Bacteria activity discovery could help in fight against AMR

A breakthrough in bacteria research by microbiologists at Queen’s University Belfast (QUB), could lead to increased effectiveness of currently available antibiotics. 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, explained: “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.”

The Valvano Research Group, including Dr Inmaculada Garcia Romero, Dr Julia Monjaras Feria, Mr Samuel Korankye and Mr Lewis Macdonald, working in collaboration with researchers from Wurzburg University and the University of Melbourne have been investigating responses to a group of ‘last resort’ antibiotics by one of the most dangerous species of bacteria, Enterobacter bugandensis.

This bacteria is among one of six highlighted by the World Health Organisation that are of major concern in relation to growing antibiotic resistance. Known as ESKAPE pathogens, they 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, are the biggest cause of life-threatening hospital-acquired infections.

In this study, the researchers looked at the responses of Enterobacter bugandensis to a last resort antibiotic group called polymyxins. 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, preventing it from attacking its host.

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.”

Funded by the Biotechnology and Biological Sciences Research Council, the study was published in the Journal of Global Antibiotic Resistance

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