5 ms·

As I said, completing your course is useful in eliminating residual disease. How does it help in preventing drug resistance? If anything it seems by increasing

As I said, completing your course is useful in eliminating residual disease. How does it help in preventing drug resistance? If anything it seems by increasing exposure to the drug it encourages the development of resistance, since it gives the (otherwise less-fit) resistant bacteria a fitness advantage. Completing a course of a drug that the bacteria is already-resistant to will accomplish nothing other than eliminating its non-resistant competitors, so what's the logic?

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 ago
  The 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 ago
    DNA 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.
hga 10y ago
Errr, the theory I'm relating is that continuing the pressure of the antibiotic will make it easier for the body, and perhaps non-susceptible benign bacteria, to finish them off (perhaps not all, but to a de minimus number where they won't pose a problem). Remove that pressure, and the resistant population has a chance to rebound. More likely than having an ecology of other bacteria to fight with is that the field is somewhat or all but completely cleared. The body may not also have had a chance to clear up whatever condition allowed it to get a grip in the first place. Etc. Again, as I understand it TB is a great example to look at, and depending on where you live it might even be a real danger to your and yours, so maybe read up on it?

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 ago
The 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 ago
  DNA 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.

hga 10y ago

Errr, the theory I'm relating is that continuing the pressure of the antibiotic will make it easier for the body, and perhaps non-susceptible benign bacteria, to finish them off (perhaps not all, but to a de minimus number where they won't pose a problem). Remove that pressure, and the resistant population has a chance to rebound. More likely than having an ecology of other bacteria to fight with is that the field is somewhat or all but completely cleared. The body may not also have had a chance to clear up whatever condition allowed it to get a grip in the first place. Etc. Again, as I understand it TB is a great example to look at, and depending on where you live it might even be a real danger to your and yours, so maybe read up on it?