Differences Between Aminoglycosides and Macrolides

Very warm welcome to today's discussion. I just want to tell you that many of my very curious students have asked a question that how to differentiate between a monoglycosides and macrolides which share the same suffix myosin. What they're really asking that many of the monoglycosides at the end of their name they have myosin. In the same way, some of the rather most of the macrolide also at the end of their name they have mycin. So how to differentiate if those are monoglycoside which are having mycin at the end and those macrolide which are having mycin in the end, if they are put together, how do you differentiate between them, right? Let me tell you. This is the basic concept we are going to talk today. As we know that the first minoglycoside which was discovered was streptomycin. That was streptomycin and after that then there are other important minoglycosides for example tobramycin. Streptomycin was the very first drug which was successfully used in treatment of the tuberculosis. Then tobramycin About Tobramycin, you need to remember that those patients with cystic fibrosis, when they have infections in their lungs, we can use Tobramycin in inhalational form also and many other uses of course. So there's streptomycin, there's Tobramycin, there's canamycin and of course then there is neomycin and all of them are having in the end Mycin, right? Now the question is, number one, why these monoglycosides are having mycin at the end? And number two, how to differentiate these monoglycosides with the mycin as a suffix from the macrolides which are having mycin? As we know, the macrolide drugs which are having mycin at the end, classically the first of The first one to be discovered, the prototype was erythromycin. Okay, I will just write mycin everywhere. Erythromycin, then after that, molecular modification of erythromycin. produced better drugs. I will tell you in what way better, right? But prototype drug and the first one to be discovered was erythromycin and after that then we came up with clarithromycin and then we came with azithromycin and one of the more drug which is used that is roxymicin. Roxy throw, yes Roxy throw. Now you look at it. Erythro suffix at the end is myosin. As there was streptomycin, tobramycin, canamycin, neomycin. Here you see erythromycin, clarithromycin, azithromycin and roxithromycin. Now how do you differentiate them? for especially the medical students who are in third year or who are newly studying the antibiotic remember even though mycine is common and so common suffix on both sides but there is something very special which has been added to the macrolide group and that is throw that is throw now it is a throw mycin so if the word at the end is not mycin throw mycin You must think of that it is macrolide, right? And again, Clary is, yes, from here, what is this? Thromycin. Azine, Thromycin. Roxy, Thromycin. So, a very simple thing is that monoglycosides have a fix at the end, mycin. which i have written on the board right these are my no glycosides and these macrolides even though have mycin as the sphix but they have something just before that, that is throw. So, macrolides can be recognized and differentiated from aminoglycosides that they are not having only myosin, but just before the myosin, they are having throw. So, throw myosin, right? So, if I see XYZ drug and myosin, look. If I say there is XYZ drug ending up with myosin and I say that it is either a minoglycoside or macrolide, tell me what it is. So it must be? It must be? Yes, that must be a minoglycoside. But if I say there is another drug that is XYZ ending up with thromycin, then can it be a monocleicocyte? No, it is a macrolide. And here I would love to mention one more point. The one more point is all of these drugs, these are derived from soil bacteria called actinomycetes. Mycetes is the soil bacteria Actinomycetes. Now let me tell you something very interesting about these soil bacteria or environmental bacteria that Actinomycetes is are the source of most of the antibiotics which we are using presently. Most of the natural antibiotics which are derived, they are derived from actinomycetes and its subgroups, subgenus. 70 to 80% of the antibiotics. or their derivatives because actinomycetes are an inexhaustible source of bioactive products including many drugs which we use today. For example, from actinomycetes we drive yes antibacterial drugs we even drive antiviral drugs we drive antifungal drug From this we drive immunosuppressive drugs, even some of the anti-cancer drugs. So actinomycetes, this type of soil bacteria is a huge blessing for humanity that they are an inexhaustible source of different bioactive compounds which can be derived from actinomycetes and many of them are being used as medicinal drugs. Right? Now, actually, from where streptomycin, tobramycin, canamycin, neomycin and similar amino glycosides are derived? They are derived from Okay, I just want to make it. It's very proud because of its services. Yes, now one genus that is streptomyces genus, right? This streptomyces genus, which is a subtype of actinomycetes, you know, This is responsible for all these aminoglycosides which end up with mycin. Which are ending up with mycin. Right? And again, macrolides, erythromycin was also originally discovered and isolated from and other genus of actinomycetes and the new name of that genus is yes the new name of that genus is Sacropolispora erythrine. Sacro-polysporarythri-genus. Now, this genus is actually responsible to produce erythromycin and then with different chemical modifications of erythromycin we end up with better drugs like clarithromycin, azithromycin and even some other roxithromycin. I want to say one thing here the most common macrolide which is being used in the world is presently erythromycin. Why? I will tell you in few minutes. I will go back there and explain it to you but let's come back. Because one of the students also asked me that some of the minoglycosides, they don't end up at mycin, they end up at the mycin. Actually, for this purpose, for example, they end up not at mycin, right? Some of the minoglycosides, they end up with... Me-cine. Why is so? For example, these are which one? Yes. These are also myoclacocytes. I'm going to write. But they don't end up at mycine. They end up at mecine. For example, there is gentamicine. Gentamicine. Then there is nettle. and then there is yes what you are saying siso siso siso mesin and we can also put plazo mesin plazo mesin now question is these are monocleicocytes ending up with mycin These are also minoglycosides which are ending up with mycin. Why is so? Answer is that it is about their source. That is about their source. As I told you, minoglycosides which end up with mycin, they are basically derived from a genus, streptomyces genus. But... Those amino glycosides which end up not with mycin but end up with mycin, they are derived with a different genus of actinomycetes. And that different genus of streptomycetes is called micromanospora. Micromanospora. genus. So this genus is responsible for, this genus is the source of gentamicin, netalmicin, cisomicin or plasmicin. Gentamicin was the original to be discovered, others are derivatives of that. Right? Now... Let's have very few words about erythromycin, clarithromycin and azithromycin. As we know, the first drug which was discovered was, macrolide which was discovered was erythromycin. Erythromycin. But then what got popular? Clarithromycin. And then what got most popular? Azithromycin. Actually... Erythromycin was approved in 1952. Then, Calarythromycin was approved around 1991. And then Azithromycin was approved around 1992. Actually, I don't know, mother drug or father drug or parent drug, whatever its gender is, Erythromycin was the original drug. Then chemical modification is in its structure. resulted in formation of clarithromycin and further modification resulted in formation of azithromycin. Now The major question here I want to answer is why all over the world the use of parent compound erythromycin is progressively decreasing and why all over the world the use of erythromycin is progressively increasing? The answer lies in actually all of them work with the same mechanism of action. They inhibit the protein synthesis by acting on the inhibiting the function of 50S-tryposome. Even though the mechanism of action is same, but they have different pharmacokinetics, they have different side effect profile, and they have different propensity for drug to drug interaction. Let's start with it. Number one, when we altered Erythromycin chemically and resulted into clarithromycin and azithromycin from this position as you move down, pharmacokinetics favorably change. Even though erythromycin can be taken per oram, clarithromycin can also be taken per oram, and azithromycin can also be taken per oram. But there is difference. You know, erythromycin has a trouble. It is When you take it orally, if it is not enteric coated, it will be significantly destroyed by gastric acid. Secondly, it also produces lot of GIT irritation due to which, because before from GIT it gets absorbed, lot of it is destroyed. So its bioavailability is less. Not only bioavailability is less, But it's of course the result is half life is less, right? The result will be that when half life is less, you have to give multiple doses per day. So when we prescribe erythromycin, we have to use it every 6 hourly or 8 hourly. It means it may be TDS or QID, right? More frequent dosing. which of course reduces the compliance. Secondly, as I told you, but as you move down, these drugs are acid stable. So they don't need to be enterically coated. And as they are not destroyed within the GIT by the acid, so their absorption is better. So bioavailability is better. Then what happens? Serum levels go up, half-life is better, their tissue penetration is better, even calerithromycin and azithromycin better enter into bacteria. And azithromycin in good concentration enters even in macrophages if some bacteria are there. So what does it mean? It means that... As calarythromycin and azithromycin have longer half-life and better penetration, so we need to give less frequent doses. For example, calarythromycin rather than TDS, we can do 12-hourly, BD, right? And azithromycin is having even longer half-life, even we have extended formulation. due to that reason we can give it once a day. So this was the first thing which I wanted to impress on my students mind, right? That why erythromycin is becoming less popular and why clarithromycin and even azithromycin especially is becoming very popular. There are many reasons. One reason I told you that erythromycin is not acid stable. So bioavailability is less, then absorb, of course, what is this? Half-life is less, tissue penetration is less, cellular penetration is less, right? And we need to give more frequent doses which translate into less tolerability and less compliance. Erythromycin has more side effects. As you move down, right, even side effects decrease, right? As calarythromycin, azithromycin, I told you they are acid stable. So they are better absorbed, they have better bioavailability, better half-life, and better penetration in the tissues, better penetration and distribution. not only into whole body but even in the cells, even in bacteria, even in macrophages. So this is one thing that we have to do it three to four times a day. This we can give it twice a day and here the dosing can be once in a day. Of course, it's a significant advantage. Second thing is not only about its pharmacokinetics, there's another thing and that is about spectrum of activity. You know erythromycin mainly act on gram positive bacteria, right? Aerobic gram positive bacteria. But calarythromycin and azithromycin, they have broader spectrum of activity. I will not go into detail of this thing in this lecture, right? Because this lecture is really only I intended in the beginning to teach that how to differentiate between those amino glycoside and macrolide which have a shearless fix myosin. But I thought just give few words about this. Now let me come back. So what I was talking about that as compared to erythromycin, erythromycin has broader antimicrobial spectrum and erythromycin is still more broad. antimicrobial spectrum so that is another plus point right so that makes azithromycin more popular than erythromycin then side effects profile yes side effects gastrointestinal side effects for example i will not narrate and differentiate all side effects but i will just mention touch the two number one erythromycin very common gastrointestinal side effects but as compared to that Clarithromycin and azithromycin have far less gastrointestinal side effects or gastrointestinal irritability and if we go for serious side effects yes now listen with your both ears if you talk about serious side effects erythromycin can produce side effects which act on the cardiac heart rhythm Long QT interval and arrhythmias can precipitate dangerous arrhythmias. But when you move from erythromycin to clarithromycin to azithromycin, the tendency to produce dangerous cardiac side effects is also reduced. Dangerous cardiac side effects are also reduced. Then another thing which I would love to mention is drug-drug interaction. Erythromycin and Clarithromycin. These two drugs are very notorious to produce drug-drug interaction because Erythromycin and Clithromycin, both of them affects the function of cytochrome p. Right? In the special subset of cytochrome p, which also deals with many other drugs right so when you are using taking these two drugs erythromycin and clarithromycin erythromycin or clarithromycin and if you are taking some other drugs like lipid lowering drugs or some other drugs or there's already there's already some pathology in the liver you should not take these drugs right because If there is already some pathology in the liver, they can act as a petrotoxic. They interfere with the function of the cytochrome P subsets which lead to drug-drug interactions also. But when you come to the azithromycin, yes the beautiful, the king, the king macrolide, azithromycin, it has the minimal interaction with the cytochrome P450 subset. which also handles many other drugs due to that reason azithromycin has minimal drug drug interaction and especially minimal prolonged qt interval arrhythmia precipitating tendency right so these are few words that in a nutshell you should remember that Erythromycines, clarithromycine, azithromycine, roxithromycine Actually don't remember that mycine is in the end Keep in mind throw also So remember they are throw mycines through my sins right so my sins gone but the important thing you need to remember first drug was erythromycin and now it is being less commonly used and now most commonly used drug is azithromycin which is derivative from the erythromycin why azithromycin is so popular because azithromycin has better pharmacokinetics has better side effects and less side effects and it is having broader spectrum of antimicrobial activity and of course it is having yes less drug drug interaction. In the end I would say don't forget aminoglycosides and macrolides both work on both work on ribosomal protein synthesis machinery in the bacteria and Both of them are concerned with the mechanism of infection is to reduce the protein synthesis in susceptible bacteria. Right? Here we can draw a simple picture like 30S unit and here it is. Yes, 50S unit and this is 50S and this is 30S unit. This is in bacteria. Actually, minoglycosides attack at 30s unit one way to remember is buy at buy at 30 if you are good businessman buy at 30 add stand aminoglycoside and tetracyclines so buy at 30 means that aminoglycosides mainly act on 30s subunit and tetracyclines also mainly act on the 30s unit and sell at sell at if you have bought at 30 if you're good businessman sell at yes 50. so 50s that includes erythromycin that include what is this chloramphenicol c for chloramphenicol e for erythromycin this is for lincosamize see it which is basically your clindamycin and this is linezo lead so drug groups what is this c stands for chloramphenicol act on 50s subunit erythromycin and associates act on 50s unit lincosamide especially clindamycin act on 50s subunit and then we talk about linezolid it's a new drug and that's also act on 50s unit right but even though aminoglycoside also inhibits the protein synthesis in bacteria by acting at 30s unit macrolide inhibits the protein synthesis in susceptible bacteria by acting at 50s subunit but there is still big difference you know what is that that this drug, yes, this drug is bactericidal. It kills the bacteria by inhibiting protein synthesis. It means it inhibits the protein synthesis in a very aggressive way. Right? That I will explain in the next lecture, upcoming lecture, that mechanism of action of Aminoglycoside because most of the protein synthesis inhibitors are bacteriostatic. But it is one of the exception which is bactericidal. Why it is so? That will be seen in next lecture and macrolide of course they are bacteriostatic. Right? Like most of the protein synthesis inhibitors. Right? So that's all for today. Thank you very much. See you later.

In the same way, some of the rather most of the macrolide also at the end of their name they have mycin. So how to differentiate if those are monoglycoside which are having mycin at the end and those macrolide which are having mycin in the end, if they are put together, how do you differentiate between them, right? Let me tell you.

This is the basic concept we are going to talk today. As we know that the first minoglycoside which was discovered was streptomycin. That was streptomycin and after that then there are other important minoglycosides for example tobramycin. Streptomycin was the very first drug which was successfully used in treatment of the tuberculosis.

Then tobramycin About Tobramycin, you need to remember that those patients with cystic fibrosis, when they have infections in their lungs, we can use Tobramycin in inhalational form also and many other uses of course. So there's streptomycin, there's Tobramycin, there's canamycin and of course then there is neomycin and all of them are having in the end Mycin, right? Now the question is, number one, why these monoglycosides are having mycin at the end?

And number two, how to differentiate these monoglycosides with the mycin as a suffix from the macrolides which are having mycin? As we know, the macrolide drugs which are having mycin at the end, classically the first of The first one to be discovered, the prototype was erythromycin. Okay, I will just write mycin everywhere.

Erythromycin, then after that, molecular modification of erythromycin. produced better drugs. I will tell you in what way better, right?

But prototype drug and the first one to be discovered was erythromycin and after that then we came up with clarithromycin and then we came with azithromycin and one of the more drug which is used that is roxymicin. Roxy throw, yes Roxy throw. Now you look at it.

Erythro suffix at the end is myosin. As there was streptomycin, tobramycin, canamycin, neomycin. Here you see erythromycin, clarithromycin, azithromycin and roxithromycin. Now how do you differentiate them?

for especially the medical students who are in third year or who are newly studying the antibiotic remember even though mycine is common and so common suffix on both sides but there is something very special which has been added to the macrolide group and that is throw that is throw now it is a throw mycin so if the word at the end is not mycin throw mycin You must think of that it is macrolide, right? And again, Clary is, yes, from here, what is this? Thromycin.

Azine, Thromycin. Roxy, Thromycin. So, a very simple thing is that monoglycosides have a fix at the end, mycin.

which i have written on the board right these are my no glycosides and these macrolides even though have mycin as the sphix but they have something just before that, that is throw. So, macrolides can be recognized and differentiated from aminoglycosides that they are not having only myosin, but just before the myosin, they are having throw. So, throw myosin, right?

So, if I see XYZ drug and myosin, look. If I say there is XYZ drug ending up with myosin and I say that it is either a minoglycoside or macrolide, tell me what it is. So it must be?

It must be? Yes, that must be a minoglycoside. But if I say there is another drug that is XYZ ending up with thromycin, then can it be a monocleicocyte? No, it is a macrolide.

And here I would love to mention one more point. The one more point is all of these drugs, these are derived from soil bacteria called actinomycetes. Mycetes is the soil bacteria Actinomycetes.

Now let me tell you something very interesting about these soil bacteria or environmental bacteria that Actinomycetes is are the source of most of the antibiotics which we are using presently. Most of the natural antibiotics which are derived, they are derived from actinomycetes and its subgroups, subgenus. 70 to 80% of the antibiotics. or their derivatives because actinomycetes are an inexhaustible source of bioactive products including many drugs which we use today. For example, from actinomycetes we drive yes antibacterial drugs we even drive antiviral drugs we drive antifungal drug From this we drive immunosuppressive drugs, even some of the anti-cancer drugs.

So actinomycetes, this type of soil bacteria is a huge blessing for humanity that they are an inexhaustible source of different bioactive compounds which can be derived from actinomycetes and many of them are being used as medicinal drugs. Right? Now, actually, from where streptomycin, tobramycin, canamycin, neomycin and similar amino glycosides are derived? They are derived from Okay, I just want to make it. It's very proud because of its services.

Yes, now one genus that is streptomyces genus, right? This streptomyces genus, which is a subtype of actinomycetes, you know, This is responsible for all these aminoglycosides which end up with mycin. Which are ending up with mycin.

Right? And again, macrolides, erythromycin was also originally discovered and isolated from and other genus of actinomycetes and the new name of that genus is yes the new name of that genus is Sacropolispora erythrine. Sacro-polysporarythri-genus. Now, this genus is actually responsible to produce erythromycin and then with different chemical modifications of erythromycin we end up with better drugs like clarithromycin, azithromycin and even some other roxithromycin.

I want to say one thing here the most common macrolide which is being used in the world is presently erythromycin. Why? I will tell you in few minutes. I will go back there and explain it to you but let's come back. Because one of the students also asked me that some of the minoglycosides, they don't end up at mycin, they end up at the mycin.

Actually, for this purpose, for example, they end up not at mycin, right? Some of the minoglycosides, they end up with... Me-cine.

Why is so? For example, these are which one? Yes. These are also myoclacocytes.

I'm going to write. But they don't end up at mycine. They end up at mecine.

For example, there is gentamicine. Gentamicine. Then there is nettle.

and then there is yes what you are saying siso siso siso mesin and we can also put plazo mesin plazo mesin now question is these are monocleicocytes ending up with mycin These are also minoglycosides which are ending up with mycin. Why is so? Answer is that it is about their source.

That is about their source. As I told you, minoglycosides which end up with mycin, they are basically derived from a genus, streptomyces genus. But... Those amino glycosides which end up not with mycin but end up with mycin, they are derived with a different genus of actinomycetes.

And that different genus of streptomycetes is called micromanospora. Micromanospora. genus.

So this genus is responsible for, this genus is the source of gentamicin, netalmicin, cisomicin or plasmicin. Gentamicin was the original to be discovered, others are derivatives of that. Right? Now... Let's have very few words about erythromycin, clarithromycin and azithromycin.

As we know, the first drug which was discovered was, macrolide which was discovered was erythromycin. Erythromycin. But then what got popular? Clarithromycin.

And then what got most popular? Azithromycin. Actually...

Erythromycin was approved in 1952. Then, Calarythromycin was approved around 1991. And then Azithromycin was approved around 1992. Actually, I don't know, mother drug or father drug or parent drug, whatever its gender is, Erythromycin was the original drug. Then chemical modification is in its structure. resulted in formation of clarithromycin and further modification resulted in formation of azithromycin.

Now The major question here I want to answer is why all over the world the use of parent compound erythromycin is progressively decreasing and why all over the world the use of erythromycin is progressively increasing? The answer lies in actually all of them work with the same mechanism of action. They inhibit the protein synthesis by acting on the inhibiting the function of 50S-tryposome. Even though the mechanism of action is same, but they have different pharmacokinetics, they have different side effect profile, and they have different propensity for drug to drug interaction. Let's start with it.

Number one, when we altered Erythromycin chemically and resulted into clarithromycin and azithromycin from this position as you move down, pharmacokinetics favorably change. Even though erythromycin can be taken per oram, clarithromycin can also be taken per oram, and azithromycin can also be taken per oram. But there is difference.

You know, erythromycin has a trouble. It is When you take it orally, if it is not enteric coated, it will be significantly destroyed by gastric acid. Secondly, it also produces lot of GIT irritation due to which, because before from GIT it gets absorbed, lot of it is destroyed.

So its bioavailability is less. Not only bioavailability is less, But it's of course the result is half life is less, right? The result will be that when half life is less, you have to give multiple doses per day.

So when we prescribe erythromycin, we have to use it every 6 hourly or 8 hourly. It means it may be TDS or QID, right? More frequent dosing.

which of course reduces the compliance. Secondly, as I told you, but as you move down, these drugs are acid stable. So they don't need to be enterically coated. And as they are not destroyed within the GIT by the acid, so their absorption is better.

So bioavailability is better. Then what happens? Serum levels go up, half-life is better, their tissue penetration is better, even calerithromycin and azithromycin better enter into bacteria. And azithromycin in good concentration enters even in macrophages if some bacteria are there. So what does it mean?

It means that... As calarythromycin and azithromycin have longer half-life and better penetration, so we need to give less frequent doses. For example, calarythromycin rather than TDS, we can do 12-hourly, BD, right? And azithromycin is having even longer half-life, even we have extended formulation. due to that reason we can give it once a day.

So this was the first thing which I wanted to impress on my students mind, right? That why erythromycin is becoming less popular and why clarithromycin and even azithromycin especially is becoming very popular. There are many reasons. One reason I told you that erythromycin is not acid stable. So bioavailability is less, then absorb, of course, what is this?

Half-life is less, tissue penetration is less, cellular penetration is less, right? And we need to give more frequent doses which translate into less tolerability and less compliance. Erythromycin has more side effects. As you move down, right, even side effects decrease, right?

As calarythromycin, azithromycin, I told you they are acid stable. So they are better absorbed, they have better bioavailability, better half-life, and better penetration in the tissues, better penetration and distribution. not only into whole body but even in the cells, even in bacteria, even in macrophages. So this is one thing that we have to do it three to four times a day.

This we can give it twice a day and here the dosing can be once in a day. Of course, it's a significant advantage. Second thing is not only about its pharmacokinetics, there's another thing and that is about spectrum of activity.

You know erythromycin mainly act on gram positive bacteria, right? Aerobic gram positive bacteria. But calarythromycin and azithromycin, they have broader spectrum of activity. I will not go into detail of this thing in this lecture, right? Because this lecture is really only I intended in the beginning to teach that how to differentiate between those amino glycoside and macrolide which have a shearless fix myosin.

But I thought just give few words about this. Now let me come back. So what I was talking about that as compared to erythromycin, erythromycin has broader antimicrobial spectrum and erythromycin is still more broad.

antimicrobial spectrum so that is another plus point right so that makes azithromycin more popular than erythromycin then side effects profile yes side effects gastrointestinal side effects for example i will not narrate and differentiate all side effects but i will just mention touch the two number one erythromycin very common gastrointestinal side effects but as compared to that Clarithromycin and azithromycin have far less gastrointestinal side effects or gastrointestinal irritability and if we go for serious side effects yes now listen with your both ears if you talk about serious side effects erythromycin can produce side effects which act on the cardiac heart rhythm Long QT interval and arrhythmias can precipitate dangerous arrhythmias. But when you move from erythromycin to clarithromycin to azithromycin, the tendency to produce dangerous cardiac side effects is also reduced. Dangerous cardiac side effects are also reduced.

Then another thing which I would love to mention is drug-drug interaction. Erythromycin and Clarithromycin. These two drugs are very notorious to produce drug-drug interaction because Erythromycin and Clithromycin, both of them affects the function of cytochrome p. Right?

In the special subset of cytochrome p, which also deals with many other drugs right so when you are using taking these two drugs erythromycin and clarithromycin erythromycin or clarithromycin and if you are taking some other drugs like lipid lowering drugs or some other drugs or there's already there's already some pathology in the liver you should not take these drugs right because If there is already some pathology in the liver, they can act as a petrotoxic. They interfere with the function of the cytochrome P subsets which lead to drug-drug interactions also. But when you come to the azithromycin, yes the beautiful, the king, the king macrolide, azithromycin, it has the minimal interaction with the cytochrome P450 subset.

which also handles many other drugs due to that reason azithromycin has minimal drug drug interaction and especially minimal prolonged qt interval arrhythmia precipitating tendency right so these are few words that in a nutshell you should remember that Erythromycines, clarithromycine, azithromycine, roxithromycine Actually don't remember that mycine is in the end Keep in mind throw also So remember they are throw mycines through my sins right so my sins gone but the important thing you need to remember first drug was erythromycin and now it is being less commonly used and now most commonly used drug is azithromycin which is derivative from the erythromycin why azithromycin is so popular because azithromycin has better pharmacokinetics has better side effects and less side effects and it is having broader spectrum of antimicrobial activity and of course it is having yes less drug drug interaction. In the end I would say don't forget aminoglycosides and macrolides both work on both work on ribosomal protein synthesis machinery in the bacteria and Both of them are concerned with the mechanism of infection is to reduce the protein synthesis in susceptible bacteria. Right?

Here we can draw a simple picture like 30S unit and here it is. Yes, 50S unit and this is 50S and this is 30S unit. This is in bacteria. Actually, minoglycosides attack at 30s unit one way to remember is buy at buy at 30 if you are good businessman buy at 30 add stand aminoglycoside and tetracyclines so buy at 30 means that aminoglycosides mainly act on 30s subunit and tetracyclines also mainly act on the 30s unit and sell at sell at if you have bought at 30 if you're good businessman sell at yes 50. so 50s that includes erythromycin that include what is this chloramphenicol c for chloramphenicol e for erythromycin this is for lincosamize see it which is basically your clindamycin and this is linezo lead so drug groups what is this c stands for chloramphenicol act on 50s subunit erythromycin and associates act on 50s unit lincosamide especially clindamycin act on 50s subunit and then we talk about linezolid it's a new drug and that's also act on 50s unit right but even though aminoglycoside also inhibits the protein synthesis in bacteria by acting at 30s unit macrolide inhibits the protein synthesis in susceptible bacteria by acting at 50s subunit but there is still big difference you know what is that that this drug, yes, this drug is bactericidal. It kills the bacteria by inhibiting protein synthesis.

It means it inhibits the protein synthesis in a very aggressive way. Right? That I will explain in the next lecture, upcoming lecture, that mechanism of action of Aminoglycoside because most of the protein synthesis inhibitors are bacteriostatic. But it is one of the exception which is bactericidal. Why it is so?

That will be seen in next lecture and macrolide of course they are bacteriostatic. Right? Like most of the protein synthesis inhibitors. Right? So that's all for today.

Thank you very much. See you later.

Transcript for:Differences Between Aminoglycosides and Macrolides

Transcript for:
Differences Between Aminoglycosides and Macrolides