Bacteria present within a wound can be divided into four distinct categories.

Contamination - defined as the presence of non-replicating microorganisms within the wound.

Colonization - defined as the presence of replicating microorganisms, which do not cause injury to the host. Examples of bacterial wound colonization would be Staphylococcus epidermis and Corynebacterium sp. whose presence have been shown to increase the rate of wound closure(³⁷).

Critical colonization - defined as the presence of replicating microorganisms, which are beginning to cause local tissue damage.

The concept of critical colonization has recently been introduced to describe wounds with an increased bacterial burden, moving between the category of colonization and local infection. During critical colonization, subtle clinical signs of infection may be present before the classical signs associated with infection appear(^{38, 39}).

These clinical signs and symptoms of local infection are listed below.

• Delayed healing
• Change in color of the wound bed
• Friable granulation tissue
• Absent or abnormal granulation tissue
• Abnormal odor
• Increased serrous exudate
• Increased pain at the wound site

Infection - defined as the presence of replicating microorganisms in the wound, which cause injury to the host.

This type of infection is regarded as systemic infection and the traditional signs and symptoms are listed below.

• Advancing redness (erythema)
• Fever
• Warmth
• Edema (swelling)
• Pain
• Foul odor
• Pus

Risk of wound infection = (bacterial dose x virulence) / Host resistance

Although bacterial quantity and virulence are significant in assessing whether a wound is infected, host factors are also of critical importance. Factors such as immunosuppression, diabetes and medication can all influence whether bacteria present in a wound will impair wound healing(⁴). In fact, in some cases of underlying diabetes, a chronic wound may exhibit only subtle signs of infection, yet the bacteria present may be very damaging to the skin and delay the healing process.

Increased bacterial burden within a wound can lead to reduced formation of granulation tissue and re-epithelialization. Experimental studies have demonstrated that regardless of the type of microorganism, the quantity of organisms is important; impairment of wound repair may occur when there are more than 1 x 105 microorganisms per gram in a wound bed(⁴). However, it has also been shown that many chronic wounds with a bacterial load greater than 1 x 105 will heal normally(40). Therefore, it is likely that the type and pathogenicity of organisms increase the risk of infection, rather than the number of microorganisms alone. For example, low numbers (< 1 X 105) of very virulent Streptococcal organisms may prevent the wound from healing.

Recently, the importance of 'biofilms' as an element of wound infection has come to light(²). When bacteria proliferate in wounds they form microcolonies, which attach to the wound bed and secrete a glycocalyx or biofilm that protects the organisms. These bacterial colonies undergo several changes, expressing different genes, which can then alter the organisms' antimicrobial sensitivity(⁴¹). Organisms may exist as clusters of individual bacterial types or as mixed bacterial colonies such as Pseudomonas and Staphylococcus sp. and it is thought that these biofilms may be a form of colonization. However, the periodic release of motile bacteria from these colonies may result in infection and therefore, the presence of biofilms may be a factor in non-healing wounds. Biofilms are protected foci of infection and bacterial resistance within the wound, which protect bacteria from the effects of antimicrobial agents such as antibiotics and antiseptics(⁶).

Antiseptics are important antimicrobial agents. Without the appropriate use of antiseptics wound bed preparation may be inadequate because bacteria may continue to thrive, thereby delaying wound closure⁽⁴²⁾. Antibiotics are also commonly used as antimicrobial agents but due to the growing concerns about bacterial resistance, their use has been restricted in many situations⁽²⁾. 

However, topical antiseptic products can also be used very effectively as antimicrobial agents⁽²⁾. In contrast to antibiotics, which have a more specific mode of action, antiseptics target bacteria at the cell membrane, cytoplasmic organelle and nucleic acid level. This multi-target antimicrobial action reduces the likelihood of bacterial resistance developing.

One of the newer topical antimicrobials is ionized silver, which offers selective advantages for wound care. ACTICOAT^◊ is an example of an ionized silver coated dressing comprised of a high-density absorptive polyethylene mesh. The silver coated polyethylene film maintains an effective concentration of silver over several days. The silver ions are maintained at sustained levels within the dressing, which provide an effective, long lasting antimicrobial barrier to bacterial penetration.

Laboratory studies (data on file, Smith & Nephew, Inc) have shown that ACTICOAT^◊dressings destroy microorganisms more quickly than conventional antimicrobial products, such as silver sulfacliazine (1% cream) or silver nitrate (0.5% solution). In vitro studies, comparing the long-term efficacy of ACTICOAT^◊ to other silver dressings, have shown ACTICOAT^◊ to be more effective in destroying antibiotic resistant bacteria including methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin resistant Enterococcus (In vitro data on file, Smith & Nephew, Inc). Thus, ACTICOAT^◊ delivers fast-acting, long-lasting infection control, which is a crucial element of wound bed preparation and a major step towards achieving wound closure.

Bacterial balance is a critical component of wound bed preparation together with debridement and exudate management. The factors effecting bacterial burden are not just confined to the number of microorganisms, but also induce host resistance, virulence and type of bacteria. ACTICOAT^◊ provided an effective, long-lasting antimicrobial barrier to fit into the clinical platform of wound bed preparation.