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The Anomalous Features of the Dick Reaction

Published online by Cambridge University Press:  15 May 2009

J. P. McGibbon
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About one-fourth of the cases in a series of 160 patients suffering from scarlet fever appeared to be Dick-negative in the acute stage of the disease.

Throughout the illness there was a progressive decrease in the number of positives and in the intensity of the reactions, till in the second week two-thirds and in the fourth week nine-tenths of the total cases were negative. Almost 90 per cent, of the original positives showed this characteristic loss of the Dick-positive state. It would appear that this change occurs less readily in young children. Fluctuations in the reaction during the course of the illness are very uncommon, if indeed they occur at all.

Of eleven cases which failed to show the above change two relapsed. In the other 149 cases no relapses occurred.

Pseudo-reactions are uncommon. Two examples have been described. It is suggested that the use of heated filtrate may be unsatisfactory and that the mechanism of these reactions requires further study.

Some of the anomalous features of the Dick reaction have been briefly discussed. In the opinion of the writer these difficulties have been exaggerated, and they do not in themselves form sufficient grounds for concluding that the test is fallacious.

On the evidence at present available one must continue to regard scarlet fever as a specific toxaemia. The allergic conception of the disease is less convincing.

Type
Research Article
Information
Journal of Hygiene , Volume 34 , Issue 1 , February 1934 , pp. 30 - 37
Copyright
Copyright © Cambridge University Press 1934

References

REFERENCES

Ando, K. (1930). J. Immunol. 18, 223.CrossRefGoogle Scholar
Benson, W. T. and Simpson, G. W. (1927). Lancet, 1, 281.CrossRefGoogle Scholar
Brockman, H. and Mayzner, M. (1927). C.R. Soc. Biol. 96, 1480.Google Scholar
Brown, W. A. (1925). Brit. J. Child. Dis. 22, 171.Google Scholar
Cooke, Jean V.et al. (1927). Amer. J. Dis. Child. 34, 969.CrossRefGoogle Scholar
Cooke, Jean V.et al. (1928). Amer. J. Dis. Child. 35, 762, 784, 974, 983, 991.Google Scholar
Dick, G. F. and Dick, G. H. (1923). J. Amer. Med. Assoc. 81, 1166.CrossRefGoogle Scholar
Gibson, H. J. and McGibbon, J. P. (1932). Lancet, 2, 729.CrossRefGoogle Scholar
Glenny, A. T., Pope, G. and Waddington, H. (1928). J. Path. and Bact. 28, 471.Google Scholar
v. Gröer, F. (1927). Klin. Wochenschr. 6, 97.CrossRefGoogle Scholar
v. Gröer, F. and Redlich, F. (1928). Zeitschr. f. d. gesamte Exper. Med. 62, 391.CrossRefGoogle Scholar
Joe, Alexander (1925). Lancet, 2, 1321.CrossRefGoogle Scholar
Lichtenstein, A. (1926). Acta. Med. Scand. Supplt. 16, 326.CrossRefGoogle Scholar
Mair, W. (1923). Lancet, 2, 1390.CrossRefGoogle Scholar
Moriwaki, G. (1927). Japan Med. World, 7, 65.Google Scholar
O'Brien, R. A. and Okell, C. C. (1926). Public Health, 39, 246.CrossRefGoogle Scholar
O'Brien, R. A., Okell, C. C. and Parish, H. J. (1928). Public Health 41, 181.Google Scholar
Okell, C. C. (1932). Lancet, 1, 761.CrossRefGoogle Scholar
Peters, B. A. and Allison, S. F. (1928). Brit. Med. J. 2, 4.CrossRefGoogle Scholar
Rosen, P. S. and Korobicina, L. A. (1925). J. Amer. Med. Assoc. 84, 1476.CrossRefGoogle Scholar
Toomey, J. A. (1926). J. Amer. Med. Assoc. 87, 941.CrossRefGoogle Scholar
Toyoda, T., Moriwaki, J. and Futagi, Y. (1930). Lancet, i, 73.Google Scholar
Zingher, A. (1924). J. Amer. Med. Assoc. 83, 432.CrossRefGoogle Scholar