Key Points
- Scientists have traced the 100-year history of multidrug resistance in bacteria.
- They found that a small group of genetic structures called “plasmids” is the main culprit.
- These plasmids evolved to carry resistance genes only after the widespread use of antibiotics became common.
- The discovery could lead to new therapies that target these plasmids directly.
Scientists have mapped 100 years of bacterial evolution to pinpoint the genetic culprits behind the rise of deadly, drug-resistant superbugs. In a groundbreaking new study, researchers found that a small group of “plasmids”—tiny, transferable pieces of DNA—is responsible for spreading the majority of multidrug resistance worldwide.
The team, which included experts from the UK and the University of Bath, analyzed a massive dataset of over 40,000 bacterial samples, some dating back to 1917, before the discovery of antibiotics. They found that the original, ancestral plasmids didn’t carry any resistance genes. It was only after the widespread use of antibiotics that these plasmids evolved to become the global super-spreaders of drug resistance we see today.
The research, published in Science, identified two primary mechanisms by which these dangerous plasmids originated. Either they picked up resistance genes and incorporated them into their own structure, or they fused with other plasmids to become more powerful and more easily transferable between different types of bacteria.
This is a breakthrough because it gives scientists a clear target. By understanding how these specific plasmids function, we may be able to develop new therapies that target the plasmids themselves, rather than just the bacteria. This could be a novel approach to combating a wide range of drug-resistant infections.
The study also created a new model for how these plasmids evolve, which could help us predict how superbugs will spread in the future. This could be a powerful tool for public health officials trying to stay one step ahead of the next big outbreak.
