Weber is now investigating how fertilizer derived from human sewage may contribute to the spread of antibiotic-resistant genes. “We’ve done a good job designing our treatment plants to reduce conventional contaminants,” he says. “Unfortunately, no one has been thinking of DNA as a contaminant.” In fact, sewage treatment methods used at the country’s 18,000-odd wastewater plants could actually affect the resistance genes that enter their systems.
Every tested strain in a dirt sample proved resistant to multiple antibiotics.
Most treatment plants, Weber explains, gorge a relatively small number of sludge bacteria with all the liquid waste they can eat. The result, he found, is a spike in antibiotic-resistant organisms. “We don’t know exactly why,” he says, “but our findings have raised an even more important question.” Is the jump in resistance genes coming from a population explosion in the resistant enteric, or intestinal, bacteria coming into the sewage plant? Or is it coming from sewage-digesting sludge bacteria that are taking up the genes from incoming bacteria? The answer is important because sludge bacteria are much more likely to thrive and spread their resistance genes once the sludge is discharged into rivers (in treated wastewater) and onto crop fields (as slurried fertilizer).
Weber predicts that follow-up studies will show the resistance genes have indeed made the jump to sludge bacteria. On a hopeful note, he has shown that an alternative method of sewage processing seems to decrease the prevalence of bacterial drug resistance. In this process, the sludge remains inside the treatment plant longer, allowing dramatically higher concentrations of bacteria to develop. For reasons that are not yet clear, this method slows the increase of drug-resistant bacteria. It also produces less sludge for disposal. Unfortunately, the process is expensive.
Drying sewage sludge into pellets—which kills the sludge bacteria—is another way to contain resistance genes, though it may still leave DNA intact. But few municipal sewage plants want the extra expense of drying the sludge, and so it is instead exported “live” in tanker trucks that spray the wet slurry onto crop fields, along roadsides, and into forests.
Trolling the waters and sediments of the Cache la Poudre, Storteboom and Pruden are collecting solid evidence to support suspicions that both livestock operations and human sewage are major players in the dramatic rise of resistance genes in our environment and our bodies. Specifically, they have found unnaturally high levels of antibiotic resistance genes in sediments where the river comes into contact with treated municipal wastewater effluent and farm irrigation runoff as it flows 126 miles from Rocky Mountain National Park through Fort Collins and across Colorado’s eastern plain, home to some of the country’s most densely packed livestock operations.
“Over the course of the river, we saw the concentration of resistance genes increase by several orders of magnitude,” Pruden says, “far more than could ever be accounted for by chance alone.” Pruden’s team likewise found dangerous genes in the water headed from local treatment plants toward household taps.
Presumably, most of these genes reside inside live bacteria, but a microbe doesn’t have to be alive to share its dangerous DNA. As microbiologists have pointed out, bacteria are known to scavenge genes from the spilled DNA of their dead.
“There’s a lot of interest in whether there’s naked DNA in there,” Pruden says of the Poudre’s waters. “Current treatment of drinking water is aimed at killing bacteria, not eliminating their DNA.” Nobody even knows exactly how long such free-floating DNA might persist.
All this makes resistance genes a uniquely troubling sort of pollution. “At least when you pollute a site with something like atrazine,” a pesticide, “you can be assured that it will eventually decay,” says Graham, the Kansas environmental engineer, who began his research career tracking chemical pollutants like toxic herbicides. “When you contaminate a site with resistance genes, those genes can be transferred into environmental organisms and actually increase the concentration of contamination.”
Taken together, these findings drive home the urgency of efforts to reduce flagrant antibiotic overuse that fuels the spread of resistance, whether on the farm, in the home, or in the hospital.
For years the livestock pharmaceutical industry has played down its role in the rise of antibiotic resistance. “We approached this problem many years ago and have seen all kinds of studies, and there isn’t anything definitive to say that antibiotics in livestock cause harm to people,” says Richard Carnevale, vice president of regulatory and scientific affairs at the Animal Health Institute, which represents the manufacturers of animal drugs, including those for livestock. “Antimicrobial resistance has all kinds of sources, people to animals as well as animals to people.”
The institute’s own data testify to the magnitude of antibiotic use in livestock operations, however. Its members sell an estimated 20 million to 25 million pounds of antibiotics for use in animals each year, much of it to promote growth. (For little-understood reasons, antibiotics speed the growth of young animals, making it cheaper to bring them to slaughter.) The Union of Concerned Scientists and other groups have long urged the United States to follow the European Union, which in 2006 completed its ban on the use of antibiotics for promoting livestock growth. Such a ban remains far more contentious in North America, where the profitability of factory-farm operations depends on getting animals to market in the shortest possible time.