Antibiotics: Cell Wall Synthesis Inhibitors: Part 1

Summary

このビデオでは、抗生物質に関する基本的な知識と、主に細胞壁に作用する抗生物質について解説しています。ペニシリンやアモキシシリン、头孢菌素類をはじめとするβラクタム系抗生物質のメカニズムと抗性菌への対応方法を紹介。さらに、鎮痛剤ヴァンコマイシンの効能と、結核治療に用いるイソニアジドの働きについても触れています。

Takeaways

• 🔬 このビデオでは、抗生物質について説明され、特に細胞壁に作用する抗生物質に焦点が当てられています。
• 🌟 抗生物質のカテゴリーは多岐にわたりますが、全てを網羅することは困難であり、特にβラクタム系抗生物質に注目されています。
• 📚 グラム陽性菌とグラム陰性菌の細胞壁の違いについて説明され、それぞれ異なるペプチドグリカン層と細胞膜の構造に注意が喚起されています。
• 💊 ペニシリンは、主にグラム陽性菌と一部のグラム陰性菌に作用し、ペニシリン結合蛋白に結びつき、細胞壁の合成を妨害します。
• 🛡️ βラクタム系抗生物質は、ペニシリン結合蛋白を刺激して自壊酵素を活性化し、細胞壁の構造を崩壊させることで細菌を殺菌します。
• 💔 一部の細菌はβラクタムアゼを産生し、ペニシリンのβラクタム環を切断することで抗生物質の作用を無効にすることができます。
• 💊 アモキシシリンはペニシリンに似た作用機構を持ちますが、βラクタムアゼに対して非常に敏感であり、通常クロバニル酸と一緒に使用されます。
• 🌐 セファロスポリンは4つの世代に分類されており、第1世代と第2世代は主にグラム陽性菌に作用し、第3世代と第4世代はグラム陰性菌にも広範に作用します。
• 💪 バンコマイシンは、グラム陽性菌に特化しており、特にMRSA（メチシリン耐性金黄色葡萄球菌）やC.diff（クローストリジウム難病）に効果的です。
• 🛠️ バンコマイシンは、ペプチドグリカン層のカルボキシル末端に結びつき、ペプチド結合を妨害することで細胞壁の合成を中断し、細菌を殺菌します。
• 💊 イソニアジドは結核を治療するために使用され、マイコリック酸合成酵素を阻害して細胞壁の整合性を損なうことで細菌を殺菌します。

Q & A

βラクタム系抗生物質とはどのような構造を持つ物質ですか？

βラクタム系抗生物質は、5つのリング構造と4つのリング構造を持ち、カーボンと窒素を含む特別な構造を持っています。これはβラクタムという名称の由来で、一般的に環状アミドという構造を持っています。

ペニシリンGやアモキシシリン、および頭孢菌素類はどのように細菌を殺菌するのですか？

これらの抗生物質はペニシリン結合蛋白に結びつき、自己分解酵素を活性化させたり、トランスペプチダーゼの交差リンキングを阻害することで、細菌の細胞壁構造を破壊します。細胞壁が破壊されると、水分が細菌細胞内に漏れ出し、最終的には細胞が溶解して細菌を殺菌します。

ペニシリンの抗生物質作用はどのようにして細菌に抵抗性を持たせることができますか？

βラクタムアーゼという酶を発現させることで、細菌はペニシリンのβラクタムリングを切断し、ペニシリン結合蛋白に結合できなくなります。これにより、ペニシリンの殺菌効果が失われるため、細菌は抗生物質に耐性が持ちます。

アモキシシリンはなぜクローワラン酸と一緒に使用されるのですか？

アモキシシリンはβラクタムアーゼに対して非常に敏感で、この酶によってβラクタムリングが切断されます。クローワラン酸はβラクタムアーゼの抑制剤であり、共用することでアモキシシリンの効果を高めることができます。

頭孢菌素類にはいくつの世代がありますか？それぞれ何の特徴がありますか？

頭孢菌素類には4つの世代があります。第1世代と第2世代は主に革陽性菌に作用し、第3世代と第4世代は革陰性菌にも効果があります。各世代の頭孢菌素類は、細菌に対する広範な抗生物質効果を提供しています。

バンコマイシンはどのような細菌に対抗するために使用されますか？

バンコマイシンは、メチシリン耐性黄色ブドウ球菌（MRSA）やクローストリジウムジフシレン感染症（C.diff）など、革陽性菌に対抗するために使用されます。

バンコマイシンはどのように細胞壁の合成を妨害するのですか？

バンコマイシンはペプチドチェーンのカーボキシル末端に結合し、ペプチドボンド形成を阻害します。これにより、細胞壁の構造が破壊され、細菌細胞が溶解して死滅します。

イソニシアジドは結核を治療するためにどのように作用しますか？

イソニシアジドは、結核菌のマイコリック酸合成酵素を阻害し、細胞壁のマイコリック酸の合成を妨害します。細胞壁の整合性が失われると、細菌細胞は死亡します。

ペニシリン結合蛋白とは何であり、抗生物質の作用にどのように関与しますか？

ペニシリン結合蛋白は、細菌の細胞壁合成に関与する酵素であり、βラクタム系抗生物質が結合する標的です。これらの抗生物質がペニシリン結合蛋白に結合することで、細胞壁の合成が妨害され、細菌を殺菌する効果が得られます。

細菌が抗生物質に耐性を持つメカニズムにはどのようなものがありますか？

細菌はβラクタムアーゼを産生することでβラクタム系抗生物質に耐性を持つことができます。また、他の抗生物質に対しても、抗生物質排出系、抗生物質分解酵素、または抗生物質標的の変異など、様々なメカニズムを通じて耐性を獲得する可能性があります。

Outlines

00:00

🔬 抗生物質の基礎知識とβラクタム系抗生物質

この段落では、抗生物質の基礎知識とβラクタム系抗生物質について説明しています。抗生物質は細菌の細胞壁に作用し、主にグラム陽性菌とグラム陰性菌の細胞壁の違いについて触れています。βラクタム系抗生物質は、ペニシリン、アモキシシリン、およびセフェム系を含み、細胞壁の合成を阻害することで細菌を殺菌します。ペニシリン結合蛋白に結びつき、オートリティック酵素を活性化し、細胞壁の構造を破壊します。

05:02

🛡️ 抗生物質による細胞壁構造の破壊メカニズム

この段落では、ペニシリンが細胞壁をどのように破壊するかについて詳しく説明しています。ペニシリンはペニシリン結合蛋白に結びつき、オートリティック酵素を刺激して細胞壁の構造を変化させ、細菌を殺菌するメカニズムを説明しています。また、抗生物質の耐性、特にβラクタム酶によるペニシリンの無効化についても触れられています。

10:02

💊 アモキシシリンとセフェム系抗生物質の治療範囲

アモキシシリンはβラクタム酶に対する敏感性があり、クローヴュラン酸と併用することで有効性を高めています。この段落では、アモキシシリンが治療できる疾患の範囲、例えば尿路感染や呼吸器感染、髄膜炎、サルモネラ感染、中耳炎などについて説明しています。セフェム系抗生物質も同様の作用機序を持っており、世代ごとに異なる細菌に対する治療効果があります。

15:02

🌟 セフェム系抗生物質の世代別特徴と治療対象

セフェム系抗生物質には4つの世代があり、それぞれ異なる細菌に対する治療効果を持っています。この段落では、第1世代と第2世代のセフェム系抗生物質が主にグラム陽性菌に作用し、第3世代と第4世代はグラム陰性菌にも効果があることを説明しています。具体的な抗生物質の名前と治療対象についても触れられています。

20:03

💥 ガンコマイシンの作用機序と抗生物質の他効果

ガンコマイシンは、グラム陽性菌に特に有効で、MRSAを含む耐性菌にも作用する抗生物質です。この段落では、ガンコマイシンが細胞壁の合成に必要なペプチドブオンド形成を阻害し、細菌を殺菌するメカニズムについて説明しています。さらに、他の抗生物質が細胞壁合成に作用する以外にも、フォリク酸経路を阻害する抗生物質も存在することを示唆しています。

🤒 抗結核薬イソニアジドの作用と抗生物質の応用

最後の段落では、結核を引き起こすマイコバクテリアに対する抗結核薬イソニアジドの作用機序について説明しています。マイコバクテリアの細胞壁はペプチドグリカンではなく、マイコリック酸から成り立っており、イソニアジドはこのマイコリック酸合成酵素を阻害して細胞壁の整合性を損なうことで細菌を殺菌します。

Keywords

💡抗生物質

抗生物質とは、微生物や細菌などの成長や繁殖を抑制する物質を指し、このビデオでは主に細菌に対する作用について説明しています。ビデオでは抗生物質が細菌の細胞壁や他の細胞構造を妨害し、細菌を殺菌するメカニズムに焦点を当てています。

💡β-ラクタン

β-ラクタンは、抗生物質の一種で、細菌の細胞壁合成を阻害する化学構造を持つ物質です。ビデオでは、ペニシリンやアモキシシリン、頭胞菌類がこのグループに属し、細菌のペニシリン結合蛋白に結びつき、細胞壁の合成を妨害する作用機序について説明しています。

💡ペニシリン結合蛋白

ペニシリン結合蛋白は、細菌の細胞壁合成に関与する酵素であり、β-ラクタン抗生物質が結びつく標的です。ビデオでは、ペニシリンがこの蛋白に結びつき、細胞壁の構造を破壊し、細菌を殺菌するプロセスを解説しています。

💡細菌の耐性

細菌の耐性とは、細菌が抗生物質の作用を回避する能力を獲得した状態です。ビデオでは、β-ラクタン酶という酵素によって細菌がβ-ラクタン抗生物質の作用を無効にしてしまう耐性メカニズムに言及しています。

💡アモキシシリン

アモキシシリンは、β-ラクタン抗生物質の一種で、広範な細菌感染に対する治療に用いられます。ビデオでは、アモキシシリンがβ-ラクタン酶に対して非常に感受性があり、クローワラン酸と併用することでその耐性を克服することができると説明しています。

💡頭胞菌類

頭胞菌類は、β-ラクタン抗生物質の一種で、複数の世代に分類され、細菌の細胞壁合成を阻害します。ビデオでは、1世代から4世代までの頭胞菌類が異なる細菌に対する効果を持つと説明し、特に3世代と4世代がグラム陰性細菌にも効果があると述べています。

💡β-ラクタン酶

β-ラクタン酶は、細菌が抗生物質のβ-ラクタン環を切断し、その抗生物質の作用を無効にする酵素です。ビデオでは、この酵素が細菌がβ-ラクタン抗生物質に耐性を持つメカニズムとして働くプロセスを解説しています。

💡クローワラン酸

クローワラン酸は、β-ラクタン酶を阻害するβ-ラクタン酶抑制剤です。ビデオでは、アモキシシリンとクローワラン酸を併用することで、β-ラクタン酶の作用を抑制し、アモキシシリンの抗生物質効果を高める方法について説明しています。

💡バニコマイシン

バニコマイシンは、グリコペプチドの一種で、特にMRSA（メチシリン耐性黄色葡萄球菌）に対する治療に用いられます。ビデオでは、バニコマイシンが細胞壁の合成を妨害し、細菌を殺菌するメカニズムについて述べています。

💡イソニアジド

イソニアジドは、結核を引き起こすマイコバクテリウムに対して使用される抗生物質です。ビデオでは、この薬剤が細菌の細胞壁のマイコリック酸の合成を阻害し、細胞壁の整合性を損なう作用について解説しています。

Highlights

视频讨论了多种抗生素及其作用机制，但无法涵盖所有类型。

介绍了革兰氏阳性和阴性细菌的细胞壁结构差异。

β-内酰胺类抗生素，如青霉素和头孢类，通过影响细胞壁合成来杀菌。

青霉素通过结合青霉素结合蛋白，激活自溶酶，破坏细胞壁。

细菌对青霉素的抗药性主要是通过产生β-内酰胺酶实现。

阿莫西林与克拉维酸合用可抑制β-内酰胺酶，增强药效。

头孢类抗生素有四代，每代对革兰氏阳性和阴性细菌的覆盖范围不同。

第一代和第二代头孢类主要治疗革兰氏阳性细菌。

第三代和第四代头孢类增加了对革兰氏阴性细菌的治疗能力。

万古霉素作为糖肽类抗生素，用于治疗甲氧西林耐药金黄色葡萄球菌(MRSA)。

万古霉素通过结合肽链的羧基末端，阻止细胞壁合成，导致细菌死亡。

异烟肼是治疗结核病的主要药物，通过抑制结核分枝杆菌的细胞壁合成。

抗生素的作用机制包括激活自溶酶、抑制转肽酶，导致细胞壁破裂和细菌死亡。

抗生素的抗药性问题日益严重，需要合理使用以减缓抗药性发展。

视频将在未来讨论针对叶酸途径的抗生素。

抗生素的分类和使用需根据细菌类型和感染情况来决定。

视频提供了对抗生素作用机制的深入理解，有助于合理用药。

Transcripts

all right engineers in this video we're

going to talk about antibiotics all

right so the way we're going to do this

is we're going to go through at 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 it's

going to start there so if you look here

now bacterial if we're talking about

grandpa's anima gram-negative bacteria

we'll make a video on this but

gram-negative and gram-positive bacteria

really just differ and their 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

the bacteria and here's the bacteria

let's say this is gram-negative and

let's say this is gram positive the real

big difference between gram-negative and

gram-positive is that when you to look

at gram-negative bacteria they have a

very thin peptidoglycan layer so they're

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

pores 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 grand positive so 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 an

overall cell structure is consisting of

okay so again one more time

gram-negative has a very thin

peptidoglycan layer but as an outer cell

membrane it also has what's called

lipopolysaccharides with lipid a and let

me probably saccharides and stuff like

that that are the toxins and I'm here

grand positive bacteria just as 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 5 ring

structure here and then you have a

little 4 ring structure right here and

then you have a little carbon eel 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 you

usually have this beta-lactam ring which

is incorporated into it okay 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

okay 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 the

peptidoglycan you see these blue

structures right here

those blue structures are specific

derivatives of carbohydrates like

glucose so what do I mean there are made

up of structures which is called NAMM

and nag so they're just derivatives of

glucose n am NAMM stands for in acetyl

uric acid in Ag stands for in acetyl

glucosamine 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 bond is

actually a pentapeptide and then across

from that again you're going to have

another what would this be this would be

another an acetyl Meramec acid and this

could be another and acetyl glucosamine

these black proteins are coming

downwards from this part to 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

right

so this is the basic structure of our

peptidoglycan 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 going to

what he's really what a lot of these

actual beta lactams are binding on to

alright next thing if you look here

these brown scissors those are little

auto lytic enzymes so we're going to

talk about them and then these little C

like orange enzymes there they're called

beta lactam ASIS ok so this little

orange structure up here this orange

structure here is called beta lactamase

and then these little brown structures

they are actually going to be called

Auto lytic enzymes okay now that we've

done that let's go over these

antibiotics here alright penicillin

first so penicillin it's it is able to

treat in general gram-positive and

gram-negative bacteria however over the

past you know 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 it today 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 the 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 though 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 that this will

be rendered ineffective

so that is the importance is that

certain bacteria become resistant by

developing beta-lactam Isis

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 a recover if you may it

can cover streptococcal okay that's the

main one it can cover streptococcal

bacteria so any type of streptococcal

bacteria okay it was able to develop you

know in the past treat you know

staphylococcal bacteria but again

they've developed resistance also so

streptococcal bacteria it's also able to

treat syphilis okay

so just a little bit on the penicillin

so what does penicillin actually do how

does it mediate these effects that it

can actually kill these bacteria because

it's bacteria SCYTL meaning you can kill

the bacteria so let's say here here's

the penicillin what the penicillin does

is it comes in and it binds on to this

penicillin binding protein so let's say

that we draw that here here's the

penicillin and he binds on to this

penicillin binding protein when he binds

to the penicillin binding protein he

stimulates the penicillin binding

protein and what this penicillin binding

protein does is it takes its hand and it

comes up there and it stimulates these

brown enzymes so then what does it do it

comes up here and stimulates these auto

lytic enzymes if these auto analytic

enzymes are activated what are they

going to do they're going to start

cutting up these bonds these peptide

bonds these glycosidic bonds and it's

going to start altering the overall

structure of the cell wall that's one

thing that happens second thing that

happens there's a lot of other enzymes

here there is other enzymes that

actually link these peptide bonds

together between these little

pentapeptides

so you get for having different types of

transpeptidase enzymes

whenever the penicillin binding protein

is stimulated he inhibits the

transpeptidase is from cross linking

these pentapeptides and if these are no

longer cross-linked the cell wall starts

becoming disrupted now when the cell

wall is disrupted it allows for water to

start leaking into the bacterial cells

and when water leaks into the

Piersol eventually can cause the cell to

lyse that is the way penicillin works so

again one more time because all the rest

of them are gonna do the same thing so

once we know penicillin we know what

these functions are - so one more time

what does penicillin do penicillin comes

in binds onto the penicillin binding

protein stimulates him when he becomes

stimulated he stimulates these Auto

lytic enzymes who start cleaving and

breaking up the cell wall then he also

inhibits let's say that I draw this

enzyme out here I'm just going to draw

some little dude out here here's this

little dude and he's got his hand in

this bond right there okay these are

transpeptidase enzyme what are these

transpeptidase enzymes doing they're

helping to link these actual

pentapeptides

he will inhibit these transpeptidase

enzymes so now they can no longer cross

link these little peptide chains and

because that the cell wall will be

disrupted

once it's disrupted water can leak in

when water leaks in to cell lysis okay

so we're set there amoxicillin same

mechanism of action cephalosporins same

mechanism of action but now amoxicillin

he is very very susceptible to these

beta lactamase is very very susceptible

so when you give someone a moxa stealing

you usually want to give it to them with

clavulanic acid

clavo lonex acid why do you want to give

that because clavulanic acid is a

beta-lactamase inhibitor so if you give

them clavulanic acid what is it going to

do it's going to inhibit the beta

lactamase enzyme if the beta lactamase

is inhibited now this amoxicillin is

going to have more available to start

exhibiting this effect okay so that's

the job of clavulanic acid

what can a moxa sill entreat it can

treat a lot of different things so

amoxicillin is good at being able to

treat urinary tract infections he's

going to being able to treat respiratory

tract infections he's also good at being

able to treat meningitis and he can also

treat infections that are caused by

salmonella - so we can also treat

infections caused by salmonella and you

know he's also really good at being able

to treat

middle ear infections on Titus media too

so Titus media middle ear infections

right okay so that is going to be the

amok Ahsan so he's going to be able to

treat urinary tract infections

respiratory tract infections meningitis

salmonella otitis media okay

cephalosporins mechanism of action same

thing activates the penicillin binding

proteins and inserts all those effects

cephalosporins though are very

interesting okay so there's four

generations of cephalus horns right so

let's go ahead and go over those real

quickly so their first generation

so we could say first generation so

first generation is actually going to be

we could take for example

cephalexin so cephalexin is one example

here of a first generation cephalosporin

then we could take for example a second

generation now a second generation will

be like Seth a rock scene set for rock

scene okay and then we could take for

example a third-generation cephalosporin

so a third-generation cephalosporin

could be like ceftriaxone and then

there's even fourth generation so fourth

generation would be like cefepime so

fourth generation would be like cefepime

now why am i mentioning this well the

reason why is cephalosporins the first

and second generation are really only

good at being able to treat mainly gram

positive bacteria so these are really

only good at being able to treat gram

positive bacteria okay whereas what's

happened over the years is that the

ceftriaxone and the SEPA pean have

actually had a little bit more ability

to treat more of the gram-negative

bacteria okay so again first generation

could be like cephalexin and second

generation could be like cefuroxime but

the big takeaway is these aren't really

used anymore but they're good to treat

gram positive third generation fourth

generation have a little bit more gram

negative coverage so except try Oksana

cefepime

okay so what would be the coverage so

for example let's say that I used

cephalexin and cefuroxime they really

only have grand positive coverage so

what I really use these guys for I would

probably use these guys for more of your

Staphylococcus aureus and streptococcus

pyogenes so even streptococcus pyogenes

okay now if we use ceftriaxone and

cefepime they can treat gram-negative so

what can I use that for I could use that

to treat them they have a lot of good

things that they could treat

now Pseudomonas is a really big one they

can treat Pseudomonas so like

Pseudomonas aeruginosa they can treat

certain types of bacteria that cause

meningitis um they're also pretty good

at being able to treat infections caused

by Klebsiella so Klebsiella which is

very common a bacteria that can cause

pneumonia so pneumonia so this is

actually a bacteria that cause pneumonia

more commonly it can cause other

infections but more commonly pneumonia

and even other different types of entero

bacteria so even different types of

inteiro bacteria all right so that's our

cephalosporins there is other beta

lactams and different types of

penicillin derivatives that I could have

mentioned like pip Tazo I could have

been to mention carbapenems you know a

pip Tazo can treat Pseudomonas

carbapenems are actually going to be

able to treat very very problematic

abdominal infections so they can treat

that too all right but that's pretty

much going to cover our beta lactam so a

quick review and we're going to move on

to the next ones really here we go

penicillins what do they actually do

they're going to come down here by onto

the penicillin binding proteins then

what activate the auto lytic enzymes

which we're going to cut up some of the

cell wall structures disrupting cell

wall also penicillin binding proteins

are going to inhibit these enzymes that

are called trans peptidases so if you

inhibit them they can't cross link these

actual peptide chains cell walls

disrupted what happens as a result water

leaks in and then eventually cause the

cell

to lice and kills itself so these are

bacteria sidle you need to kill the

bacteria what could be certain types of

beta lactams penicillin amoxicillin

cephalosporins right and I can even

included carbapenems or pepper selling

with hazel back in like pip Tazo but

again what is penicillin treating grand

positive and gram-negative mainly

streptococcal because there's a

staphylococcal bacteria become resistant

he can also treat syphilis

what about amoxicillin he's very very

sensitive to the beta lactamase is who

cleaved the beta lactam rings so in

order to make them effective what are

you give them with clavulanic acid what

can they treat UTIs respiratory tract

infections bacteria that cause

meningitis salmonella otitis media okay

and then cephalus points you said there

are four main generations there is five

fifth I said can you eat Marissa first

generation second generation are mainly

for gram positive first generation could

be like cefalexin second generation

could be like cefuroxime so they can

treat Staphylococcus aureus and

streptococcus pyogenes okay and then

third and fourth generation are more for

the gram-negative coverage and so those

third generations to be like ceftriaxone

and cefepime right what can they treat

like Pseudomonas aeruginosa meningitis

Klebsiella which can cause pneumonia as

well as entero bacteria okay what other

kind of drugs affect the cell wall

because there is other drugs besides

these ones very very powerful one we

have to mention this one this very very

powerful one is actually called it's

like glycol peptide

so let's actually put that down so let's

actually this is actually a group under

the glycol peptides

so what glycol peptide is this this

glycol peptide is very very strong this

is called Vanko Mison and vancomycin is

actually really good at being able to

treat mersa what is what is Marissa

Marissa stands for methicillin-resistant

Staphylococcus aureus now methicillin is

an antibiotic but they don't really use

that anymore okay but certain bacteria

have become resistant right to

penicillin or methicillin so you have to

give Vanko because that can kill the

Marissa

okay now venko is actually really good

mainly at being able to treat gram

positive bacteria okay so like MRSA and

c-diff so Clostridium difficile colitis

so it's good at being able to treat c

diff so c diff is the one that makes you

pee out your butthole all right so it's

really nasty one really really

infectious diarrhea and it also can

retreat certain types of bacteria which

are like resistant resistant coagulase

so coagulase negative now remember i'm

saying negative resistant coagulates

negative bacteria okay and this is Vanko

so vanko's are pretty powerful

antibiotic now what does vancomycin do

he does something different he has the

overall same effect of these beta

lactams but different mechanism of

action what exactly is he doing thank ou

is very very interesting so you know

that every protein usually has what's

called a carboxy terminus and then as an

amino terminus right and then really if

I were to show the peptide bond

correctly it's really what's linking in

this part together right here's what's

interesting let's say I take Vanko if I

give someone Vanko look what it's doing

it's binding onto this carboxyl end when

it binds onto the carboxyl end this

can't form a peptide bond so now what

happens is vancomycin binds onto the

carboxyl end of these actual peptide

chains and if it blocks onto it Xterra

Clee hinders that peptide bond formation

so now if you can't form a peptide bond

this cell wall is disrupted if this cell

wall is disrupted what happens water

flows in as water flows in what happens

the cell lysis so this is a bacterial

cell antibiotic okay so one more time

what does Vanko doing it's binding onto

the carboxyl end of these peptide chains

as it binds on to the carboxyl end it's

sterically hindered this amine group

from being able to form a peptide bond

and as a result of cell wall is

disrupted water enters in and the cell

lysis so it's a bacterial Seidel

antibiotic okay so we've covered our

glycol peptides now let's go over here

let's cover a very

weird type of bacteria that's not for

grandpas and for gram negative bacteria

okay so this one that I'm going to talk

about is mainly important for being able

to treat tuberculosis okay so it's

mainly used to treat tuberculosis so

caused by the Mycobacterium now

Mycobacterium don't have a cell wall

that's made up of peptidoglycan they are

made up of these little orange

structures you know what these orange

structures are called they're called

mycolic acid so can you see this enzyme

right here this blue enzyme this blue

enzyme is called a mycolic acid synthase

source in space it's called I so nyeh

SID and again what is this antibiotic do

this antibiotic is mainly treating

tuberculosis caused by the Michel

bacterium so what it does is it has a

specific point word actually here let's

say here's the isoniazid it's actually

going to come in and inhibit this

mycolic acid synthase our synthetase

enzyme if this enzyme is inhibited can

it synthesize the mycolic acids to make

up the cell walls no and if it can't

synthesize this mycolic acid the cell

wall integrity is altered if the cell

walls integrity is altered can that cell

survive no water might flush into it and

cause the bacteria to die so again

isoniazid is used to treat tuberculosis

caused by the micro bacterium it's cell

walls consisting of these mycolic acid

residues what happens is if you give

ionize it and hits the mycolic acid

synthesis or synthase enzyme which then

can no longer synthesize mycolic acid if

it can't synthesize mycolic acid the

cell walls integrity is altered and then

what happens the bacterial cell dies

okay alright guys so that pretty much

covers on this part the antibiotics that

are treating for specifically the cell

wall synthesis and structure in the next

video we're going to talk about the

antibiotics that are mainly used to

target the folic acid pathway