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Treating Chronic Wounds With Hypochlorous Acid Disrupts Biofilm

Pearls for Practice

Treating Chronic Wounds With Hypochlorous Acid Disrupts Biofilm


Wound healing is a complex process; many factors, including the presence of bacteria, can potentially delay actual healing. Increasing evidence shows that some bacteria within chronic wounds live within biofilm communities in which bacteria are protected from host defenses and develop resistance to systemic antibiotic treatment.1 Bacteria in biofilm behave differently from planktonic bacteria of the same organism in terms of their response to antibiotic treatment and human immunity.2,3 The biofilm is formed when a group of microorganisms stick to each other and become embedded within a self-produced matrix of extracellular polymeric substance composed of extracellular DNA, polysaccharides, and proteins.3 Among the most common biofilm-forming bacteria are Staphylococcus aureus and Pseudomonas aeruginosa.2 In order to disrupt biofilm within a wound, an agent must kill the bacteria and decrease the polysaccharides and proteins in the extracellular matrix of the biofilm.

Although the exact role of biofilm in chronic wound healing remains unclear, treatments that kill microorganisms within biofilms and disrupt the extracellular matrix of the biofilm may aid in the healing of chronic wounds.4 Hypochlorous acid (HOCl) is a naturally occurring small molecule generated by white blood cells in the human body. In vitro testing has shown hypochlorous acid can rapidly kill important wound pathogens, including antibiotic-resistant, methicillin-resistant S aureus and P aeruginosa. The time for inactivating these organisms is extremely rapid (<30 seconds).

An important attribute of the human body’s immune system is its ability to instigate a rapid attack against invading pathogens by releasing highly potent oxidizing substances such as hypochlorous acid. After engulfing the invading pathogens, neutrophils release an oxidative burst of hypochlorous acid that very quickly destroys the engulfed bacteria, virus, or fungi. The HOCl, produced by neutrophils, kills microorganisms by binding to critical cell membrane components and affecting cell permeability. This leads to the rupture of the cell membrane and subsequent disintegration of cells.4

Efficacy Study

A study was conducted to test the efficacy of HOCl (Vashe Wound Cleanser, Urgo Medical) as an agent to disrupt S aureus biofilm in a recognized biofilm model.5 S aureus biofilms were produced by circulating nutrient broth (casamino acid [0.1 g/L], yeast extract [0.1 g/L], MgS0₄.2H2O [0.2 g/L], FeSO4.7H2O [0.0005 g/L], Na2HPO4 [1.25g/L], KH2PO4 (0.5 g/L], and lactose [0.025 g/L]) through Tygon tubing (Saint Gobain Corporation) for 12 hours. Between 5 mL and 10 mL of S aureus culture (108 colony-forming units [CFU]/mL) was circulated through the tubing. Biofilms were treated with hypochlorous acid for 1, 3, 5, 7, and 10 minutes. 

After each treatment, 2 cm2 pieces of tube were cut and neutralized, and bacterial numbers, residual protein, and carbohydrate content measured.4 

Results. S aureus bacterial counts were reduced by greater than log 5 CFU/cm3 following a 1-minute exposure to HOCl. A reduction of  greater than log 6 CFU/cm3 was observed after 3, 5, 7, and 10 minutes of exposure to HOCl (see Figure 1). This log reduction represented complete removal of the S aureus biofilm. Furthermore, approximately 70% of biofilm polysaccharide and > 90% of the biofilm protein were removed after 5, 7, and 10 minutes of contact time (see Figure 2 and Figure 3).4


HOCl was effective at reducing S aureus bacterial numbers and at disrupting the polysaccharide and protein matrix within the biofilm model. Similar data have been reported in a P aeruginosa biofilm model using HOCl.6 The current study indicates that HOCl may assist in the management of hard-to-heal chronic wounds by decreasing the bacterial numbers and by penetrating and disrupting the polysaccharide/protein matrix of wound pathogen biofilms.


Martin C. Robson, MD, is emeritus professor of surgery at the University of South Florida, Tampa.  Pearls for Practice is made possible through the support of Urgo Medical, Fort Worth, TX ( The opinions and statements of the clinicians providing Pearls for Practice are specific to the respective authors and not necessarily those of Urgo Medical, Wound Management & Prevention, or HMPGlobal. This article was not subject to the Wound Management & Prevention peer-review process. The article was originally published in the 2014 November/December issue of Today’s Wound Clinic.