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> those strains will gradually lose their resistance once no longer exposed to antibiotics,

I've never heard this. Can you cite an example or source for this? How could we be losing if medicine can afford to "wait out" a strain? MRSA's been around 80 years. Call me skeptical.



> Can you cite an example or source for this?

“We previously reconstructed a 1,000-year-old remedy containing onion, garlic, wine, and bile salts, known as ‘Bald’s eyesalve’, and showed it had promising antibacterial activity. In this current paper, we have found this bactericidal activity extends to a range of Gram-negative and Gram-positive wound pathogens in planktonic culture and, crucially, that this activity is maintained against Acinetobacter baumannii, Stenotrophomonas maltophilia, Staphylococcus aureus, Staphylococcus epidermidis and Streptococcus pyogenes in a soft-tissue wound biofilm model” [1].

> How could we be losing if medicine can afford to "wait out" a strain?

In general, “mutations that confer larger” resistance “are more costly” in terms of fitness [2].

Absent the selection pressure of a particular antibiotic, the bugs without that resistance generally outcompete the ones weaving chainmail against Tomahawks.

[1] https://www.nature.com/articles/s41598-020-69273-8

[2] https://pmc.ncbi.nlm.nih.gov/articles/PMC4380921/


To prove the claim we need to see that the salve is useful and that it used to be less useful because of resistance. Is that proven somewhere? This just looks like a "new" antibiotic.

And the more important part is losing resistance in a meaningful timeframe, much smaller than 1000 years. Also the relevant genes can't be easy to reactivate.


> we need to see that the salve is useful and that it used to be less useful because of resistance. Is that proven somewhere?

No proof, but when I came across this it was suspected the treatment fell out of use due to resistance.


Salves are antibiotic in the sense that they are antimicrobial. Bald's is effective in the same way that bleach, chlorhexidine, iodine, etc are. They are for external and external wound use and have no function against an existing deep or systemic infection.


I don't have a source or example and I don't have the time to properly search, but I can provide a quick explanation:

The vast majority of resistance mechanisms are detrimental to the cell that has them.

  1. The bacteria consumes energy to be resistant by pumping out the antibiotic, blocking it with a protein or breaking it down with an enzyme.
  2. Alters it's billion-years-optimized metabolism or structure to be resistant and this affects it's efficiency.
  3. Forgoes on a source of energy because it can't use it anymore.
You can read about these mechanisms here: https://en.wikipedia.org/wiki/Antimicrobial_resistance#Mecha...

When in a competition with regular bacteria (no antibiotic around), these resistant cells will be outcompeted and gradually replaced.




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