A new study has revealed the mechanisms that enabled one of the world's most dangerous antibiotic-resistant bacteria to silently infiltrate hospitals and dominate the global epidemiological landscape.
The international team, led by the University of East Anglia in Britain and including scientists from the British Quadram Institute and universities in Canada and Mexico, relied on laboratory samples dating back to the 1970s to reconstruct the genetic history of Acinetobacter baumannii, a stubborn hospital pathogen that is a nightmare for health systems due to its extreme resistance to treatment.
The researchers found that these bacteria did not suddenly emerge as a super threat, but rather evolved and adapted quietly over many decades, with small but cumulative genetic changes that eventually made them capable of resisting most available antibiotics.
In this context, Dr. Benjamin Evans, the lead researcher from Norwich Medical School at the University of East Anglia, explained that bacteria that cause infections in humans can adapt to antibiotics, rendering them ineffective. He noted that his team focused on this particular type because it thrives in hospital environments and causes infections that are extremely difficult to treat, especially for the most vulnerable patients.
He added that understanding the mechanism by which this microbe became a threat of this magnitude is crucial to stopping its spread, but the genetic events that led to its success have remained a mystery until now.
The study showed that bacteria evolved in successive waves, with each wave producing strains more resistant to antibiotics than the previous one, providing one of the clearest scientific pictures of how resistance gradually accumulates, then the balance suddenly tips in favor of the pathogen.
Researchers confirm that this superbug was "made" over decades and is still in a state of continuous evolution.
To achieve this breakthrough, the team collected a unique set of 226 bacterial samples, dating from the 1970s to the early 2000s, and cultured them in the laboratory. They then extracted their DNA and sequenced it using the advanced Oxford Nanopore technology.
To obtain a global picture, the researchers combined these historical genomes with more than a thousand modern genomes from six continents, and compared all 1,281 chromosomes, enabling them to build a detailed evolutionary tree, along with a comprehensive survey of antibiotic resistance genes, to track the emergence, disappearance, and remodeling of these genes over time.
By matching genetic changes with the dates and locations of samples, the team was able to determine when key resistance traits emerged and how they spread globally. They concluded that the bacteria did not suddenly appear as a super-threat, but rather gradually infiltrated and gained dominance, becoming by 2005 the most widespread strain of its kind in the world.
The key lies in identifying a crucial turning point, which was the bacteria's acquisition of two key genetic elements, one of which is a gene known as oxa23, which confers resistance to powerful antibiotics, thus enhancing its ability to survive treatments and making it more difficult to eliminate.
The study revealed that this bacterium is not a single, unified strain, but rather divided into at least four distinct groups, each with its own evolutionary trajectory. Three of these groups exhibited gradual, step-by-step evolution, akin to a slow genetic arms race against modern medicine. The fourth group stands out as a different case, appearing to have branched independently and being detected with increasing frequency in modern samples, raising concerns that a newer and potentially more adaptive variant may be on the rise.
The researchers emphasize the importance of these findings in guiding current and future antibiotic use policies, especially with bacteria such as Acinetobacter baumannii, which pose a serious threat to global health systems, warning that there is an urgent need to develop new approaches to combat it, otherwise the infections it causes will become untreatable.
