Study reveals rapid evolution and global spread of Pseudomonas aeruginosa

A new study has found that Pseudomonas aeruginosa — an environmental bacterium that can cause devastating multidrug-resistant infections, especially in people with underlying lung disease — evolved rapidly and then spread around the world over the past 200 years, likely driven by changes in human behavior.

The job will appear in the journal Science.

P. aeruginosa is responsible for more than 500,000 deaths annually worldwide, of which more than 300,000 are associated with antimicrobial resistance (AMR). People with conditions such as COPD (smoking-related lung damage), cystic fibrosis (CF) and non-CF bronchiectasis are particularly susceptible.

How P. aeruginosa evolved from an environmental organism to a specialized human pathogen was previously unknown. To investigate, an international team led by scientists from the University of Cambridge examined DNA data from nearly 10,000 samples collected from infected individuals, animals and environments around the world.

By mapping the data, the team was able to create phylogenetic trees – “family trees” – that show how the bacteria in the samples are related. Remarkably, they found that nearly seven out of ten infections are caused by just 21 genetic clones, or “branches” of the family tree, that evolved rapidly (by acquiring new genes from neighboring bacteria) and then spread around the world over the past 200 years.

This spread most likely occurred as a result of humans starting to live in densely populated areas where polluted air made our lungs more susceptible to infection and where there were more opportunities for infections to spread.

These epidemic clones have an intrinsic preference for infecting certain types of patients, with some preferring CF patients and others non-CF individuals. It turns out that the bacteria can take advantage of a previously unknown immune defect in people with CF, allowing them to survive in macrophages. Macrophages are cells that “eat” invading organisms, breaking them down and preventing the spread of infection. But a previously unknown flaw in the immune system of CF patients means that once a macrophage has ingested P. aeruginosa, it is unable to get rid of it.

After lung infection, these bacteria evolve in different ways to become even more specialized for the particular lung environment. As a result, certain clones may be transmitted in CF patients and other clones in non-CF patients, but almost never between CF and non-CF patient groups.

Professor Andres Floto, director of the UK Cystic Fibrosis Innovation Hub at the University of Cambridge and Royal Papworth Hospital NHS Foundation Trust, and lead author of the study, said: “Our Pseudomonas research has taught us new things about the biology of cystic fibrosis and revealed important ways in which we might be able to improve immunity against invading bacteria in these and potentially other conditions.

“From a clinical perspective, this study revealed important information about Pseudomonas. The focus has always been on how easily this infection can spread among CF patients, but we have shown that it can spread with alarming ease among other patients. This has a very important implications for infection control in hospitals where it is not uncommon for an infected individual to be in an open ward with someone potentially very vulnerable.

“We are incredibly lucky at Royal Papworth Hospital where we have single rooms and we have developed and evaluated a new ventilation system that reduces airborne bacteria and protects all patients.”

Dr. Aaron Weimann, from the Victor Phillip Dahdaleh Heart & Lung Research Institute at the University of Cambridge and first author of the study, said: “It’s remarkable to see the speed at which these bacteria can evolve and become epidemic, and how they can specialize. indeed, for the specific lung setting, we need systematic, proactive screening of all at-risk patient groups to detect and hopefully prevent further epidemic clones.