The research has been published in the Journal of Global Antimicrobial Resistance.

The study was carried out at the Wellcome-Wolfson Institute for Experimental Medicine at Queen’s University Belfast by the Valvano Research Group including Dr Inmaculada Garcia Romero, Dr Julia Monjaras Feria, Mr Samuel Korankye and Mr Lewis Macdonald, in collaboration with researchers from Wurzburg University and the University of Melbourne.

Antimicrobial resistance (AMR) is one of the top global public health threats. It is estimated that bacterial AMR was directly responsible for 1.27 million global deaths in 2019 and contributed to 4.95 million deaths. AMR happens when germs like bacteria and fungi develop the ability to defeat the drugs designed to kill them.

Professor Miguel A Valvano, Chair in Microbiology and Infectious Diseases at the Wellcome-Wolfson Institute for Experimental Medicine at Queen’s University Belfast and Lead Researcher on the study, explains: “Antimicrobial resistance is one of the greatest challenges to human health. Deadly infections like pneumonia, wound or bloodstream infections are becoming untreatable as the bacteria are becoming resistant to current antibiotics.”

A major concern in relation to antibiotic resistance, as highlighted by the World Health Organisation, are “ESKAPE pathogens”. The term “ESKAPE” encompasses six pathogens with growing antibiotic resistance.

These ESKAPE pathogens can “escape” last-resort antibiotics (antibiotics that are used to treat infections with bacteria that are resistant against more common antibiotics), and as a result, they are the biggest cause of life-threatening hospital-acquired infections, such as pneumonia, in critically ill patients.

One of these last resort antibiotics belongs to the family of polymyxins, which are used to treat various bacterial infections.

In this study, the researchers looked at the responses to polymyxin by one of the most dangerous species of the bacteria Enterobacter bugandensis.

They discovered a set of genes within the bacteria that are expressed more frequently in the antibiotic's presence and identified a small protein encoded by one of these genes that interacts with a pump to “send” out the antibiotic to the outside of the bacteria’s cell, which stops it from being able to destroy the bacteria.

Professor Valvano continues: “Our research has discovered that high-level antibiotic resistance to polymyxin antibiotics happens not only by preventing the binding of the antibiotic to the bacterial surface, as previously known, but also by the interaction of the pump that forces the antibiotic to the outside of the bacterial cell, providing it with two layers of resistance against the antibiotic.

"This new information can prove useful to develop ways to destroy this pump action to make existing antibiotics more effective and help in the fight against antibiotic resistance.”

This research was funded by the Biotechnology and Biological Sciences Research Council.

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Media inquiries to Sian Devlin at s.devlin@qub.ac.uk