A new study from researchers at the Trinity Translational Medicine Institute (TTMI) and the Irish Mycobacterial Reference Laboratory at St James’s Hospital has revealed how a hard-to-treat lung bacterium, Mycobacterium avium, changes and adapts inside patients over many years.
Their work helps explain why this infection often comes back and why antibiotics sometimes fail.
Mycobacterium avium is part of a group of germs known as non-tuberculous mycobacteria. Unlike the bacteria that cause tuberculosis, these ones are found naturally in water and soil.
They can infect people when the germs are breathed in, especially those who already have weak lungs or immune systems. Once inside the lungs, they can cause chronic infections that are very difficult to cure. This problem is becoming more common around the world.
Treating M. avium infections takes a long time—usually more than a year of several antibiotics taken together. Even then, up to half of patients don’t fully recover, and many become sick again later. Doctors have long wondered how this bacterium manages to survive for so long inside the lungs and how it develops resistance to treatment.
To find out, the research team studied nearly 300 bacterial samples collected from patients in Ireland, the UK, and Germany, including 20 Irish patients treated at St James’s Hospital in Dublin.
They used a powerful technique called whole-genome sequencing, which allows scientists to read every letter of the bacteria’s DNA. By comparing samples taken from the same patients over several years, the researchers could see exactly how the bacterium evolved and adapted inside the human body.
The results were fascinating. Instead of one single infection lasting for years, many patients were repeatedly infected with new strains of the bacterium.
Some of these strains were closely related to ones found in other European countries, suggesting that people might be picking them up from shared environmental sources like water or soil. This discovery challenges the idea that recurring infections always come from the same bacteria hiding in the lungs.
The scientists also found that the bacterium changes its DNA slowly—about one new genetic mutation per year. More importantly, they identified 13 specific genes that showed signs of adapting to survive in the harsh environment of the lungs.
These genes help the bacteria resist antibiotics, fight off the immune system, and survive in low-oxygen conditions. Some of them had never before been linked to the survival of this microbe.
Dr. Aaron Walsh, lead researcher at TTMI, explained that the study shows how M. avium evolves in real time inside the lungs. Understanding which genes help it survive could lead to new treatment targets.
His colleague, Dr. Emma Roycroft, added that some of the genes were involved in processes like forming biofilms—a sticky layer that helps bacteria cling to surfaces and resist drugs—and managing stress inside the body.
The researchers plan to continue their work by testing how these 13 genes function in the lab, using more advanced DNA sequencing to spot even smaller genetic changes, and studying environmental samples to find out where reinfections come from.
They also hope to include more patient groups in future studies to confirm whether the same genetic patterns appear elsewhere.
When reviewing these findings, one thing becomes clear: M. avium is not just a simple infection that lingers—it’s a shape-shifting survivor that can change and return even after long treatments.
This explains why some antibiotics lose their power over time and why new approaches are needed. Understanding how this bacterium adapts could help scientists develop smarter drugs and prevent repeated infections.
The study, published in Genome Medicine, offers hope for better ways to fight this stubborn infection. But it also serves as a reminder of how clever and persistent microbes can be—and how science must keep evolving to stay one step ahead.
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The study is published in Genome Medicine.
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