A glimmer of hope
The use of antibiotics exerts a Darwinian selection pressure for acquisition of resistance by the target bacteria, and resistance arising anywhere in the microbial world can ultimately be transferred to disease-causing bacteria. In addition, the antibiotic discovery process is now in terminal decline. The golden age of antibiotics took place in the 1930s to 1970s, with at least 11 new classes discovered; since then there have been only two new classes of antibiotics.
What’s worse is that many antibiotics are ‘broad spectrum’, meaning they kill loads of different bacteria, good or bad. Consider them weapons of mass destruction, dropped on a precision target – the ‘collateral damage’ can be huge and even lead to new infections (e.g. C. difficile).
But there is hope:
My research over 37 years involved the study of a number of bacteriocins that can kill a range of clinically important bacteria. I – and many other researchers – did not believe they could be useful clinically because injecting a “foreign” bacterial protein into a patient is likely to induce a severe immune response that would make the antibiotic inactive. There were therefore gasps of amazement in Beijing at data presented from several animal studies showing this was not the case.
If you consider a killing domain as a red Lego brick and a targeting domain as a yellow Lego brick, you can make hundreds of different hybrid proteins consisting of one red and one yellow brick to make what I refer to as a series of novel bacteriocin-derived antibiotics (BDAs). In fact, several BDAs have already been designed to kill target bacteria, fungi and even tumour cells.
The ability to use the BDA system to continually make novel antibiotics significantly de-risks the development of antibiotics process and in my opinion offers a significant ray of hope in the present gloom. It is now for governments and health organisations to make sure they make the most of this unexpected breakthrough.