Antibiotics!

I have three questions (so far), but the first one might answer the second one.

1. How do antibiotics work? Obviously they "kill bacteria" but how do they do it? What do they disrupt? Do all antibiotics work the same way?

2. Why do you have to take a course of antibiotics? Why doesn't one big dose do the trick, why do you have to take a lot of smaller doses? Wouldn't something that's there on day one kill off all of it (if the dose was large enough), and why does something that didn't kill it on day one kill it on day five?

3. What happens to "good bacteria" when you take antibiotics? Does it die in the same proportion as the "bad bacteria"? Last time I was on antibiotics I was supposed to eat yogurt every day to keep my digestive system from malfunctioning, but why didn't the antibiotics kill the yogurt bacteria too? I mean they were both in my belly, right? How'd they not interact when they were in such close proximity?

Antibiotics are designed with a specific purpose, if I remember correctly.

I don't think they kill the good cells in your body, just the bacteria they were designed to kill. I think that antibiotics generally inhibit important things that living bacteria need to thrive...like it needs to keep creating energy and it needs it's cell wall and all that good stuff.

It's a relatively slow process depending on how you look at it. I think of it as a war of sorts. Each pill you take sends in some new troops. I'd think if you just gave someone one big dose, it'd be like putting a red blood cell in pure water. (results in explosion of sorts)


Someone feel free to correct me.

I think the purpose of eating yogurt is that you keep adding "good" bacteria to your stomach continuously while you're on AB.

There are several types of AB, I think the most usual ones attack the bacterial membrane, ultimately making the bacteria autolyse. Some are more effective on Gram+ and some takes out almost all.

Not sure why one large dose isn't enough, and there are some different opinions whether you should take AB the full period even if you're well. I think it's to be sure that all the bad bacterias are out, so the remaining don't develop resistance against the AB in use.

There's some, a lot among the doctors, worry here in Sweden about the increase of AB-resistant bacteria in the world. Not sure how it's viewed in the rest of the world...

Yeah, around here it's standard that if you've got a script for a week's worth, you shouldn't stop after three days when the problem seems fixed, you're supposed to take the whole week.

I want to know specifically what they break. Is it the cell wall? Is it the metabolism? Do they block absorption of some critical substance?

Wikipedia lists some stuff but it's not terribly non-specialist-friendly.

How about this?

http://www.wisegeek.com/why-do-i-have-to-keep-taking-antibiotics-after-i-feel-better.htm

I'd think they specifically break a process.
If the antibiotic is going after killing the whole cell division process, it'll attack the things that go along with cell division.

Cell division= mitosis -> occurs in the nucleus ->occurs in the nucleolus -> messing with chromosomes. Errors during cell division can cause mutations or apoptosis. (cell death)



Metabolism can be broken down into catabolism and anabolism. The first breaks down large molecules for energy and the latter uses that energy to construct things like protein and nucleotides. Protein production. You think about where proteins are manufactured. They're manufactured in ribosomes.

Ribosomes are inside the cell, so somehow this antibiotic is getting through the cell wall via endocytosis (maybe?) and is unleashing chaos inside of it. But now I'm just completely guessing/going off previous knowledge.

Generally antibiotics target molecules in a bacterial cell that are crucial to the cell's existence. It can be imperfect in that a bacterial cell and the host's (patient's) cell might be similiar enough that the antibiotic targets the patient as well, causing side-effects. Thankfully, there is a bit of evolutionary difference between most bacteria and most mammals that there are targets that minimize side-effects.

The main reason for taking a full duration of an antibiotic is basically micro-evolution. Since microorganisms reproduce quickly, they can evolve quickly, and some even have methods for transferring genes directly without reproduction. If you take a short dose of antibiotics, what you're doing is actually only killing a majority of the bacteria, reducing the disease's strength of symptoms, but you're not killing all of the bacteria. Most importantly, the short dose may act as a selection pressure that will promote the remaining bacteria to evolve resistance to the antibiotics (e.g. by modifying it's target molecules). Eventually the evolved bacteria will spread and make the disease less treatable. This is an issue with newer antibiotic resistant diseases like MRSA.
But even without evolution, the bacteria may simply repopulate, so think of the full course of antibiotics, beyond disease symptoms, as an insurance policy.

The death of 'good bacteria', a.k.a. your natural intestinal microflora, is similar to antibiotics causing side-effects in the patient. If the antibiotic isn't specific enough in its target, there is 'collateral damage'. Normally, we tend to have lots of E.coli in our intestines which block out other, less friendly, micro-organisms. Accidentally killing the E. coli may make room for other organisms, that we normally eat in small quantities in our food,etc..., which may cause a separate disease if they are able to populate in large numbers.


Firstlady is pointing in the right direction. There are many categories of antibiotics based on what they target. To get a better idea, you'll have to study some cellular biology on the parts of a cell and the cellular molecules involved.

Bacteria and human cells differ in the cell wall, and in the plasmid version of DNA transmission. Many antibiotics target related processes, in order to avoid killing human cells as well as they do bacteria.
However, they still cause side-effects: your liver is often unable to process these compounds at a high rate, and they become toxic to you as well. Bacteria may still survive at this toxic level and so you need to keep the level at almost toxic (for you) in order to eliminate the bacteria.
The selection pressure is not an either-or thing; hence being exposed to a long burst of a toxic substance will kill bacteria which have a slight advantage, just a little more slowly, but not those with absolute resistance. Since resistance builds up in increments of slight advantage, completing the course helps prevent bacterial resistance.

GoodGame said:

Firstlady is pointing in the right direction. There are many categories of antibiotics based on what they target. To get a better idea, you'll have to study some cellular biology on the parts of a cell and the cellular molecules involved.

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My attempts were weak in comparison to yours and brighteye's, but I guess it is good to at least be pointing in the right direction.

Firstlady said:

My attempts were weak in comparison to yours and brighteye's, but I guess it is good to at least be pointing in the right direction.

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These guys are good. You had more than I did, anyway!

Brighteye said:

However, they still cause side-effects: you liver is often unable to process these compounds at a high rate, and they become toxic to you as well. Bacteria may still survive at this toxic level and so you need to keep the level at almost toxic (for you) in order to eliminate the bacteria.

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That's right on the money.

Is that always the case? The other stuff about some of the buggers surviving... if the level was high enough, they wouldn't, would they?

Most antibiotics (penecilines, cephalosporines, carbanapenemes) exhibit a beta-lactame ring (4-cycle with an amide bond in the ring) and their tatget is afaik a protein neccessary for bacteria reproduction. The cyclic amide is reactive -> the bond breaks and the molecule bonds to the proteine rendering it inactive.

The reason for such a variety of those antibiotics is that bacteria possess also enzymes to break those beta lactames so they can not attack vital proteins.
-> different sidechains on antibiotics mean different resistance to those beta-lactamases, different intake, different lifetime inside the body (you also have those lactamases, your liver also oxidises/ transforms those molecules so they can be excreted) and better suitability for certain applications (pills, injections, salves,..)
Also, people can build up allergies to those antibiotics so you need variety there.

LucyDuke said:

Is that always the case? The other stuff about some of the buggers surviving... if the level was high enough, they wouldn't, would they?

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Supposedly. If you cultured some bacteria and then exposed them to a ridiculously high dose, you probably would destroy your culture. But you could do the same with a great number of compounds that are simply toxic, such as bleach, so you wouldn't have shown too much.