Deadly bacteria can share antibiotic resistance faster than we thought

Antibiotics have saved countless lives over the decades. But according to the pathogens they kill, antibiotics are an old enemy, one they are already capable of fighting.

It turns out that the spread of antibiotic resistance may not be as limited as we assumed, giving more species much easier access to antibiotic resistance than previous models would have us believe.

The findings come from a study conducted by bio-informatics researcher Jan Zrimec of Chalmers University of Technology in Sweden, which looked at signs of mobility among elements of DNA called plasmids.

If a genome is a cookbook, plasmids can be represented as loose pieces of paper with precious recipes stolen from friends and family members. Many contain instructions for making materials that can help bacteria survive under stressful conditions.

And for bacteria, a dose of antibiotics is about as stressful as it gets.

Although we have been using it for a better part of a hundred years as a form of medicine, it is true that we have simply been inspired by a microbial arms race that can be almost as old as life itself.

As different types of microbes have devised new ways to stimulate the growth of their bacterial competitors over the centuries, bacteria have devised new ways to overcome them.

These defenses are often preserved in the encoding of a plasmid, allowing bacterial cells to share resistance through a process called conjugation. If the word evokes thoughts about encounters during prison visits, you just have to stretch your imagination to imagine it … between unicellular organisms.

To spread plasmids widely between cells in an act of bacterial hanky-panky, they must possess a region of genetic coding called an origin.oftransfer order, or oriT.

This sequence is associated with an enzyme that cuts the plasmid open for easy copying, and then reseals it. Without oriT, the secret recipe of a plasmid is destined to remain in the possession of its owner.

In the past it was believed that each plasmid must possess both oriT and a code for the enzyme in order to divide it into conjugation sections.

Today, it is clear that the enzyme is not necessarily specific for a specific oriT sequence, which means that if a bacterial cell contains numerous plasmids, some may benefit from the enzymes encoded by others.

If we want to compile a catalog of plasmids that can be shared – including those containing antibiotic resistance instructions – we simply need to know how much an oriT sequence contains.

Unfortunately, finding and quantifying these series is a time-intensive and arduous task. Thus, Zrimec has developed a much more efficient way of searching for oriT, based on unique properties of the physical properties of the coding.

He applied his findings to a database of more than 4,600 plasmids, calculating how common mobile plasmids were based on the occurrence of oriT.

It seems that we were probably far from the point in how common this essential series is, with the results of Zrimec eight times higher than those of previous estimates.

If we consider other transmission factors, it could mean that there are twice as many mobile plasmids among bacteria as we thought, with twice as many bacterial species in possession. And that is not all.

There was another discovery that Zrimec made that is a cause for concern.

“Plasmids belong to different mobility groups, or MOB groups, so they can not just transmit any bacterial species,” says Zrimec.

However, his research now points to half of the oriT series that he said found entirely conjugation enzymes from another MOB group, suggesting that the boundaries between bacterial species would be more permeable to plasmids than we also thought. has.

All of this is worrying news in light of the race to develop new antibacterial treatments.

“These results may imply that there is a robust network for the transmission of plasmids between bacteria in humans, animals, plants, soil, aquatic environments and industries, to name a few,” says Zrimec.

“Resistance genes naturally occur in many different bacteria in these ecosystems, and the hypothetical network could mean that genes from all of these environments could be transferred to bacteria that cause disease in humans.”

It’s an arms race in which we started saving lives – and we never imagined how skilled bacteria would be to match our firepower.

This technology will help us better understand what we are facing. And even if it does not look pretty.

This research was published in Microbiology open.

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