The antibiotic era was barely 20 years old when people started raising concerns about using the new “miracle drugs” in agriculture. Penicillin first entered use in 1943, streptomycin in 1944, tetracycline in 1948 — and by 1965, the United Kingdom’s Agricultural Research Council was hearing testimony that organisms common in food animals, especially Salmonella, were becoming resistant to the antibiotics being used on the animals while they were alive. By 1969, the UK government had compiled an official report outlining the danger, and by 1973, a task force of the US Food and Drug Administration had concurred, and concluded the only safe action was to withdraw approval to use antibiotics in animals. (At which, as we now know, they would never be successful.)

The policy difficulty regarding this long-recognized problem has never been the emergence of resistant bacteria on farms; no one seriously disputes that resistance emerges whenever antibiotics exert selective pressure on bacteria, killing the vulnerable and opening an ecological niche into which the surviving not-vulnerable can expand. The  sticking point has been the difficulty of proving that those resistant bacteria depart from farms, cross to humans, and cause resistant illness in them. Stuart Levy demonstrated it in 1976, on an experimental farm plot he set up just to make the proof. Most of the rest of the research, though — and after decades, there are hundreds of pieces of research — has been observational and retrospective: Looking at the drugs administered to populations of animals (about which we have very little data), measuring the antibiotic-resistant illness that arises in the human population, and making increasingly sophisticated backward matches between the resistance factors that show up in humans and the drugs that are deployed primarily on farms.

Demonstrating the bacterial traffic prospectively and experimentally, as Levy did, is challenging not just logistically but also ethically. It is difficult to imagine a study design that could trace specific animals, their meat, and their eaters in a large group of free-living humans; and unless you have volunteers, as Levy did, the study would push ethical boundaries as well. But having that lack of definition in the middle of the animal-to-human bacterial flow permits uncertainty — which proponents of continued ag antibiotic use exploit.

A new study of Danish farmers and their livestock may have ended that uncertainty. It is still retrospective, but its observations — using whole-genome sequencing — are so fine-grained that their tracing of the bacterial traffic seems to me to be difficult to challenge.

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A paper released recently, by the University of Iowa team that is the lone US research group tracking “pig MRSA” ST398, caused a ripple. (It came out while I was at ScienceOnline and it’s taken me a while to catch up.) The paper compares the occurrence of MRSA, drug-resistant staph, on various cuts of retail pork from pigs that were raised either conventionally in confinement, with routine use of antibiotics, or in an alternative rearing scheme with no antibiotics. (NB: Not “organic,” despite what some headlines said; that’s a separate issue of USDA licensure.) The team found that both conventionally raised and antibiotic-free meat carried MRSA, both the human-associated kind and the pig-adapted kind.

The TL;DR over the past week has been: There’s just as much resistant bacteria on drug-free meat as there is on conventional meat, so why spend the money — or raise the alarm over farm antibiotic use?

My interpretation is a little more nuanced. But my takeaway is that, in its underlying data, the study proves what campaigners against ag antibiotic use keep saying: that once you use antibiotics indiscriminately and drive the emergence of resistant organisms, you have no way of predicting where that resistance DNA will end up.

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