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What's curious about this view, is that it ignores how researchers create AMR bugs in the lab. Namely low doses of Antibiotics to allow time for the bacteria t
by photoJ 10y ago
What's curious about this view, is that it ignores how researchers create AMR bugs in the lab. Namely low doses of Antibiotics to allow time for the bacteria to mutate and develop resistance. If you're interested you can look up MIC Minimal Inhibitory Concentration, I think you would find it illuminating. Also the assertion that the resistant phenotype is "otherwise less-fit" is not accurate.
- astazangasta 10y agoThe resistant phenotypes often ARE less fit, as the guy above me said - if you have to run a solute pump in order to remove drug from your cytoplasm, that has a cost in energy and protein. EVERY phenotype has a cost that must be paid. You don't get to hang onto a useless genotype in the absence of a selective pressure that maintains it. Low doses allow you to provide a continuous challenge that doesn't kill the entire population. That's not what's happening when you stop your drug course early.
- photoJ 10y agoDNA absolutely hangs on to useless genotypes for some period of time. Horizontal gene transfer allows for redundant genes to exist. They have increased mutation which MIGHT lead to some productive change, but for an extended period of time they don't. Not to mention biological mechanism which exist for many many generations even though they aren't used in some grow medium. The disagreement here is about time scale. If it were true that resistant phenotypes often ARE dramatically less fit to the degree you imply we could simply stop taking Antibiotics and everything would revert back to it Susceptible state. When you stop a dosage early you've very likely applying a low dosage to some subpopluation. Dosages are not linear, nor evenly applied throughout the entire population of bacteria in a human body.