science

Killer bacteria could participate in antibiotic resistance faster than we thought

Killer bacteria could participate in antibiotic resistance faster than we thought

Antibiotics have saved countless lives over the decades. However, for the pathogens that kill it, antibiotics are an old enemy, and they are already adept at fighting.

It turns out that the spread of antibiotic resistance may not be as restricted as we assumed, giving more species much easier access to antibiotic resistance than we previously thought.

The results came from a study conducted by bioinformatics researcher Jan Zrimmek from Chalmers University of Technology in Sweden, which looked for markers of movement between DNA elements called plasmids.

If the genome is a cookbook, then the plasmids can be imagined as loose scraps of paper containing valuable recipes stolen from friends and relatives. Many of them contain instructions for making materials that can help bacteria survive stressful conditions.

And for bacteria, the dose of antibiotics is as cumbersome as it is.

While we have been using it as a form of medicine for the better part of a hundred years, the truth is that we have simply been inspired by a microbial arms race that may be as old as life itself.

As different types of microbes have devised new ways to stunt the growth of their bacterial competitors through the ages, bacteria have invented new ways to overcome them.

These defense measures are often preserved in plasmid encoding, allowing bacterial cells to easily share resistance through a process called conjugation. If this word raises thoughts of encounters during prison visits, you need to expand your imagination a little to portray it … among single-celled organisms.

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In order to widely distribute plasmids between cells to make bacterial tissues, they must possess a region of genetic coding called the parentFromTransfer sequence, or oriT.

This sequence is what It deals with an enzyme Which cuts the plasmid to open it for easy copying, and then closes it again. Without oriT, the confidential plasmid recipe would remain in its possession.

In the past, it was thought that each plasmid needed to possess both oriT and the enzyme code in order to participate in conjugation work.

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

If we want to come up with a catalog of plasmids that can be shared – including those that contain instructions for antibiotic resistance – we simply need to know how many contain the oriT sequence.

Unfortunately, finding and measuring these sequences is a daunting and time-consuming task so Zrimec has developed a more efficient method for searching for oriT based on the unique properties of the physical properties of the encoder.

He applied his findings to a database of more than 4,600 plasmids, and calculate how common mobile plasmids were based on oriT prevalence.

It turns out we might have been too far off the mark in how common this basic sequence was, with Zrimec’s scores being eight times higher than the results of previous estimates.

Taking other conversion factors into account, it could mean that there are twice as many mobile plasmids among bacteria than we imagine, with twice the number of bacterial species having. And this is not all.

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Another discovery Zrimec made is cause for concern.

“Plasmids belong to different kinetic groups, or MOB groups, so they cannot switch between any bacterial type.” Zrimec says.

However, his research now suggests that half of the oriT sequences he found suitable for conjugation enzymes from the MOB group are very different, suggesting that the boundaries between bacterial species may be more permeable to plasmids than we also thought.

All this is worrying news in the race to develop new anti-bacterial treatments.

“These results could indicate a robust network of plasmids transport between bacteria in humans, animals, plants, soil, aquatic environments, and industries, to name but a few.” Zrimec says.

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

It’s an arms race we got into in order to save lives – we never imagined how adept bacteria could match our firepower.

Technology like this will help us better understand what we are facing. Indeed, it doesn’t look pretty.

This research was published in Microbiology is open.

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