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Microbe Found In Grassy Field Contains Powerful Antibiotic
sciencehabit writes For much of the last decade, a team of researchers in Boston has eagerly exhumed and reburied dirt. It's part of a strategy to access an untapped source of new antibiotics—the estimated 99% of microbes in the environment that refuse to grow in laboratories. Now, their technique has yielded a promising lead: a previously unknown bacterium that makes a compound with infection-killing abilities. What's more, the team claims in a report out today, the compound is unlikely to fall prey to the problem of antibiotic resistance. That suggestion has its skeptics, but if the drug makes it through clinical trials, it would be a much needed weapon against several increasingly hard-to-treat infections.
Even by Slashdot's own TL;DR: summary, the title of this is wrong. Its not the new antibiotic in 30+ years that's astonishing, its the technique used in the experiment because it allows scientists to get easier access to those microbes that wouldn't grow in a lab. That hurdle is now a thing of the past.
That's exactly what they claim to have found (at least so far in tests on mice). They also assert that they think it would be extremely difficult for MRSA to adapt to this drug, as it would require a fundamental change in the structure of it as being a gram positive bacteria.
Finding things that kill bacteria is easy. Finding things that kill bacteria and do not significantly harm the host, now that is the hard part.
That's exactly what they claim to have found (at least so far in tests on mice). They also assert that they think it would be extremely difficult for MRSA to adapt to this drug, as it would require a fundamental change in the structure of it as being a gram positive bacteria.
I should have specified a human host. Biotech is littered with drugs that seems to work great on test animals but have serious side effects on humans.
You didn't read the paywalled article, did you?
The antibiotic blocks the bacterial cell wall synthesis. Animals don't have this particular cellular component, so the drug is essentially inactive against humans. This was shown by doing tests on mice. There is the possibility that the drug may elicit allergic response in humans (penicillin often does), but this will be tested in clinical trials.
The more exciting part of the work that did not get any mention in the summaries is how they found the antibiotic. They developed an approach to grow on a large scale microorganisms that were previously impossible to culture in lab conditions. They capture the microorganisms on a chip and then put the chip back into the environment from which the samples was isolated. This means that they did not need to guess what kind of nutrients each microorganism will need (they tested ~10,000 different microbes). The approach allowed them to grow 50 fold more microorganisms compared to what was possible using the current state of the art. To me this is the big news, because antibiotic discovery has been limited by our ability to grow microorganisms in the lab.
That's exactly what they're claiming. From TFA:
Moreover, these pathogens failed to develop resistance to the compound: There were no surviving individuals that had evolved to withstand its attack. (Resistance usually develops when a small percentage of microbes escape an antibiotic because of a mutation and then those bacteria multiply.) Lewis initially took this total devastation as a discouraging sign—the mark of “another boring detergent.” (Bleach, after all, is a strong antibiotic, but it’s a little too effective at killing any surrounding cells.) However, it turned out that the new compound, which the group named teixobactin, was not toxic to human cells in a dish.
Yes there haven't been human trials yet, but that's very promising.
If we keep taking natural antibiotics from nature, mass manufacture them, won't we just train the world's bacterial populations to be immune to practically anything we can throw at them?
You are making a very good point. Currently antibiotic resistance is a serious problem, mostly because we are very slow in discovering new antibiotics. What is very exciting about this research is that it significantly shifts the odds in our favor by allowing very large scale screens for new antibiotics. It will allow us to outpace the rate of resistance development. The probability that a particular infection will be resistant to multiple different antibiotics drops exponentially with the number of antibiotics you have. If you have a tool chest of 5-6 antibiotics sooner or later you will have pathogens that are resistant to a significant proportion of these antibiotics. Make the tool chest 10 times larger, and you will have a lot less to worry about.
As others have suggested this disrupts a part of Gram (+) cell wall synthesis which is difficult for bacteria to alter. Most antibiotics disrupt the protein constituents of the wall. Mutate one gene and the protein changes so it's relatively "easy" for bacteria to develop resistance. This new drug binds lipid constituents of the wall which are produced in a long synthesis pathway rather than a 1 to 1 gene to protein synthesis. Bacteria would need to mutate multiple genes coding multiple parts of the pathway simultaneously and in a complementary way to alter the structure of the target lipid without completely disrupting the pathway. So it's a much "harder" (meaning less likely to happen frequently) mutation to achieve.