Hostname: page-component-78c5997874-4rdpn Total loading time: 0 Render date: 2024-11-03T08:42:19.291Z Has data issue: false hasContentIssue false

The value of antiseptics as prophylactic applications to recent wounds

Published online by Cambridge University Press:  15 May 2009

J. Gordon
Affiliation:
Department of Pathology and Bacteriology, Leeds University
J. W. McLeod
Affiliation:
Department of Pathology and Bacteriology, Leeds University
Anna Mayr-Harting
Affiliation:
Department of Pathology and Bacteriology, Leeds University
J. W. Orr
Affiliation:
Department of Pathology and Bacteriology, Leeds University
K. Zinnemann
Affiliation:
Department of Pathology and Bacteriology, Leeds University
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.

There have been groups of observers both in this country and in Germany who have been entirely sceptical about the value of the prophylactic application of antiseptics to wounds and who seem to incline to the opinion that such medication is likely to be more harmful than useful; e.g. Colebrook in a special report to the Medical Research Council (1928) stated that ‘the ordinary “antiseptics” have a higher affinity for the leucocytes than for the microbes, and by combining with the former forfeit their microbicidal potential’. Further, he stated that with the exception of optochin and neosalvarsan, substances which have been tried as antiseptics are so rapidly fixed on serum proteins, blood cells, and the fixed tissues, that they fail to impart bactericidal power to the serum. Fleming (1924, 1931) in a number of ingenious experiments showed that injury to leucocytes is the most likely outcome of antiseptic applications to wounds, and has argued that they are more likely to be harmful than useful for that reaon; later (1938), he pointed out the superiority of the sulphonamides to the older antiseptics as tested by his ‘slide cell’ technique and in penicillin he has discovered an antiseptic which in respect of a high ratio of bactericidal potency to its toxicity to mammalian tissues approaches the ideal. This has given the clinical results which would be expected on theoretical grounds. There are, however, limitations to the use of penicillin as a general prophylactic antiseptic application which depend on (a) its failure to destroy some types of bacteria which cause suppuration, (b) its relative lability, (c) its present cost. There is therefore ground for further careful assessment of the best prophylactic antiseptic. Fleming (1940) has in fact admitted that there may be a place for proflavine in the interim dressing of wounds pending surgical treatment. The German opinion on the question of the prophylactic use of antiseptics seems to have been considerably influenced by the observations of Schimmelbusch, who had demonstrated that mice inoculated on a scarified area of the tail with anthrax bacilli could not be saved when the tail was amputated at a point proximal to the site of inoculation even 10 min. after the wound had been infected. It was concluded on this account that the penetration of bacteria from a wound into the deeper tissues was so rapid that local treatment of the wound was obviously futile. Schiemann & Wreschner (1922) and Weise (1922), however, who record these observations of Schimmelbusch, made similar observations with streptococci but showed that with this micro-organism not only tail amputation but also local application of antiseptics was often successful in saving mice so infected. They did not dispute the rapid penetration of the bacteria but concluded that in the case of the streptococcus the body could deal with limited numbers of these micro-organisms, if the local lesions from which they were reaching the general circulation were eliminated. Further, Browning (1943) in a discussion of the antiseptic action of the amino acridine compounds made an extensive survey of the literature on the influence of these substances on leucocytes and concluded that in view of the wide variations in results the particular technique adopted must be an important factor. Hence he suggests there is need for much caution in accepting such results as an indication of what will actually happen in the animal body.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1947

References

REFERENCES

Albert, A., Francis, A. E., Garrod, L. P. & Linnell, W. H. (1938). Brit. J. Exp. Path. 19, 41.Google Scholar
Armitage, G., Gordon, J., Cohen, J. B. & Elling-worth, S. (1929). Lancet, 2, 968.CrossRefGoogle Scholar
Baker, L. D. (1942). J. Bone Jt Surg. 24, 641.Google Scholar
Berger, E. (1937). Klin. Wschr. 16, 53.CrossRefGoogle Scholar
Bisgard, J. D. & Baker, C. P. (1942). Surg. Gynec. Obstet. 74, 20.Google Scholar
Bonney, V. & Browning, C. H. (1918). Brit. Med. J. 1, 562.CrossRefGoogle Scholar
Bonnin, N. J. & Fenner, F. (1941). Med. J. Aust. 1, 134.CrossRefGoogle Scholar
Botterel, E. H., Carmichael, E. A. & Cone, W. V. (1941). J. Neurol. Psych. 4, 163.CrossRefGoogle Scholar
Boxall, G. N., Happold, F. C. & Lloyd, Ll. (1934). Parasitology, 26, 44.CrossRefGoogle Scholar
Browning, C. H. (1943). Brit. Med. J. 1, 341.CrossRefGoogle Scholar
Browning, C. H., Cohen, J. B., Ellingworth, S. & Gulbransen, R. (1926). Proc. Roy. Soc. B, 100, 293.Google Scholar
Browning, C. H., Cohen, J. B., Ellingworth, S. & Gulbransen, R. (1931). J. Path. Bact. 34, 592.Google Scholar
Browning, C. H. & Gulbransen, R. (1925). Brit. Med. J. 1, 688.CrossRefGoogle Scholar
Colebrook, L. (1928). A Study of some Organic Arsenical Compounds with a view to their Use in certain Streptococcal Infections. Report to the Medical Research Council. London: H.M. Stationery Office.Google Scholar
Colebrook, L. (19401941). Proc. Roy. Soc. Med. 34, 337.Google Scholar
Colebrook, L. & Francis, A. E. (1941). Lancet, 1, 271.CrossRefGoogle Scholar
Collier, W. A. & Bernhagen, I. (19281929). Z. Hyg. InfektKr. 109, 382.CrossRefGoogle Scholar
Evans, D. G., Fuller, A. T. & Walker, J. (1944). Lancet, 2, 523.CrossRefGoogle Scholar
Fleming, A. (1924). Proc. Roy. Soc. B, 96, 171.Google Scholar
Fleming, A. (1931). Brit. Dent. J. 52, 105.Google Scholar
Fleming, A. (1938). Lancet, 2, 74.CrossRefGoogle Scholar
Fleming, A. (1940). Proc. Roy. Soc. Med. 33, 487.Google Scholar
Garrod, L. P. (1940). Lancet, 1, 798.CrossRefGoogle Scholar
Goldberger, H. A. (1942). Amer. J. Surg. 56, 353.CrossRefGoogle Scholar
Gordon, J. & McLeod, J. W. (1941). Lancet, 1, 407.CrossRefGoogle Scholar
Heggie, R. M. & Heggie, J. F. (1942). Lancet, 2, 604.Google Scholar
Jensen, N. K., Johnsrud, L. W. & Nelson, M. C. (1939). Surgery, 6, 1.Google Scholar
Key, J. A. & Burford, T. H. (1941). Surg. Gynec. Obstet. 73, 324.Google Scholar
Legroux, R. (1940). Mem. Acad. Chir. 66, 415.Google Scholar
McIntosh, J. & Selbie, F. R. (1942). Lancet, 2, 750.CrossRefGoogle Scholar
McIntosh, J. & Selbie, F. R. (1943). Lancet, 1, 793.CrossRefGoogle Scholar
McLeod, J. W. & Bevan-Brown, R. E. (1918). J. Path. Bact. 22, 74.Google Scholar
McSwain, B. & Glenn, F. (1942). Arch. Surg. 44, 231.CrossRefGoogle Scholar
Mitchell, G. A. G. & Buttle, G. A. H. (1942). Lancet, 2, 416.CrossRefGoogle Scholar
Porritt, A. E. et al. (1945). Penicillin Therapy and Control in 21st Army Group.CrossRefGoogle Scholar
Reinhardt, A. (1922). Z. Hyg. InfektKr. 95, 27.CrossRefGoogle Scholar
Rubbo, S. D., Albert, A. & Maxwell, M. (1942). Brit. J. Exp. Path. 22, 69.Google Scholar
Russell, Dorothy S. & Beck, J. (1944). Lancet, 1, 112.Google Scholar
Russell, Dorothy S. & Falconer, M. A. (19401941). Brit. J. Surg. 28, 472.CrossRefGoogle Scholar
Russell, D. S. & Falconer, M. A. (1943). Lancet, 1, 580.CrossRefGoogle Scholar
Schiemann, O. (1922). Z. Hyg. InfektKr. 97, 280.CrossRefGoogle Scholar
Schiemann, O. & Wreschner, H. (1922). Z. Hyg. InfektKr. 95, 424.CrossRefGoogle Scholar
Schneider, L. (1941). Amer. J. Med. Sci. 201, 208.CrossRefGoogle Scholar
Weise, K. (1922). Z. Hyg. InfektKr. 97, 56.CrossRefGoogle Scholar