Ok, so this is nothing new. We’ve been hearing about returning to the “pre-antibiotic” era for years now. So when I first heard the news news out of China, about resistance to polymyxin antibiotics (a resistance found in both food animals treated with the stuff, and patients hospitalized with infections) I wondered why all the fuss over this one?
To begin with, the polymyxins are an old class of antibiotics (discovered in the late 1940s) and used to treat a range of infections until a few decades ago following reports that the drug also caused serious kidney disease. But then, with the rise of antibiotic resistant bacteria and the fall one antibiotic after another – polymyins were revived.
Since they hadn’t been used in decades – bacteria remained sensitive. Combined with research suggesting that the drug could be used without the high risk of kidney disease, colistin, a type of polymyxin antibiotic, once again became popular.
Unfortunately Chinese pig farmers (and, others around the globe) had been using colistin too, by the ton. Here’s a quote from an article in the Guardian:
“China is one of the world’s largest users and producers of colistin for agriculture and veterinary use. Worldwide, the demand for colistin in agriculture is expected to reach almost 12,000 tonnes a year by the end of 2015, rising to 16,500 tonnes by 2021.”
And so, inevitably, bugs like E. coli which normally resides peacefully in our intestines (although some strains can be quite nasty) as well as the intestines of other animals — like those pigs in China — began resisting the stuff. Mutating, surviving, evolving.
But here’s the catch. Usually, according to these reports, resistance arises in populations by mutation. Bad enough, but it meant that the mutation was relatively contained to that particular population (although could still spread if you happened to become infected by a member of that resistant population.)
What’s new here is that researchers have found a gene for resistance that resides on a plasmid in E. coli. Plasmids are circular bits of DNA that bacteria can pass like a bit of gossip from one bacterium to another. While bacteria reproduce by splitting apart (making little clones) they aren’t completely celibate. Sometimes bacteria engage in microbial hanky-panky and actually conjugate, joining together passing plasmids from one to the other.
One E. coli may pass its plasmid – and its resistance – to another strain of E. coli (like the infamous E. coli 0157). Or, it may even engage with an all-together different kind of bacterium, like Klebsiella pneumoniae – notorious for causing pneumonia and other hospital acquired infections.
The concern of course is that colistins have become an antibiotic of last resort. Now we not only have resistance in a common bacterium but one that is ready and able to share.
Despite the gloom and doom scenario there is hope. And it may not come in the form of a traditional antibiotic (though there is at least one new one out there.)
From bacteriocins, highly specific killer chemicals produced by bacteria (in contrast to most of our broadly acting antibiotics) to bacteriophages, viruses that attack specific bacteria (see phage therapy used across the Atlantic for nearly a century) the end of the antibiotic era may usher in an era of more directed and effective treatment (good news for our microbiome!). But more on that later.