Wound Biofilm Development and Virulence

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wound biofilm virulence

By the WoundSource Editors

Wound biofilms not only impede healing but also increase the risk of infection. It is essential that wound biofilms be addressed and treated in a prompt, consistent manner. Biofilms have been an ongoing challenge because of the majority of resistant bacteria. Research in antibiofilm technology continues to grow, and it is essential to keep up on the most recent evidenced-based practice literature for improving patients’ outcomes.

Biofilm Generation

Wound chronicity is costing the health care system millions of dollars every year. Microbial communities known as biofilms are generally composed of bacteria, fungi, viruses, proteins, extracellular DNA, biogenic factors, and other types of microorganisms. The organisms are microscopic, but as the biofilm matures it attaches the microbial community to a wet or moist surface as a viscous substance. This viscous substance is referred to as exopolymeric material (EPM). The biofilm protects the microorganisms from the body’s natural immune response and then prevents antibodies from reaching them. The body attempts to fight biofilm through the inflammatory response but is unsuccessful. Healing tissue is damaged, and in return there is delayed wound healing.1,2

Biofilms in Drug Resistance and Antimicrobial Tolerance

Biofilms’ polymicrobial nature and dense EPM matrix paralyze large antibodies and neutralize microbicides. Bacterial cells that are encased in EPM are much different from free-living, planktonic bacteria. These bacterial cells have reduced motility and activity. This action is referred to as sessile (non-motile) and increases antimicrobial tolerance. A biofilm can promote anaerobic bacterial growth and synergism among different bacteria, thus generating methicillin-resistant Staphylococcus aureus (MRSA) resistant proteins and producing negative charges of polysaccharides and DNA that bind cationic molecules such as cationic silver, antibiotics, and polyhexamethylene biguanide.3 Antimicrobial tolerance is increased by many antibiotic classes that target only peptidoglycan produced in the cell wall (β-lactams), protein (aminoglycoside) synthesis, or DNA replication (quinolones).4 The transfer of antimicrobial-resistant genes carries moving genetic elements. This transfer can occur between or among bacteria and/or cells from the same or different species. The potential for virulent infection therefore increases.5

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Wound exudate amount and consistency can be useful indicators of a biofilm. There has been a correlation among moisture imbalance, translucent or opaque film above the wound bed, recalcitrance, and local wound infection.6

Antibiotics can disturb and eradicate bacteria, but once the antibiotic is suspended, the remaining cells can stimulate infection once again, causing antibiotic resistance. Antibiotic resistance genes carry mobile genetic elements, such as plasmids. Resistance causes irreversible genotype changes in the bacteria, apart from resistance genes harbored on mobile genetic elements.5

On the other end of the spectrum of antibiotic resistance is antimicrobial tolerance. Bacterial cells that survive antibiotics are known as persister cells. Persister cells block synthesis of peptidoglycan or DNA. The cells then remain sensitive to the antibiotic, and regrowth of the biofilm will occur with a susceptibility profile similar to that of the original biofilm. Persister cells win and are maintained.6

Debridement in Biofilm Reduction

The most important step in chronic wound care is to remove necrotic tissue and the microbial bioburden by surgical or sharp debridement.7 Given the strong attachment of EPM, removal of all the underlying biofilm is difficult. The remaining attached cells allow the biofilm an opportunity to regrow and start the biofilm growth cycle again, thereby increasing the risk of wound infection.5


More antibiofilm research is needed to better determine antimicrobial susceptibility patterns, test old and new antibiofilm agents, and improve current available treatments. We know that biofilms delay healing, but the mechanism remains to be identified. Sharp debridement of wound biofilm is considered the “gold standard,” but it is not effective in removing and preventing regrowth of biofilm. Quorum sensing inhibitors and molecular diagnostic techniques are proving to help increase the ability to treat biofilms, but they do not differentiate the biofilm type. Innovations in biofilm eradication-type technology are needed to improve effective and cost-effective antibiofilm treatments.

2. Donlan RM. Biofilms: microbial life on surfaces. Emerg Infect Dis. 2002;8(9):881–90.
3. Carver C. How to identify biofilm in a wound. WoundSource. http://www.woundsource.com/blog/how-identify-biofilm-in-wound. Published August 18, 2015. Accessed December 20, 2017.
4. Peterson LR. Squeezing the antibiotic balloon: the impact of antimicrobial classes on emerging resistance. Clin Microbiol Infect. 2005;11 Suppl 5:4–16.
5. James GA, Swogger E, Wolcott R, et al. Biofilms in chronic wound. Wound Repair Regen. 200816(1):37–44.
6. Fauvart M, De Groote VN, Michiels J. Role of persister cells in chronic infections: clinical relevance and perspectives on anti-persister therapies. J Med Microbiol. 2011;60(Pt 6):699–709.
7. Wolcott RD, Cox SB, Dowd SE. Healing and healing rates of chronic wounds in the age of molecular pathogen diagnostics. J Wound Care. 2010;19(7);272–8, 280–1.

Suggested Reading
Hurlow J, Bowler PG. Potential implications of biofilm in chronic wounds: a case series. J Wound Care. 2012;21(3):109–10, 112, 114 passim.


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