Leading Antibiotic Doomsayer Mellows on Infection Armageddon
A new realm of narrow-spectrum antibiotics offers new hope, Richard James explains.
In 2007, Richard James, then a microbiologist at the University of Nottingham in the UK, began raising some of the first warnings of an impending cataclysm. The antibiotics that have largely enabled the modern world—turning once-deadly bacterial infections into something eminently treatable—were failing. It was beginning in hospital patients, but as a potential threat, increasingly drug-resistant bacteria were something far more general and far more lethal.
At the time, James was pilloried as a "sensationalist and scaremonger" by the UK Department of Health's chief nursing officer. He was soon enough vindicated, as the antibiotic resistance problem became an increasingly public and increasingly deadly concern. Drug development had stalled, but the bacteria were just getting started. Two years ago, England's chief medical officer declared that, "the rise in antibiotic resistance is comparable to the threat of global warming," while a 2014 report estimated that by 2050 superbugs would be killing 390,000 annually in Europe and 310,000 annually in the US.
James recounts all of this in a new op-ed for the Guardian, but his larger point is unexpectedly optimistic. The OG doomsayer has found not just hope but something like assurance about the bacterial infection future thanks to a new class of "exquisitely narrow-spectrum" antibiotics, revealed recently at a workshop in Beijing.
The new narrow-spectrum antibiotics are able to target specific varieties of bacteria thanks to proteins called bacteriocins. These are what the bacteria themselves use to knock off other bacteria, especially ones that happen to be really similar to themselves and, thus, competing for the same resources.
"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," James writes. "There were therefore gasps of amazement in Beijing at data presented from several animal studies showing this was not the case."
The number of potentially useful protein combinations is vast. A single target bacteria and a single killing bacteria could have hundreds of possible bacteriocins between them, with each one offering a novel bacteriocin-derived antibiotic (BDA).
"The ability to use the BDA system to continually make novel antibiotics significantly de-risks the development of antibiotics process," James concludes, "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."
And if you're going to take hope from anybody, Richard James is probably a sure bet.