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Biofilm

What is a biofilm?

The biofilm barrier

Biofilm is a cluster of attached bacteria embedded in a matrix of proteins and sugars which offers protection from host defences and antimicrobials.1

Biofilm formation
Biofilm form with the initial attachment of single planktonic bacteria, creating a coherent cluster of cells within a protective matrix.2

EPS matrix
This matrix, composed of protein, DNA and sugars, is known as Extracellular Polymeric Substance, or EPS.1-3 Biofilm is difficult to treat as it provides tolerance to antimicrobial treatments4-6 and the host immune response.7-9

Delayed healing
An impaired immune response leads to a vicious cycle of tissue damage and low level inflammation.10,11

To effectively disrupt biofilm and promote healing, an antimicrobial must penetrate the EPS and attack the bacteria within2, with a sustained action that stops biofilm reformation.4,5


 

  Biofilm is difficult to identify as it is invisible to the naked eye, non-uniformly distributed across the wound12 and often present in deeper tissues.13,14


Biofilm is thought to be present in up to 78% of all chronic wounds15 and is thought to be  directly linked to delayed healing16-18


Learn more about biofilm

 

References

1. Burmølle, M. et al., FEMS Immunol. Med. Microbiol. 59,(2010);
2. Stoodley, P et al. Annu. Rev. Microbiol. (2002); 56: 187–209;
3. Flemming HC et al. Nature Rev Microb. (2010); 8,623-633;
4. Phillips P, et al. Int Wound J. 2013:1-15;
5. Wolcott, R. D. et al. J. Wound Care. 2010 .19, 320–8;
6. Stewart PS & Costerton JW. 2001. Lancet (London, England) 358, 135–8;
7. Jesaitis AJ, et al. 2003. J. Immunol. 171, 4329–4339;
8. Bjarnsholt, T. et al. Microbiology 2005. 151, 373–383;
9. Cochrane, DM, et al. 1998. J. Med. Microbiol. 27, 255–61;
10. Bjarnsholt T et al. Wound Repair Regen (2008); 16: 2–10;
11. Costerton, J. W. et al. Science 284, 1318–22 (1999);
12. Thomsen T. R. et al.l Wound Rep Reg 18 38–49,(2010);
13. Kirketerp-Møller, K. et al. J. Clin. Microbiol. 46, 2717–22 (2008);
14. Fazli, M. et al. J. Clin. Microbiol. (2009). 47, 4084–9.
15. Malone, M. et al. J. Wound Care 25,12, 20–25 (2016);
16. Roche ED, et al. Wound Repair Regen 2012; 20: 537–43.
17. Schierle CF, et al. Wound Repair Regen. 2009;17: 354–9.
18. Zhao G. et al. Wound Repair 2012; 20: 342–352

Biofilm in chronic wounds

Despite the best care some wounds struggle to heal

Biofilm is thought to be present in up to 78% of all chronic wounds1 and is thought to be  directly linked to delayed healing2-4

  • Biofilms are difficult to treat as they provide tolerance to antimicrobial treatments5-7 and the host immune response8-10
  • Periodic release of motile bacteria from colonies can result in recurrent infections11

Detection is difficult since classic signs of infection may not be present, but indirect signs and symptoms may include:

  • Antimicrobial therapy failure5-7
  • Delayed wound healing2-4
  • Recurrent infections11
  • Chronic, low-level inflammation4

 

  24%* of patients with chronic wounds lived with their wound
for at least 6 months, 16% have remained unhealed for a year
or more12
 

The patient care cost of a non-healing** wound was a mean
135% more than that of a healed wound13

  Biofilm is present in 78% of chronic wounds1 and believed
to play a significant role in non-healing2-4
  Wounds that contain biofilm may not be identified, resulting
in ineffective treatment and delayed healing2,3, 14
  Most topical antimicrobials fail to disrupt biofilm5,15
  *European data
**non-healing wound defined as non-progression after 12 weeks

 

  Why silver is not effective against biofilm
Charged ions, such as silver or chlorides are more easily neutralised by the EPS matrix.16 Moreover the concentration of silver required to eradicate biofilm is estimated to be 10 to 100 times higher than that used to eradicate planktonic bacteria.15 Such concentrations are currently unavailable in any silver dressing.

 

 

References

1. Malone, M. et al. J. Wound Care 25,12, 20–25 (2016);
2. Roche ED, et al. Wound Repair Regen 2012; 20: 537–43.
3. Schierle CF, et al. Wound Repair Regen. 2009;17: 354–9.
4. Bjarnsholt T, et al. Wound Rep Reg. 2008;16:2-10 ;
5. Phillips P, et al. Int Wound J. 2013:1-15.
6. Wolcott, R. D. et al. J. Wound Care. 2010 .19, 320–8.
7. Stewart PS & Costerton JW. 2001. Lancet (London, England) 358, 135–8.
8. Jesaitis AJ, et al.. 2003. J. Immunol. 171, 4329–4339.
9. Bjarnsholt, T. et al. Microbiology 2005. 151, 373–383;
10. Cochrane, DM, et al. 1998. J. Med. Microbiol. 27, 255–61.
11. Costerton JW. Science. 1999;284:1318-1322.
12. Lindholm C, Searle R. Int Wound J. (2016) Jul;13 Suppl 2:5-15;
13. Guest JF et al; Int. Wound J. 14, 2 322-330. (2016);
14. Zhao G. et al. Wound Repair (2012); 20: 342–352;
15. Bjarnsholt et al. APMIS (2007).115: 921–8;
16. Stewart, P. S. et al. J. Appl. Microbiol. (2001). 91, 525–32

The biolfilm barrier

Biofilms are linked to delayed wound healing1-3

Around 78% of chronic wounds contain a biofilm4. Biofilms are difficult to treat as they provide tolerance to antimicrobial treatments5-7 and the host immune response8-10

Superior efficacy against biofilm proven across different lab models5,11-13

IODOSORB™ has a long history of effectiveness against biofilm with superior results compared to other topical antimicrobials such as PHMB, silver and povidone iodine.5

In line with the biofilm experts’ recommendations14 on selecting an effective anti-biofilm dressing, IODOSORB has been tested and shown to be more effective than AquacelTM Ag+ across five challenging and clinically relevant biofilm models.11-13

Evidence: IODOSORB against biofilm

 

 
‡ Staphylococcus aureus mature biofilms; $ MRSA biofilms; § Mixed bacterial cultures. Pseudomonas aeruginosa PA01, Staphylococcus aureus Mu50, and Enterococcus faecalis V583; ¥ Treatment every 24 h for 48 h total.
* Model 1: Colony; Model 2: DripFlow; Model 3: Lubbock; Model 4: Mouse; Model 5: Porcine explant
** AquacelTM Ag+ is a product formerly known as AquacelTM Ag+ Extra.

References

1.Roche ED, et al. Wound Repair Regen 2012; 20: 537–43;
2. Schierle CF, et al. Wound Repair Regen. 2009;17: 354–9;
3. Bjarnsholt T, et al. Wound Rep Reg. 2008;16:2-10;
4. Malone, M. et al. J. Wound Care 25,12, 20–25 (2016);
5. Phillips P, et al. Int Wound J. 2013:1-15;
6. Wolcott, R. D. et al. J. Wound Care. 2010 .19, 320–8;
7. Stewart PS & Costerton JW. 2001. Lancet (London, England) 358, 135–8;
8. Jesaitis AJ, et al. 2003. J. Immunol. 171, 4329–4339;
9. Bjarnsholt, T. et al. Microbiology 2005. 151, 373–383;
10. Cochrane, DM, et al. 1998. J. Med. Microbiol. 27, 255–61;
11.Fitzgerald, D. J. et al. Wound Repair Regen. 25: 13-24 (2016) ;
12. Schultz, G. & Yang. Poster presented at WUWHS Florence (2016);
13. Oates J.L. et al. Poster presented at SAWC, Atlanta.(2016);
14.Schultz et al. Wound Repair Regen (2017); approved article;
15. Malone, M. et al. J Antimicrob Chemother 2017; 00: 1–9;

New consensus recommendations on treatment of biofilm

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