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Researchers reveal how bacteria can adapt to resist treatment by antibiotics
In a joint collaboration, researchers from Denmark and Switzerland have shown that bacteria produce a specific stress molecule, divide more slowly, and thus save energy when they are exposed to antibiotics. The new knowledge is expected to form the basis for development of a new type of antibiotics.
All free-living organisms are under constant pressure to survive. Darwin dubbed this "survival of the fittest" and thus described how the best adapted species would have most offspring and therefore eventually end up propagating itself.
This fundamental principle is particularly prominent in the world of microorganisms, where free-living bacteria live in a constant fight to be the most well adapted and thus those who divide fastest in any given natural habitat. But when bacteria at the same time are exposed to deadly antibiotics, this fight becomes a question of balancing fitness, i.e. the ability to divide fast, with tolerance towards antibiotics. This amazing adaptability of bacteria is a contributing factor to the severity of infectious diseases in humans, including tuberculosis and severe urinary tract infection, for which the disease often resurfaces after treatment has ended.
In a new research paper, just published in the high-impact journal Molecular Cell, researchers from Aarhus University have collaborated with experts from the University of Copenhagen and the technical university ETH Zürich in Switzerland and taken a close look at how bacteria handle this difficult balancing act. The results show that bacteria very quickly reduce their rate of cell division when exposed to antibiotics in order to maintain the highest possible tolerance, but quickly start growing again when the substances are removed and fitness is the most important factor.
[...] It is expected that the new knowledge about the molecular basis for the reaction of bacteria to antibiotics can be used to develop a whole new type of antibiotics that prevent bacteria from saving up energy and thus adapt to the treatment.
Yong Everett Zhang, René Lysdal Bærentsen, Tobias Fuhrer, Uwe Sauer, Kenn Gerdes, Ditlev Egeskov Brodersen. (p)ppGpp Regulates a Bacterial Nucleosidase by an Allosteric Two-Domain Switch. Molecular Cell, 2019; DOI: 10.1016/j.molcel.2019.03.035
(Score: 2) by JoeMerchant on Monday April 29 2019, @01:06PM (2 children)
Agree that this adaptation to shift into "survival mode" is a good thing to describe and a possible target for attack, maybe not as important as biofilms, but... the headline:
would seem to be drawing the obvious conclusion from relatively well known book [wikipedia.org] published nearly 160 years ago.
🌻🌻 [google.com]
(Score: 2) by ikanreed on Monday April 29 2019, @05:28PM (1 child)
In context, they were actually using survival of the fittest as a metaphor for on-the-fly in-a-single-cell adaptation. As stress levels rise, the molecules that regulate antibiotic resistance increase, because the stress alarmones "kill" the chemicals that increase the growth rate of the cell(which somehow protects the cell from antibiotics? Unclear).
It's not actually about cells that have resistance surviving.
(Score: 2) by JoeMerchant on Monday April 29 2019, @07:04PM
No: you do the hokey pokey and you turn yourself about that's what it's all about.
All these fancy mechanisms to shelter-in-place or whatever, surviving to spawn another generation, whether you're using alarmones or hardwired fear of serpents, or higher cognitive functions deducing the location of snipers in the trees and cover along your route to safety, those adaptations were all developed through "Preservation of favored races in the struggle for life."
But, yeah, they are focused on an adaptation that they think might be defeatable, making the bacteria more vulnerable to antibiotics that can suppress their ability to proliferate.
What I think most of these researchers are missing is that interventions like they are hoping to develop challenge the bacteriome, piss it off, and make it develop faster and stronger than it ever would without such highly targeted attacks. Eventually, they may throw things far enough out of whack that new super-strains emerge which are not at all compatible with the ~39 trillion bacterial cells that you carry within your body, and we may find ourselves dramatically altered (most likely not for the better) by the new balance of microbial power in our environment and ourselves.
🌻🌻 [google.com]