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by pcrh
4178 days ago
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Without having read the article too closely, teixobactin appears to be binding the lipids of the bacterial cell wall. It might be hard to evolve simple resistance to this (and the authors support this by experiment) as this would require that the bacterium changes the composition of its membranes, rather than evolve a mutated enzyme, which is how most spontaneous resistance occurs. However, that does not exclude the possibility of the bacterium acquiring a plasmid or phage carrying an enzyme that inactives teixobactin. This particular mode of acquiring antibiotic resistance is quite common. Nevertheless, this finding does seem to be quite a big deal. A novel broad-spectum antibiotic where spontaneous resistance is unlikely is a pretty powerful addition to the pharmacopeia. |
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Right, which is why I said the bit about bacteria kicking out genes that they don't need. Bacteria will "eject" a plasmid within a generation or two if they no longer need the gene(s) in question. Replicating a big gob of easily-ejectable DNA is not something bacteria do unless there's a good reason to do it.
Basically, for plasmid resistance to propagate, you need to have constant exposure to the antibiotic in question, or the resistance gene needs to be stably integrated into the bacterial genome. The former doesn't happen until an antibiotic is in extremely wide use, and the latter is one more rare step on top of an already unlikely chain of events.
It's not impossible, it's just unlikely.