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Why does taking too much antibiotics create resistance?

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Hello everyone,

 

Ok I have an infection due to to X bacteria. I take too much antibiotics. How does the X bacteria develop resistance then? For the commensals I can understand. I take antibiotics commensals die and the minority that are resistance will survive and multiply and now the new commensals would be resistant. But I'm asking about outside bacteria. Thanks :)

Edited by scilearner

Bacteria develop resistance via evolution. There are literally millions of pounds of bacterium covering the Earth every second, one of them is bound to randomly develop a gene that will allow it to survive the drug that it is exposed to. If just that one bacterium survives, it will multiply and create a whole colony that will survive the drug and eventually spread unless contained.

Edited by questionposter

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I'm not asking about the mechanism exactly, I know it is about evolution and survival of the fittest. But for example, when u take antibiotics for a viral infection. Why do they say bacteria will develp resistance? What bacteria are they referring to, the bacteria living inside your body (commensals), but they are not harmful so even if they are resistant why does it matter? Thanks for replies so far :)

It's not taking to much antibiotics that's likely to lead to resistance, it's taking not enough.

The other issue is people taking antibiotics for infections that are not bacterial.

 

Aren't there many complaints by doctors of taking too much anti-biotics, since taking too many increases the likelihood of a bacterium developing a resistance?

 

I'm not asking about the mechanism exactly, I know it is about evolution and survival of the fittest. But for example, when u take antibiotics for a viral infection. Why do they say bacteria will develp resistance? What bacteria are they referring to, the bacteria living inside your body (commensals), but they are not harmful so even if they are resistant why does it matter? Thanks for replies so far :)

 

They are referring to whatever bacterium that the drug targets or whatever it effects. If the drug targets bacterium in a wound, then the bacterium in your wound might possibly develop a resistance when exposed to the drug. Most often though it will get them. Really any bacteria colony that is exposed has a chance of being resistant, but most of the time you put antibiotics inside of your body, which is often where bacterium also are, so its not likely they are talking about bacterium outside your body unless they say specifically on your skin or in the air or something.

Edited by questionposter

I'm not asking about the mechanism exactly, I know it is about evolution and survival of the fittest. But for example, when u take antibiotics for a viral infection. Why do they say bacteria will develp resistance? What bacteria are they referring to, the bacteria living inside your body (commensals), but they are not harmful so even if they are resistant why does it matter? Thanks for replies so far :)

 

Here's an example:

 

Many antibiotics have a certain functional group called a beta-lactam:

 

Blacta3.gif

Image cred: beta-lactams

 

Some bacteria have these enzymes on the surface of their cell walls/membranes that can hydrolyze the beta lactam rings (the four-membered N-containing ring) of antibiotics.

 

Fig1.jpg

 

Image cred: beta-lactamase mechansim

 

This of course deactivates the drug. Evolutionarily I'm not sure how this happens but I know that bacterial populations can develop more aggressive beta-lactamase enzymes over time with exposure to beta-lactam antibiotics. Some drugs have even begun to incorporate other beta-lactam molecules in the pill formulations as "sacrificial substrates" so that the bacterial beta-lactamases "bite" the sacrificial substrates first leaving the active drug intact.

Edited by mississippichem

It is not that bacteria develop resistances upon encountering antibiotics. This is a common misconception. What happens is that in any large bacterial population you will find a few that have that resistance due to random mutations. Without antibiotics their amount will be relatively low.

However, once you add antibiotics to the mix you kill off those that do not have the resistance. Thus, allowing the resistant ones to spread. The result is that the number of resistant strains spread, rather that they suddenly develop the resistance.

 

But for example, when u take antibiotics for a viral infection.
Viral infections are a different thing, you do not take antibiotics against viruses.

It is not that bacteria develop resistances upon encountering antibiotics. This is a common misconception. What happens is that in any large bacterial population you will find a few that have that resistance due to random mutations. Without antibiotics their amount will be relatively low.

However, once you add antibiotics to the mix you kill off those that do not have the resistance. Thus, allowing the resistant ones to spread. The result is that the number of resistant strains spread, rather that they suddenly develop the resistance.

 

Viral infections are a different thing, you do not take antibiotics against viruses.

 

Evolutionarily I'm not sure how this happens but I know that bacterial populations can develop more aggressive beta-lactamase enzymes over time with exposure to beta-lactam antibiotics

 

My keyword was populations. I never said that any single bacteria could develop a resistance. Perhaps my use of the word "develop" implied what you seem to be replying to.

Edited by mississippichem

My keyword was populations. I never said that any single bacteria could develop a resistance. Perhaps my use of the word "develop" implied what you seem to be replying to.

 

A single bacterium does develop a resistance, it only takes one bacterium to form a resistant colony.

My keyword was populations. I never said that any single bacteria could develop a resistance. Perhaps my use of the word "develop" implied what you seem to be replying to.

 

Well, it is more accurate to state that resistance spread faster throughout a population, rather than develop it. The "development" part, i.e. the rise of enzymes that have beta-lactamase activities occurs more or less independently of the presence of antibiotics (this is not entirely accurate as stress can lead to error-prone DNA repair, which in turn increases mutation rates).

 

Mechanistically, single bacteria develop or acquire resistance in different ways that can range form mutations in the target site of antibiotics (so that they cannot interact anymore) up to acquiring proteins that either inactivate the antibiotics or reduce the accumulation of it.

In the latter case the efficiency of the enzymes can then increase over time by precisely the same mechanism as its initial spread. I.e. those with a low level resistant will mutate, and if there are variant that are more resistant, they will spread, outcompeting the less resistant ones.

Antibiotics essentially just add a strong selective pressure to the population.

Edited by CharonY

Well, it is more accurate to state that resistance spread faster throughout a population, rather than develop it. The "development" part, i.e. the rise of enzymes that have beta-lactamase activities occurs more or less independently of the presence of antibiotics (this is not entirely accurate as stress can lead to error-prone DNA repair, which in turn increases mutation rates).

 

Mechanistically, single bacteria develop or acquire resistance in different ways that can range form mutations in the target site of antibiotics (so that they cannot interact anymore) up to acquiring proteins that either inactivate the antibiotics or reduce the accumulation of it.

In the latter case the efficiency of the enzymes can then increase over time by precisely the same mechanism as its initial spread. I.e. those with a low level resistant will mutate, and if there are variant that are more resistant, they will spread, outcompeting the less resistant ones.

Antibiotics essentially just add a strong selective pressure to the population.

 

Well stated. Thanks for the clarification.

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