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The behaviour of a mutant strain of Salmonella typhimurium in experimental mouse typhoid

Published online by Cambridge University Press:  15 May 2009

Derek Hobson
Affiliation:
The Wright-Fleming Institute of Microbiology, St Mary's Hospital Medical School, London, W. 2
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A streptomycin-resistant mutant of a virulent strain of Salm. typhimurium was less virulent to mice than the parent strain. The difference in virulence was only observed when mice were infected with small numbers of organisms. Although the mutant strain caused fewer deaths than the parent strain it remained capable of establishing persistent infection in the majority of animals.

The significant difference in the behaviour of the two strains in vivo was that after clearance from the blood multiplication in the tissues began more rapidly with the virulent strain and was progressive, whereas multiplication of the mutant was delayed, was less in degree and was apparently suppressed within a few days of infection.

The mutant strain was apparently identical antigenically with the parent strain, and was equally toxic. The mice dying of infection with this strain did so when the bacterial population had reached a level similar to that in the terminal stage of infection with the virulent strain.

The essential difference between the two strains was the speed and probability of attaining a critical final population. The mutant strain of Salm. typhimurium, both in vitro and in vivo, had a slower growth rate than the parent strain. A possible hypothesis to explain the importance of this finding in relation to the outcome of infection has been discussed.

I am indebted to the Medical Research Council for the provision of a grant towards the expenses of this investigation and to Mr T. Norris and Miss Italia S. Alderton for technical assistance.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1957

References

Bacon, G. A., Burrows, T. W. & Yates, M. (1950). Brit. J. exp. Path. 31, 714.Google Scholar
Boivin, A. (1939). C.R. Soc. Biol., Paris, 132, 370.Google Scholar
Challice, C. E. & Gorrill, R. H. (1954). Biochim. biophys. Acta, 14, 484.CrossRefGoogle Scholar
Davis, B. D. & Mingioli, E. S. (1950). J. Bact. 60, 17.CrossRefGoogle Scholar
Felix, A. (1952). J. Hyg., Camb., 50, 515.Google Scholar
Felix, A. & Bensted, H. J. (1954). Bull. World Hlth Org. 10, 919.Google Scholar
Felix, A. & Pitt, R. M. (1951). J. Hyg., Camb., 49, 92.CrossRefGoogle Scholar
Gorrill, R. H. (1952). J. Path. Bact. 64, 857.CrossRefGoogle Scholar
Greenwood, M., Hill, A. B., Topley, W. W. C. & Wilson, J. (1936). Spec. Rep. Ser. med. Res. Coun., Lond., no. 209.Google Scholar
Hill, A. B., Hatswell, J. M. & Topley, W. W. C. (1940). J. Hyg., Camb., 40, 538.Google Scholar
Hobson, D. (1956). Brit. J. Exp. Path. 37, 20.Google Scholar
Hobson, D. (1957 a). J. Path. Bact. 73, 399.CrossRefGoogle Scholar
Hobson, D. (1957 b). J. Hyg., Camb., 55, 334.CrossRefGoogle Scholar
Mackenzie, G. M., Pike, R. M. & Swinney, R. E. (1940). J. Bact. 40, 197.CrossRefGoogle Scholar
Ørskov, J., Jensen, K. & Kobayashi, K. (1928). Z. Immunforsch. 55, 34.Google Scholar
Reed, L. J. & Muench, H. (1938). Amer. J. Hyg. 27, 493.Google Scholar
Schütze, H., Gorer, P. A. & Findlayson, M. H. (1936). J. Path. Bact. 53, 443.CrossRefGoogle Scholar
Smith, P. H., Oginsky, E. L. & Umbreit, W. W. (1949). J. Bact. 58, 761.CrossRefGoogle Scholar
Wilson, G. S. (1930). J. Hyg., Camb., 30, 40.CrossRefGoogle Scholar
Wilson, G. S. & Miles, A. A. (1955). Topley and Wilson's Principles of Bacteriology and Immunology, 4th ed.London: Arnold.Google Scholar
Wright, H. D. (1927). J. Path. Bact. 30, 184.CrossRefGoogle Scholar