[Specific antitoxic therapy of botulism].
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The method for obtaining the neurotoxin, or alpha-fraction of the toxin, of Cl. botulinum, type B, is described. In accordance with this method, the toxin was precipitated three times with hydrochloric acid in the isoelectric zone with subsequent extraction with phosphate (pH 6.8) and citrate-phosphate (pH 5.6) buffers, then fractionated in columns with DEAE cellulose (pH 5.6), DEAE Sephadex A-50 (pH 7.2) and Sephadex G-200 (pH 7.2). The homogeneous neurotoxin preparations with molecular weights ranging from 145,000 to 160,000 and having the isoelectric point at pH 5.5 and toxicity 5.0--10.0 x 10(7) Dlm per 1 mg protein were obtained.
A column chromatography method was employed to obtain a monospecific botulinus type A toxin. The latter was found to be a homogeneous product via column chromatographic and electrophoretic studies. The immunodiffusion test after Ouchterlony with a serum obtained with the use of a native toxin yielded one precipitation line. No such lines were produced with a serum obtained from animals immunized with a type B toxin. The purified toxin could be detoxicated by routinely applied methods. When injected to rabbits it induced the production of monospecific antibodies.
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A double antibody version of CLISA was demonstrated to be a rapid method (1 h) for detection and quantitative determination of Clostridium botulinum toxin antigens in biological samples. The sensitivity of this assay is about ten-fold higher than both ELISA and passive hemagglutination test. Thus, the double antibody version of CLISA appeared to be useful for the control of food products contaminated with Cl. botulinum type A bacteria.
Botulism is a rare disease which usually is caused by preformed botulinum toxin in food. However, this article describes a case of wound botulism in a 29-year-old male heroin addict who developed progressive diplopia, dysphagia and proximal weakness of skeletal limb muscles. He needed mechanical ventilation for two weeks. The clinical diagnosis of botulism was supported by neurophysiological tests. Assays for detection of botulinum toxin and Clostridium botulinum were negative. The patient had not eaten any contaminated food the last two weeks before symptoms appeared, but he had multiple contaminated skin wounds. After treatment with botulinum antitoxins and antibiotics he gradually recovered, and six weeks later he was discharged from hospital in good condition. To the best of our knowledge this is the first case of wound botulism reported in Norway.