There’s been excitement this week at the announcement of a new antibiotic. Called teixobactin by its discoverers, it is produced by a soil bacterium, also new to science because it needed the development of a novel system to enable it to grow and be tested in the laboratory for antibiotic production.
Teixobactin binds to lipid precursors of the bacterial cell wall. It protects mice against an experimental septicaemia caused by MRSA. Because of the way it works it could have a very broad spectrum of antibacterial activity. Its discoverers have not found mutants of Staphylococcus aureus (the SA in MRSA) or Mycobacterium tuberculosis that are resistant to it, and because it binds to a lipid and not to a mutable protein, they suggest that the development of resistance might be avoided.
So far so good. Teixobactin shows real promise. Of course clinical trials are needed to ensure safety and establish efficacy.
But it would be wise not to be too optimistic. There is a pattern that repeats itself depressingly often with a new therapeutic agent. It starts life as a wonder drug. It cures everything in sight. Side effects then emerge, and the mantra is ‘wouldn’t give it to a dog’. After further studies it is established in the pharmacopoeia as ‘useful with care for the following conditions’.
And as a firm believer in the power of evolution I reserve judgment about the possible inability to develop resistance. Bacteria beat antibiotics not just by selecting mutations in the targets themselves. Some change non-protein targets by selecting mutations in proteins that are involved in their synthesis. Others keep the antibiotics out by making the cell wall impermeable. Yet others fight them by speeding up excretion from inside the cell.
The only way to find out whether teixobactin resistance develops in clinical practice will be to use it. It will be good if it passes the safety and efficacy tests to enable that to happen. The need for new antibiotics is growing.