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The study suggests antibiotic-resistant bacteria can pump the antibiotics out of their systems – information that could help researchers find new ways to kill bacteria.
A new study at Queen’s University Belfast (QUB) could make existing antibiotics more effective and reduce the impact of antibiotic resistance.
This issue – also known as antimicrobial resistance (AMR) – is a serious and growing issue in healthcare globally, which occurs when bacteria, fungi, viruses or parasites become resistant to drugs that are designed to kill them.
These changes make infections harder to treat and increase the risk that diseases will spread and kill people. It is estimated that in 2019, bacterial AMR was directly responsible for 1.27m global deaths and contributed to 4.95m deaths, according to the World Health Organization.
Prof Miguel A Valvano, lead researcher on the QUB study, described AMR as “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,” Valvano said.
But Valvano and his team have discovered how a certain bacteria reacts to a strong antibiotic, which could improve our understanding of how to tackle this issue.
Multiple layers of defence
The researchers highlighted the danger of ‘ESKAPE pathogens’, which are certain pathogens that are able to deal with last-resort antibiotics – powerful medicines used to tackle antimicrobial-resistant bacteria.
One of these last-resort antibiotics belongs to the family of polymyxins, which are used to treat serious infections. The researchers looked how polymyxin interacted with Enterobacter bugandensis, which is an ESKAPE pathogen.
The researchers discovered a set of genes within the bacteria, which were expressed more frequently in the antibiotic’s presence. They also identified a small protein encoded by one of these genes that causes the bacteria to pump the antibiotic out of its cell, protecting itself from being destroyed.
“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,” Valvano said.
“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.”
Last year, a study led by Trinity College Dublin was able to “look under the bacterial bonnet” and make a blueprint that could help design bespoke drugs.
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