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How to Identify & Fight Biofilm to Advance wound Healing- My Clinical Experiences

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Dr Rajendra Prasad    05 May 2020

Dr. Rajendra Prasad, Associate Professor, Institute of Vascular Sciences Ramaiah Hospital, Bangalore

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Why Biofilms Can Be a Challenge

Antibiotics are designed to attack bacteria, and may only partially eliminate the bacteria contained within a biofilm. The dense exopolymeric material (EPM) matrix actually paralyzes large antibodies and neutralizes microbicides. A biofilm is capable of promoting anaerobic bacteria growth, synergism between different bacteria, generating MRSA-resistant proteins, producing negative charges of polysaccharides and DNA bind cationic molecules like Ag+, antibiotics. This is why clinical studies show 60% of chronic wounds contain a biofilm, and can again reform in three days after sharp debridement. The wound appears to be healing, then becomes stagnant again.

Ways to Manage a Biofilm

Sequential sharp debridement of wounds will disrupt the biofilm growth and promote faster healing. Treating wounds with an antimicrobial or bacteriostatic dressing in an alginate or polymeric foam form will help prevent reformation of biofilms. Dressings impregnated with Ionic silver, EDTA (Ethylene Di Amine Tetra Acetic Acid) & BEC (Benzethonium Chloride) are at the top of the list. Stay away from gauze impregnated dressings and skin graft application, as this is the perfect food source environment for biofilms. Systemic antibiotics are used to destroy the biofilm microbes and prevent reseeding of bacteria on the wound surface. Maggot debridement therapy has been reintroduced for the treatment of chronic wounds. Studies have shown that the excretions/secretions of maggots contain many bioactive compounds.

Infection and biofilm

Microorganisms are commonly divided into two distinct phenotypes: single cells (i.e. planktonic) or sessile aggregates (i.e. the biofilm mode of growth). Research into bacterial pathogenesis has previously focused primarily on acute — or planktonic — infections, which result from invasion by free-floating, solitary microorganisms, as has the development of prevention and treatment control measures. However, a new category of chronic infection caused by microorganisms growing as biofilm has become an increasingly important focus in wound care1. Hard-to-heal wounds are often chronically infected, producing a distinct pattern of growth associated with biofilm2, which can be 500 to 5,000 times more tolerant to antimicrobials3. Chronic biofilm based infections have a slower progression than acute infections are characterised by an adaptive inflammatory response and are typically extremely resistant to antibiotics and many other conventional antimicrobial strategies and have an innate ability to evade the host’s defences1. Regardless of phenotype, microbial cells have multiple mechanisms to attach to specific host epitopes4-6. Within minutes, over 800 biofilm genes may be expressed5, providing genetic capability for microbial cells to communicate and develop protection (self-secreted matrix polymers) 10-11, and secrete molecules preventing host immunity counter measures 12-14

An innovative, advanced strategy that targets local barriers to healing

Management of microbial load is vital in the prevention of infection. Moreover, although moist wound healing strategies are no more likely to promote infection than earlier dry wound healing strategies15, the combination of pooled exudate associated with fully saturated dressings9 and the corrosive nature of chronic wound exudate may be linked to biofilm development and resulting infection. Prior to the discovery that keeping wounds moist would improve healing16, the traditional approach was to soak up fluid and leave the wound to dry. As understanding increased regarding the optimum wound healing environment, the first film dressings with polyurethane technology were developed17, followed by alternatives such as alginates and hydrocolloids18, and later, Hydrofiber™ Technology. Since the first Hydrofiber™ Technology was developed 20 years ago, various products have been developed based on its unique physicochemical properties

What is Hydrofiber™ Technology and how does it work?

Hydrofiber™ Technology is a soft, conformable material composed of sodium carboxymethycellulose, which can absorb a large amount of wound fluid that is transformed into gel to create a moist environment. While Hydrofiber™ Technology is neither hydrocolloids nor alginates, it incorporates benefits from both while addressing their weaknesses, including cohesive gelling and aggressive adhesion (as demonstrated in vitro) 19 Mode of action-Hydrofiber™ Technology allows rapid permeation of fluid and full expansion of fibres, creating a gel that resists wicking within fibres and prevents wicking between fibres, by way of gel blocking (as demonstrated in vitro) 20. This gel provides intimate contact with the wound bed, filling ‘dead space’ where microbes could grow. Excess fluid is retained, locking in harmful components such as endogenous proteinases and exogenous microorganisms found in wound exudate and reducing transmission to the surrounding skin21

Summary

For healthcare professionals, initiating effective therapeutic strategies in a timely and cost-effective manner to reduce wound complexities, manage the patient’s symptoms and expectations and, where possible, achieve healing, remains a challenge. Indeed, the drive towards securing funding for efficacious and cost-effective wound care therapies continues apace. Innovative strategies for diagnosis and treatment are critical. Making changes in approach to wound care could lead to improved symptom control and long-term outcomes, reduced economic costs, and better patient quality of life. Exciting developments in the field of point-of-care diagnostic testing, which have been identified above, have the potential to facilitate improvements in practice and offer a more targeted and effective approach to wound management.

The evolution of Hydrofiber™ Technology in dressings with the addition of anti-biofilm Ag+ Technology also presents the case for an innovative advanced technology for hard-to-heal wounds that combats certain factors with a considerable influence on healing: biofilm, exudate and risk of infection.

References

  1. Bjarnsholt T (2013) The role of bacterial biofilms in chronic infections. APMIS 121 (Suppl 136): 1–51
  2. Läuchli S, Swanson T, Serena T, Harding K. The use of a point-of-care test for bacterial protease activity in chronic wounds. Wounds International 2015; 6(4).
  3. Watters C, Everett J, Haley C, Clinton A, Rumbaugh K. Insulin treatment modulates the host immune system to enhance Pseudomonas aeruginosa wound biofilms. Infect. Immun 2014, 82(1):92-100.
  4. Souza MC, dos Santos LS, Sousa LP, Faria YV, Ramos JN, Sabbadini PS, et al. Biofilm formation and fibrinogen and fibronectin binding activities by Corynebacterium pseudodiphtheriticum invasive strains. Antonie van Leeuwenhoek. 2015 Jun 1; 107(6):1387-99
  5. Sillanpaa J, Chang C, Singh KV, Montealegre MC, Nallapareddy SR, Harvey BR, et al. Contribution of individual Ebp Pilus subunits of Enterococcus faecalis OG1RF to pilus biogenesis, biofilm formation and urinary tract infection. PloS one 2013; 8(7):e68813
  6. Chavakis T, Wiechmann K, Preissner KT, Herrmann M. Staphylococcus aureus interactions with the endothelium: the role of bacterial ‘secretable expanded repertoire adhesive molecules’ (SERAM) in disturbing host defense systems. Thrombosis and haemostasis 2005; 94(2):278-85
  7. Singh R, Ray P. Quorum sensing-mediated regulation of staphylococcal virulence and antibiotic resistance. Future microbiology 2014; 9(5):669-81
  8. Laverty G, Gorman SP, Gilmore BF. Biomolecular mechanisms of staphylococcal biofilm formation. Future microbiology 2013; 8(4):509-24.
  9. Coggan KA, Wolfgang MC. Global regulatory pathways and cross-talk control pseudomonas aeruginosa environmental lifestyle and virulence phenotype. Current issues in molecular biology 2012; 14(2):47-70.
  10. Swanson T, Grothier L, Schultz G. Wound Infection Made Easy. Wounds International 2014. Available from: www. woundsinternational.com
  11. Whitfield GB, Marmont LS, Howell PL. Enzymatic modifications of exopolysaccharides enhance bacterial persistence. Front Microbiol 2015; 6:471.
  12. Moyat M, Velin D. Immune responses to infection. WJG 2014; 20(19):5583-93.
  13. Durand E, Cambillau C, Cascales E, Journet L. VgrG, Tae, Tle, and beyond: the versatile arsenal of Type VI secretion effectors. Trends in microbiology 2014; 22(9):498-507.
  14. Raymond B, Young JC, Pallett M, Endres RG, Clements A, Frankel G. Subversion of trafficking, apoptosis, and innate immunity by type III secretion system effectors. Trends in microbiology 2013; 21(8):430-41.
  15. Hutchinson JJ and Lawrence JC . Wound infection under occlusive dressings 1991 Feb 28; 17(2):83-94.
  16. Winter G. Formation of the Scab and the Rate of Epithelisation of Superficial Wounds in the Skin of the Young Domestic Pig. Nature 1962; 293-294
  17. Jones VJ. The use of gauze: Will it ever change? I Wound 2006; 3:79-86
  18. Thomas S. Hydrocolloid dressings in the management of acute wounds: a review of the literature. Int Wound J 2008; 5:602-13.
  19. Queen D. Technology update: Understanding Hydrofiber® Technology. Wounds International 2010; 1(5).
  20. Waring MJ, Parsons D. Physicochemical characterisation of carboxy-methylated spun cellulose fibres. Biomaterials 2000; 22: 903–12
  21. Walker M, Hobot JA, Newman GR, Bowler PG. Scanning electron microscopic examination of bacterial immobilisation in a carboxymethyl cellulose (AQUACEL®) and Alginate Dressing. Biomaterials 2003; 24: 883–90.

Additional References

  1. Harris LG, Bexfield A, Nigam Y, Rohde H, Ratcliffe NA, Mack D. Disruption of Staphylococcus epidermidis biofilms by medicinal maggot Lucilia sericata excretions/secretions. Int J Artif Organs. 2009 Sept;32(9):555-64.
  2. Phillips PL, Yang Q, Davis S, et al. Antimicrobial dressing efficacy against mature Pseudomonas aeruginosa biofilm on porcine skin explants. Int Wound J. 2015 Aug;12(4):469-83. doi: 10.1111/iwj.12142
  3. Stechmiller JK, Schultz G. Implementing Biofilm and Infection 2014 Guidelines. National Pressure Ulcer Advisory Panel. Available athttp://www.npuap.org/wp-content/uploads/2015/02/3-Treating-Biofilms-J-St...
  4. Wolcott RD, Rhoads DD. A study of biofilm-based wound management in subjects with critical limb ischemia. J Wound Care. 2008 Apr;17(4):145-8, 150-2, 154-5.

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