Advancements in molecular microbiology, microscopy technology, and techniques for study of bacteria have increased the ability to identify the existence of biofilms, but there still remains the unknown, such as differentiating between planktonic bacteria and biofilm.1 Chronic non-healing wounds harbor bacteria across the wound etiology classification.2–4 Malone et al. determined that the prevalence of biofilms in chronic wounds was 78.2% (confidence interval, 61.6–89, P < 0.002).2 The development of biofilms moves through a common pattern: attachment, microcolony formation, maturation, and dispersion. The initial attachment is reversible, but the attachment becomes stronger as cells multiply and change their gene expressions. This cell communication process is referred to as quorum sensing, allowing cells to survive.
Clinicians evaluating wounds should be thorough and detailed, including the clinical history, any signs and symptoms, and microscopic culture and tissue examination to help identify causative microorganisms.5 Conventional culturing methods lack sensitivity, and studies have proved the consistent failure of identifying types of organisms present within biofilm. DNA-based technology and molecular methods are better suited that conventional culturing methods for identifying biofilm colonies.6–10 Using a multidisciplinary approach, with good wound cleansing and established principles of wound care, will provide better healing outcomes. Research shows that microorganisms rarely invade healthy tissue unless the wound bed is compromised by drying out.11
Many strategies and therapies are most effective in suppressing biofilm activity in a wound. The goal is to target only the biofilm and not the defense and healing mechanisms of the body. Aggressive debridement, topical antiseptics, systemic antibiotics, DNA identification of microorganisms, and management of host factors (offloading, compression, diabetes, nutrition) are all components of a biofilm-based wound care approach. Debridement methods used to aid in biofilm eradication are utilized to prepare the wound bed to move toward healing. Keeping the wound bed clear of devitalized tissue and biofilm is imperative in enhancing wound healing progress. If biofilm colonies contaminate the wound bed, the transition to wound closure becomes complex.12,13
Combining debridement methods has been found to be an advantage in managing complex wounds and different pathological tissues since 2006.4 Developed biofilms harbor physical and metabolic defenses. These defenses enable the biofilm to resist antimicrobials that usually alienate planktonic cells and include resistance to host defenses, biocides, antibiotics, and ultraviolet light. Sequential sharp debridement of wounds disrupts biofilm growth and inhibitory factors and can promote faster healing. It is difficult to predict the outcome because we still do not know the depth needed to remove the entire biofilm colony.14
Finding the pieces of the puzzle to biofilms is an ongoing process. However, we know more now than a decade ago. Biofilms are known for their considerable defense protection from host immunities and utmost tolerance to antimicrobial agents. There are no normal standard signs and symptoms or precise methods to identify biofilms. Key essentials to preventing, disrupting, and suppressing biofilm regrowth are aggressive debridement, topical antibiofilm strategies, and host factor management strategies.
References
1. Wolcott RD, Hanson JD, Rees EJ, et al. Analysis of the chronic wound microbiota of 2,963 patients by 16S rDNA pyrosequencing. Wound Repair Regen. 2016;24(1):163–74.
2. Malone M, Bjarnsholt T, McBain AJ, et al. The prevalence of biofilms in chronic wounds: a systematic review and metaanalysis of published data. J Wound Care. 2017;26(1):20–5.
3. Seth AK, Geringer MR, Hong SJ, Leung KP, Mustoe TA, Galiano RD. In vivo modeling of biofilm-infected wounds: a review. J Surg Res. 2012;178(1):330–8.
4. Kalan L, Loesche M, Hodkinson BP, et al. Redefining the chronic-wound microbiome: fungal communities are prevalent, dynamic, and associated with delayed healing. MBio. 2016;7(5):e01058–16.
5. Høiby N, Bjarnshold T, Moser C, et al. ESCMID guideline for the diagnosis and treatment of biofilm infections 2014. Clin Microbiol Infect. 2015;21(1):1-25.
6. Hoffman LR, Déziel E, D’Argenio DA, et al. Selection for Staphylococcus aureus small colony variants due to growth in the presence of Pseudomonas aeruginosa. Proc Natl Acad Sci U S A. 2006;103(52):19890–5.
7. Fux CA, Costerton JW, Stewart PS, Stoodley P. Survival strategies of infectious biofilms. Trends Microbiol. 2005;13(1):34–40.
8. Rhoads DD, Wolcott RD, Sun Y, Dowd SE. Comparison of culture and molecular identification of bacteria in chronic wounds. Int J Mol Sci. 2012;13(3):2535–50.
9. Han A, Zenilman JM, Melendez JH, et al. The importance of a multifaceted approach to characterizing the microbial flora of chronic wounds. Wound Repair Regen. 2011;19(5):532–41.
10. Human Microbiome Project Consortium. Structure, function and diversity of the healthy human microbiome. Nature. 2012; 486(7402):207–1
11. Brölmann FE, Eskes AM, Goslings JC, et al; REMBRANDT study group. Randomized clinical trial of donor-site wound dressings after split-skin grafting. Br J Surg. 2013;100(5):619–27.
12. Sherman RA. A new dressing design for use with maggot therapy. Plast Reconstr Surg. 1997;100(2):451–6.
13. Liu WL, Jiang YL, Wang YQ, Li YX, Liu YX. Combined debridement in chronic wounds: a literature review. Chin Nurs Res. 2017;4(1):5–8. https://www.sciencedirect.com/science/article/pii/S2095771817300063. Accessed November 30, 2018.
14. Grey JE, Enoch S, Harding KG. Wound assessment. BMJ. 2006;332(7536):285–8.
15. WoundSource. Debridement Devices. https://www.woundsource.com/product-category/debridement/debridement-de…. Accessed November 30, 2018.
16. Crone S, Garde C, Bjarnsholt T, Alhede M. A novel in vitro wound biofilm model used to evaluate low-frequency ultrasonic-assisted wound debridement. J Wound Care. 2015;24(64):64, 66–69, 72.
17. Runyan CM, Carmen JC, Beckstead BL, Nelson JL, Robison RA, Pitt WG. Low-frequency ultrasound increases outer membrane permeability of Pseudomonas aeruginosa. J Gen Appl Microbiol. 2006;52(5):295–301.
Suggested Reading
Leaper D. Sharp technique for wound debridement. World Wide Wounds. 2002. http://www.worldwidewounds.com/2002/december/Leaper/Sharp-Debridement.h…. Accessed November 30, 2018.
Schultz G., Bjarnsholt T, James GA, et al; Global Wound Biofilm Expert Panel. Consensus guidelines for the diagnosis and treatment of biofilms in chronic non-healing wounds. Wound Repair Regener. 2017;25(5):744–57.
The views and opinions expressed in this blog are solely those of the author, and do not represent the views of WoundSource, HMP Global, its affiliates, or subsidiary companies.