TUBERCULOSIS can "lurk" in patients' bone marrow where it is protected from drugs, according to a study which could explain why the disease often recurs years after treatment.
Taking antibiotics can spare sufferers the symptoms of tuberculosis, but doctors have never been able to prevent the condition resurfacing years or decades after the initial therapy.
Now researchers from Stanford University have discovered that the disease is capable of "infiltrating" cells in bone marrow which may protect it from treatments.
The cells have qualities like a natural resistance to drugs, infrequent division and a privileged immune status which could allow them to survive various types of treatment, the scientists explained.
In a study published in the Science Translational Medicine journal, the researchers reported that they had found active tuberculosis bacteria in the cells of human patients who had been treated for the disease.
It is possible that a host of other infectious diseases may use a similar "wolf-in-stem-cell-clothing" tactic to hide away from therapies, they suggested, although any new treatments will take many years to develop.
Traces of the bacteria were identified in mesenchymal stem cells, which can produce specialised cell types including bone, fat and cartilage.
Although the stem cells are typically found in the bone marrow they are also capable of moving to the lungs – the ideal environment for tuberculosis bacteria.
After testing their theory on mice in a previous study, the researchers carried out a small clinical trial in India where bone marrow biopsies were taken from nine patients who had been treated for tuberculosis and who had no traces of the bacteria in their respiratory tract.
In eight of the nine patients, bacterial DNA could still be found in bone marrow stem cells, and in two of these cases living bacteria were found.
Dr Bikul Das, lead author of the study, said: "Not only is this strong evidence that the tuberculosis can remain dormant in stem cells, but it shows that the living bacteria could be recovered from these cells after a long period of time.
"It's also very suggestive of how the reactivation could be triggered: These stem cells are known to migrate to sites of injury or inflammation and begin dividing. So, migrating stem cells harbouring dormant bacteria might reactivate the disease in the lung."
Dr Dean Felsher, co-senior author, added: "Other infectious agents might use stem cells in a similar manner. We'd like to further characterise whether and how these stem cells provide a protective niche for other infectious agents."
Nick Collins Telegraph.co.uk