Abstract
Antibiotic resistant bacteria are a worldwide health concern and it is essential to develop new antimicrobial agents to kill these bacteria and to reduce the use of antibiotics. Staphyloccus aureus (S.aureus) an important medical pathogen is responsible for many wound infections and up to 25% of all strains produce the toxic shock syndrome toxin (TSST-1) which stimulates the release of inflammatory cytokines which cause fever and shock. Here we report on the inhibition of two penicillin resistant TSST-1 producing strains of S.aureus by seven different honeys. Bacterial growth was reduced after 24 hours at 37oC, from 10.0 log 10 in the TSB growth control to less than 1.0 log 10 in Highland, Chilean and Manuka honey. TSST-1 production was reduced from 256ng/ml in the TSB growth control to less than 30 ng/ml in sub inhibitory concentrations of all honeys.
Highlights
Staphylococcus aureus is a common pathogen associated with a large proportion of nosocomial and community acquired infections resulting in high morbidity and mortality
The observed decrease in the amount of toxin in the supernatant from the subinhibitory concentration of each honey was not the result of a decrease in cfu/ml of bacteria as there was no significant decrease in cfu/ml in honey treated bacteria compared to the number of bacteria cfu/ml in the Tryptone Soy Broth (TSB) control
For Manuka honey at 5%, there were more bacteria 9.19 log 10 in this culture compared to 8.93 log 10 in the TSB growth control yet there was a significant decrease in Toxic Shock Syndrome Toxin -1 (TSST-1) production to 29.33 ng/ml in the Manuka culture compared to > 256 ng/ml in the TSB growth control
Summary
Staphylococcus aureus is a common pathogen associated with a large proportion of nosocomial and community acquired infections resulting in high morbidity and mortality. Diseases caused by this microbe include skin and soft tissue abscesses, toxic shock syndrome (TSS), scalded skin syndrome, food poisoning, pneumonia and septicaemia [1,2].Treatment of diseases caused by S. aureus is difficult because of the emergence of multi- antibiotic resistant strains, including methicillin resistant S. aureus (MRSA) and vancomycin resistant S. aureus (VRSA) [3,4,5]. The ability of S.aureus to cause disease is largely dependent on the presence of extracellular virulence factors, including surface and secreted toxins [2]. The pathophysiology of TSS includes a release of cytokines and T-cell activation induced by TSST-1 and its direct effect on endothelial cells causing vasodilation resulting in hypotension [8]
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