Microbes have developed a quick and effective way to exchange genetic information coding for antibiotic resistance, other functions.

Just as the digital age allows people to exchange information instantly, bacteria linked to humans and their livestock also seems to freely and rapidly exchange genetic material related to human disease and antibiotic resistance through a mechanism called horizontal gene transfer (HGT).

Research leader Eric Alm of MIT’s Department of Civil and Environmental Engineering and Department of Biological Engineering says in a paper published in Nature online that he and his team have found evidence of an enormous network of recent gene exchange that connects bacteria from around the world: 10,000 unique genes flowing via HGT among 2,235 bacterial genomes.

Scientists have long known about HGT, an ancient method for bacteria from different lineages to acquire and share useful genetic information that they did not inherit from their parents. They know, that when a transferred gene is bestowed with a desirable trait, for example antibiotic resistance or pathogenicity, it may undergo positive selection and be passed on to a bacterium’s own descendant. This can be detrimental to humans, as seen in the proliferation of antibiotic-resistant bacteria strains in so-called “super bugs.”

Until now, scientists did no know how much or how rapidly this information was being exchanged, however, MIT researchers have managed to illustrate the vast scale and rapid speed with which genes can proliferate across bacterial lineages.

Alm, the Karl Van Tassel Associate Professor explains:

“We are finding [completely] identical genes in bacteria that are as divergent from each other as a human is to a yeast. This shows that the transfer is recent; the gene hasn’t had time to mutate.”

Computational systems biology graduate student Chris Smillie, one of the lead authors of the paper says:

“We were surprised to find that 60% of transfers among human-associated bacteria include a gene for antibiotic resistance.”

These resistance genes might be associated with using antibiotics in industrial agriculture because researchers discovered 42 antibiotic-resistance genes that were shared between livestock- and human-associated bacteria. This demonstrates a crucial link that connects pools of drug resistance in human and agricultural populations.

Alm comments:

“Somehow, even though a billion years of genome evolution separate a bacterium living on a cow and a bacterium living on a human, both are accessing the same gene library. It’s powerful circumstantial evidence that genes are being transferred between food animals and humans.”

The researchers furthermore identified 43 independent cases of antibiotic-resistance genes crossing between nations. Mark Smith, microbiology graduate student and also a lead author of the study warns:

“This is a real international problem. Once a trait enters the human-associated gene pool, it spreads quickly without regard for national borders.”

The U.S. has a widespread practice of adding prophylactic antibiotics to animal feed to promote growth and prevent the spread of disease in densely housed herds and flocks. This is banned in many European countries. The Federal Drug Administration states that over 80% of the 33 million pounds of antibiotics, including penicillins and tetracyclines commonly used as human medicines, were sold in the U.S. in 2009 for agricultural use, with 90% being administered sub therapeutically through food and water.

The researchers discovered that HGT occurs more frequently amongst bacteria occupying the same body site, share the same oxygen tolerance or have the same pathogenicity. This leads to the conclusion that ecology, or environmental places, are more important to whether a transferred gene will be incorporated into a bacterium’s DNA and passed on to its descendants than either lineage or geographical proximity in determining.

Alm explains:

“This gives us a rulebook for understanding the forces that govern gene exchange.”

By applying these rules in order to discover genes that are linked to the ability to cause meningitis and other diseases, the team hopes that transferred traits and the genes encoding those traits might pave the way for especially promising targets for future drug therapies.

They are continuing their work and are currently comparing exchange rates amongst bacteria living in separate sites on the same person and amongst bacteria living on or in people who suffer from the same disease. They are also studying an environmentally contaminated site to establish which swapped genes might facilitate microbial cleanup by metal-reducing bacteria.

Co-authors of the Nature paper are graduate student Jonathan Friedman, postdoc Otto Cordero and former graduate student Lawrence David, now at Harvard University.

The research is part of the National Institutes of Health’s Human Microbiome Project and was funded by the Department of Energy’s ENIGMA Scientific Focus Area and the National Science Foundation.

Written by: Petra Rattue