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Comment by vosper | Hacker News Reader

> "It changed our understanding because it means antibiotic resistance didn't evolve in the clinic through our use. The resistance is hardwired," she says.

But if that was true wouldn't bacteria always have been resistant to these "natural" antibiotics (the majority of those that we use, according to this article) and this they never would have been effective in the first place? And if that's true, how was this built-in resistance suddenly switched on to the extent that scientists are now talking about a future where bacteria we could easily treat a few decades ago will be unstoppable? I think either I'm missing some important details, or this article is.

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Bacteria can share DNA, there is a plasmid that sort of infects bacteria, and it causes bacteria to create connections with other bacteria. https://en.wikipedia.org/wiki/Plasmid It shares the plasmid DNA, but it also shares other DNA from that one bacteria to another. This allows bacteria to rapidly modify by mixing and matching DNA from other bacteria around them. Obviously bacteria that have traits that are beneficial are selected for. So some pathogenic bacteria that don't have this resistance will be killed by the antibiotic. Some nonpathogenic bacteria that have natural resistance will at some point share the relevant DNA with the pathogenic bacteria, which will then be selected for by the antibiotic, and then you have the new pathogenic antibiotic resistant strain. Or it could happen with some minor mutation, depending on how the antibiotic works, the article is deceptive in saying that resistance doesn't come from antibiotic use.

Well for starters you can't use this bacteria and all bacteria interchangeably.

Secondly bacteria of all sorts live in different eco systems. But all bacteria doesn't live in every eco system. They're not subject to the same stresses, attacks, and naturally don't develop immunity to things they're not exposed to and all bacteria aren't always exposed to everything...

You're kind of going all or nothing for millions of species of bacteria and that's obviously overly simplistic. You might as well make the argument that because cheetahs can run 60mph, so shouldn't all vertebrates be capable of that?

I would think that having a resistance an antibiotic meant that a bacteria was losing out on a different advantage. This is why resistant bacteria only exist in places where having the resistance, hospitals etc., is more beneficial than what it lost to get the resistance.

For example if a cheetah developed a larger body at the cost of speed. It wouldn't survive as well unless there was a benefit to being larger but slower.

As the article hints at, it depends on environment; this particular bacteria was in a very hostile environment, where it had to compete with other bacteria for nutrients. Outside, there's enough room and food for everyone, so there was less of a need to develop resistances.

My thoughts exactly.

I'd speculate that they're saying that all bacteria had some resistance to start with, rather than the various types of bacteria all having mutated to have this characteristic. The implication being that if a large number of bacteria were already immune then evolution favouring this immunity requires a lower rate of evolution to if that characteristic was a recent mutation which then immediately became favoured and spread; as each mutation having any success would be less likely, and therefore implying that this is such a significantly beneficial mutation (given human use of antibiotics) that evolution has favoured this attribute far more than otherwise would have been required.

From what I learned in my microbiology class... the genes which confer resistance to antibiotics are present in bacterial populations, but not necessarily every individual bacterium. Additionally, through a process that is sort of like the bacterial version of sex, called Horizontal Gene Tranfer, one microbe can transfer the genes which confer resistance to antibiotics to another bacterium on plasmids, which are basically small circular rings of DNA.

So basically, it takes energy and resources to turn that gene into the proteins which will deactivate the specific antibiotic, so if the bacteria is never coming into contact with the antibiotics, there's not really a reason to keep that gene around. But if suddenly a bacteria population were to find itself in a hospital environment, where surfaces are being disinfected very frequently, not only is it extremely beneficial to keep the antibiotic resistance genes around, but also they are being actively selected for, since all bacteria without those genes are being killed off.

Horizontal Gene Transfer can happen between bacteria that are not even the same species. So for example, the Hero Bug that this article is talking about, if it were present in the hospital environment, might be able to send over a methicillin-resistance plasmid to a possibly pathogenic bacteria like Staph, and create MRSA. But if the pressure to remain resistant to methicillin was removed from the staph populations, by no longer using that antibiotic to treat the infection for several years, the staph cells would eventually mostly "forget" how to resist that antibiotic by no longer ensuring that the resistance gene is included in every bacteria in the subsequent generations. Probably about .01% of the bacterial cells would keep the gene even if it was not required for their survival, and once we start using the antibiotic again a few years later, wiping out most of the bacteria is usually good enough to help the immune system take care of the ones that are left.

This idea of holding off on using a specific antibiotic for a while is called antibiotic rotation. Here's a paper where they tested the efficiency of the idea: https://www.ncbi.nlm.nih.gov/pubmed/17693828

Here's the wikipedia article on horizontal gene transfer: https://en.wikipedia.org/wiki/Horizontal_gene_transfer

Plasmids: https://en.wikipedia.org/wiki/Plasmid

And antibiotic resistance: https://en.wikipedia.org/wiki/Antimicrobial_resistance

tl;dr: The overuse of antibiotics can lead to bacterial populations developing resistance to those drugs, but since the chemicals in "natural antibiotics" have been around for a long time before we started using them, the genes to counteract them already exist, but are not always expressed.

Thanks for the info on Plasmids... I guess that has an impact on evolution where you start having to look at whole bacteria populations rather than just the evolution via individuals or species to the point where the model becomes similar to the evolution of knowledge within a society.

You're right! Between plasmids and viruses, there's lots of ways that DNA can get moved around on the microscopic scale that you wouldn't expect when your intuition is concerned with multicellular organisms like us.

It's sort of a balance. Multicellular organisms get a lot of benefits that single-celled organisms don't, but in exchange, multicellular organisms give up the plasticity to improve themselves on demand by aquiring new DNA to better fit their environment.

Extended phenotypes?

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