Biofilm-Based Wound Management: Implications for Clinical Practice

Over the last 10 ten years, knowledge expansion regarding the presence and action of biofilm in hard-to-heal wounds has contributed to a new paradigm of wound bed preparation. Understanding the role biofilm plays in chronic infection and delayed wound healing allows clinicians to proactively choose interventions that address biofilm and promote expedited wound healing.

Biofilm is a complex, often polymicrobial, structure that can form on an array of surfaces including teeth, implanted medical devices, showers and bathtubs, and notably chronic and hard-to-heal wounds.¹ In hard-to-heal wounds, planktonic bacteria, which are bacteria in their free-floating form, seed onto the surface of the wound and attach themselves to the wound base. They begin to form polymicrobial communities that can contain other species of bacteria and often fungal and viral components as well. These communities cover themselves with a protective coating known as an extrapolymeric substance (EPS).

The EPS is typically a polysaccharide. This sugary shell protects microbes within the biofilm from antibiotics and antimicrobials.^2,3 This is a reason why not all topical or systemic antibiotics and antiseptics will work on hard-to-heal wounds, and why some may be chosen over others when designing biofilm-based wound management strategies. Within the EPS, polymicrobial communities of microbes communicate via a process known as quorum sensing. Quorum sensing allows communities to distribute resources, alert other microbes, induce virulence, and even share antibiotic resistance genes, all within the protection of the EPS.⁴

While disrupting biofilm is an important component in any wound treatment strategy, biofilm is known to begin to form and reform in as little as 24 hours.^1,5 The speed at which biofilm forms and reforms means that these wound treatment strategies are most effective when implemented as part of a protocol in which evidence-based anti-biofilm interventions are used repetitively, at each patient encounter.

Biofilm is known to be present in most, if not all, chronic and hard-to-heal wounds^5-7 but is generally not visible to the naked eye. It is not uncommon for failed extracellular matrix, slough, exudate, and general wound debris to be mistaken for biofilm even by experts in wound healing.³ Although the human eye typically cannot see biofilm, biofilm does tend to grow into these types of necrotic tissue. This is another reason why debridement is an important component of wound treatment. Removing necrotic tissue lessens the overall bioburden and associated inflammation.⁸ Although biofilms are known to be located on the surface of hard-to-heal wounds, they also have the ability to integrate deeper into the tissue itself.^3,9 The speciation of planktonic microbes often differs compared to species within biofilms; therefore, culturing a wound via a swab may produce a false-negative result, or the swab may only culture the planktonic bacteria, which would not provide clinically meaningful information.³

IMPLICATIONS FOR WOUND HEALING

Managing biofilm has important implications on healing outcomes in chronic and hard-to-heal wounds as its presence is known to impact wound healing.^3,5 After controlling for host factors associated with persistent delayed healing (ie, compression, offloading, debridement, addressing any acute soft tissue infection), biofilm is considered the most important single cause of delayed wound healing.³ Wound care protocols that incorporate evidence-based wound bed preparation, control for host factors, and incorporate anti-biofilm treatment strategies are known collectively as wound hygiene.⁵

Emerging evidence indicates a number of interventions are associated with disruption of biofilm in wounds. These technologies include non-contact low-frequency ultrasound, sharp debridement, and some dressings.^3,5,6,10-12 Sharp debridement is considered one of the most important treatment strategies to combat biofilm and expedite wound healing.^3,12,13 Once the EPS of biofilm is disrupted through a thorough sharp debridement, microbes are exposed and a window of time is opened during which antimicrobials can be more effective.^12,13 Additionally, continuing anti-biofilm treatment after this initial disruption can help slow the reformation of biofilm, and limit its negative effects on wound healing.

SUMMARY

Biofilm is known to be present in most, if not all, chronic and hard-to-heal wounds. It usually cannot be seen by the naked eye, so its presence is presumed. Disrupting biofilm is an important component in any wound treatment strategy. Because biofilm is associated with delayed wound healing, incorporating evidence-based anti-biofilm strategies into a proactive wound healing protocol of care that is delivered regularly and repeatedly can expedite wound healing and improve patient outcomes.^5,14

REFERENCES

1. Mancl KA, Kirsner RS, Ajdic D. Wound biofilms: lessons learned from oral biofilms. Wound Repair Regen. 2013;21(3):352-362. doi:10.1111/wrr.12034

2. Wolcott RD, Rumbaugh KP, James G, et al. Biofilm maturity studies indicate sharp debridement opens a time- dependent therapeutic window. J Wound Care. 2010;19:320-328. doi:10.12968/jowc.2010.19.8.77709

3. Schultz G, Bjarnsholt T, James GA et al. Consensus guidelines for the identification and treatment of biofilms in chronic nonhealing wounds. Wound Repair Regen. 2017;25(5):744-757. doi:10.1111/wrr.12590

4. Zhao X, Yu Z, Ding T. Quorum-sensing regulation of antimicrobial resistance in bacteria. Microorganisms. 2020;8(3):425. doi:10.3390/microorganisms8030425

5. Murphy C, Atkin L, Vega de Ceniga M, et al. Embedding wound hygiene into a proactive wound healing strategy. J Wound Care. 2022;31:S1-S24. doi:10.12968/jowc.2022.31.Sup4a.S1

6. Malone M, Bjarnsholt T, McBain AJ, et al. The prevalence of biofilms in chronic wounds: a systematic review and meta-analysis of published data. J Wound Care. 2017;26(1):20-25. doi:10.12968/jowc.2017.26.1.20

7. Johani K, Malone M, Jensen S, et al. Microscopy visualisation confirms multi-species biofilms are ubiquitous in diabetic foot ulcers. Int Wound J. 2017;14(6):1160-1169. doi:10.1111/iwj.12777

8. Bryant R, Nix D. Acute & Chronic Wounds: Current Management Concepts. 4th ed. Elsevier; 2012.

9. Schaber JA, Triffo WJ, Suh SJ, et al. Pseudomonas aeruginosa forms biofilms in acute infection independent of cell-to-cell signaling. Infect Immun. 2007;75(8):3715-3721.

10. Seth AK, Nguyen KT, Geringer MR, et al. Noncontact, low-frequency ultrasound as an effective therapy against Pseudomonas aeruginosa-infected biofilm wounds. Wound Repair Regen 2013;21(2):266-274. doi:10.1111/wrr.12000

11. Phillips PL, Yang Q, Davis S, et al. Antimicrobial dressing efficacy against mature Pseudomonas aeruginosa biofilm on porcine skin explants. Int Wound J. 2015;12(4):469-483. doi:10.1111/iwj.12142

12. Malone M, Swanson T. Biofilm-based wound care: the importance of debridement in biofilm treatment strategies. Br J Community Nurs. 2017;22(suppl 6):S20-S25. doi:10.12968/bjcn.2017.22.Sup6.S20

13. Wolcott RD, Rumbaugh KP, James G, et al. Biofilm maturity studies indicate sharp debridement opens a time- dependent therapeutic window. J Wound Care. 2010;19(8):320-328. doi:10.12968/jowc.2010.19.8.77709

14. Rajpaul K. Biofilm in wound care. Br J Community Nurs. 2015;(suppl Wound Care):S6-S11. doi:10.12968/bjcn.2015.20.Sup3.S6

Dr Swoboda is a wound care coordinator/nurse practitioner, Froedtert and the Medical College Community Hospital Division, Menomonee Falls, WI; and professor
of translational science, Clinical Translational Science Institute of Southeastern Wisconsin, Milwaukee, WI.
The opinions and statements expressed herein are specific to the respective author and not necessarily those of Wound Management & Prevention or HMP Global.
This article was not subject to the Wound Management & Prevention peer-review process.