Compound destroys MRSA and makes it vulnerable to other antibiotics

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Transmission electron microscope image of a clinical MRSA isolate at 300,000x magnification. Credit: Maisem Laabei/University of Bath

Key points:

  • A compound that both inhibits the MRSA superbug and makes it more vulnerable to antibiotics has been discovered.
  • The compound tested was effective against 10 different antibiotic resistant strains of S. aureus.
  • Although further research is needed, the compound could have important implications in a clinical setting as a new treatment option.

Researchers at the University of Bath (UK) have discovered a compound that not only inhibits the MRSA virus but, more importantly, makes it vulnerable to established antibiotics.

The new compound, a polyamine, destroys Staphylococcus aureus, the bacteria responsible for MRSA, by disrupting the pathogen’s cell membrane. Polyamines are natural compounds present in most living organisms. Until a decade ago they were thought to be essential for all life, but scientists now know they are both absent and toxic to, S. aureus. Since this discovery, researchers have been trying to exploit the pathogen’s unusual vulnerability to polyamines to inhibit bacterial growth.

In a book published in Frontiers in microbiology, which is exactly what Maisem Laabei and his team did. They found that a modified polyamine (called AHA-1394) is much more effective at destroying antibiotic-resistant strains of S. aureus than even the most active natural polyamine.

The compound has been tested in vitro against 10 different antibiotic resistant strains S. aureus, including some that are known to be resistant to vancomycin, the latest drug of choice given to patients battling an MRSA infection. The compound was successful against all strains resulting in no additional bacterial growth.

The study shows that in addition to destroying S. aureus Directly, the compound is able to restore the sensitivity of multi-resistant strains of the bacterium to three important antibiotics: daptomycin, oxacillin and vancomycin. This could mean that antibiotics that have become ineffective after decades of overuse could, over time, regain their ability to control serious infections.

“With our new compound, the pathogen is destroyed when used at a concentration more than 128 times lower than that required to destroy the pathogen when we use a natural polyamine,” Laabei said. “This is important because drugs that have the lowest minimum inhibitory concentration are likely to be more effective antimicrobial agents and safer for the patient.”

“Preliminary research suggests the compound is not toxic to humans, which of course is critical,” Laabei said. “In our next study, for which we are seeking funding, we hope to focus on the precise mechanisms used by the compound to inhibit S. aureus. We believe that the compound attacks the membrane of S. aureus, which makes the membrane permeable, leading to bacterial death.

The compound was also tested against biofilm, the thin, hard-to-treat layer of microorganisms that grows on hard surfaces and can lead to serious infection. The results were promising here too, with the compound preventing the formation of new biofilm, but not disrupting established biofilm.

Information courtesy of University of Bath.

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