Biofilms and Their Potential Role in Wound Healing

Steven L. Percival, PhD; Philip G. Bowler, MPhil


Wounds. 2004;16(7) 

In This Article

The Potential Significance of Biofilms in Wounds

Based on the authors' hypothesis, it is likely that a wound environment is able to support the development of bacterial biofilms, although at the present time, there is very little clinical evidence to support this. Wounds have been shown to possess many of the characteristics that suggest the existence of biofilms. In fact, an investigation by Serralta and colleagues[28] provided evidence that biofilms may form in wounds, and it is probable that biofilms could have a significant effect on inflammation, infection, and healing.

Wounds are susceptible to microbial contamination from both exogenous and endogenous sources including the nose, skin, mouth, and the gut, and it is likely that such organisms are involved in the evolution of microbial communities in wounds. The development of microbial communities and their variation over time previously has been demonstrated in an acute full-thickness porcine wound model.[29] In this study, the authors found that the microbial ecology changed from a predominantly Gram-positive bacterial population during the early days after wounding to a predominantly Gram-negative population by Day 6 with anaerobes becoming evident between Days 6 and 8. It is likely that a similar microbial progression and community development occurs in human cutaneous wounds, and biofilms are likely to play an important role in this. Microbial progression within a wound is thought to consist of a number of stages (Figure 1) and if this process is not controlled, the probability of infection increases.[30] It is proposed by the authors that this model is in fact a model of a progressing biofilm.

The relationship between microbial progression and biofilm formation in wounds.

Early contaminants on a wound surface are most likely to be skin flora (e.g., Staphylococcus epidermidis) that adhere to the wound, proliferate, synthesize EPSs, and form a "healthy" biofilm. It is at this point that the host initiates a normal immune response and maintains a "homeostasis" at the site of contamination. It is conceivable, based on documented evidence,[29] that Gram-negative bacilli may then colonize the biofilm -- these organisms utilize available oxygen and provide growth factors that enable anaerobes to establish within the biofilm thus forming a complex but stable polymicrobial "climax" community[31] often termed microbial homeostasis.[32] A climax community is a collection of microorganisms within a "quasi" steady state, implying stable associations and integrations of function between microbial populations. In this situation, the progression to wound healing may become compromised by the biofilm community, i.e., the microbial to host balance is weighted in favor of the microorganisms, and the term critically colonized has been used to describe this state. At this stage, the microorganisms, while interfering with the wound healing process, may not necessarily induce any clinical signs of infection, although there may be subtle signs that indicate bacterial imbalance (e.g., change in wound color or odor together with the presence of devitalized tissue and ischemia). It may be appropriate to consider the use of a broad-spectrum topical antimicrobial agent at this stage to control the microbial challenge. The combined effects of the antimicrobial agent and the host immune response are likely to improve conditions for healing where bacterial imbalance is evident. Without control of microbial progression, a transition from an early "healthy" biofilm to a "pathogenic" wound biofilm may develop and ultimately lead to clinical infection. While the net pathogenic effect of the biofilm community exceeds the host's immune response, wound healing is likely to be compromised.

Scientific and clinical research in the area of wound biofilms and the associated bacterial interactions is now warranted to better understand the impact on wound healing.


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