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The pathogenicity of the spores of Clostridium botulinum

Published online by Cambridge University Press:  15 May 2009

J. Keppie
Affiliation:
From the Microbiological Research Department, Porton, near Salibury
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1. The injection of mice with botulinum spores, freed from all traces of superficial toxin, can cause death but only if a very large number is given. This number was found in the case of a highly toxic strain to be of the order of 20 million spores given intramuscularly. This dose was fatal in the absence of spore germination.

2. In human botulism it is concluded that the spores of Clostridium botulinum persent in spoiled foodstuffs are not of importance compared with the toxin produced by the initial growth of the contaminating organisms.

3. Toxin could be demonstrated in the cytoplasm of botulinum spores when these were disintegreted by mechanical means. This is of theoretical interest as the toxin within the spores is more heat-stable than the extracellular form.

4. A local anaerobic myositis could be produced in mice by the intramuscular injection of spores plus 2·5% CaCl2. The number of viable spores in the LD50 was of the order of 50,000.

5. Calcium chloride solution in the commonly used strength of 2·5% was shown regularly to cause a drop in the number of botulinum spores in a given suspersion of some 40% and a parallel loss of viability of about 60%.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1951

References

REFERENCES

Coleman, G. E. (1929). Amer. J. Hyg. 9, 47.Google Scholar
Coleman, G. E. & Meyer, K. F. (1922). J. infect. Dis. 31, 622.CrossRefGoogle Scholar
Edmondson, R. B., Giltner, L. T. & Thom, C. (1920). Arch. int. Med. 26, 357.CrossRefGoogle Scholar
Ermengem, E. van (1897). Z. Hyg. Infektr. 26, 1.Google Scholar
Geiger, J. C., Dickson, E. C. & Meyer, K. F. (1922). Bull. U.S. Publ. Hlth Serv., Publ. Hlth Lab. 127, 1.Google Scholar
Hall, I. C. & Davis, N. C. (1923). J. exp. Med. 37, 585.CrossRefGoogle Scholar
Mickle, H. (1948). J. R. micr. Soc. 68, 10.CrossRefGoogle Scholar
Miles, A. A. & Misra, S. S. (1938). J. Hyg., Camb., 38, 732.Google Scholar
Orr, P. F. (1922). J. infect. Dis. 30, 118.CrossRefGoogle Scholar
Reed, L. J. & Muench, H. (1938). Amer. J. Hyg. 27, 493.Google Scholar
Starin, W. A. & Dack, G. M. (1925). J. infect. Dis. 36, 383.CrossRefGoogle Scholar
Thom, C., Edmondson, R. B. & Giltner, L. T., (1919). J. Amer. med. Ass. 73, 907.CrossRefGoogle Scholar