Shadowing Practice: Antibiotics: Cell Wall Synthesis Inhibitors: Part 1 - Learn English Speaking with Video

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320 משפטים

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Alright engineers, in this video we're going to talk about antibiotics.

Alright, so the way we're going to do this is we're going to go through multiple different types of antibiotics.

We're not going to cover all of them.

It would just be impossible to cover all of them and all their different effects and mechanisms of action.

We're going to start off by looking at antibiotics that are affecting the cell wall.

So let's go ahead and start there.

So if you look here, now bacteria, if we're talking about gram positive or gram negative bacteria, we'll make a video on this,

but gram negative and gram positive bacteria really just differ and they're overall, like if I were to have, let's say I take for example here,

I take two bacterial cells, just real quickly.

Let's say here's a bacteria and here's a bacteria.

Let's say this is gram negative and let's say that this is gram positive.

The real big difference between gram negative and gram positive is that when you look at gram negative bacteria, they have a very thin peptidoglycan layer.

So their peptidoglycan layer that we're going to talk about that is very thin.

And another thing is that they have a cell membrane, an outer cell membrane surrounding that peptidoglycan layer.

And they have little porins inside of it, right?

So little porins.

A gram positive bacteria is the exact opposite.

It has a very very thick peptidoglycan layer, a very thick peptidoglycan layer.

Okay and that is going to be our gram positive.

So when we're looking at gram positive

and gram negative bacteria

it really is important to kind of have a basic idea of what their overall cell wall looks like

and overall cell structure is consisting of.

Okay so again one more time gram negative has a very thin peptidoglycan layer but has an outer cell membrane.

And it also has what's called lipopolysaccharides with lipid A and lipopolysaccharides and stuff like that that are the toxins.

And then over here, gram -positive bacteria just has a very thick peptidoglycan layer, but no outer cell membrane.

Okay, so now that we know that, let's go ahead and dig into antibiotics.

So the first antibiotics that we're going to talk about here, we're going to talk about the beta -lactams.

Okay, so we're going to focus here on our beta -lactams.

Now what is a beta -lactam?

Now just really really quickly it has a specific structure.

So if you look at a beta -lactam usually you have a five ring structure here

and then you have a little four ring structure right here

and then you have a little carbonyl and then you have this little nitrogen group here.

So it's kind of like a cyclic amide.

This right here is the beta -lactam, this component here, this is the beta -lactam.

So these beta -lactam antibiotics usually have this beta -lactam ring which is incorporated into it.

The beta -lactams we're going to focus on here, we're going to focus specifically on the penicillins.

So we'll talk about penicillin, specifically like penicillin G, and then we're going to talk about amoxicillin,

so amoxicillin, and then we're going to talk about cephalosporins.

And we'll talk about all the generations of cephalosporins okay before I do

that let's take a look at the overall cell wall structure

again just a little bit more in depth zooming in on

that peptidoglycan layer

if we look in the peptidoglycan layer what is a peptidoglycan

you see these blue structures right here those blue structures are specific derivatives of carbohydrates like glucose

so what do I mean they're made up of structures which is called NAM and NAG.

So they're just derivatives of glucose.

NAM, NAM, stands for N -acetylmuramic acid.

NAG stands for N -acetylglucosamine.

All these are, these blue structures here, they're just derivatives of our carbohydrates, like glucose.

Okay?

Now coming up off of these carbohydrate residues you see this like a violet structure coming up out of this

that right there is like peptide bonds actually a pentapeptide

and then across from

that again you're gonna have another what would this be this would be another anacetylmuramic acid

and this could be another anacetylglucosamine

these black proteins are coming downwards from this part too this is another pentapeptide

and if you look there this little orange structure that's the cross link between them that's the peptide bond between them

So this is the basic structure of our peptidoglycine layer in a zoomed look.

You see this little orange guy just kind of sitting down?

That's our penicillin binding protein.

So that little red structure right there, which is actually going to be sitting down there on the cell membrane,

is going to be the penicillin binding protein.

So what is this guy here called?

He's called the penicillin binding protein.

Okay, he's a pretty important structure here because he's really what a lot of these actual beta -lactams are binding onto.

Alright, next thing.

If you look here, these brown scissors, those are little autolytic enzymes.

We're going to talk about them.

And then these little C -like orange enzymes there, they're called beta -lactamases.

Okay, so this little orange structure up here, this orange structure here is called beta -lactamase.

and then these little brown structures there are actually going to be called autolytic enzymes.

Okay now that we've done that let's go over these antibiotics here.

All right penicillin first.

So penicillin it's it is able to treat in general gram -positive and gram -negative bacteria.

However However, over the past years,

certain bacteria have become resistant to penicillin.

Okay?

How have they become resistant to penicillin?

Okay.

This beta -lactamase, there's a specific part of its name, beta -lactamase.

So it's an enzyme, right?

So look what it can actually do.

I'm going to draw that beta -lactam ring over here.

And it's got that double bond right there with the NH and then it's got that little five -membered ring there.

This is our penicillin.

If we give someone penicillin who already has bacteria that are very resistant to the penicillin, what do I mean?

Maybe they have plasmids that allow for them to produce this enzyme called beta -lactamase.

What will the beta -lactamase do?

Boom.

It'll break the beta -lactam ring.

If it cuts the beta -lactam ring, this penicillin is not going to be able to bind to this penicillin binding protein and mediate its effects.

So because of this would be rendered ineffective.

So that is the importance as a certain bacteria become resistant by developing these beta -lactamases.

So really it's more effective now just being able to treat gram -positive bacteria with a little bit of gram -negative coverage.

So what type of bacteria is it able to cover?

It can cover streptococcal, okay that's the main one.

It can cover streptococcal bacteria.

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So any type of streptococcal bacteria.

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It was able to develop in the past treat staphylococcal bacteria but again they've developed resistance also.

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So streptococcal bacteria it's also able to treat syphilis.

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So just a little bit on the penicillin.

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So what is penicillin actually do?

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How does it mediate these effects that it can actually kill these bacteria because it's bactericidal meaning it can kill the bacteria.

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So let's say here here's the penicillin.

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What the penicillin does is it comes in and it binds on to this penicillin binding protein.

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So let's say that we draw that here.

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Here's the penicillin and he binds on to this penicillin binding protein.

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When he binds to the penicillin binding protein he stimulates the penicillin binding protein

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and what this penicillin binding protein does is it takes its hand

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and it comes up there and it stimulates these brown enzymes.

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So then what does it do?

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It comes up here and stimulates these autolytic enzymes.

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If these autolytic enzymes are activated, what are they gonna do?

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They're gonna start cutting up these bonds, these peptide bonds, these glycosidic bonds, and it's gonna start altering the overall structure of the cell wall.

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That's one thing that happens.

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Second thing that happens, there's a lot of other enzymes here.

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There is other enzymes that actually link these peptide bonds together between these little pentapeptides, so you're having different types of transpeptidase enzymes,

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whenever the penicillin binding protein is stimulated, he inhibits the transpeptidases from cross -linking these pentapeptides.

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And if these are no longer cross -linked, the cell wall starts becoming disrupted.

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Now, when the cell wall is disrupted, it allows for water to start leaking into the bacterial cells.

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And when water leaks into the bacteria cell eventually can cause the cell to lice.

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That is the way penicillin works.

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So again one more time because all the rest of them are gonna do the same thing.

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So once we know penicillin we know what these functions are too.

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So one more time what does penicillin do?

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Penicillin comes in binds onto the penicillin binding protein, stimulates him.

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When he becomes stimulated he stimulates these autolytic enzymes who start cleaving and breaking up the cell wall.

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Then he also inhibits, let's say that I draw this enzyme out here I'm just gonna draw some little dude out here.

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Here's this little dude and he's got his hand in this bond right there.

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Okay these are transpeptidase enzymes.

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What are these transpeptidase enzymes doing?

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They're helping to link these actual pentapeptides.

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He will inhibit these transpeptidase enzymes.

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So now they can no longer cross -link these little peptide chains and because that the cell wall will be disrupted.

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Once it's disrupted water can leak in.

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When water leaks in to cell lysis.

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Okay so we're set there.

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Amoxicillin, same mechanism of action.

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Cephalosporin, same mechanism of action.

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But now, Amoxicillin, he is very, very susceptible to these beta -lactamases.

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Very, very susceptible.

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So when you give someone Amoxicillin, you usually want to give it to them with clavulonic acid.

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Clavulonic acid.

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Why do you want to give that?

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Because clavulonic acid is a beta -lactamase inhibitor.

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So if you give them clavulonic acid, what is it going to do?

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It's going to inhibit the beta -lactamase enzyme.

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If the beta -lactamase is inhibited, now this amoxicillin is going to have more available to start exhibiting this effect.

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Okay, so that's the job of clavulonic acid.

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What can amoxicillin treat?

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It can treat a lot of different things.

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So amoxicillin is good at being able to treat urinary tract infections.

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He's good at being able to treat respiratory tract infections.

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He's also good at being able to treat meningitis.

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and he can also treat infections that are caused by salmonella too.

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So he can also treat infections caused by salmonella, and he's also really good at being able to treat middle ear infections, otitis media too.

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So otitis media, middle ear infections, right?

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Okay, so that is going to be the amoxicillin.

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So he's good at being able to treat urinary tract infections, respiratory tract infections, meningitis, salmonella, otitis media, okay?

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Cephalosporins, mechanism of action, same thing, activates the penicillin binding proteins and exerts all those effects.

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Cephalosporins though are very interesting.

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Okay, so there's four generations of cephalosporins, right?

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So let's go ahead and go over those real quickly.

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So they're first generation, so we could say first generation.

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So first generation is actually going to be, we could take for example, Cephalexin.

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So Cephalexin is one example here of a first generation Cephalosporum.

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Then we could take for example a second generation.

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Now a second generation would be like Cephiroxine.

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Okay and then we could take for example a third generation Cephalosporum.

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So a third generation Cephalosporum could be like ceftriaxone.

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And then there's even fourth generation.

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So fourth generation would be like cefepine.

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So fourth generation would be like cefepine.

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Now why am I mentioning this?

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Well the reason why is cephalosporins, the first and second generation,

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are really only good at being able to treat mainly gram positive bacteria.

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So these are really only good at being able to treat gram positive bacteria.

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Okay whereas what's happened over the years is that the ceftriaxone

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and the sepapine have actually had a little bit more ability to treat more of the gram negative bacteria.

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Okay so again first generation could be like cefalexan

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and second generation could be like cefiroxan but But the big takeaway is these aren't really used anymore, but they're good to treat gram -positive.

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Third generation, fourth generation have a little bit more gram -negative coverage.

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So like ceftriaxone and cefepine.

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Okay, so what would be the coverage?

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So for example, let's say that I used cefalexan and cefiroxine.

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They really only have gram -positive coverage.

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So what would I really use these guys for?

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I would probably use these guys for more of your Staphylococcus aureus and Streptococcus pyogenes.

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So even Streptococcus pyogenes.

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Okay?

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Now if we use Ceftriaxone and Cefepime, they can treat Gram -negative.

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So what could I use that for?

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I could use that to treat, they have a lot of things that they could treat.

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Pseudomonas is a really big one.

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They can treat Pseudomonas, so like Pseudomonas aeruginosa.

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They can treat certain types of bacteria that cause meningitis.

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They're also pretty good at being able to treat infections caused by Klebsiella.

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So Klebsiella, which is very common bacteria that can cause pneumonia.

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So pneumonia, this is actually a bacteria that can cause pneumonia.

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More commonly, it can cause other infections, but more commonly pneumonia.

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and even other different types of enterobacteria.

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So even different types of enterobacteria.

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All right.

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So that's our cephalosporins.

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There is other beta -lactams and different types of penicillin derivatives that I could have mentioned, like Piptazo.

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I could even have mentioned carbopanems.

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You know, Piptazo can treat pseudomonas.

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Carbopanems are actually good at being able to treat very, very...

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problematic abdominal infections so they can treat that too.

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Alright but that's pretty much going to cover our beta -lactam

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so quick review and then we're gonna move on to the next ones.

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Really?

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Here we go.

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Penicillins.

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What do they actually do?

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They're gonna come down here, bind onto the penicillin binding proteins, then what?

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Activate the autolytic enzymes which are gonna cut up some of the cell wall structures, disrupting the cell wall.

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Also penicillin binding proteins are going to inhibit these enzymes which are called transpeptidases.

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So if you inhibit them they can't cross -link these actual peptide chains.

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Cell walls disrupted.

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What happens as a result?

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Water leaks in and then eventually causes the cell to lice and kills the cell.

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So these are bactericidal, meaning they kill the bacteria.

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What could be certain types of beta -lactams?

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Penicillin, amoxicillin, cephalosporins, right?

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And I could even include carbapandums or pipericillin with tazobactam like piptazo.

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But again, what is penicillin treating?

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Gram positive and gram negative, mainly streptococcal because there's staphylococcal bacteria become resistant.

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He can also treat syphilis.

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What about amoxicillin?

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He's very very sensitive to the beta -lactamases who cleave the beta -lactam rings.

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So in order to make them effective, what do you give them with?

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Calavulonic acid.

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What can they treat?

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UTIs, respiratory tract infections, bacteria that cause meningitis, salmonella, otitis media.

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Okay, and then cephalosporins we said there are four main generations.

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There is five.

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Fifth I said can treat MRSA.

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First generation and second generation are mainly for gram -positive.

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First generation could be like cephalexin, second generation could be like cefiroxime, so they can treat staphylococcus aureus and streptococcus pyogenes.

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Okay, and then third and fourth generation are more for the gram -negative coverage, and so those third generations would be like ceftriaxone

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and cefepime, right? what can they treat like Pseudomonas aeruginosa meningitis Klebsiella

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which can cause pneumonia as well as enterobacteria okay what other kind of drugs affect the cell wall

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because there is other drugs besides these ones very very powerful one

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we have to mention this one this very very powerful one is actually called it's a glycopeptide

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so let's actually put that down

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so let's actually this is actually a group under the glycopeptides so what glycopeptides Glycopeptide is this.

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This glycopeptide is very very strong.

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This is called vancomycin.

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And vancomycin is actually really good at being able to treat MRSA.

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What is MRSA?

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MRSA stands for Methicillin Resistant Staphylococcus Aureus.

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Now Methicillin is an antibiotic but they don't really use that anymore.

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okay but certain bacteria have become resistant right to penicillins

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or methicillin so you have to get vanco because

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that can kill the MRSA okay

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now vanco is actually really good mainly at being able to treat gram -positive bacteria okay

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so like MRSA and C diff so Clostridium difficile colitis

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so it's good at being able to treat C diff

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so C diff is the one that makes you pee out your butthole all right

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so it's really nasty one really really infectious diarrhea

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and it also can treat certain types of bacteria

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which are like resistant resistant coagulase

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so coagulase negative now remember I'm saying negative resistant coagulase negative bacteria okay

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and this is vanco

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so vanco is a pretty powerful antibiotic

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now what is vancomycin do he does something different he has the overall same effect as these beta -lactams

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but different mechanism of action what exactly is he doing?

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Vanko is very very interesting so you know

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that every protein usually has what's called a carboxy terminus

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and then it has an amino terminus right and then really

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if I were to show this peptide bond correctly

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it's really what's linking this part together right here's what's interesting let's say I take Vanko if I give someone vanco,

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look what it's doing.

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It's binding onto this carboxyl end.

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When it binds onto the carboxyl end, this can't form a peptide bond.

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So now what happens is vancomycin binds onto the carboxyl end of these actual peptide chains.

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And if it blocks onto it, it hysterically hinders that peptide bond formation.

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So now if you can't form a peptide bond, this cell wall is disrupted.

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If the cell wall is disrupted what happens?

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Water flows in.

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As water flows in what happens?

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The cell lysis.

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So this is a bacteriocidal antibiotic.

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Okay so one more time.

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What is vanco doing?

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It's binding onto the carboxyl end of these peptide chains.

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As it binds onto the carboxyl end it sterically hinders this amine group from being able to form a peptide bond.

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And as a result the cell wall is disrupted, water enters in and the cell lysis.

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So it's a bacteriocidal antibiotic.

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Okay, so we've covered our glycopeptides.

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Now let's go over here

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and let's cover a very weird type of bacteria that's not for gram positive or gram negative bacteria.

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Okay, so this one that I'm going to talk about is mainly important for being able to treat tuberculosis.

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Okay, so it's mainly used to treat tuberculosis.

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So caused by the mycobacterium.

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Now mycobacterium don't have a cell wall that's made up of peptidoglycans.

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They are made up of these little orange structures.

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You know what these orange structures are called?

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They're called mycolic acid.

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So, and you see this enzyme right here, this blue enzyme?

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This blue enzyme is called a mycolic acid synthetase or synthase.

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It's called isoniazid.

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and again what is this antibiotic do this antibiotic is mainly treating tuberculosis caused by the mycobacterium

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so what it does is it has a specific point where it actually here let's say here's the isoniazid

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it's actually going to come in and inhibit this mycolic acid synthase

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or synthetase enzyme

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if this enzyme is inhibited can it synthesize the mycolic acids to make up the cell wall no

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and if it can't synthesize this mycolic acid the cell wall integrity is altered.

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If the cell wall's integrity is altered, can that cell survive?

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No. Water might flush into it and cause the bacteria to die.

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So again, isoniazid is used to treat tuberculosis caused by the mycobacterium.

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Its cell walls consisting of these mycolic acid residues.

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What happens is if you give isoniazid, it inhibits the mycolic acid synthetase or synthase enzyme, which then can no longer synthesize mycolic acid.

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If it can't synthesize mycolic acid, the cell walls integrity is altered and then what happens the bacterial cell dies.

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Okay all right guys so that pretty much covers on this part the antibiotics

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that are treating for specifically the cell wall synthesis and structure.

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In the next video we're going to talk about the antibiotics that are mainly used to target the folic acid pathway.

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אוצר מילים והערות הגייה לשיעור הזה

שיעור הדיבור הזה מבוסס על הסרטון “Antibiotics: Cell Wall Synthesis Inhibitors: Part 1”. המילים שחוזרות הכי הרבה: penicillin, cell, bacteria, treat, gram. בסרטון הזה יש 320 משפטים ו-3467 מילים לתרגול Shadowing. הדיבור נמשך 22:08. הדובר מדבר בקצב טבעי של כ-157 מילים בדקה, קרוב לשיחה יומיומית. רק 76% מהמילים נמצאות בין 3,000 המילים הנפוצות ביותר באנגלית, כך שאוצר המילים מאתגר.

אוצר מילים מרכזי בסרטון הזה

15 מילים מהסרטון שכדאי ללמוד, עם ההגייה והמשמעות שלהן:

מילה	הגייה	משמעות
gram שם עצם	/ˈɡɹæm/	גְרַם
beta שם עצם	/ˈbeɪtə/	בֵּיתָא
enzyme שם עצם	/ˈɛn.zaɪm/	אנזים
acid שם עצם	/ˈæsɪd/	חוּמצָה
antibiotic שם עצם	/ˌæn.taɪ.baɪˈɑ.tɪk/	אַנְטִיבְּיוֹטִיקָה
infection שם עצם	/ɪnˈfɛkʃən/	זיהום, זִהוּם
layer שם עצם	/ˈleɪ̯ɚ/	רוֹבֶד, שִׁכְבָה
mechanism שם עצם	/ˈmɛk.ə.nɪ.zəm/	מַנְגָּנוֹן
leak שם עצם	/liːk/	נְזִילָה
membrane שם עצם	/ˈmɛm.bɹeɪn/	קרום
pneumonia שם עצם	/njuˈməʊniə/	דַּלֶּקֶת רֵאוֹת
alter פועל	/ˈɔl.təɹ/	שינה, שִׁנָּה
tuberculosis שם עצם	/tʃuːˌbɜː(ɹ)kjʊˈləʊsɪs/	שחפת
thin שם תואר	/ˈθɪn/	דַּק
thick שם תואר	/θɪk/	עבה

Phrasal verbs שתשמעו

מילה	משמעות
sit down פועל	התיישב \ הִתְיַשֵּׁב

משפטים שכדאי לחזור עליהם

משפטים קצרים ושלמים מהסרטון שאפשר להשתמש בהם בשיחה יומיומית:

We're not going to cover all of them.
Let's say here's a bacteria and here's a bacteria.
You see this little orange guy just kind of sitting down?
Why do you want to give that?
You know what these orange structures are called?

דקדוק בסרטון הזה

המבנים שהדובר משתמש בהם הכי הרבה, עם המילים המדויקות מהסרטון:

מבנה	בסרטון
סביל (Passive voice) be + past participle — הדגש הוא על מה שקורה, לא על מי שעושה את הפעולה	is incorporated · is called · be called
הווה מושלם (Present perfect) have/has + past participle — פעולה שקרתה בעבר ועדיין יש לה חשיבות או השפעה עכשיו	we've done · have become · have they become
משפטי זיקה (Relative clauses) who / which + clause — מידע נוסף על אדם או דבר	ring which is · structures which is · there, which is

הגייה ששווה לשים לב אליה

הדובר משתמש ב-61 קיצורים וצורות מקוצרות, כמו we're, they're, gonna. אמרו אותם בצורה הקצרה, כפי שאתם שומעים אותם.

הצלילים של “th”: thin /ˈθɪn/, thick /θɪk/, synthesis /ˈsɪnθəsɪs/, pathway /ˈpæθˌweɪ/, synthesize /ˈsɪnθəsaɪz/
הצלילים של “sh” ו-“zh”: infection /ɪnˈfɛkʃən/, infectious /ɪnˈfɛk.ʃəs/, flush /ˈflʌʃ/
מילים ארוכות — שימו לב להטעמה: antibiotic /ˌæn.taɪ.baɪˈɑ.tɪk/, mechanism /ˈmɛk.ə.nɪ.zəm/, derivative /dɪˈɹɪvətɪv/, tuberculosis /tʃuːˌbɜː(ɹ)kjʊˈləʊsɪs/, integrity /ɪnˈtɛɡɹəti/

צלילים שדוברי עברית מתקשים בהם:

/w/ — שפתיים מעוגלות, לא /v/: whereas /(h)wɛɹˈæz/, pathway /ˈpæθˌweɪ/, downwards /ˈdaʊnwɚdz/, takeaway /ˈteɪkəweɪ/
/æ/ — פתוח יותר מה-“אֶ” העברית, לא כמו “a” ב-“cup”: gram /ˈɡɹæm/, acid /ˈæsɪd/, antibiotic /ˌæn.taɪ.baɪˈɑ.tɪk/, tract /tɹækt/, activate /ˈæktɪˌveɪt/
/r/ — הלשון לא נוגעת בשום מקום, לא ה-“ר” הגרונית: gram /ˈɡɹæm/, resistant /ɹəˈzɪstənt/, disrupt /dɪsˈɹʌpt/, membrane /ˈmɛm.bɹeɪn/, tract /tɹækt/

איך לתרגל עם הסרטון הזה

הקשיבו לכל הסרטון פעם אחת בלי לדבר, ורשמו את המילים שאתם לא מכירים.
התחילו במהירות 0.75×, תרגלו Shadowing משפט אחר משפט, וחזרו למהירות רגילה כשזה מרגיש קל.
הקליטו את עצמכם והשוו למקור, תוך תשומת לב למילים כמו gram, beta, enzyme.

מהי טכניקת השאדואינג?

שאדואינג היא טכניקת למידת שפה מבוססת מדע שפותחה במקור להכשרת מתורגמנים מקצועיים ופופולרית על ידי הפוליגלוט ד"ר אלכסנדר ארגואלס. השיטה פשוטה אך עוצמתית: אתה מקשיב לאודיו באנגלית ילידית וחוזר עליו בקול רם מיד — כמו צל העוקב אחרי הדובר עם עיכוב של 1–2 שניות בלבד. בניגוד להאזנה פסיבית או תרגילי דקדוק, שאדואינג מכריח את המוח והשרירים בפה לעבד ולשחזר דפוסי דיבור אמיתיים בו זמנית. מחקרים מראים שזה משפר משמעותית את דיוק ההגייה, האינטונציה, הקצב, הדיבור המחובר, הבנת השמיעה ושטף הדיבור — מה שהופך אותו לאחת השיטות היעילות ביותר להכנה לIELTS Speaking ולתקשורת באנגלית בעולם האמיתי.

טכניקת Shadowing: קרא את המדריך המלא שלב אחר שלב →

Shadowing Practice: Antibiotics: Cell Wall Synthesis Inhibitors: Part 1 - Learn English Speaking with Video

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