Harmless bacteria from American soils carry the same antibiotic-resistance genes as many pathogenic microbes around the world, suggesting there is a secret arms trade running between the bacteria in our soils and those that ravage our bodies with disease. Such a trade has long been suspected, but Gautam Dantas from the Washington University School of Medicine in St. Louis has now found the clearest evidence for it. “The genes are 100 percent identical,” he said.
The research, published today (August 30) in Science, confirms that soil bacteria are an important reservoir of resistance genes, serving as an ancient stockpiles of shields and armor that disease-causing microbes can tap into. This may have contributed to the recent rise in multidrug-resistant microbes. “[The movement of] resistance between environment and clinic becomes a certainty rather that a hypothetical threat,” said Gerry Wright, a microbiologist at McMaster University, who was not involved in the research.
Both Dantas and Wright have previously shown that soil bacteria are loaded with antibiotic-resistance genes, which were similar to those responsible for clinical resistance. The idea was that the use of antibiotics to rear livestock or control plant bacteria creates a strong evolutionary pressure for drug resistance among soil microbes. Genes conferring that resistance can find their way into the microbes that infect humans.
But proof of transfers from soil to clinic has been scarce. After all, Wright has shown that these resistance reservoirs are thousands, if not millions, of years old. And until now, scientists have only documented two examples of free-living bacteria with identical resistance genes to clinical pathogens.
Dantas has now found several more with resistance genes that match base pair-for-base pair with bacterial strains isolated in the clinic. Together with lab members Kevin Forsberg and Alejandro Reyes, he isolated antibiotic-resistant bacteria from 95 cultures derived from soils at 11 sites throughout the United States. They then extracted fragments of DNA from the resistant microbes, and tested them for their ability to confer antibiotic resistance in the common gut bacterium Escherichia coli. In this way, the researchers found 110 resistance genes, around half of which were new to science.
Seven of these genes were exactly identical to those previously recovered from pathogens in clinical samples from all major continents, including common opportunists like Pseudomonas aeruginosa and the plague bacterium Yersinia pestis. These genes allow bacteria to resist five different classes of antibiotics, by hiding from the drugs, pumping them out, modifying them, or destroying them outright.
These results clearly show that soil bacteria are trading genes with their clinical counterparts. “It’s strong confirmation of suggestive data that we’ve been seeing for the last 4 to 5 years,” said David Graham, a microbiologist at Newcastle University who did not participate in the study.
These transfers probably happened recently. Five of the shared genes are flanked by extensive pieces of DNA that are also a match between soil and clinical samples. Since bacteria accumulate mutations very quickly, such perfect similarity suggests that these sequences are fresh trades, which have not had much time to diverge.
Bacteria can also swap many genes at a time. Some of the seven genes that Dantas identified sit in large clusters, flanked by sequences which make it easier for them to move between microbial species. This means that a susceptible bacterium could pick up the ability to resist many different antibiotics in one fell swoop.
Dantas cautioned that while his study “shows that gene flow is occurring,” it does not indicate “the direction in which it occurs.” Human pathogens could have made their way into the environment and shared their genes with the soil bacteria there, or conversely, soil microbes could have somehow ended up in patients. “The likeliest scenario in my mind is that resistance genes are moving in both directions,” said Dantas.
One possible route to gene sharing is the beneficial bacteria in our guts act, which could as couriers for resistance genes, handing them from soil bacteria we ingest with contaminated food to the pathogens that are infecting us at the same time. Indeed, one of the genes that Dantas identified has also been found in a human gut bacterium.
“There still isn’t a proven pathway from sites like soils to an organism in your gut that’ll make you ill,” Graham said.
K. Forsberg et al., “The shared antibiotic resistome of soil bacteria and human pathogens,” Science, doi: 10.1126/science.1220761.