Methicillin-resistant Staphylococcus aureus (MRSA) is the most common drug-resistant pathogen that can infect skin, soft tissues, major organs and the blood. MRSA infections are often resistant to conventional antibiotics compromising effective treatment meaning new and reliable therapies are urgently required.
Patients colonised by S. aureus or MRSA are more likely to b einfected and so patients, identified as carriers prior to surgery, are treated to eradicate these pathogens. However, resistance to mupirocin, the antibiotic of choice for reducing such carriage, is increasing and treatment failure is more often encountered. Hence a particularly attractive opportunity exists to provide an alternative de-colonisation cream.
The new treatment is a combination of a peptide (ranalexin) with a bacteria cell wall-digesting protein (lysostaphin), which specifically targets and kills Staphylococcus aureus, including MRSA. The combination is synergistic;these components are more active together compared to the components on their own against lysostaphin-resistant S. aureus and also vancomycin-intermediate resistant (VISA) isolates. Furthermore, unlike conventional antibiotics the combination kills non-multyplying bacteria.
The combination is highly efficacious in vivo in an animal model, ex vivo on the surface of human skin and when dried on the surface of catheter tubing. In animals, we demonstrated that when the combination is impregnated into dressings and applied to MRSA-infected wounds for 5 days it reduces MRSA in these lesions by >99% compared to untreated controls and wounds treated with the individual components. The combination was more effective compared to vancomycin-treated animals. The combination can be used topically to treat MRSA-infected wounds.
Similarly, the combination demonstrated enhanced efficacy for reducing MRSA on living human skin compared to the individual components alone. The combination is an effective de-colonisation agent specifically capable of reducing MRSA carriage without adversely affecting the skin's normal protective microflora.
The University of St. Andrews has applied for International (PCT) patent protection (No. PCT/GB2007/001157) and US patent protection (no. 12/225441)
The University would welcome enquiries from commercial parties interested in entering into a licensing arrangement and/or collaboration to further develop this technology.