The nationwide experiment will initially include around 100,000 volunteers.
Wildebeest, science advice for Trump, antibiotics, and more
September 1, 2017|
IMAGE COURTESY OF CHRISTOPHER DUTTON
—Grant Hopcraft, landscape ecologist at the University of Glasgow, who studies wildebeest migration in order to understand the animals’ interaction with their ecosystems (The Scientist, August 15)
—Evolutionary biologist and author Richard Dawkins, when asked in a Scientific American interview what advice he would give to Donald Trump if he had the chance (August 10)
—A memo, penned by software engineer James Damore, decrying what he calls “arbitrary social engineering” aimed at increasing workplace diversity at Google, which fired him after the document circulated first inside then outside the company (August 5)
—University of Washington particle physicist and philosopher of science Chanda Prescod-Weinsten, criticizing what she calls the “shoddy science” that propped up Damore’s argument (August 9)
—MIT biologist Jim Collins, on the emerging understanding of the effects of finishing courses of antibiotics on the development of resistance in pathogens (The Scientist, August 11)
September 5, 2017
" - That’s never made any sense to me. Why would resistance arise if you stop using your antibiotics? In fact, I think the adage should be that in order to ensure increased likelihood that you will successfully treat your infection, you should complete your full course of antibiotics, but bear in mind that the risk you run is, the longer you use antibiotics, you increase your risk of developing resistance. "
Actually this makes a lot of sense, although Collins's counter argument does also. It is not a case of black and white, but one where pros and cons have to be weighed. People should still follow doctors' orders. Consider:
When you start taking the drug, you have a large population of the pathogen, with a lot of diversity in sensitivity to the drug, but lets say none that are completely resistant. When you start taking the drug, you rapidly kill off most of the pathogens. Say 99% are killed and 1% is still viable, but not growing or reproducing, or doing so very slowly (bacteriostasis). Under these conditions the chances for further resistance mutations to arise is very low, both due to the small number of organisms and the low rate of replication. Now you feel better and stop taking the drug. If you stop before 100% are killed, the remaining 1%, which will be the 1% with the highest resistance, will begin to multiply and repopulate the niche. Now the numbers and turnover rate are high, and new mutations will arise, with the population diversifying with respect to resistance. You could transmit these partially resistant bugs to someone else, or you might start feeling sick again (relapse due to premature termination of regimen). The doctor prescribes the same antibiotic, but this time it doesn't seem to work as well. After a week you're still not feeling so hot. Doc says increase the dose 5-fold, and that does seem to help. You start feeling better and stop taking the drug. Again 1% of the pathogens are still viable, and they are the ones with the highest level of resistance. You relapse again, and this time nothing works.
When scientists select for resistance mutations in the lab, for example to determine the target of a drug, the procedure is to start with a sublethal dose and gradually increase it. If you don't want to select for resistance, be sure to take a high enough dose and take it for long enough to eradicate the pathogen.
Of course there are counter-arguments. As long as you are taking the antibiotic, you are passing most of it into the sewer where it can induce drug resistance which can be transferred between various species and end up back in a pathogen. We have to hope that dilution in the sewer is such that it has no effect, which is probably the case in city sewers but maybe not in individual septic tanks.