Hostname: page-component-78c5997874-s2hrs Total loading time: 0 Render date: 2024-11-09T15:51:25.907Z Has data issue: false hasContentIssue false
  • English
  • Français

The incidence of brucellosis clinical and latent among various groups of the population

Published online by Cambridge University Press:  15 May 2009

C. P. Beattle
C. P. Beattle
Affiliation:
From the Bacteriology Department, University of Edinburgh
Rights & Permissions [Opens in a new window]

Extract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

1. The population as a whole is exposed to Brucella infection by the consumption of infected milk. This does not appear to be a very potent source of infection as relatively few clinical cases of brucellosis occur, nor are many latent infections discovered by the agglutination reaction.

2. Those exposed to contact with infected animals or meat, as are farm workers, slaughterers and butchers, run a greater risk of contracting infection. The risk is not, however, markedly increased when the contact is limited to the handling of carcasses or meat, milking or ordinary animal husbandry.

3. Members of the veterinary profession, who assist in calving and remove placentas from infected cows are exposed to the greatest risk of infection. They come in contact with the greatest natural concentration of Br. abortus through the most dangerous route, the skin. Clinical brucellosis is not common among them, but many contract latent infection. 58·3% of post-graduate and 10·8% of undergraduate veterinary students were found to have agglutinins for Br. abortus in their serum. This should be borne in mind when a diagnosis of undulant fever is considered in a member of the veterinary profession.

Type
Research Article
Information
Journal of Hygiene , Volume 38 , Issue 2 , March 1938 , pp. 260 - 268
Copyright
Copyright © Cambridge University Press 1938

References

REFERENCES

Bang, O. & Bendixen, H. C. (1932). Medlemsblad. fur den Danske Dyrlaegefarening, 15, 1. abs. Cornell Vet. 22, 195.Google Scholar
Beattle, C. P. (1932). Lancet, i, 1002.CrossRefGoogle Scholar
Beattle, C. P., Smith, J. & Tulloch, W. J. (1935). Lancet, i, 1427.CrossRefGoogle Scholar
Burnet, E. (1922). Arch. Inst. Pasteur Afrique Nord, 2, 187.Google Scholar
Carpenter, C. M. (1926). J. Inf. Dis. 39, 220.CrossRefGoogle Scholar
Carpenter, C. M., Boak, R. & Chapman, O. D. (1929). J. Immunol. 17, 65.CrossRefGoogle Scholar
Cruickshank, R. & Barbour, W. J. (1931). Lancet, i, 852.CrossRefGoogle Scholar
Dalrymple-Champneys, W. (1933). Proc. Roy. Soc. Med. 26, 99.Google Scholar
Dalrymple-Champneys, W. (1934). Lancet, i, 95.CrossRefGoogle Scholar
Dalrymple-Champneys, W. (1935). Lancet, ii, 1449.CrossRefGoogle Scholar
Dible, J. H. & Pownall, M. (1932). J. Hygiene, 32, 349.CrossRefGoogle Scholar
Dooley, P. (1932). Arch. Int. Med. 50, 373.CrossRefGoogle Scholar
Gilbert, R. & Dacey, H. G. (1932). J. Lab. and Clin. Med. 17, 345.Google Scholar
Hardy, A. V., Hudson, M. G. & Jordan, C. F. (1929). J. Inf. Dis. 45, 271.CrossRefGoogle Scholar
Hardy, A. V., Jordan, C. F., Bork, I. H. & Hardy, G. C. (1930). U.S. Treasury Dept., Nat. Inst. Health Bull. 158.Google Scholar
Hill, I. C. & Learmonth, R. (1934). J. Inf. Dis. 55, 184.CrossRefGoogle Scholar
Huddleson, I. F. & Johnson, H. W. (1930). J. Amer. Med. Assoc. 94, 1905.CrossRefGoogle Scholar
Johns, E. P., Campbell, F. J. H. & Tennant, C. S. (1932). Canad. Med. Assoc. J. 27, 490.Google Scholar
Jordan, C. F. (1931). J. Inf. Dis. 48, 526.CrossRefGoogle Scholar
Kristensen, M. & Holm, P. (1929). Zbl. Bakt. Abt. 1, Orig. 112, 281.Google Scholar
Kristensen, M. (1931). 2me Congres Internat. Path. Comp. 68.Google Scholar
Kruger, H. (1932). Deut. Tierärzt. Woch. 40, 481.Google Scholar
Larson, W. P. & Sedgwick, J. P. (1913). Am. J. Dis. Child. 6, 326.Google Scholar
Laun, R. H. & Herde, E. (1934). Ztchr. f. Hyg. u. Infektionskr. 116, 315.CrossRefGoogle Scholar
Lentze, F. A. (1930). Zbl. Bakt. Abt. 1, Orig. 118, 360.Google Scholar
Maclean, F. S. (1932). New Zealand Med. J. 262, cited Brit. Med. J. ii, 105.Google Scholar
Morales-Otero, P. (1933). J. Inf. Dis. 52, 54.CrossRefGoogle Scholar
Morgan, W. P. (1932). Lancet, i, 1067.CrossRefGoogle Scholar
Peterson, C. E. (1935). J. Lab. & Clin. Med. 20, 727.Google Scholar
Priestley, F. W. (1934). J. Comp. Path. and Ther. 47, 181.CrossRefGoogle Scholar
Pullinger, E. J. (1934). Lancet, i, 967.CrossRefGoogle Scholar
Rossi, P. (1935). C. R. Soc. Biol. 118, 1053.Google Scholar
Sasano, K. T., Caldwell, D. & Medlar, E. M. (1931). J. Inf. Dis. 48, 576.CrossRefGoogle Scholar
Smith, J. (1932). J. Hygiene, 32, 354.CrossRefGoogle Scholar
Smith, J. (1934). J. Hygiene, 34, 242.CrossRefGoogle Scholar
Taylor, R. M., Lisbonne, M. & Vidal, L. F. (1934). Mouvement Sanitaire, 130.Google Scholar
Thomsen, A. (1931). J. Inf. Dis. 48, 484.CrossRefGoogle Scholar
Wilson, G. S. & Nutt, M. N. (1926). J. Path. Bact. 29, 141.CrossRefGoogle Scholar
Wilson, G. S. (1932). Vet. Record, 12, 1240.Google Scholar