Clinical Experience with Wound Biofilm and Management: A Case Series

Start Page: 
End Page: 
Jennifer Hurlow, GNP, CWOCN; and Philip G. Bowler, MPhil, BSc

Despite attaching firmly to wound tissue, biofilm can be carefully peeled away without causing damage to underlying tissue. Although biofilm will reform, a protocol of care that includes its repeated removal is likely to support wound progression over time.

     Biofilm and alginate. In the cases described, the use of a silver-containing alginate dressing coincided with the rapid development of viscous, green-colored exudate; P. aeruginosa commonly was implicated. Although silver is used for antimicrobial protection, in this study it was observed that use of the silver alginate dressing was associated with the formation of thick, green exudate. Clinicians may want to consider 1) why silver (and in some cases, systemic antibiotics) appears to be ineffective as an antimicrobial agent in certain situations; 2) whether exudate may be too viscous to trigger release of the silver ions from the alginate dressing; and 3) whether exudate absorption is compromised by the quantity of the fluid (in each case the dressing looked like a wet blanket over the wound, but even a wet blanket can bleed its dye) or the presence of biofilm (ie, viscous alginate exopolysaccharide produced by P. aeruginosa).

     Possibly, dressing components (eg, alginate and calcium) could have contributed to formation of the viscous exudate. In the authors’ scientific experience, alginate has been found to be an important component of biofilm EPS (notably in the presence of P. aeruginosa), rendering it hydrophobic, robust, and difficult to disperse. Calcium likely strengthens the bonds between alginate polysaccharide chains in the EPS8 and enhances pyocyanin production in P. aeruginosa.11 A base wound pH likely enhances fluorescence of the P. aeruginosa-produced fluorescein dye, inducing a bright green-blue-yellow coloration in the wound. Interestingly, with regard to silver, one in vitro study12 demonstrated the ability of silver ions to disrupt the biofilm (EPS) structure formed by Staphylococcus epidermidis at low concentration (50 parts per billion). However, regarding the current case studies, clinical wound conditions such as viscosity of the EPS produced by P. aeruginosa may have compromised the ability of the silver dressing to interact with and combat biofilm bacteria.

     Biofilm and MMPs. In the cases described, the slimy, cloudy film often seemed to be associated with wounds that did not exhibit clinical signs of infection but appeared to be fighting something that manifested as persistent inflammation. This observation may relate to the state of “silent infection” or “critical colonization,” a concept described as a state in which bacteria are established within a biofilm community and compromise wound healing without inducing clear signs of clinical infection.13

     Inflammation, a natural and essential part of any healing process, manages potential infection and clears the wound of devitalized tissue. However, clinical studies have shown that chronic wounds often exist in a prolonged inflammatory state involving elevated pro-inflammatory cytokine, proteinase, and oxidative activity — all of which may play a role in delayed wound healing.5 It is widely acknowledged that pathogenic bacteria stimulate inflammation through activation and proliferation of macrophages and pro-inflammatory cytokines.14,15 Recently, biofilm has been considered to be a primary cause of the prolonged inflammation that exists in chronic wounds16 and the cause of silent chronic inflammation in hemodialysis patients due to repeated stimulation of macrophages.17 The persistence of biofilm in chronic wounds may be associated with elevated production of proteinases (MMPs) and subsequent delayed healing.


1. Fux CA, Costerton JW, Stewart PS, Stoodley P. Survival strategies of infectious biofilms. TRENDS in Microbiol. 2005;13(1):34–40.
2. Costerton JW, Geesey GG, Cheng KJ. How bacteria stick. Scientific American. 1978;238(1):86–95.
3. Donlan RM, Costerton JW. Biofilms: survival mechanisms of clinically relevant microorganisms. Clin Microbiol Rev. 2002;15(2):167–193.
4. Kievit TR, Iglewski BH. Bacterial quorum sensing in pathogenic relationships. Infect Immun. 2000;68(9):4839–4849.
5. Enoch S, Harding K. Wound bed preparation: the science behind the removal of barriers to healing. WOUNDS. 2003;15(7):213–229.
6. Costerton JW. A short history of the development of the biofilm concept. In: Ghannoum M, O’Toole GA (eds). Microbial Biofilms. Washington, DC: ASM Press;2004:4–19.
7. Purevdorj-Gage LB, Stoodley P. Biofilm structure, behavior and hydrodynamics. In: Ghannoum M, O’Toole GA (eds). Microbial Biofilms. Washington, DC: ASM Press;2004:160–173.
8. Starkey M, Gray KA, Chang SI, Parsek MR. A sticky business: the extracellular polymeric substance matrix of bacterial biofilms. In: Ghannoum M, O’Toole GA (eds). Microbial Biofilms. Washington, DC: ASM Press;2004:174–191.
9. Sheffield PJ. Tissue oxygen measurements. In: Davis JC, Hunt TK (eds). Problem Wounds. The Role of Oxygen. New York, NY: Elsevier; 1988:17–51.
10. Rooke T. TcPO2 in non-invasive vascular medicine. Blood Gas News. 1998;7(2):21–23.
11. Sarkisova S, Patrauchan MA, Berglund D, Nivens DE, Franklin MJ. Calcium-induced virulence factors associated with the extracellular matrix of mucoid Pseudomonas aeruginosa biofilms. J Bacteriol. 2005;187(13):4327–4337.
12. Chaw KC, Manimaran M, Francis EHT. Role of silver ions in destabilization of intermolecular adhesion forces measured by atomic force microscopy in Staphylococcus epidemidis biofilms. Antimicrob Agents Chemother. 2005;49(12):4853–4859.
13. Percival SL, Bowler PG. Biofilms and their potential role in wound healing. WOUNDS. 2004;16(7):234–240.
14. Roberts FA, Richardson GJ, Michalek SM. Effects of Porphyromonas gingivalis and Escherichia coli lipopolysaccharides on mononuclear phagocytes. Infect Immun. 1997;65(8):3248–3254.
15. Rabehi L, Irinpoulou T, Cholley B, Haeffner-Cavaillon N, Carreno M-P. Gram-positive and Gram-negative bacteria do not trigger monocytic cytokine production through similar intracellular pathways. Infect Immun. 2001;69(7):4590–4599.
16. Wolcott RD, Rhoads DD, Dowd SE. Biofilms and chronic wound inflammation. J Wound Care. 2008;17:333–341.
17. Cappelli G, Tetta C, Canaud B. Is biofilm a cause of silent chronic inflammation in haemodialysis patients? A fascinating work hypothesis. Nephrol Dialysis Transplant. 2005;20:266–270.
18. Tsuneda S, Aikawa H, Hayashi H, Yuasa A, Hirata A. Extracellular polymeric substances responsible for bacterial adhesion onto solid surface. FEMS Microbiol Letters. 2003;223:287–292.
19. Lindfors J. A comparison of an antimicrobial wound cleanser to normal saline in reduction of bioburden and its effect on wound healing. Ostomy Wound Manage. 2004;50(8):28–41.
20. Shakeri S, Kermanshahi RK, Moghaddam MM. Assessment of biofilm cell removal and killing and biocide efficacy using the microtiter plate test. Biofouling. 2007;23(2):79–86.
21. Hunt TK, Hennestall RB, Pines E, et al. Impairment of microbicidal function in wounds: correction with oxygen. In: Hunt TK (ed). Soft and Hard Tissue Repair, Biological and Clinical Aspects. New York, NY: Praeger;1984:455–468.

Post new comment

  • Web page addresses and e-mail addresses turn into links automatically.
  • Lines and paragraphs break automatically.
  • Use to create page breaks.

More information about formatting options

Enter the characters shown in the image.