Pseudomonas aeruginosa is a type of bacteria found in the environment that can cause severe infections which are difficult to treat with multiple drugs, especially in individuals with pre-existing lung conditions. A recent study has shown that this bacteria has evolved rapidly and spread worldwide in the past two centuries, possibly due to changes in human behavior.
P. aeruginosa is responsible for more than 500,000 deaths globally each year, with over 300,000 attributed to antimicrobial resistance (AMR). People with conditions like Chronic Obstructive Pulmonary Disease (COPD), cystic fibrosis (CF), and non-CF bronchiectasis are at higher risk of infection.
The transformation of P. aeruginosa from an environmental organism to a specialized human pathogen was previously unknown. To investigate this, an international team of researchers, led by scientists from the University of Cambridge, analyzed DNA data from nearly 10,000 samples taken from infected individuals, animals, and various environments worldwide. Their findings have been published in the journal Science.
By analyzing the data, the team was able to create phylogenetic trees that illustrate the genetic relationships among the bacteria in the samples. They discovered that nearly 70% of infections are caused by 21 genetic clones that have rapidly evolved by acquiring new genes from other bacteria and then spread globally over the last 200 years. This spread is believed to be linked to the increasing population density, air pollution affecting lung vulnerability to infections, and greater opportunities for transmission.
These epidemic clones tend to target specific patient groups, with some more prevalent in CF patients and others in non-CF individuals. It was found that the bacteria exploit an immune deficiency unique to CF patients, enabling them to evade the body’s defenses and persist within cells known as macrophages. Macro-phages are responsible for eliminating invading pathogens, but in CF patients, they struggle to eradicate P. aeruginosa once it enters the cells.
Following lung infection, the bacteria continue to adapt to the lung environment, leading to specialized clones that are more adept at infecting specific patient groups. Interestingly, transmission between CF and non-CF patient groups is rare.
Professor Andres Floto, Director of the UK Cystic Fibrosis Innovation Hub at the University of Cambridge and Royal Papworth Hospital NHS Foundation Trust, and the senior author of the study, stated: “Our research on Pseudomonas has provided insights into cystic fibrosis and potential strategies to enhance immunity against invading bacteria.”
Dr. Aaron Weimann from the Victor Phillip Dahdaleh Heart & Lung Research Institute at the University of Cambridge, and lead author of the study, highlighted the rapid evolution of these bacteria into epidemic forms and their ability to adapt to specific lung environments. He stressed the need for proactive screening of vulnerable patient groups to detect and prevent the emergence of new epidemic clones.
The study was supported by funding from Wellcome and the UK Cystic Fibrosis Trust.
