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Antibiotics have saved countless lives over the decades. Yet for the pathogens they kill, antibiotics are an old enemy, an enemy they are already adept at fighting.
It turns out that the spread of antibiotic resistance may not be as limited as we have assumed, giving more species much easier access to antibiotic resistance than previous models did. would suggest.
The findings come from a study conducted by bioinformatics researcher Jan Zrimec of Chalmers University of Technology in Sweden, which looked for signs of mobility among pieces of DNA called plasmids.
If a genome were a cookbook, plasmids could be imagined as slips of paper with prized recipes stolen from friends and relatives. 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.
While we’ve been using them as a form of medicine for almost a hundred years, the truth is, we were simply inspired by a microbial arms race that might be almost as old as life itself.
While different species of microbes have concocted new ways to prevent the growth of their bacterial competitors through the ages, bacteria have come up with new ways to overcome them.
These defenses are often preserved in the encoding of a plasmid, allowing bacterial cells to easily share resistance through a process called conjugation. If the word conjures up thoughts of meeting on prison visitation, you have to push your imagination a little further to imagine it … between single-celled organisms.
In order for plasmids to be widely distributed among cells in a bacterial speckle act, they must have a genetic coding region called the origin.–of–transfer sequence, or oriT.
This sequence is what engages with an enzyme that cuts the plasmid for easy copying and then closes it. Without oriT, a plasmid’s secret recipe is destined to remain in the possession of its owner.
In the past, it was believed that each plasmid had to have both oriT and a code for the enzyme in order for it to be shared in acts of conjugation.
Today, it is clear that the enzyme is not necessarily specific to a particular oriT sequence, which means that if a bacterial cell contains many plasmids, some could benefit from the enzymes encoded by others.
If we want to create a catalog of plasmids that can be shared – including those with instructions for antibiotic resistance – we just need to know how many contain an oriT sequence.
Unfortunately, finding and quantifying these sequences is a long and laborious job. Zrimec has therefore developed a much more efficient way of finding oriT based on unique characteristics of the physical properties of the encoding.
He applied his findings to a database of over 4,600 plasmids, calculating the frequency of motile plasmids based on the prevalence of oriT.
It turns out that we were probably far off the mark in how often this essential streak is found, with Zrimec’s results being eight times higher than previous estimates.
Taking other transfer factors into account, it could mean that there are twice as many motile plasmids among bacteria as we imagined, with twice as many bacterial species in their possession. And that’s not all.
There was another discovery made by Zrimec which is of concern.
“Plasmids belong to different mobility groups, or MOB groups, so they cannot be transferred between any bacterial species,” Zrimec explains.
Yet his research now suggests that half of the oriT sequences he found matched to conjugating enzymes from a different MOB group, suggest that the boundaries between bacterial species may be more permeable to plasmids than we also thought.
All of this is disturbing news in light of the race to develop new antibacterial treatments.
“These results could imply that there is a strong network of plasmid transfer between bacteria in humans, animals, plants, soil, aquatic environments and industries, to name 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 transferred to bacteria that cause disease in humans.”
It is an arms race we have entered to save lives – never imagining how competent bacteria would be to match our firepower.
Technology like this will help us better understand what we are facing. And already, it is not pretty.
This research was published in Open microbiology.
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