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How to tell if a drug is bacteriostatic or bactericidal

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RussianJoo

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I am having trouble with this concept.. what makes it bacteriostatic vs. bactericidal?

anyone have a good way of reasoning this out? I'd like to keep memorization to a minimum.

thanks in advance for replying.
 

Blesbok

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We're ECSTaTiC about bacteriostatic
Very Finely Proficient At Cell Murder

and all that good stuff.


Although reasoning can help you figure out some of them, there is no really good way to tell which drugs are bacteriostatic and which are cidal just based on the drug mechanism. The best is just to remember the mnemonics.
 

mercaptovizadeh

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I am having trouble with this concept.. what makes it bacteriostatic vs. bactericidal?

anyone have a good way of reasoning this out? I'd like to keep memorization to a minimum.

thanks in advance for replying.

I just looked them up in wikipedia and FA. This is how I understand it:

The bacteriostatics are erythromycin, clindamycin, sulfamethoxazole, trimethoprim, tetracycline, and chloramphenicol

Note that erythromycin, clindamycin, tetracycline, and chloramphenicol all target the ribosome (tetracycline does 30s and the others do 50s). Macrolides also inhibit the 50s. They inhibit bacterial protein synthesis before bacteria can even attempt a cell division. So bacteria are "static" - they can still use the proteins they have, but can't get to the replication step because they can't make new proteins necessary for a proper division.

TMP/SMX act against dihydrofolate reductase and thus reduce the ability to make thymidine, which is necessary for DNA synthesis. Without necessary new thymidine, bacteria won't even try to replicate.

The bactericidals are vancomycin, fluoroquinolones, penicillin, aminoglycosides, cephalosporins, and metronidazole. I'm not sure, but you could probably also include polymyxins and quinolones here.

You can treat penicillin, cephalosporins, and vancomycin all together here. They all target the cell wall. The way I understand this is that an intact cell wall will not be affected but if bacteria attempt to replicate (and they will, since they have the protein and DNA apparatus to do so) these antibiotics will wreck the formation of new cell walls so the progeny is nonviable.

Quinolones and fluoroquinolones block DNA gyrase, so once the bacteria try to replicate, they are blocked in the midst of DNA synthesis and die. They don't "know" about the quinolones/fluoroquinolones until they've started DNA synthesis and then it's too late.

Metronidazole also attacks DNA, breaking the helical structure. I'd bet that it does this more so when the DNA is "vulnerable" i.e. during DNA synthesis (towards replication) than on DNA that's just sitting there.

Polymyxins destroy the cell membrane directly, so that would be toxic and bacteriocidal.

Aminoglycosides seem to have multiple mechanisms. They do target the 30s ribosome, but it also seems that they break up the external gram negative cell membrane. This is what I found on wikipedia:

The protein synthesis inhibition of aminoglycosides does not usually produce a bactericidal effect, let alone a rapid one as is frequently observed on susceptible Gram-negative bacilli. Aminoglycosides competitively displace cell biofilm-associated Mg2+ and Ca2+ that link the polysaccharides of adjacent lipopolysaccharide molecules. "The result is shedding of cell membrane blebs, with formation of transient holes in the cell wall and disruption of the normal permeability of the cell wall. This action alone may be sufficient to kill most susceptible Gram-negative bacteria before the aminoglycoside has a chance to reach the 30S ribosome[3]."

So, aminoglycosides are bactericidal due to the membrane effect, not the ribosomal effect.

So, in recap, I would say that agents that target protein and nucleotide (TMP/SMX) synthesis are bacteriostatic whereas those that target DNA synthesis (metro, f/quin), the cell wall (vanc, pen, ceph), or the cell membrane (aminoglyc, polymyx) are bactericidal.
 

SOUNDMAN

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Aminoglycosides seem to have multiple mechanisms. They do target the 30s ribosome, but it also seems that they break up the external gram negative cell membrane. This is what I found on wikipedia:



So, aminoglycosides are bactericidal due to the membrane effect, not the ribosomal effect.

Isn't this what also gives aminoglycosides there synergistic effects when used with beta-lactam antibiotics?
 

mercaptovizadeh

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Isn't this what also gives aminoglycosides there synergistic effects when used with beta-lactam antibiotics?

Yes. It breaks up the membrane so that beta-lactams can then penetrate more easily and attack the cell wall.
 

RussianJoo

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I just looked them up in wikipedia and FA. This is how I understand it:

The bacteriostatics are erythromycin, clindamycin, sulfamethoxazole, trimethoprim, tetracycline, and chloramphenicol

Note that erythromycin, clindamycin, tetracycline, and chloramphenicol all target the ribosome (tetracycline does 30s and the others do 50s). Macrolides also inhibit the 50s. They inhibit bacterial protein synthesis before bacteria can even attempt a cell division. So bacteria are "static" - they can still use the proteins they have, but can't get to the replication step because they can't make new proteins necessary for a proper division.

TMP/SMX act against dihydrofolate reductase and thus reduce the ability to make thymidine, which is necessary for DNA synthesis. Without necessary new thymidine, bacteria won't even try to replicate.

The bactericidals are vancomycin, fluoroquinolones, penicillin, aminoglycosides, cephalosporins, and metronidazole. I'm not sure, but you could probably also include polymyxins and quinolones here.

You can treat penicillin, cephalosporins, and vancomycin all together here. They all target the cell wall. The way I understand this is that an intact cell wall will not be affected but if bacteria attempt to replicate (and they will, since they have the protein and DNA apparatus to do so) these antibiotics will wreck the formation of new cell walls so the progeny is nonviable.

Quinolones and fluoroquinolones block DNA gyrase, so once the bacteria try to replicate, they are blocked in the midst of DNA synthesis and die. They don't "know" about the quinolones/fluoroquinolones until they've started DNA synthesis and then it's too late.

Metronidazole also attacks DNA, breaking the helical structure. I'd bet that it does this more so when the DNA is "vulnerable" i.e. during DNA synthesis (towards replication) than on DNA that's just sitting there.

Polymyxins destroy the cell membrane directly, so that would be toxic and bacteriocidal.

Aminoglycosides seem to have multiple mechanisms. They do target the 30s ribosome, but it also seems that they break up the external gram negative cell membrane. This is what I found on wikipedia:



So, aminoglycosides are bactericidal due to the membrane effect, not the ribosomal effect.

So, in recap, I would say that agents that target protein and nucleotide (TMP/SMX) synthesis are bacteriostatic whereas those that target DNA synthesis (metro, f/quin), the cell wall (vanc, pen, ceph), or the cell membrane (aminoglyc, polymyx) are bactericidal.


great thanks a lot that's exactly what i was looking for.
 

Blesbok

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Isn't this what also gives aminoglycosides there synergistic effects when used with beta-lactam antibiotics?
I think they are synergistic, because like you know the big limiting factor with aminoglycosides is their inability to enter the cell (hence the reason they only work on aerobes), but if you break up the cell wall it helps them enter the cell more effectively and therefore synergizes their effect. I am not 100%, but I am pretty sure I remember this being the reason.
 
7

78222

I just looked them up in wikipedia and FA. This is how I understand it:

The bacteriostatics are erythromycin, clindamycin, sulfamethoxazole, trimethoprim, tetracycline, and chloramphenicol

Note that erythromycin, clindamycin, tetracycline, and chloramphenicol all target the ribosome (tetracycline does 30s and the others do 50s). Macrolides also inhibit the 50s. They inhibit bacterial protein synthesis before bacteria can even attempt a cell division. So bacteria are "static" - they can still use the proteins they have, but can't get to the replication step because they can't make new proteins necessary for a proper division.

TMP/SMX act against dihydrofolate reductase and thus reduce the ability to make thymidine, which is necessary for DNA synthesis. Without necessary new thymidine, bacteria won't even try to replicate.

The bactericidals are vancomycin, fluoroquinolones, penicillin, aminoglycosides, cephalosporins, and metronidazole. I'm not sure, but you could probably also include polymyxins and quinolones here.

You can treat penicillin, cephalosporins, and vancomycin all together here. They all target the cell wall. The way I understand this is that an intact cell wall will not be affected but if bacteria attempt to replicate (and they will, since they have the protein and DNA apparatus to do so) these antibiotics will wreck the formation of new cell walls so the progeny is nonviable.

Quinolones and fluoroquinolones block DNA gyrase, so once the bacteria try to replicate, they are blocked in the midst of DNA synthesis and die. They don't "know" about the quinolones/fluoroquinolones until they've started DNA synthesis and then it's too late.

Metronidazole also attacks DNA, breaking the helical structure. I'd bet that it does this more so when the DNA is "vulnerable" i.e. during DNA synthesis (towards replication) than on DNA that's just sitting there.

Polymyxins destroy the cell membrane directly, so that would be toxic and bacteriocidal.

Aminoglycosides seem to have multiple mechanisms. They do target the 30s ribosome, but it also seems that they break up the external gram negative cell membrane. This is what I found on wikipedia:



So, aminoglycosides are bactericidal due to the membrane effect, not the ribosomal effect.

So, in recap, I would say that agents that target protein and nucleotide (TMP/SMX) synthesis are bacteriostatic whereas those that target DNA synthesis (metro, f/quin), the cell wall (vanc, pen, ceph), or the cell membrane (aminoglyc, polymyx) are bactericidal.

Well, I guess I can applaud your verbose posts so long as they aren't in the sociopolitical forum:thumbup::thumbup:
 

auburnO5

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I know this is an old thread... but it seems pretty helpful.

I have a question though:

We were told that Rifampin is bactericidal.

The mechanism of action for Rifampin is that it bind to the B subunit of bacterial RNA polymerase which inhibits RNA synthesis.

By using the logic above (which seems to be correct), wouldn't that make Rifampin bacteriostatic?

If anybody has an opinion on this, I would like to hear it!
 

dozitgetchahi

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I think they are synergistic, because like you know the big limiting factor with aminoglycosides is their inability to enter the cell (hence the reason they only work on aerobes), but if you break up the cell wall it helps them enter the cell more effectively and therefore synergizes their effect. I am not 100%, but I am pretty sure I remember this being the reason.

This is true.

Reading other posts, it is also worth noting that the combination of trimethoprim with sulfamethoxazole is generally considered to be bactericidal...and chloramphenicol is usually considered to be bactericidal as well (it may only be bacteriostatic against certain species).
 

aspiringdoc09

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I know this is an old thread... but it seems pretty helpful.

I have a question though:

We were told that Rifampin is bactericidal.

The mechanism of action for Rifampin is that it bind to the B subunit of bacterial RNA polymerase which inhibits RNA synthesis.

By using the logic above (which seems to be correct), wouldn't that make Rifampin bacteriostatic?

If anybody has an opinion on this, I would like to hear it!


Well my background is in biochemistry (B.S.) and soon to be microbiology (B.S.) by this spring, so hopefully it makes since.

Auburn, bacteriostatic = bacteria growth suppression and bactericidal = bacteria cell death. Think about these concepts in terms of the Central Dogma (DNA --> RNA --> Proteins). Rifampin works by preventing RNA synthesis, which means it will prevent protein synthesis. All cells rely on proteins for cellular functions, so no proteins = CELLULAR DEATH. What is the purpose of having genes? Answer: Protein production. Any cellular function you think of relies on a protein to carry it out/produce an effect. I hope this helps. Again, as mention earlier in this post, it is bacteriostatic if the antibiotic actions are reversible.
 
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