A deadly hospital bacterium spent decades quietly accumulating antibiotic resistance before becoming one of the most feared pathogens in the world, according to a study published in the journal Microbial Genomics. The research traces how Acinetobacter baumannii evolved in waves, with resistance peaking in the mid-2000s.
The study was led by researchers at the University of East Anglia, working alongside scientists at the Quadram Institute and teams in Canada and Mexico. They assembled a collection of 226 bacterial samples dating from the 1970s to the early 2000s, grew them in the lab, extracted their DNA, and sequenced it using long-read Oxford Nanopore technology. Those genomes were then merged with more than 1,000 more recent genomes from six continents, giving researchers a dataset of 1,281 chromosomes to compare.
Lead researcher Dr. Benjamin Evans, from UEA's Norwich Medical School, described what made the bacterium so difficult to catch: "This bacterium particularly thrives in hospital environments and can cause infections that are extremely difficult to treat — particularly for vulnerable patients."
The picture that emerged from the data was not one of a sudden outbreak. Instead, the bacterium changed slowly and steadily across multiple generations. Each wave of evolution produced strains that were better at surviving antibiotic treatment than the ones before.
Evans said the pattern was gradual but carried a tipping point. "What we found is that it has adapted in waves, with each wave producing bacteria that were better adapted to resist antibiotics than the previous wave." He added that the research offers "one of the clearest pictures yet of how antibiotic resistance can accumulate gradually — and then suddenly tip the balance in favor of the pathogen."
The full title of the study, published in Microbial Genomics, is "New isolates from the 1970s to early 2000s provide insights into the evolution of Acinetobacter baumannii international clone 2 and its resistome." The focus is specifically on international clone 2, one of the dominant strains that spread across hospitals worldwide.
The researchers used high-performance computing to build a detailed evolutionary tree from all 1,281 chromosomes. They paired that analysis with a comprehensive scan of antimicrobial resistance genes to track how and when specific resistances appeared.
What the study makes clear is that this pathogen did not emerge from nowhere. Evans put it directly: "One thing is clear — this superbug didn't just appear. It was decades in the making, and it's still evolving."
The researchers say that understanding the genetic events behind the bacterium's rise is critical to containing it. Until this study, those events were poorly understood. The work provides a foundation for tracking how the pathogen may continue to change and for identifying what future resistance patterns might look like.
