The effect of manuka honey on the structure of Pseudomonas aeruginosa.

The purpose of this study was to investigate the effects of manuka honey on the structural integrity of Pseudomonas aeruginosa ATCC 27853. The minimum inhibitory concentration (MIC) and the minimum bactericidal concentration (MBC) of manuka honey for P. aeruginosa were determined by a microtitre plate method, and the survival of bacteria exposed to a bactericidal concentration of manuka honey was monitored. The effect of manuka honey on the structure of the bacteria was investigated using scanning and transmission electron microscopy (SEM and TEM, respectively). The MIC and MBC values of manuka honey against P. aeruginosa were 9.5% (w/v) and 12% (w/v) respectively; a time-kill curve demonstrated a bactericidal rather than a bacteriostatic effect, with a 5 log reduction estimated within 257 min. Using SEM, loss of structural integrity and marked changes in cell shape and surface were observed in honey-treated cultures. With TEM, these changes were confirmed, and evidence of extensive cell disruption and lysis was found. Manuka honey does not induce the same structural changes in P. aeruginosa as those observed in staphylococci. Our results indicate that manuka honey has the potential to be an effective inhibitor of P. aeruginosa.

The intracellular effects of manuka honey on Staphylococcus aureus.

The purpose of this study was to investigate the effect of manuka honey on Staphylococcus aureus in order to identify the intracellular target site. The mode of inhibition of manuka honey against S. aureus NCTC 10017 was investigated by determining the minimum inhibitory concentration (MIC), minimum bactericidal concentration (MBC) and the effect of time on viability. Structural changes were observed by scanning (SEM) and transmission electron microscopy (TEM) of cells suspended for 4 h at 37 degrees C in 0.05 mM Tris buffer containing 10% (w/v) manuka honey and were compared to cells in buffer alone or buffer containing 10% (w/v) artificial honey (to assess osmotic damage). A bactericidal mode of inhibition for manuka honey on S. aureus was established. Marked structural changes in honey-treated cells were seen only with TEM, where a statistically significant increase in the number of whole cells with completed septa compared to untreated cells were observed (P < 0.05). Structural changes found with TEM suggest that honey-treated cells had failed to progress normally through the cell cycle and accumulated with fully formed septa at the point of cell division without separating. Sugars were not implicated in this effect. The staphylococcal target site of manuka honey involves the cell division machinery.

Absence of bacterial resistance to medical-grade manuka honey.

Clinical use of honey in the topical treatment of wounds has increased in Europe and North America since licensed wound care products became available in 2004 and 2007, respectively. Honey-resistant bacteria have not been isolated from wounds, but there is a need to investigate whether honey has the potential to select for honey resistance. Two cultures of bacteria from reference collections (Staphylococcus aureus NCTC 10017 and Pseudomonas aeruginosa ATCC 27853) and four cultures isolated from wounds (Escherichia coli, methicillin-resistant S. aureus (MRSA), Pseudomonas aeruginosa and S. epidermidis) were exposed to sub-lethal concentrations of manuka honey in continuous and stepwise training experiments to determine whether the susceptibility to honey diminished. Reduced susceptibilities to manuka honey in the test organisms during long-term stepwise resistance training were found, but these changes were not permanent and honey-resistant mutants were not detected. The risk of bacteria acquiring resistance to honey will be low if high concentrations are maintained clinically.