Comment by hodder | Hacker News Reader

Comment by hodder | Hacker News Reader

The anthropomorphism of bacterial evolution makes the article hard to follow for the layman (me). Can someone familiar with bacterial evolution please explain to me how the use of antibiotics leads to superbugs? I am clearly misunderstanding something.

I was under the impression that in a population of bacteria, genes express themselves in any number of random ways. If we expose the bacterial culture to antibiotics, the bacteria susceptible to the antibiotic dies, while the resistant bacteria lives on free to reproduce, leaving the descendant bacteria with resistive characteristics...

My question to the HN scientists is, doesn't this just destroy some subset of bacteria? Is new genetic information produced that did not exist before? Taking this trimming tree down the line, wouldn't the "superbug" antibiotic resistant bacteria have been created/survived and thrived anway? Or does the antibiotic exposure actually cause, "the bacteria to want to survive", in the sense that exposing them to antibiotics leads to more rapid mutation of descendants? Why wouldnt the antibiotic resistant bacteria be created with or without overuse of antibiotics? Isn't the spectrum of the genetic tree just trimmed?

Let's suppose that in an antibiotic-resistant future some, very small, number of people develop a mutation that produces 2 effects: antibiotic resistance and VERY ugly nose warts. Since other people live for 25 years and the uglies for 100 years, I suppose they would be desirable mates with lots of offspring despite the ugliness. In a few centuries, they would be the majority. Now, if there weren't the antibiotic resistance, do such mutations have the same chance to appear? Yes, but they'd have hard trouble finding mates. Their mutation has only drawbacks, and no advantages. As soon as the advantage appears, the mutation has more chance to spread through offspring. The same with bacteria. It is not necessary that they mutate more, it is just that those mutations that help the bacteria survive spread quickly. But if the danger is not present, the mutation is not significant.

My guess: before the antibiotic, the minority resistant bacteria have to compete with the majority non-resistant. After, they can proliferate freely. Repeat with the next antibiotic, and soon all the ones we see are resistant to all the antibiotics we have.

You pretty much nailed it in a very succinct manner.

That's why it's so important to complete a course of antibiotics rather than stopping once you feel better. Once you've started antibiotics, you're basically enriching the population in bacteria that aren't affected by the antibiotic. This is normally a very small population, but if you stop half-way, the pressure on those bacteria from other bacteria (the ones that died) is lower, allowing the resistant population to flourish.

If you finish a course of antibiotics, you not only kill the susceptible bacteria, but you also give your own immune system a chance to take down the few remaining bacteria that are resistant.

This is an unconvincing argument to me - if antibiotic resistant bacteria survive, why would finishing the course of antibiotics make a difference?

Does it clinically happen that stopping a course of antibiotics early causes an antibiotic resistant form of the infection?

(I couldn't find evidence either way, but I did find a few articles saying typically prescribed course lengths could be safely reduced in the effort to reduce antibiotic use generally)

This gives a much better summary of the theory...

http://blog.oup.com/2011/11/antibiotics/

Yes, I get the theory, but I think it's probably false. No clinical evidence is offered.

Care to share it?

Just to be clear:

I can't share because that's exactly my point - as far as I can find, there isn't a single clinical example of stopping antibiotics early causing any problem of antibiotic resistance.

>> if antibiotic resistant bacteria survive, why would finishing the course of antibiotics make a difference?

I can only speculate, but here's how I imagine it.

Your body can kill a certain number of bacteria on its own. Antibiotics help reduce the infection to the point where your body can do the rest.

If the resistant bacteria are a small minority, taking antibiotics long enough to kill most of the non-resistant ones will let your body kill the remaining resistant ones.

If you stop too early, the battle tide has not yet turned. Instead, by killing, say, half the non-resistant ones, you've made the resistant ones a larger proportion of the whole infection. Then both groups continue to multiply.

If you repeat this several times, starting and stopping the antibiotics depending on how you feel, the resistant bacteria could go from being 1% of your infection to 50%.

That's a good question.

I have no credentials or background to know the answer, but I wonder if this is something where the use of antibiotics decimates most the bacteria population so that it's easier for the resistant ones to thrive, as opposed to cohabitate and possibly be overtaken by the non-resistant ones. I'm thinking of it like Conway's Game of Life where a cell dies if surrounded by more than 3 cells. With antibiotics, you limit the number of living cells around and are more likely to keep others living.

Or maybe the non-resistant ones would have another trait that make them thrive more than the resistant ones if both are mixed?

Theoretically, non-resistant bacteria should have a competitive advantage over resistant bacteria in an environment without antibiotics - they don't have to spend energy producing useless resistance enzymes, and instead can grow better.

That means, in theory, with no antibiotics, you should have very few resistant organisms.

The problem is that's all "in theory". Right now, the level of evidence for community-acquired MRSA and the competitive advantages of susceptible versus resistant S. aureus has thrown that all into question.

There are some situations where an organism can evolve overnight to exposure to an antibiotic. See Inducible Extended Beta lactamase resistance in E Coli. HOWEVER. Bacteria evolve just as any organism does via random genetic mutations that may or may not lead to resistance. It's Darwinism on the cellular level. The vast majority of antibiotic resistance occurred regardless of exposure. There is a segment of society that wants to blame humans for every problem it seems.

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