Defining, dealing with and solving the controversial issue of the role that food animal production plays in antibiotic-resistant bacteria should be simple. All you have to do is answer four simple questions, says Randy Singer, an epidemiologist in the College of Veterinary Medicine at the University of Minnesota: what is resistance, how does it develop, where does it come from, and when is it going away?
While those are simple questions, easy answers have thus far proved elusive. In fact, answers of any kind have proved to be nearly impossible to find.
For example, Singer says to consider the question of how antibiotic resistance develops. Conventional wisdom would have you believe that non-therapeutic antibiotic use in food animal production is causing antibiotic-resistant bacteria that somehow wind up in humans.
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But is that the real answer or just the most convenient? He says researchers went into a cave that hadn’t seen any human activity for 4 million years, collected bacterial samples and cultured them. “We see plenty of resistance to the same antibiotics we’re using today. So resistance isn’t new. Resistance has always been there.”
The problem, he suggests, is in how we look at bacterial resistance. We assume naturally-occurring antimicrobial compounds did back then what we want them to do now – conduct germ warfare.
“What we’re actually seeing now is these compounds are more like signaling modules, communities of bacteria interacting with each other and these antibiotic-like compounds seem to be molecules that inform others in the community about changes to the environment so they can respond to those changes.”
Thus, you have bacteria that are intrinsically resistant to antibiotics. “It’s not because of anything that developed over time,” he says.
Conventional wisdom which holds that antibiotic use creates resistant bacteria just got blown away. However, Singer says that while antibiotic use may not cause resistance, it may help in the spread of antibiotic-resistant bugs.
“What it looks more like is everyone is carrying some bacteria in them that have some resistance,” he says. “If you apply a treatment, you may amplify the amount of resistance that individual is carrying (by killing the susceptible bugs and leaving the resistant ones) which would give more opportunity for spread. But it’s not resistance that is developing.”
So, he says, the question is what kind of drug application is going to select for that resistant population? If you hit hard and hit early with a high dose of a medically-important antibiotic, you will select for the population of resistance that is already there.
“If you give a low dose of an antibiotic that is being used for growth promotion and feed efficiency, perhaps the selection pressure is a lot less and it wouldn’t have the effect on the resistant population as strongly as the hit-hard, hit-early drugs that you would use in therapy.”