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Antibiotics resistance Q&A
30 June 2016 • Author(s): Caroline Richards
With the rise in drug-resistant bacterial infections heralding a new, dark era of medicine, antibiotics alternatives could one day become the first-line defence against infectious diseases. With the urgent need to find new approaches clear, Caroline Richards, Editor of European Pharmaceutical Review, interviewed Dr. Bjorn Herpers, Chief Medical Advisor of the Dutch biotechnology firm Micreos, to find out more about the company’s targeted antibacterial products. Micreos is developing a lysin called Staphefekt, which specifically targets Staphylococcus aureus, including meticillin-resistant Staphylococcus aureus (MRSA). Dr. Bjorn also serves as Clinical Microbiologist at Public Health Laboratory, Kennemerland.
How does Micreos’ novel, targeted antibacterial product work and which strains of Staphylococcal species is it effective against?
Micreos has developed the world’s first endolysin registered for human use on intact skin. This endolysin is a recombinantly produced bacteriophage-derived cell-wall hydrolase that represents a new class of antibacterial agent. Micreos’ endolysin, Staphefekt, specifically targets both methicillin-resistant and methicillin-susceptible strains of Staphylococcus aureus. It is used for inflammatory skin and soft tissue infections where S. aureus is an aggravator and/or the causal bacterium. Endolysins work by instantaneously digesting peptidoglycan crosslinks in a bacterial cell wall causing irreversible lysis. The newly formed hole in the bacterial cell wall causes the host bacterium to be killed. Since this process is independent of the bacterial metabolism, it is also effective in biofilms.
Can you explain why bacteria are unable to develop resistance to endolysins over time?
Endolysin activity is a crucial step in the life cycle of phages. During a billion years of co-evolution of phages and their bacterial host, natural selection has yielded endolysins that target parts of the bacterial cell wall that the bacteria cannot change. This is because the targeted area is so essential to their structure that the bacteria cannot survive if a mutation, great enough to interfere with endolysin activity, occurs. Therefore, bacterial resistance has not been observed and is not expected…
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