Are you saying the adaptations bacteria make to become resistant to antibiotics causes them to be easier targets for the immune system? Do you have a link I could read more about this?
The discussion here seems to have ignored what seems like the interesting/new part of this. There has been plenty of prior research and media around blanket use of antibiotics creating _drug resistant_ bacteria which are harder to fight with drugs. But this is saying that additionally because some antibiotics are similar to chemicals endogenously produced within our own bodies, they also produce bacteria which our bodies are less effective at fighting on their own.
I.e. this isn't just about the use of antibiotics -- this is about the use of antibiotics which are _similar to parts of our own immune systems_. Using antibiotics which are more dissimilar to our own immune responses would create _drug resistant_ bacteria but not _immune resistant_ bacteria.
Potentially - though it's a lot harder to evolve resistance to physical destruction than it is to a given antibiotic. The other aspect, aka 'the hygiene hypothesis' still holds, killing more pathogens may well lead to weakened immune response from lack of exposure.
To my knowledge, antibiotics inhibit crutial bacterial functions such as protein synthesis in bacterial ribosomes which causes cell death. To survive, the cell mutates its ribosomes which costs energy and makes them less efficient but functional again. If you are lucky, the bacteria need a long time before finding an efficient mutation. A combination of multiple such attack vectors can further decrease the efficiency at which the bacteria operate, giving your body an advantage. However, finding new attack vectors (which don't interact with human cells) takes on the order of ten years. So resistance is still a big Problem.
> I've never understood why a longer course of antibiotics would kill a resistant bacteria, while a shorter one won't. It's either resistant or it's not.
The thing you're missing is that bacteria share genes. So if you have a high proportion of resistant bacteria, but non-resistant bacteria are still around, the genes survive and spread. But if only the (few) resistant ones are around, the (weakened) immune system can kill them and the genes don't.
(And also, “it's either resistant or it's not” is an oversimplification in many real-world cases.)
One comment. With bacteria, resistance is to specific (or multiple) antibiotics. This doesn't mean necessarily that the strongest bacteria in general terms get selected. For example MRSA tends to affect people who for some reason have weakened immune systems because healthy people do a decent job of fighting it off.
Aren't drug resistant bacteria weaker though? Like reproducing slower, spreading less, being more likely to be defeated by your own immune system?
Also antibiotics would still be good against most bacteria since only some have evolved antibiotic resistance. I know they can sometimes spread to other species of bacteria, but they still would be at a disadvantage outside of places that use antibiotics. If you just got cut or something with random bacteria in it wouldn't you probably be ok?
You realize people died from bacterial infections before antibiotics, right? Bacterial resistance to antibiotics doesn't make the bacteria more likely to kill us than before.
This is an amazing video[1] from Harvard Medical School released couple of days ago showing evolution of bacteria that evolve in 10 days to become resistant to antibiotics.
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