Hi everybody, Dr Mike here. In this video I'm going to help you memorize all the different antibiotic classes, whether they target gram-negative or gram-positive bacteria, some examples of each and also their mechanism of action. So let's begin with a mnemonic. The mnemonic to remember all the classes of antibiotics is going to be, the Queen's Guidance Counselor said antibiotics can protect many, if not most, royal members.
So just like every other mnemonic, take the first letter of each That's going to be the first letter of each of the antibiotic classes. So let's take a look. So for the, the T stands for tetracycline. The Q stands for quinolone and fluoroquinolone.
Fluoroquinolone. The G stands for glycopeptides. The C stands for Cephalosporins.
The S stands for Sulfonamides. The A stands for Aminoglycosides. The C stands for Carbopenem. The P stands for penicillin. The M, now here's the thing, we've got M, M, M. So, how do we remember?
So, I've made this a bit easier for you. The first two letters will help you here. So, M-A, macrolide.
So, I've got the macrolides. M-O, monobactam. R is rifampin and ME is metronidazole.
And here we go. We have the Queen's Guidance Council. I said antibiotics can protect many, if not most, royal members. And here are our antibiotic classes. Tetracycline, quinolone, fluoroquinolone, glycopeptide.
cephalosporin, sulfonamides, aminoglycosides, carbapenem, penicillin, macrolides, monobactin, rifampin, and metronidazole. Now, do they target gram-negative, gram-positive bacteria or both? So firstly, remember that bacteria have a cell wall.
We do not. This cell wall is a whole bunch of sugars packed on top of each other with proteins linking them together. Now you can have bacteria that has a really thick cell wall or bacteria that has a really thin cell wall. If you were to expose both of them to a purple dye, the one with the thick cell wall will absorb that dye and they look purple and we call that gram positive. The other one doesn't.
It comes up pinkish and we call that gram negative. And that's one way for us to classify bacteria. So Which of these affect gram positive or negative or both? Let's take a look.
Firstly, tetracycline. Both gram positive and gram negative. That's what it targets. Quinlone fluoroquinlone, also positive and negative. Glycopeptide, positive.
Cephalosporin, positive negative. Sulfonamides, positive negative. Aminoglycosides, negative only. Carbapenem, positive negative. Penicillin, both positive and negative.
Macrolides, positive only. Monobactam, negative only. refampin positive negative and metronidazole positive negative so what you can see is two positive negative than a positive two positive negative a negative two positive negative a positive than a negative and two positive negative so now what we've got is our classes and whether they target gram positive negative or both now here are some examples of each and I've pre loaded them up on the board so I don't misspell them and we have for tetracycline tetracycline and doxycycline. For quinolone, fluoroquinolone, we've got naledixic acid and ciproflaxacin respectively.
Glycopeptide, vancomycin, cephalosporin, ceftanil, sulfonamides, sulfamethoxazole. Aminoglycosides, the common gentamicin and streptomycin. For carbopenem, meropenem.
For penicillin, the common penicillin and amoxicillin. And the common erythromycin for macrolides. Yeah, for macrolides.
And then for monobactin, we've got the aztrionum. And for rifampin, we've got rifampin or rifampicin. And then for metronidazole, metronidazole. Now, most importantly, we need to take a look at how do these antibiotics work? What is their mechanism of action?
So like I said earlier with gram positive negative, bacteria have a cell wall. We don't. So what we need to do is exploit the differences.
When we have some sort of bacterial infection, we want to give ourselves a drug that don't kill our cells, but just kills the bacterial cells. So we need to exploit the differences between us. One of those differences is bacteria has a cell wall. If we damage that cell wall, basically the cell bursts. Now remember, inside of a bacteria, It is hyperosmotic.
That means it likes to drag water towards it. And the thing that stops it from dragging water towards it, and then swelling up and bursting, is that cell wall. So if we destroy the cell wall, either stop it from being synthesized, or we stop it from being maintained, it will burst. Let's have a look at the antibiotics that can do this.
So, first of which is going to be the glycopeptides. That inhibits cell wall synthesis. Then we've got the cephalosporins, they also inhibit cell wall synthesis. Then we've got the carbapenems, they also inhibit cell wall synthesis. Penicillins, we all know, inhibits cell wall synthesis.
And then we've got the monobactams, inhibits cell wall synthesis as well. Now they don't all do it the same way, they all do it slightly differently, yet in a similar fashion, but they're inhibiting that bacterial cell wall from being made or being maintained, which ends up making the bacteria burst. So that's one way we've exploited the cell wall.
What's another way? So remember that we have DNA that needs to go to RNA that needs to go to amino acids or pro-that fall to proteins. So DNA to RNA is transcription. RNA to proteins is translation. And bacteria do both of these different to us.
So first of which is the translation going, so reading the RNA to turn into amino acids that can fold into proteins. We have ribosomes, right? Ribosomes have two subunits, and basically the mRNA feeds into the subunits, we read it and spit out amino acids. So for us humans, our two subunits are 60S and 40S. But for bacteria, it's 30S and 50S.
So we can target specifically the ribosomal subunits, stopping translation from happening. So what we've got here is tetracycline. That specifically stops the 30S subunit of the ribosome.
Brilliant. We've also got the aminoglycosides. That stops the 30S subunit as well.
Again, stopping translation. And we've got the macrolides. This stops the 50S subunit. Brilliant. So, we can stop translation.
What else can we do? Well, let's take a look. If we look at the quinolones and fluoroquinolones, what we can do is in order, remember, if we take a look at the DNA of humans, our DNA is linear, but it's double stranded and it's wrapped around each other. But for bacteria, it's circular, but it's also double stranded and wrapped around each other. So in order for us to read our DNA, we need to unwind it.
So bacteria need to do that as well. But because they're slightly different, they use different enzymes to do this. Now both of those enzymes are called topoisomerases, topoisomerases, but they're different. Now here, the quinolones and fluoroquinolones, this is important. So for DNA synthesis to occur, we need to unwind it.
And the topoisomerase that bacteria use is topoisomerase 2 and topoisomerase 4. So we can inhibit. those two topoisomerases inhibiting DNA synthesis and that's what quinolones and fluoroquinolones do. Then if we take a look at the sulfonamides, what they actually do is they target folic acid synthesis.
So we need folic acid for survival. Now the difference is we get our folic acid from our food, bacteria has the enzyme to synthesize it. So since we don't have that enzyme, we can target that enzyme and if it doesn't work, No folic acid synthesis, no survival.
So we can target folic acid synthesis through the sulfonamides. Now the last two mechanisms is for rifampin and for metronidazole. How do they work?
So we've spoken about DNA synthesis, right? And we've spoken about here the 30S and 50S subunits, so translation. What about transcription, turning DNA to RNA? So this is using an RNA polymerase.
Now... That's what rifampin does, is it inhibits RNA polymerase. So you can say RNA polymerase.
So DNA transcription, that's what it inhibits. That's what rifampin does. And again, they use different polymerases to us. And then finally, metronidazole, very effective antibiotic. It works by actually just damaging.
The DNA. DNA damage. How does it do it? It oxidizes the DNA.
When you oxidize DNA, you pull electrons away from it. And then the DNA is damaged and cannot be read and no longer can be used. So what we've just worked through is... A mnemonic to remember all the classes of antibiotics.
Here they are here. Whether they target gram-positive, gram-negative bacteria. Some examples of each and also the mechanism of action of each. Hi everyone, Dr. Mike here.
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