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In a groundbreaking study, researchers have mapped the evolution of Pseudomonas aeruginosa, a deadly environmental bacterium that has rapidly adapted to become a significant threat to human health over the past 200 years. This bacterium, responsible for over 500,000 deaths annually, particularly affects individuals with underlying lung conditions and is a major contributor to antimicrobial resistance (AMR), accounting for over 300,000 of these deaths.
The study, led by an international team of scientists from the University of Cambridge and published in Science, reveals how P. aeruginosa evolved from an environmental organism into a specialized human pathogen. This transformation was driven by changes in human behavior, such as increased urbanization and air pollution, which have made human lungs more susceptible to infection.
To trace the evolutionary path of P. aeruginosa, researchers analyzed DNA from nearly 10,000 samples collected from infected individuals, animals, and environments globally. By constructing phylogenetic trees, the team discovered that nearly 70% of infections are caused by just 21 genetic clones that have rapidly evolved and spread worldwide. This global spread coincides with the rise of densely populated areas, where the bacteria found ample opportunities to infect susceptible populations.
Professor Andres Floto, Director of the UK Cystic Fibrosis Innovation Hub at the University of Cambridge and Royal Papworth Hospital NHS Foundation Trust, and senior author of the study, highlighted the clinical implications of their findings. “Our research on Pseudomonas has taught us new things about the biology of cystic fibrosis and revealed important ways we might be able to improve immunity against invading bacteria in this and potentially other conditions,” Floto said.
One of the study’s significant revelations is the bacteria’s ability to exploit a previously unknown immune defect in cystic fibrosis (CF) patients. Normally, macrophages, a type of immune cell, ingest and destroy invading organisms. However, in CF patients, a flaw in their immune systems allows P. aeruginosa to survive inside macrophages, leading to persistent infections. These bacteria then further evolve to specialize in different lung environments, resulting in distinct clones that infect CF and non-CF patients differently.
Dr. Aaron Weimann from the Victor Phillip Dahdaleh Heart & Lung Research Institute at the University of Cambridge, and first author of the study, emphasized the need for systematic, proactive screening of at-risk patient groups to detect and prevent the emergence of more epidemic clones. “It’s remarkable to see the speed with which these bacteria evolve and can become epidemic and how they can specialize for a particular lung environment,” Weimann noted.
The study underscores the importance of rigorous infection control measures in hospitals, especially for vulnerable patient populations. The researchers advocate for improved air-handling systems and single-room accommodations to reduce the risk of airborne bacterial transmission.
Funded by Wellcome and the UK Cystic Fibrosis Trust, this research not only enhances our understanding of P. aeruginosa but also provides critical insights into preventing the spread of this deadly pathogen and improving patient outcomes in the face of evolving bacterial threats.
