Critical Colonization — The Concept under Scrutiny
- 0 Comments
- 12673 reads
The term critical colonization has attracted increasing attention over the past 5 years. Accepted by some and viewed with derision by others, critical colonization has been regarded by a number of publications as synonymous with local infection1-4 through its association with the criteria for wound infection developed by Cutting and Harding,5 a benchmark for diagnosis that appears to have gained relatively broad acceptance. Others have dismissed the concept of critical colonization as a myth, expressing the view that a wound is either infected or not, with no prodromal phase of infection.6 In order to advance understanding of delayed healing in the absence of an obvious clinical cause, the basic concept of critical colonization deserves consideration.
If alternative explanations for delayed healing can be identified, patient morbidity potential can be reduced; therefore, delayed healing must be placed accurately into context to help avoid making or perpetuating inappropriate assumptions. This paper reviews the emergence of the concept of critical colonization from an historical perspective, discusses assumptions that have been made, and presents scientific evidence collated from the literature. This approach draws some parallels with the criteria for wound infection developed by Cutting and Harding5 where a review of the literature led to the collation of traditional and additional diagnostic features of wound infection and the development of an entirely new approach to identifying clinical wound infection.
Development of the Concept
The term critical colonization was first coined in 1996 by Davis7 in a poster presented to a joint meeting of the Wound Healing Society and the European Tissue Repair Society. Using case studies, Davis demonstrated how delayed healing in wounds could be reversed through appropriate use of topical antiseptics. She also defined the condition of the wound in relation to bacterial presence. Using a modified model for infection first published by Ayton,8 Davis introduced the notion of critical colonization within the infection spectrum (from sterile to contaminated to colonized to critically colonized to infection) and defined it as “multiplication of organisms without invasion but interfering with wound healing.”
Davis also stated that “the classic signs of infection must be reassessed to include the ‘critically colonized’ wound,”7 offering the first association with local infection. In support of her treatise, Davis cited Danielson9 and a clinical study with microbiological screening by Trengove10 espousing the notion that the presence of pathogens, with or without host reaction, could interfere with healing. Currently, the absence of a host response is viewed as a fundamental link to understanding the concept of critical colonization.
Davis continued to champion the term critical colonization but little if any notice was taken until Kingsley11 renamed her model of wound infection “the Wound Infection Continuum.” This model would appear to bear the most relevance to acute wounds because even though the first stage — sterility — is not a feature or even a therapeutic goal in chronic wounds, the wound infection continuum is most closely associated with chronic wounds.
1. Sibbald RG, Meaume S, Kirsner RS, Munter KC. Review of the clinical RCT evidence and cost-effectiveness data of a sustained-release silver foam dressing in the healing of critically colonised wounds. Available at: http://www.worldwidewounds.com/2005/december/Sibbald/Silver-Foam-Dressin.... Accessed May 16, 2006.
2. Edwards R, Harding KG. Bacteria and wound healing. Curr Opin Infect Dis. 2004;17(2):91–96.
3. Jorgenson B, Price P, Anderson KE, et al. The silver-releasing foam dressing, Contreet Foam, prompts faster healing of critically colonised venous leg ulcers: a randomised controlled trial. Int Wound J. 2004;2(1):64–73
4. Schultz GS, Sibbald RG, Falanga V, et al. Wound bed preparation: a systematic approach to wound management. Wound Rep Regen. 2003;11(suppl 1):S1–S28.
5. Cutting KF, Harding KG. Criteria for identifying wound infection. J Wound Care. 1994;3(4):198–201.
6. Gilchrist B. Finding bacteria in wounds: are you being misled? Presented at: European Wound Management Association Conference Proceedings, Pisa, Italy; May 22–24, 2003
7. Davis E. Don’t deny the chance to heal! Presented at: 2nd Joint Meeting of the Wound Healing Society and the European Tissue Repair Society, Boston, Mass; May 15–19, 1996.
8. Ayton M. Wounds that won’t heal. Nurs Times. 1985;81(46 suppl):S16–S19.
9. Danielson L. The role of Pseudomonas aeruginosa in chronic wounds. Proceedings of the 4th European Wound Management Association Conference on Advances in Wound Management. Copenhagen, Denmark; September 6–9, 1994.
10. Trengove NJ, Stacey MC, McGechie DF, et al. Qualitative bacteria and chronic leg ulcer healing. J Wound Care. 1996;5(6):2772–2780.
11. Kingsley A. A proactive approach to wound infection. Nurs Stand. 2001;15(30):50–58.
12. Dow G. Bacterial swabs and the chronic wound: when, how, and what do they mean. Ostomy Wound Manage. 2003;49(5 suppl A):8S–13S.
13. Sibbald RG, Orsted H, Schultz GS, et al. Preparing the wound bed 2003: focus on infection and inflammation. Ostomy Wound Manage. 2003;49(11):24–51.
14. Markus YM, Bell MJ, Evans AW. Ischemic scleroderma wounds successfully treated with hyperbaric oxygen therapy. J Rheumatol. 2006;33(8):1694–1696.
15. Hermanns JF, Paquet P, Arrese JE, et al. La cytotoxicité bénéfique des antiseptiques. Rev Med Liege. 1999;54(7):600–605.
16. Kingsley AR. The wound infection continuum and its application to clinical practice. Ostomy Wound Manage. 2003;49(7 suppl A):S1–S7.
17. Ennis WJ, Menenses P. Wound healing at the local level: the stunned wound. Ostomy Wound Manage. 2000;46(1 suppl A):39S–48S.
18. Selkon J, Cherry GW, Wilson JM, Hughes MA. Evaluation of hypochlorous acid washes in the treatment of chronic venous leg ulcers. J Wound Care. 2006;15(1):33–37.
19. Ovington L. Bacterial Toxins and wound healing. Ostomy Wound Manage. 2003;49(7 suppl A):8–12.
20. Cutting KF, White RJ. Criteria for identifying wound infection — revisited. Ostomy Wound Manage. 2005;51(1):28–34.
21. Trengove NJ, Stacey MC, McGechie D, Stingemore N, Mata S. Qualitative bacteria and chronic leg ulcer healing. Proceedings of the 4th European Wound Management Association Conference on Advances in Wound Management, Copenhagen, Denmark; September 6–9, 1994.
22 Heinzelmann M, Scott M, Lam T. Factors predisposing to bacterial invasion and infection. Am J Surg. 2002;183(2):179–190.
23. Cutting KF. Wound healing, bacteria and topical therapies. EWMA J. 2003;3(1):17–19.
24. Lookingbill D, Miller SH, Knowles RC. Bacteriology of chronic leg ulcers. Arch Dermatol. 1978;114(12):1765–1768.
25. Daltrey DC, Rhodes B, Chattwood JG. Investigation into the microbial flora of healing and non-healing decubitus ulcers. J Clin Pathol. 1981;34(7):701–705.
26. Halbert AR, Stacey MC, Rohr JB, et al. The effect of bacterial colonization on venous ulcer healing. Austral J Dermatol. 1992;33:75–80.
27. Hansson C, Hoborn J, Moler A, Swanbeck G. The microbial flora in venous leg ulcers without clinical signs of infection. Acta Derm Venereol. 1995;75(1):24–30.
28. Drosou A, Kirsner RS, Welsh E, Sullivan TP, Kerdel FA. Use of infliximab, an anti-tumor necrosis alpha antibody, for inflammatory dermatoses. J Cutan Med Surg. 2003;7(5):3823–3886.
29. Eron LJ, Lipsky B, Low D, et al. Managing skin and soft tissue infections. J Antimicrob Chemother. 2003;52(1 suppl):S3–S17.
30. Cooper RA, Morwood S, Burton N. Histamine production by bacteria isolated from wounds. J Infect. 2004;49:39.
31. Aspiroz C, Navarro C, Aguilar E, Rodriguez-Andre M. Bacteraemia in an obese patient with cellulitis and chronic ulceration in the lower extremity. Enferm Infec Microbiol Clin. 2004;22(6):363–364.
32. Isaac-Marquez AP, Lezama-Davila CM. Detection of pathogenic bacteria in skin lesions of patients with Chiclero’s ulcer. Mem Inst Oswaldo Cruz. 2003;98(8):1093–1095.
33. Bowler PG, Davies BJ. The microbiology of infected and noninfected leg ulcers. Int J Dermatol. 1999;38(8):101–106
34. Moore K. The cell biology of chronic wounds: the role of inflammation. J Wound Care. 1999;8(7):345–352.
35. Page KR, Scott AL, Manabe YC. The expanding realm of heterologous immunity: friend or foe? Cell Microbiol. 2006;8(2):185–196.
36. Abd-El-Aleem SA, Morgan C, Ferguson MW, et al. Spatial distribution of mast cells in chronic venous leg ulcers. Eur J Histochem. 2005;49(3):265–272.
37. Gray D, White RJ, Kingsley A, Cooper P. Using the wound infection continuum to assess wound bioburden. Wounds-UK. 2005;1(2 suppl):S15–S21.
38. Allen L, Dockrell DH, Pattery T, et al. Pyocyanin production by Pseudomonas aeruginosa induces neutrophil apoptosis and impairs neutrophil-mediated host defenses in vivo. J Immunol. 2005;174(6):3643–3649.
39. Serralta VW, Harrison-Balestra C, Cazzaniga AL, et al. Lifestyles of bacteria in wounds: presence of biofilms? WOUNDS. 2001;13(1):29–34.
40. Stephens P, Wall IB, Wilson MJ, et al. Anaerobic cocci populating the deep tissues of chronic wounds impair cellular wound healing responses in vitro. Br J Dermatol. 2003;148(3):456–466.
41. Lau GW, Hassett DJ, Ran H, et al. The role of pyocyanin in Pseudomonas aeruginosa infection. Trends Mol Med. 2004;10(12):599–606.
42. Costerton JW. Cystic fibrosis pathogenesis and the role of biofilms in persistent infection. Trends Microbiol. 2001;9(2):50–52.
43. Usher LR, Lawson RA, Geary I, et al. Induction of neutrophil apoptosis by Pseudomonas aeruginosa exotoxin pyocyanin; a potential mechanism of persistent infection. J Immunol. 2002;168(4):1861–1868.
44. Dacheux D, Epaulard O, de Groot A, et al. Activation of Pseudomonas aeruginosa type III secretion system. Infect Immun. 2002;70(7):3973–3977.
45. King JR, Koerber AJ, Croft JM, et al. Modelling host tissue degradation by extracellular bacterial pathogens. Math Med Biol. 2003;20(3):227–260.
46. White RJ. More research is needed before we can accurately define and understand critical colonisation. Letter. Wounds-UK. 2006;2(2):86–88.
47. Hamilton Jakobsen B, Danielsen L. Venous leg ulcer. Ugeskr Laeger. 1997;159(19):2836–2840.
48. Denning GM, Iyer SS, Reszka KJ, et al. Phenazine-1-carboxylic acid, a secondary metabolite of Pseudomonas aeruginosa, alters expression of immunomodulatory proteins by human airway epithelial cells. Am J Physiol Lung Cell Mol Physiol. 2003;285(3):584–592.
49. Zychlinsky A, Sansonetti P. Perspective series: host/pathogen interactions. Apoptosis in bacterial pathogenesis. J Clin Invest. 1997;100(3):493–495.
50. Zychlinsky A, Sansonetti P. Apoptosis as a pro-inflammatory event: what can we learn from bacteria-induced cell death? Trends Microbiol. 1997;5(5):201–204.
51. Buret A, Cripps AW. The immunoevasive activities of Pseudomonas aeruginosa. Am Rev Respir Dis. 1993;148(3):793–805.
52. Speert DP. Molecular epidemiology of Pseudomonas aeruginosa. Front Biosci. 2002;7:354–361.
53. Sio CF, Otten LG, Cool RH, et al. Quorum quenching by an N-acyl-homoserine lactone acylase from Pseudomonas aeruginosa PA01. Infect Immun. 2006;74(3):1673–1682.
54. Bowler PG, Davies BJ, Jones SA. Microbial involvement in chronic wound malodour. J Wound Care. 1999;8(5):216–218.
55. Rotstein OD, Nasmith PE, Grinstein S. The bacteroides by-product succinic acid inhibits neutrophil respiratory burst by reducing intracellular pH. Infect Immun. 1987;55(4):864–870.
56. Rotstein OD, Vittorini T, Kao J, et al. A soluble Bacteroides by-product impairs phagocytic killing of Escherichia coli by neutrophils. Infect Immun. 1989;57(3):745–753.
57. Athanasopoulos AN, Economopoulos M, Orlova V, et al. The extracellular adherence protein (EAP) of Staphylococcus aureus inhibits wound healing by interfering with host defense and repair mechanisms. Blood. 2006;107(7):2720–2727.
58. Chavakis T, Hussain M, Kanse SM, et al. Staphylococcus aureus extracellular adherence protein serves as anti-inflammatory factor by inhibiting the recruitment of host leukocytes. Nat Med. 2002;8(7):687–693.
59. Haggar A, Ehrnfelt C, Holgersson J. The extracellular adherence protein from Staphylococcus aureus inhibits neutrophil binding to endothelial cells. Infect Immun. 2004;72(10):6164–6167.
60. Reed PJ, Sanderson P. Detection of anaerobic wound infection. J Clin Path. 1979;32(12):1203–1205.
61. Cutting KF. The identification of infection in granulating wounds by registered nurses. J Clin Nurs. 1998;7(6):539–546.
62. Bowler PG. The aerobic and anaerobic microbiology of wounds: a review. WOUNDS. 1998;10(6):170–178.
63. White RJ, Cutting KF, Kingsley A. Critical colonisation: clinical reality or myth? Wounds-UK. 2005;1(1):94–95.