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The Influence Of Tuberculosis Upon The Development Of Brucella Abortus Infection

Published online by Cambridge University Press:  15 May 2009

E. J. Pullinger
E. J. Pullinger
Affiliation:
From the Research Institute in Animal Pathology, Royal Veterinary College, London
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Summary and conclusion

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1. The difficulty of isolating Br. abortus from samples of “dirty” milk by means of guinea-pig inoculation is noted. This has been shown to be due in certain instances to the presence of tubercle bacilli in the inoculum, though this is probably not the full explanation.

2. Following the simultaneous inoculation of virulent tubercle bacilli and Br. abortus into guinea-pigs, the latter infection generally failed to become established, whereas control animals inoculated under the same conditions with Brucella, but without tubercle bacilli, became infected.

Results of the inoculation of the two organisms into opposite sides of guinea-pigs indicate a generalized as well as a local increase of resistance to Br. abortus.

3. It is suggested that the mononuclear cell reaction stimulated by the tubercle bacilli destroyed Br. abortus.

I am indebted to the Directors of the United Dairies, Limited, for their interest and financial support. My thanks are due to Dr W. S. Gordon, Moredun, for sending a virulent strain of Br. abortus.

Type
Research Article
Information
Journal of Hygiene , Volume 36 , Issue 3 , July 1936 , pp. 456 - 466
Copyright
Copyright © Cambridge University Press 1936

References

REFERENCES

Beattie, C. P. (1932). Lancet, i, 1002.CrossRefGoogle Scholar
Dienes, L. (1936). Arch. Path. Washington, 21, 357.Google Scholar
Dienes, L. & Mallory, T. B. (1932). Amer. J. Path. 8, 689.Google Scholar
Gaiger, S. H. & Davies, G. O. (1933). Veterin. Rec. 13, 876.Google Scholar
Gay, F. P., Clark, A. R. & Linton, R. W. (1926). Arch. Path. Washington, 1, 857.Google Scholar
Pullinger, E. J. (1934). Lancet, i, 967.CrossRefGoogle Scholar
Rowlands, W. T. (1933). Veterin. Rec. 13, 127.Google Scholar
Schoenfeld, A. F. & Cotton, C. M. (1925). J. Inf. Dis. 37, 68.CrossRefGoogle Scholar
Schroeder, E. C. & Cotton, W. E. (1911). 28th Ann. Rep. Bureau Animal Industry, Washington, p. 139.Google Scholar
Smith, J. (1932). J. Hyg. 32, 354.CrossRefGoogle Scholar
Wilson, G. S. & Nutt, M. N. (1926). J. Path. and Bact. 29, 141.CrossRefGoogle Scholar