Five levels of the bacterial chronic wound relationship

Dear Sirs

We write in connection with your recent article entitled ‘Development of an experimental model of infected skin ulcer ^† ’.

All chronic wounds are contaminated by organisms that exist around the wound and on the dressing. Sources of contamination include the patients' own skin, their saliva, secretions from stool and the perianal area, the hands of heath care providers and the environment. When these organisms gain access to the superficial wound surface, a microbial ecosystem is set up resulting in multiplication of organisms or colonisation with these organisms attached to the tissue. The host response can still predominate in the bacterial colonisation, but there are a number of local factors such as the presence of foreign material or local debris that can lower host resistance. When lowered host resistance is combined with the production of damaging metalloproteases, chemokines and cytokines from the invading bacteria, a pro‐inflammatory environment is set up that will delay healing prior to the establishment of a clinically recognised bacterial infection. This stage is referred to as increased bacterial burden or critical colonisation as outlined in (Figure 1).

Figure 1.

The relationship between host and bacteria.

To study the effect of bacteria on chronic wounds, researchers have attempted to develop satisfactory animal models for years. In the article by Tachi et al., the authors created a chamber model for wound infection by three methods of injury: excision with and without the placement of gauze on the wound surface, a burn injury and a crush injury. Each of these wounds were then contaminated with bacteria using the common wound pathogens Staphylococcus Aureus and pseudomonas. By day 3, the host eliminated the superficial bacteria in the case of the burn and crush injury, but the gauze‐covered wounds had persistence of the bacteria and purulent discharge to day 7 with tissue bacterial counts exceeding 10⁶ colony‐forming units per gram of tissue until day 9. The ulceration persisted without wound contracture when the gauze was present. There were no subcutaneous abscesses (deep compartment) or surrounding tissue infections. In the case of the crush and burn injuries, the host was able to eliminate the surface bacteria and exudate but deep abscesses were established in 15–25% of rats representing deep tissue infection.

We need to consider the bacteria–wound relationship in a staged model as outlined in (Table 1). In practice, there is a progression of the bacterial invasion in a wound that may be halted when recognised at each stage.

Table 1.

Stages of chronic wound bacterial burden — infection and treatment

Level of invasion	Treatment to restorebacterial balance
Contamination above woundand in dressing	Infection control andantibacterial content
Superficial wound surface	Topical antimicrobial
Deep wound compartment	Systemic agents
Surrounding skin	Systemic or parental agents
Systemic infection	Parental agents

According to this study, the persistence of bacteria was enhanced in the presence of a foreign object (gauze in this model). These results should alert the clinician to remove particulate matter that will facilitate bacterial proliferation. The presence of deep abscesses related to crush and burn trauma are a reminder that surface injuries may be misleading and not reflect the true impact of the damage to the underlying deeper compartment. The model does not address the surrounding skin or systemic infection that may occur as the result of the presence of bacteria in chronic wounds.

The authors, however, are to be commended for their exploration of the relationship of bacteria and host resistance in an animal model. This study should stimulate further investigation including clinical research to further validate these concepts in persons with chronic wounds.