The skin is the largest organ of the body. Microbiologically, the primary function of the skin is to control the microbial populations that live on its surface. In fact, the skin is an effective barrier against bacterial infections. Although many bacteria reside on the skin surface, they are normally unable to cause an infection. A loss of skin integrity (i.e., a wound) alters the defense functions of the skin and creates favorable conditions to microbial colonization and proliferation.
Since wound colonization involves numerous microorganisms that are potentially pathogenic, any wound is exposed to the risk of becoming infected.
Wound contaminants are most likely to originate from the environment (i.e. exogenous microorganisms in the air), from the surrounding skin, involving members of the normal skin microflora such as Staphylococcus epidermidis and micrococci, or from the mucosae membranes.1
However, to date, Staphylococcus aureus, Pseudomonas Aeruginosa and Klebsiella Pneumoniae, are the most frequently isolated bacteria from skin lesions, causing delayed healing and infection in both chronic and acute wounds.2
The effect of the microorganisms on wound healing has been widely studied, and even if the majority of wounds are polymicrobial, involving both aerobes and anaerobes, aerobic pathogens such as S. aureus, P. aeruginosa, and Klebsiella Pneumoniae have been most frequently cited as the cause of delayed wound healing and infection. S. aureus is considered to be the most problematic bacterium in traumatic, surgical, and burn infections3. Moreover, S. aureus and K. pneumoniae are known as the principal responsible for biofilm formation, a major virulence factor contributing to the chronicity of infections4. Furthermore, several reports associating the enterobacterium Escherichia coli (E. coli) with skin and soft tissue infections (SSTIs) have been published: E. coli was found to be the causative agent of neonatal omphalitis, cellulitis localized to lower or upper limbs, necrotizing fasciitis, surgical site infections, infections after burn injuries, and others5.
Although systemic antibiotic therapy is essential for advancing cutaneous infections, wounds that exhibit only localized signs of infection or are failing to heal but do not have clinical signs of infection (i.e., an heavy colonization) may initially be treated with topical agents. Topical agents against microbial contamination include antibiotics and antiseptics.
The topical antiseptic treatment is generally favored in chronic wounds that are heavily contaminated by a variety of microorganisms. The topical antiseptic agents most commonly used include iodine-releasing agents (e.g., povidone iodine and cadexomer iodine), chlorine-releasing solutions (e.g., Dakin’s solution and sodium hypochlorite solution), hydrogen peroxide, chlorhexidine, silver-releasing agents, polyhexanide and acetic acid3.
The management of the microbial infection in wound healing is one of the most important components for an effective standard of care. In fact, the management of microbial infection is included in the TIMERS protocol for the treatment of chronic lesions, which classifies the different conditions that occur in case of chronic injuries6.
Microorganisms tend to interact with chronic wounds at four different levels: contamination, colonization, critical colonization and infection.
To accelerate wound healing, physicians use bioactive dressings which are capable of interacting with the microenvironment of the wound and of stimulating its healing. They represent the evolution of advanced dressings7.
Many bioactive dressings contain also antiseptic compounds to reduce the risk of bacterial contamination; among the most used and most effective are silver sulfadiazine and polyhexanide.
Silver sulfadiazine is the silver salt of sulfadiazine, an antiseptic belonging to the class of sulfonamides.
Clinically, metallic silver is relatively inert, but its interaction with the moisture of the skin surface and with the wound fluids results in the release of silver ions with antibacterial properties8.
The silver ions bind to the proteins present in the tissues causing structural changes of the cellular wall and of the nuclear membranes of the bacteria themselves. Silver binds to the DNA and RNA of bacteria inhibiting their replication8.
Polyhexanide biguanide (PHMB) is a synthetic polymer structurally similar to naturally occurring antimicrobial peptides (AMP).
The structural similarities between AMP and PHMB suggest that the latter can enter the membranes of bacterial cells and kill bacteria in a similar way to AMP9.
PHMB is thought to adhere and destroy target cell membranes, causing potassium ions and other cytosolic components to leak, resulting in bacterial cell death10.
This study aims to compare the antimicrobial activity of two preparations for topical use, one containing 0,1% PHMB, the other containing 1% silver sulfadiazine, against S. aureus, P. aeruginosa, K. pneumoniae, E. coli, and the combination of S. aureus and K. pneumoniae.