Streptococcus pyogenes (group A Streptococcus; GAS) is always of clinical significance in wounds where it can initiate infection, destroy skin grafts and persist as a biofilm. Manuka honey has broad spectrum antimicrobial activity and its use in the clinical setting is beginning to gain acceptance with the continuing emergence of antibiotic resistance and the inadequacy of established systemic therapies; novel inhibitors may affect clinical practice. In this study, the effect of manuka honey on S. pyogenes (M28) was investigated in vitro with planktonic and biofilm cultures using MIC, MBC, microscopy and aggregation efficiency. Bactericidal effects were found in both planktonic cultures and biofilms, although higher concentrations of manuka honey were needed to inhibit biofilms. Abrogation of adherence and intercellular aggregation was observed. Manuka honey permeated 24 h established biofilms of S. pyogenes, resulting in significant cell death and dissociation of cells from the biofilm. Sublethal concentrations of manuka honey effectively prevented the binding of S. pyogenes to the human tissue protein fibronectin, but did not inhibit binding to fibrinogen. The observed inhibition of fibronectin binding was confirmed by a reduction in the expression of genes encoding two major fibronectin-binding streptococcal surface proteins, Sof and SfbI. These findings indicate that manuka honey has potential in the topical treatment of wounds containing S. pyogenes.
INTRODUCTIONStreptococcus pyogenes (group A Streptococcus) colonizes the nasopharynx and skin of healthy individuals, forming part of the commensal microbiota. Under appropriate conditions, S. pyogenes can be transmitted to wounds and is especially problematic after surgery, following skin grafting and for military personal with traumatic or puncture wounds. Wounds provide a route of entry to the host and damaged tissues display a matrix of proteins including collagen, albumin, fibronectin and fibrinogen, which collectively provide a plethora of ligands to which opportunistic pathogens, including streptococci, adhere (Kubo et al., 2001). Surgical site infection accounts for approximately 25 % of all hospital-acquired infections and may result in the development of a non-healing or chronic wound (Werdin et al., 2009). Non-healing wounds are defined as wounds that have failed to proceed through the normal, orderly and timely reparative process that results in restoration of anatomical and functional integrity, within 3 months (Cooper, 2005;Guo & Dipietro, 2010). In the developed world, approximately 1-1.5 % of populations have non-healing wounds, and these account for 2-4 % of all health care expenses (Gottrup, 2008).Biofilms have been associated with persistent or chronic wound infections and are a major obstacle to healing (James et al., 2008;Rhoads et al., 2008). Streptococcus species readily form biofilms, by a process in which numerous cell-wall-anchored adhesins specifically attach to human tissue protein ligands and promote bacterial aggregation (Nobbs et ...