Critical Colonization — The Concept under Scrutiny
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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.
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