Magdalena Kawalec-Segond. Ineffective antibiotics and stubborn semi-live bacteria

On November 18, we celebrated the European Antibiotic Awareness Day. It passed almost unnoticed in the media preoccupied with the Cronavirus pandemic, which is clearly getting out of control (which will end up with around 50,000 excess deaths) and what is happening on our eastern border. The day before, in Nature, microbiologists from Israel described a new state of functioning of “stressed” bacterial cells, which would require even smarter approach to antibiotic therapy. Perhaps studying it in-depth will allow the development of antibiotics to which bacteria will be much more difficult to become resistant.

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The main purpose of such a day is to draw attention and raise the awareness of society, politicians and medical specialists to the phenomenon of the growth and spread of antibiotic resistance among microorganisms that cause human infections. I have written about this issue many timesbecause the problem has been growing rapidly for at least a quarter of a century.

It has many sources in our psychology and economy, and not only in the genetic variation inherent in bacteria, which is selected in hospitals with the mass use of various antibiotics. So Darwinian evolution in action, which we can see with the naked eye, although bacteria are invisible to it.

We see mainly because bacteria multiply very quickly and therefore mutate quickly. And antibiotic resistance is often due to mutations that make the battery immune to the drug. Or, it can destroy the antibiotic molecule before it works and kills the bacteria.

We are not generally learned microbiologists or physicians. However, each of us can join the rescue of antibiotics – drugs of last resort in bacterial infections. Because people are already dying of diseases caused by multiresistant bacteria, such as tuberculosis, gonorrhea, New Delhi (Klebsiella pneumoniae), meticilino- and vancomycin-resistant staphylococci, a stick of blue oil sensitive only to colistin, or to nothing, and 40 years more to this God of the spirit enterococci, which in the meantime have become immune to everything.

Bacteria have antibiotic resistance genes encoded in their DNA – often on the so-called moving parts, i.e. types of genetic suitcasesthat easily move between even unrelated bacteria. Thus, antibiotic resistance spreads not only “vertically” exponentially – from bacteria resistant to its progeny, but also “across” or horizontally, between unrelated bacteria.

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How can we save antibiotics in our everyday life? When taking antibiotics, follow your doctor’s instructions, i.e. three times a day means every eight hours instead of anytime, and two tablets means two, not one – or vice versa.

If possible, prevent infection by vaccination. Regularly wash children’s hands and hands, for example after sneezing or coughing, before touching other objects or people. Antibiotics should only be used on a prescription, do not use residues from previous treatments or over-the-counter antibiotics.

Ask your pharmacist how to dispose of any unused medicine and do not throw it away in the trash. And above all, not to force doctors to prescribe an antibiotic – they can generally tell what type of infection we are dealing with: viral where antibiotics will not work, or bacterial.

Bacteria have been here for 3.5 billion years, we – in even the most distant and original form – for 2 million years. So who has a better chance against nature? Of course, we have a brain, and this is our only advantage, because we neither multiply as fast as they do, nor evolve at a reverse pace under the pressure of selection – the massive use of antibiotics, nor quickly adapt to some new, completely alien environment.

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Thanks to the results of the work of scientists, i.e. the human brain, since Alexander Fleming was awarded the Nobel Prize for the discovery of penicillin, the world’s population has more than tripled. And that’s only 75 years. Three generations. However, Fleming said during his Nobel Prize lecture that antibiotic resistance would rise and spread.

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It was 1945, he knew nothing about DNA, about the mutations in it, and about the moving parts of the genome, like the plasmids and transposons that carry drug resistance genes en masse between bacteria.

Antibiotics put bacteria – like other agents – into a state of severe life-threatening stress. This stress, and in addition, on single bacterial cells, has been studied for years by a group of scientists from the Hebrew University in Jerusalem under the supervision of Nathalie Balaban. In an experiment reported in the latest publication, Nature, they investigated the dynamics of single cells that had been subjected to acute stress, too intense to regulate the response, but not lethal.

When bacterial growth has been arrested by acute, transient exposure to potent inhibitors (generally actions such as antibiotics), it has been observed that the same stress (same concentration of bacterial growth inhibitor), applied rapidly or gradually, can lead to completely different dynamics of regeneration. Regeneration in bacteria – since they are essentially unicellular and we study a single cell – is the state of cell division resumption. By measuring the dynamics of regeneration after exposure to stress on thousands of cells, it was shown that the mathematical model used could predict the result of antibiotic persistence measurements.

It must be understood that the action of antibiotics is most often based on inhibiting the growth of the bacterial cell (e.g. penicillins inhibit the building of the cell wall, gentamicin or streptomycin inhibit the action of the bacterial ribosome). Thus, this cell stops growing (the so-called bacteriostatic effect) and is unable to divide.

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In general, he is unable to remain in such detention for long. Thus – especially when faced rapidly with high drug concentrations – it simply cannot continue to maintain cell integrity and literally ruptures or spills beyond the cell sheaths.

However, some cells, especially those that were dormant, were not growing at any given point in time and were not dividing extensively; when the concentration of the antibiotic was below the lethal concentration, they can somehow survive the attack while dormant.

Results of Israeli researchers focused on this state of “hibernation” in response to stress can explain the ubiquitous phenotype of antibiotic resistance, which very often cannot be linked to specific ‘resistance genes’. It turns out, therefore, that under the influence of stress, two different cellular states can be observed: the regulated state, which prepares cells for quick recovery, and the state disturbed as a result of acute stress, with slow and heterogeneous dynamics of regeneration. A better understanding of the latter, the researchers say, could shed new light on cell survival and evolution under stress.

Stress reactions enable cells – including bacterial ones – to adapt to changes in external conditions by activating specific metabolic and / or developmental pathways. And what doesn’t kill us, makes us stronger, does it? Well, bacteria have the same philosophy of life, and we have to think: discoverers or developers of new antibiotics, the pharmaceutical companies that produce them, the doctors who prescribe them, and the patients who take them.

We have to think about how realistically bacteria respond to antibiotics. Because from such one tireless, stubborn cell that can handle it, a whole big infection can regenerate. The idea is to minimize this possibility. To save the miracle of modern medicine, which undoubtedly are antibiotics.

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About Peter Wilson

In love with technology, with an eye towards smartphones, he does not disdain any activity linked to the Nerd world. TV series, movies, manga, anime, and comics (Marvel addicted) are the order of the day.

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