Researchers Focus on Developing New Antibiotics to Fight Against Drug-Resistant Superbugs

drug-resistant superbugs

Researchers are positive new antibiotics can be developed from already existing medicine to fight more effectively against drug-resistant superbugs.

A team of researchers from the University College London believes existing medication can be turned into new antibiotics that would be able to kill drug-resistant superbugs in the future. Details of their report have been recently published in the journal Scientific Reports.

Study’s Highlights

Researchers say antibiotics work by breaking apart germ cells in order to stop infections and their further spreading. Up until this point, however, antibiotics require up to 24 hours to take effect. However, with the new formula the scientists are working on, the modified medication will boost the antibiotics’ effectiveness to fight against drg0resistant superbugs like MRSA.

According to the researchers, there have been only a handful of new antibiotics designed over the past decades. While modern technology was falling behind, drug-resistant superbugs grew even more aggressive, claiming more lives with each passing year.

A gloomy prediction says that the number of victims will only continue to increase in the upcoming decades. Hence, untreatable infections will be responsible for more deaths than cancer by 2050, say researchers. The good news is that the antibiotics already developed can be modified to “push” harder into the germ cells’ surface and break them apart.

Improved Efficiency

University College London’s Dr. Joseph Ndieyira describes the germ cells as having certain locks with antibiotics being the keys. Upon opening the “locks”, the germ cells would be broken apart and ultimately killed. However, drug-resistant bugs developed the ability to change these “locks”, says Dr. Ndieyira. As a result, the new antibiotics will have to break open the “doors” and take apart the germ cells’ structure by storm.

The best candidates, so far, have been vancomycin and oritavancin. However, they both work in different ways. Vancomycin causes bacteria to stop functioning and ultimately die by disrupting its vital processes. On the other hand, oritavancin employs a more aggressive behavior towards the germ cells and presses into the pathogens with a force 11,000 stronger than its counterpart, vancomycin.

Furthermore, oritavancin is great at forming clusters on the germ cells’ surface. Once these clusters exert the aforementioned force, the germ cells’ structure eventually breaks apart. More importantly, however, as opposed to vancomycin which takes from 6 to 24 hours to take effect, oritavancin engages in the battle against the superbugs within 15 minutes.

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