not react to the antibody raised against the synthetic peptide of the amino-terminal 20 residues of VAMP-2, suggesting that the toxin treatment has caused antigenical alteration in the amino-terminal region of VAMP-2. In rat brain synaptosomes, type B neurotoxin was reduced presumably with sulfhydryls in the membrane and detected in the synaptic vesicle fraction which involved the degradation of VAMP-2 and the inhibition of neurotransmitter release. The light chain in a free form was present in the cytosol fraction. These findings suggest a possibility that type B neurotoxin endocytoses into synaptic vesicles by the recycling pathway and the light chain is penetrable through synaptic vesicle membrane. However, the amount of type B neurotoxin entrapped into synaptic vesicles appears to be extremely small, which may be attributed to a lower sensitivity of the toxin to brain synaptosomes than to peripheral nerve endings.     

Clostridium perfringens type C enterotoxemia in a newborn foal

A 1-day old, full-term foal with a history of colic died 2 hours after admission. Necropsy revealed an extremely flaccid, fluid-filled intestinal tract. Histopathologically, the superficial intestinal mucosa was completely necrotic, with minimal inflammatory response. Numerous large, gram-positive rods covered the villi. Clostridium perfringens was isolated on bacteriologic culturing of the intestinal tract contents and was identified as type C by toxin neutralization tests.     

Association between Key-Gaskell syndrome and infection by Clostridium botulinum type C/D

There is growing evidence that equine dysautonomia is a toxicoinfection with Clostridium botulinum type C. The possibility that feline dysautonomia has the same aetiology was investigated by attempting to detect botulinum type C neurotoxin in the food, faeces and the contents of the ileum of affected cats, and by serology. The toxin was detected directly in four of eight affected cats and after enrichment in seven of them, and in their dried food. No toxin was detected in healthy control cats or in their tinned food. Recent exposure to the organism was assessed by the detection of immunoglobulin A (IgA) in the faeces of healthy control cats and affected cats. The levels of IgA antibodies to the toxin and to surface antigens of C. botulinum type C in the faeces of the affected cats 14 weeks after the outbreak were significantly higher than in the faeces of the control cats.     

Clostridium botulinum type B toxicosis in a herd of cattle and a group of mules

Clostridium botulinum type B toxicosis was diagnosed as the cause of generalized weakness and death in a group of cows and mules fed from the same batch of rye silage. One severely affected cow was treated and recovered, as did other less severely affected cows. All affected mules died. The remaining cattle in the herd were then vaccinated before continued feeding of the silage.     

Susceptibility of mink to Clostridium botulinum type C toxin

Investigations to determine the exact susceptibility of mink to Clostridium botulinum type C toxin clearly showed that mink were considerably less resistant to this toxin than has previously been described. Mink weighing approximately 900 g were killed by 360 MLD when toxin was mixed into the feed. By subcutaneous injection, the lethal dose was determined to be in the range of 18 to 36 MLD.When comparing the susceptibility per g of body weight after parenteral application of the toxin, mink proved to be less resistant than mice to this type of toxin. Continued feeding tests in mink with suspected material is pointed out as a preferable method for practical demonstrations of Clostridium botulinum type C toxin in cases where the toxin content in the suspected material is very low (1 MLD per g or less).     

Hemorrhagic enteritis caused by Clostridium perfringens type C in a foal

A 4-day-old foal died with bloody diarrhea. Using a mouse neutralization test, Clostridium perfringens type C was isolated from intestinal contents, and alpha and beta toxins were identified. About 4 m of the jejunum had severe necrohemorrhagic enteritis. Microscopically, large, rod-shaped, gram-positive bacteria were seen on necrotic intestinal villi by use of Brown and Hopp's stains.     

Susceptibility of mink to Clostridium botulinum type E toxin

Experiments aiming at elucidation of the toxicity of Clostridium botulinum type E for mink are described. The observations indicate that amounts in the order of 2 x10^s intraperitoneal MLD (mice) or approximately 200 MLD per g of type E toxin will kill a mink after oral administration. The symptoms observed in the animals were atypical as there was an unusually short period between administration of the toxin and the onset of symptoms and deaths of the animals. Similar results were obtained when Clostridium botulinum type E toxin was fed to Swiss mice. When mice were protected by subcutaneous injections of type E antitoxin prior to feeding the animals survived without showing any symptoms.Subcutaneous injection of type E toxin in amounts of the order of 2 x10^s intraperitoneal MLD (mice) killed mink, and typical symptoms of botulism were observed. This quantity corresponds to ap-proximately 2 intraperitoneal MLD (mice) per g.Comparison is made with previous observations obtained in similar experiments made with Clostridium botulinum type C toxin. It is shown that mink arc substantially less susceptible to type E than to type C toxin when the toxins are given by mouth. On this basis previous results in reports on outbreaks of botulism in mink caused by Clostridium botulinum type E may be regarded as questionable.     

The taxonomic position of Clostridium botulinum type c.

Experimental evidence is produced to justify abandoning the practice of subdividing Costridium botulinum Type C into type Calpha and Cbeta.     

鸡肉毒梭菌中毒的诊治

我镇某散养鸡场，07年6月28目，2月龄2000只鸡群中突然发生运动神经麻痹和延脑麻痹为主要症状的疾病，同时发生大批死亡。前后共发病928只，发病率46．4％，死亡886只，病死率89．7％。通过发病情况调查，临诊症状观察，病理剖检及动物播种试验，初步诊断为肉毒梭菌毒系中毒症。     

Clostridium botulinum type D intoxication in a dairy herd in Ontario

Thirty-four Holstein cows died after exposure to Clostridium botulinum type D toxin, presumably from contaminated haylage. The presence of type D toxin in ruminal contents was confirmed by mouse inoculation. This is the first confirmation by direct toxin isolation of C. botulinum type D toxin in cattle in North America.