Scientists led by the University of Birmingham have identified a new mechanism of antibiotic resistance in bacterial cells which could aid understanding of, and the development of solutions to, the growing problem of antibiotic resistance.
The research, published in PNAS, describes the way in which a strain Salmonella within a patient was able to develop resistance to the commonly used antibiotic drug ciprofloxacin.
The patient in question was admitted to hospital for repair of a leaking abdominal aortic aneurysm graft, and was treated for a disseminated Salmonella infection.
Through isolates taken over the course of 20 weeks, the team used whole genome sequencing to reveal a mutation in the bacterial cells that allowed them to become resistant to the effects of some antibiotics.
Dr Jessica Blair explained: “We cannot know for sure when this mutation happened within this strain. What we do know is that it developed soon after this patient was given ciprofloxacin to treat the infection. It’s further evidence that, when it comes to the issue of antibiotic resistance, we are coming up against a very capable and complex adversary.”
Laura Piddock, Professor of Microbiology at Birmingham, BSAC Chair in Public Engagement and Director of Antibiotic Action said: “Our study further highlights the need for increased understanding about antibiotic resistance, not least to inform future strategies to both minimise and prevent antibiotic-resistant bacteria arising when new treatments become available.”
The team hopes that such insights into the mechanisms by which bacteria become resistant to antibiotics will help to design smarter therapies and drugs. In this instance, the treatments would be designed to avoid the impact of the particular mutation. This is a realistic aspiration, as surprisingly the team also found that some antimicrobial compounds were pumped out poorly by the mutated pump and so had enhanced antibiotic activity.
The World Health Organisation recently warned that “many common infections will no longer have a cure and, once again, could kill unabated.”