Scientists, in a new study released on Friday, have demonstrated how Pseudomonas aeruginosa, an environmental bacterium that can cause severe multidrug-resistant infections, particularly in individuals with underlying lung conditions, has rapidly evolved and spread globally over the past 200 years.
Human behavior changes have contributed to this bacterium becoming epidemic, responsible for over 500,000 deaths annually worldwide, with more than 300,000 of those linked to antimicrobial resistance (AMR), according to a team from the University of Cambridge in the UK.
Individuals with conditions such as chronic obstructive pulmonary disease (COPD), cystic fibrosis (CF), and non-CF bronchiectasis are particularly vulnerable to P. aeruginosa. The bacterium exploits immune deficiencies to persist in cystic fibrosis patients.
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To investigate how P. aeruginosa evolved from an environmental organism into a specialized human pathogen, scientists examined DNA data from nearly 10,000 samples taken from infected individuals, animals, and environments worldwide.
Using this data, the team created phylogenetic trees, or ‘family trees,’ illustrating the relationships among the bacterial samples.
Their findings, published in the journal Science, revealed that almost 70% of infections are caused by just 21 genetic clones, or ‘branches’ of the family tree. These clones have rapidly evolved by acquiring new genes from neighboring bacteria and have spread globally over the last 200 years.
The spread of the bacteria occurred mainly as people began living in densely populated areas, where air pollution made lungs more susceptible to infection and where there were more opportunities for infections to spread.
The team also noted that P. aeruginosa spreads with alarming ease not only between cystic fibrosis patients but also between other patients.
The study on P. aeruginosa “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,” said Professor Andres Floto, Director of the UK Cystic Fibrosis Innovation Hub at the University of Cambridge.
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