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Mutations that allow the bacteria that cause tuberculosis to resist key drugs do not necessarily limit their ability to compete with non-resistant relatives as has been thought.
The finding, published today (30 June) in Science has implications for efforts to control the disease.
It suggests that bacteria with certain genetic make-ups that confer resistance to the two most potent tuberculosis (TB) drugs are more likely to spread in human populations.
Although multi-drug resistant TB is treatable, it takes up to two years and can cost 100 times more than treating regular TB.
Previous studies suggest that drug-resistance comes at a cost to bacteria, making them less likely to survive if they have to compete for scarce resources.
The authors of the new study, led by Sebastien Gagneux of Stanford University in the United States, tested the theory with TB-causing bacteria in the laboratory.
They found that the ability of the resistant bacteria to compete depended on the mutations they had acquired to become resistant, as well as their genetic strain.
Most drug resistant bacteria lost out to their non-resistant relatives when grown in the absence of drugs. But for other drug-resistant forms there was little or no loss in ability to compete.
The researchers say one of these forms accounts for 54 per cent of TB bacteria isolated in clinics worldwide that can resist the drug rifampin.
Ruth McNerney who studies TB at the London School of Hygiene and Tropical Medicine says the study is interesting but is “a small part of a big picture”.
Stephen Gillespie, a TB expert at the Royal Free Hospital in the United Kingdom, agrees. “This is an important piece of work,” he says, “but it is important to realise that bacterial [ability to survive] is context-dependent and previous work has shown that identical strains fare differently in different patients.”