Study reveals rapid evolution and global spread of Pseudomonas aeruginosa

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

The job appears in the journal science.

P. aeruginosa is responsible for over 500,000 deaths per year worldwide, of which over 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 this, an international team led by scientists at the University of Cambridge examined DNA data from almost 10,000 samples taken 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 from the samples are related to each other. Amazingly, they found that almost seven out of ten infections are caused by just 21 genetic clones, or “branches” of the family tree that have evolved rapidly (picking up new genes from neighboring bacteria) and then spread globally over the past 200 years .

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

These epidemic clones have an intrinsic preference to infect specific types of patients, with some favoring CF patients and other non-CF individuals. It turns out that the bacteria can exploit a previously unknown immune defect in people with CF, allowing them to survive inside macrophages. Macrophages are cells that “eat” invading organisms, breaking them down and preventing the spread of infection. But a previously unknown defect in the immune system of CF patients means that once the macrophage ingests P. aeruginosa, it is unable to get rid of it.

After infecting the lungs, these bacteria then evolve in different ways to become even more specialized for a particular lung environment. The result is that certain clones can be transmitted within CF patients and other clones within non-CF patients, but almost never between CF and non-CF patient groups.

Professor Andres Floto, Director of the UK Cystic Fibrosis Innovation Center at the University of Cambridge and Royal Papworth Hospital Foundation, and senior author of the study said: “Our research on Pseudomonas has taught us new things about biology of cystic fibrosis and revealed important ways we may be able to improve immunity against invading bacteria in this and potentially other conditions.

“From a clinical perspective, this study has 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 also spread with alarming ease among CF patients. This has very important implications for infection control in hospitals, where it is not unusual for an infected individual to be in an open ward with someone potentially very vulnerable.

“We are extremely fortunate at Royal Papworth Hospital that we have single rooms and have developed and evaluated a new air handling system to reduce the amount of bacteria in the air and protect all patients.”

Dr. Aaron Weimann of the Victor Phillip Dahdaleh Heart and Lung Research Institute at the University of Cambridge, and first author of the study, said: “It is remarkable to see the speed at which these bacteria evolve and can become epidemics and how they can For a particular lung setting, we really need systematic and active screening of all groups of patients at risk to detect and hopefully prevent the emergence of more epidemic clones.