Bacteria becoming resistant to ‘last chance’ antibiotic

A patient at hospital. Picture: PA Photo/JupiterImages Corporation.
A patient at hospital. Picture: PA Photo/JupiterImages Corporation.
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Bacteria are becoming resistant to the antibiotic which is the last line of defence against infection, a new study found.

Colistin is a ‘last resort’ antibiotic used to treat life-threatening bacterial infections that do not respond to other treatments because the bugs have become resistant to other groups of antibiotics.

But increasingly bacteria have evolved to include a gene which increases resistance to colistin sparking alarm across the globe.

Since the discovery of penicillin in the 1920s antibiotics revolutionised medicine, saving hundreds of millions of lives by preventing infections and allowing huge advances in surgery and the treatment of other conditions.

Colistin was introduced in the 1959 but its use has been limited as it may be toxic to kidneys but as more antibiotics became useless it was became the last antibiotic in the medic’s arsenal.

Now an international research team, led by the University of Bristol, has provided the first clues to understand how the mcr-1 gene protects bacteria from colistin.

Last year Dr Jim Spencer from the School of Cellular and Molecular Medicine and colleagues from Oxford, Cardiff, Diamond Light Source, Thailand and China, identified mcr-1 as the first colistin-resistance gene that could be passed between bacteria.

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This enabled resistance to spread rapidly within a bacterial population.

Since then, the mcr-1 gene has been detected in common bacteria, such as E. coli, in China, the US and across Europe first in farm animals and recently in human.

The use of colistin in agriculture has been blamed for the growing antibiotic resistance and the Chinese have now banned it from naimal feeds.

In the new study scientists discovered colistin acts by binding to, and disrupting, the outer surface of bacteria.

Bacteria carrying the mcr-1 gene make a protein that modifies the bacterial surface to reduce colistin binding, making the organism resistant.

The team used X-rays produced at Diamond’s crystallography beamlines to generate detailed pictures of the portion of this protein responsible for this modification, and with this information identified key features that are necessary for it to function.

They also constructed computer models of the chemical reaction that leads to resistance.

This provided the first clues as to how mcr-1 acts within the bacterial cell, as well as information essential to efforts to identify ways of blocking MCR-1 function that could restore the activity of colistin against bacteria carrying mcr-1.

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Co-author Professor Adrian Mulholland said: “The importance of understanding colistin resistance can hardly be overstated: it is rapidly emerging threat to public health.

“Our results illuminate the structural and (for the first time) mechanistic basis of transferable colistin resistance conferred by mcr-1, thanks to the combination of biological, chemical and computational expertise brought to bear on this project.

“We are confident that our findings will drive efforts to understand mcr-1-mediated resistance and ultimately help identify routes towards overcoming MCR-1 activity in harmful bacteria.”

The study was published in the journal Scientific Reports.