One of the fundamental contributions of bacteriology to the understanding of disease is the concept that a symptom or specific pathological condition may have its origin in the activity of a single compound elaborated by'a pathogenic agent. Historically this principle has been best exemplified by the exotoxins produced by certain bacteria. Among these exotoxins are the neurotoxins produced in vitro by Clostridium botulinum under suitable environmental conditions of nutrition, anaerobiosis, and temperature. The botulinal toxins have also been objects of curiosity because they are the most potent poisons known. It is my purpose to outline some of our knowledge of the nature of the botulinal toxins and to record questions of interest that remain to be answered.Clostridium botulinum is a sporeforming, strictly anaerobic, rod-shaped bacterial species. Under as yet poorly understood conditions of growth it produces intracellularly a neurotoxin which is released into the growth medium after the major increase in the bacterial culture's population has been achieved. What role, if any, the toxin plays in the economy of the parent bacterium is a complete mystery. The organism is generally unable to grow within the body of the warm-blooded animal; hence, from a medical and veterinary stand-
Among numerous published methods for the rupturing of microorganisms are grinding in any of a variety of mills, supersonic disintegration, and the sudden release of high pressure. Another effective procedure depends upon agitation in the presence of small glass beads (Curran and Evans,
On the basis of toxicity assays using partition centrifugation cells it was established that the sedimentation coefficient of type A botulinum toxin appearing in the lymph of orally poisoned rats was 7.9 x 10–18 cm. per dyne sec. with 95 per cent confidence limits of 4.4 to 11.4 x 10–13 cm. per dyne sec. This is a significantly lower value than that obtained for crystalline toxin but is well within the range of size for proteins. Exposure of crystalline toxin for 2 hours to digestive processes in a section of the duodenum of living rats did not significantly reduce the sedimentation coefficient of the toxin. The S20 of crystalline toxin employed in the present study ranged between 12 and 21 with a mean value of 17.9. While it was observed that both botulinum toxin and albumin sedimented from lymph in glycerol gradient tubes to essentially the same level no evidence was developed to indicate association between toxin in lymph and serum albumin. The electrophoretic mobility of toxin in lymph is like that of crystalline toxin and not albumin. Dialysis of toxic lymph against serum albumin does not result in the appearance of toxin in the dialysate.
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