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"Bacteria are quickly out-competed by genetic variants with fewer expressing genes that they don't need." This has not been true for MRSA, where transmission of resistant organisms in the community was sustained despite there not being particularly intense selective pressure in the community. Last I checked (I don't work in community transmission as much) we don't have a firm handle on why that's true, but I'd caution against simply assuming that resistant organisms will be out competed absent selective pressure.

Beyond that, even if they are out competed, that's not sufficient. They need to be out competed to extinction.



MRSA is due to the mecA gene, which is integrated into the S. Aureus genome. It's not plasmid-mediated resistance, which means that it's less likely to disappear from bacterial populations, even in the absence of selective pressure:

http://www.eurekaselect.com/68849/article


More than mecA, which itself doesn't sound like it's grossly maladaptive in the absence of β-Lactam antibiotics (it codes for an "replacement" enzyme that's not β-Lactam sensitive): https://en.wikipedia.org/wiki/Methicillin-resistant_Staphylo...

There's also regulatory genes that may be present, there are 6 known varieties of the whole gene cassette, with 5 further subtypes based on these regulators, so in the absence of β-Lactam antibiotics it sounds like a lot of them will be fit.

Nasty.


True - but the post I was responding to wasn't talking about plasmid-mediated resistance, but rather a broad assertion that a competitive disadvantage will take care of things. That's a strong assumption for which we have a counter example.




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