INTRODUCTION

The major human bacterial pathogen Pseudomonas aeruginosa causes multidrug-resistant infections, particularly in people with underlying immunodeficiencies or inflammatory lung diseases such as cystic fibrosis (CF). However, it remains unclear how P. aeruginosa has evolved into a highly adapted, globally disseminated pathogen.

Individuals with cystic fibrosis and other chronic inflammatory lung diseases are particularly vulnerable to colonization by Pseudomonas aeruginosa.

Epidemic clones have emerged in certain patient groups that are associated with poor clinical outcomes and antimicrobial resistance. Weimann et al. investigated when and how such clones emerge by accessing international collections of clinical and environmental strains of P. aeruginosa amassed over the past century.

The authors distinguished 21 major clones based on pairwise single-nucleotide polymorphism distances and majority multilocus sequence type. 

A series of epidemic clones emerged and expanded between 1850 and 2000, indicating recent selective pressures, possibly driven by industrialization, associated pollution, and human population change and underpinned by major changes in bacterial physiology