Author Mark O’Brien, BSc, RGN, is clinical nurse specialist tissue viability, independent consultant.
Abstract O’Brien, M. (2007) Understanding critical colonisation of wounds. Nursing Times; 103: 43, 48–50.
The effect of the presence of bacteria in wounds is complex and only partially understood. Perhaps more concerning is the level of misunderstanding among nurses about how infection and its precursors – contamination and colonisation – are defined. Understanding the distinction between infection, contamination and colonisation is critical to the delivery of clinical and cost-effective wound care, given the influence that bacteria have on the success, or lack of it, of wound healing.
Recently there has been a new addition to this continuum – ‘critical colonisation’. While this term has yet to be defined fully, it is already influencing how clinicians view aspects of wound healing and select modes of treatment (White et al, 2005).
Before reading this article, please write down a brief definition of contamination, colonisation and infection. They all involve the presence of bacteria, but what is the difference between them? When you have completed the exercise, you will find the key features in Table 1.
The perfect host
Wounds present an ideal environment for bacterial growth – they are moist, warm, and there is reduced oxygenation. Virtually all are colonised – in other words bacteria are present and replicating but there is no host reaction. However, it does not necessarily follow that they are an ideal environment for infection.
In a young patient with an otherwise clean wound, intact immune system and no other pathology, bacteria may colonise the wound without harm. The same pattern of bacteria in an older, debilitated patient with multiple pathologies could prove life-threatening. So, infection depends not just on the bacterium’s ability to cause an infection but also on whether the host is capable of preventing it.
In recent years, the term ‘critical colonisation’ has gained acceptance among clinicians and is central to Kingsley’s (2001) ‘wound care continuum’. It describes a state where ‘host defences are unable to maintain a healthy [bacterial] balance’ and bacteria are sufficient in number to delay healing but not cause a classical host reaction, such as heat, redness or swelling.
The term has arisen from clinical observation rather than microbiological study, as clinicians have observed the resolution of previously indolent wounds following the use of antibacterials (Davis, 1998). At the same time, the concept of ‘wound-bed preparation’ has established control of ‘bioburden’ or bacterial load as a priority of wound care (Sibbald et al, 2000).
Infection is considered to have occurred when populations of bacteria reach 105 colony-forming units per gram of tissue (or a bioburden of 100,000 viable organisms per gram of tissue) (Georgiade, 1983). This is not a definitive figure, as it is known that certain bacteria will cause a host reaction with smaller populations. For example, beta-haemolytic streptococci and some other bacteria work synergistically (one species enhances the effect of another) (Bowler, 2003).
How do we diagnose infection?
In most cases we rely on a clinical identification of a host reaction. In other words, ‘If it looks infected, it is infected.’ While this sounds crude compared with the ‘105’ method, it is far more practical and clinically useful if prompt treatment is to be implemented. Problems do arise, however, if clinicians fail to recognise the symptoms and do nothing or, just as importantly, misdiagnose normal inflammatory processes as infection and over-prescribe antibiotics.
In recent years the diagnostic criteria for wound infection have been the subject of significant debate, culminating in Cutting et al (2005) using a Delphi approach (a method for reaching consensus among a group of experts) to describe the key features of infection for a variety of acute and chronic wounds. While these features have not been validated, the resulting criteria may offer a framework for more accurate and timely diagnosis.
It should also be remembered that there is little benefit in performing swabs to identify bacteria in wounds that are not showing signs of infection. As mentioned, the presence of bacteria does not equate to infection. Similarly the important question is whether healthy tissue is infected, not the slough and debris lying on it. Swabs should therefore be taken after a wound has been cleansed with normal saline and any loose debris removed, the aim being to sample an area of viable wound bed (Cooper and Lawrence, 1996).
It is also extremely important to provide a detailed account of symptoms to the microbiology department, as this will direct their investigations and subsequent advice on treatment.
How do we diagnose critical colonisation?
Unfortunately ‘if it looks like critical colonisation, it is critical colonisation’ does not work. White (2003) suggests that the clinical appearance of critical colonisation can include any of the following:
- Indolent wound not responding to appropriate care with underlying pathologies and no cellulitis (when infection spreads into tissue);
- No cellulitis but with exacerbation of pain, or pain becoming present when it was not before, or change in the quality experience of pain;
- Thick slough not responding to standard techniques for removal;
- Slough quickly returns after rapid debridement techniques (for example, larval or sharp surgical);
- Intransigent odour.
Care should be taken when interpreting such findings because critical colonisation is often marked by an absence of symptoms rather than their presence. Diagnosis of critical colonisation may be speculative as a result of difficulties separating bacterial components from other factors that could obstruct healing or assessment. For example:
- Cellulitis may not be evident if a patient is significantly immuno-compromised or it may be masked by pigmentation or venous staining;
- Unsatisfactory debridement or recurrence of slough may be a consequence of poor technique or local ischaemia;
- Increased pain could be related to alterations in dressing or medication regimens.
The presentations described may have a bacterial component and this should not be neglected, but adhering too closely to fixed criteria risks focusing on the pathogen and neglecting the host.
Despite such reservations it is known that when bacteria are present in sufficient numbers they can release enzymes (matrix metalloproteinases) and other factors (cytokines, tumour necrosis factor) that promote chronic local inflammation and degrade tissue without generating a cellulitis. It is this period of surface degradation that critical colonisation may describe with the bacteria proving an irritant, rather than attacking, force. If not addressed, this irritation can lead to painfully slow healing and significant patient distress.
In wounds, bacteria collaborate to form a protective biofilm. They group together and generate a polysaccharide matrix or ‘slime’ that envelopes them, shielding them from: passing macrophages and neutrophils (the main immune cells responsible for killing bacteria); variations in wound temperature, pH and humidity; and the penetration of antibiotics. Biofilms are, however, more than just a slimy bunker in which bacteria hide. The bacteria within can communicate with each other and work in unison, in effect acting as a single multicellular organism (Cooper and Okhiria, 2006).
Protected inside their bunker, the bacteria are immune to the efforts of neutrophils trying to attack them. This does not stop the neutrophils from trying. Stimulated by the bacterial presence, neutrophils will release a stream of proteolytic (protein-splitting) enzymes that, unable to penetrate the biofilm, act instead on the wound bed, leading to chronic low-grade inflammation and degradation of tissue – in other words, another manifestation of critical colonisation.
It should also be noted that biofilms are not visible to the naked eye and, as with critical colonisation, their presence is often inferred as opposed to demonstrated. Bacteria outside a biofilm are described as ‘planktonic’ or free-floating. While they are free to cause infection they are also at the mercy of the immune system and antibacterial agents. The major significance of the biofilm is that if the free bacteria are eliminated, the biofilm can release a new wave of bacteria ready to attack the host. This ability may be responsible for the clinical scenario of recurrent infection (Cooper and Okhiria, 2006) as seen in complicated orthopaedic wounds (biofilms associated with implants) and chronic wounds such as venous leg ulcers.
It is clear that bacteria are capable of occupying a variety of states. So how can we use this knowledge to improve our clinical practice?
Objectives of wound care
If we acknowledge that bacteria can have a detrimental effect on wound healing before a host reaction occurs, then we must also acknowledge the need to minimise wound bioburden.
The objective is not to eliminate all bacteria but to return the wound to a safely colonised state where the host is able to manage the bacterial load independently. Excluding all bacteria is neither desirable or, arguably, possible, without risking damage to healthy tissue (Hampton, 1997). The use of topical antibacterials in this context may be appropriate but they should not be viewed as a universal panacea. Additional methods of optimising the local wound environment (debridement, care of surrounding skin, dressing interval) and the patient’s general health (nutrition, oedema management, diabetes control) in order to reduce susceptibility and recurrence, should always be considered.
If a wound has become static this should be a trigger to reassess all aspects of patient care, not just the topical agent/dressing used (Sibbald
et al, 2000). It is also worth reassessing personal and organisational infection control practices to limit patient exposure to pathogens. For example, when did you last audit your mattresses or dressing technique?
Recently there has been a renewed interest in the use of topical antibacterials. The reasons include:
- Treatment of MRSA and efforts to minimise its transmission;
- The need to further reduce antibiotic prescribing;
- The advent of (and attendant publicity around) silver-impregnated dressings;
- The concept of wound-bed preparation;
- The theory of critical colonisation.
There is a definite place for the use of topical antimicrobials in the right context. The importance of the new generation of silver dressings and povidone iodine for treating gross infection cannot be denied. However, use is often based on intuition (and marketing) rather than research-based evidence. Meanwhile the older, arguably as effective and often cheaper formulations, such as silver sulphadiazine and iodine-based products, are neglected.
Topical antibacterials should be considered if critical colonisation is suspected (Kingsley, 2001). When choosing which agent to use, the following criteria should be taken into account:
- Compatibility with wound (fluid handling, adherence, pain on removal, size);
- Antibacterial spectrum and duration of effect;
- Evidence base;
- Cautions and contraindications;
The concept of critical colonisation should be viewed as part of a continuum from contamination to infection. Whether it can be described as a definitive phase distinct from colonisation on one side and infection on the other, is arguable. However, the concept offers a coherent explanation for delayed wound healing in many patients and a potential framework for the appropriate use of topical antibacterials.
It must be recognised that, at present, critical colonisation is theoretical and much additional research is required, especially with regard to accurate diagnosis and appropriate treatment.
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