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Antibiotics

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Lab

Antibiotics Introduction

0:07what's up ninja nerds in this video

0:08today we're going to be talking about

0:10antibiotics and there is so much to talk

0:12about it is insane here's what i really

0:14want you guys to do i'm telling you it

0:16will really benefit you if you do this

0:18go down the description box below click

0:20on the link to our website when you get

0:22to the website download the

0:24illustrations for this video it is going

0:26to be crucial have the one where we have

0:29everything on the whiteboard where it's

0:30not filled out and then have the key

0:32where everything is already filled out

0:34and follow along we'll do it together

0:36and then i urge you guys antibiotics are

0:38tough there's so much to remember keep

0:41going through those and keep testing

0:42yourself trying to fill everything in

0:44multiple times until you fill it out on

0:46your own without having to look at the

0:47key i'm urging you guys to please do

0:49this this is a lot to cover it'll be

0:51hard to remember everything but i think

0:53i organized it in a way that will help

0:54you guys to remember so let's talk about

0:56antibiotics all right so let's talk

Mechanism of Action

0:58about how antibiotics work against

0:59bacteria particularly their mechanism of

1:01action how do they kill or reduce the

1:04actual growth of gram positive gram

1:06negative bacteria anaerobic bacteria

1:08atypical bacteria how do they do that

1:10and so i think the way that we can

1:11categorize this is based upon the

1:13structure of the bacteria there's

1:15different components of the actual

1:16bacteria the first one that is important

1:18is the cell wall so the cell wall is

1:20made up of peptidoglycans and it's

1:22cross-linked by these different types of

1:23tetrapeptides there's a lot of proteins

1:25that work in that area called like

1:26penicillin binding proteins or trans

1:29peptidases as you can call them

1:31if we can inhibit some of the enzymes

1:33that either synthesize peptidoglycan

1:35layers within the cell wall that'll

1:37inhibit the cell wall synthesis and if

1:39we don't have the cell wall the bacteria

1:42won't have the ability to divide

1:43properly and also it's susceptible to

1:46things leaking in and out of the cell

1:47introducing the opportunity for

1:49bacterial death

1:51now

1:52there's two ways within the cell wall

1:54synthesis

1:55one is we can decrease the

1:58peptidoglycan synthesis

2:00i'll say okay so we can actually just

2:02reduce the synthesis of peptidoglycans

2:05and there's two antibiotics that i want

2:07you to remember that are qualified

2:08within that category the first one is

2:11vancomycin

2:13the second one that you may not have

2:15actually heard about too often because

2:16we only really use it in like acute

2:19cystitis is phosphomycin

2:22so phosphomycin okay so that's one type

2:24of actual category of antibiotics that

2:27work to inhibit the cell wall synthesis

2:29of the actual bacteria by inhibiting the

2:31peptidoglycans that are the component of

2:33that actual cell wall the other thing

2:36is we can actually reduce the

2:37cross-linking so the cross-linking via

2:40the tetrapeptides

2:42of the peptidoglycans is crucial because

2:46this helps to stabilize the actual cell

2:48wall and if you reduce the cross-linking

2:50via the penicillin binding proteins you

2:52then reduce the ability of the cell wall

2:53to be synthesized and this is

2:55susceptible now to bacterial cell death

2:58there is a plethora of antibiotics

3:01within this category of reducing the

3:04cross-linking let's talk about these the

3:06first one that i want you to remember is

3:07your natural penicillins and there's two

3:09types of penicillins that i want you to

3:10remember the first one is your

3:12penicillin g this comes in the im or the

3:15iv form

3:16the other one is your penicillin v

3:19this is more of the p.o form okay

3:22the next group so you have your natural

3:24penicillins penicillin g penicillin v

3:26the

3:27anti-staphylococcal penicillins is how i

3:29like to remember these

3:30so this would be a couple different ones

3:32you have what's called oxacillin which

3:34is going to be in an iv form

3:36you have naphthalene which is another

3:38type of iv form and then you have the

3:40only po form which is dicloxacillin

3:45okay so these are the different groups

3:47for that one the next group that i want

3:49you guys to remember is the amino

3:50penicillins the amino penicillins are

3:53very interesting

3:54and this consists of primarily

3:56amoxicillin

3:59and ampicillin

4:02now we'll talk about these later but

4:04certain types of bacteria have developed

4:06resistance against the actual

4:08penicillinase bacteria penicillinase so

4:11they'd actually develop these different

4:12types of enzymes certain bacteria called

4:14beta-lactamases which break down the

4:16beta-lactam ring of the penicillins

4:18that's what these are called your

4:19beta-lactams

4:21they can break them down and render the

4:22antibiotic ineffective

4:24so what happens is we often take these

4:27these drugs that are penicillinase like

4:28susceptible and we add on something

4:32called a beta lactamase inhibitor that

4:34we'll talk about over there we commonly

4:36add on amoxicillin plus something called

4:37clavillonate to make amoxicillin

4:40clavillon also known as augmentin

4:42or ampicillin plus what's called

4:44sulbactum which is ampicillin sulbactum

4:47also known as unison so that is the

4:50group here natural penicillins

4:51anti-staphylococcal penicillins and

4:52aminopenicillins the next one here is

4:54your anti-pseudomonal penicillins very

4:56very commonly utilized drug category

4:59here you'll see this so many times

5:01utilized in the hospital and this is

5:04called pipicillin

5:05now pippericillin is a really

5:06interesting one because there is some

5:08types of resistance from certain types

5:10of bacteria they have what's called

5:11beta-lactamase inhibitors

5:13you can actually utilize them so they

5:14are beta-lactamases you can use an

5:16inhibitor with this actual drug here

5:18it's called tazobactum and so commonly

5:20we never give pepperocillin by itself we

5:22give it what's called pipracillin

5:24tazobactum also known as zosim and so

5:27commonly this will also get added to a

5:29beta-lactamase inhibitor which we'll

5:30talk about

5:32all right that's our penicillins again

5:34we're all talking about this whole

5:36category here we actually put them in

5:37the category called beta-lactams it's

5:40just the structure of the actual

5:41penicillin or the beta-lactams they have

5:43like a ring and that beta-lactam ring is

5:45the important component to a lot of

5:47these drugs here your penicillins your

5:48cephalosporins your carbopenems and your

5:50monobactins all right the next group

5:52within your betalactams is your

5:53cephalosporins and there is actually

5:55five generations of cephalosporins and

5:58as we go down you'll see they have they

6:00go from gram-positive coverage to more

6:02gram-negative coverage as you go down

6:04but we'll get into that when we get into

6:05antibiotic coverage in the spectrum but

6:07for the first generation cephalosporins

6:10i want you to remember here for these

6:12you have something called cefazolin and

6:14this is an interesting drug also known

6:16as anceph and the other one is

6:18cephalexin cephalexin these are the two

6:21primary antibiotics that you'll utilize

6:24second gen to be honest with you i don't

6:25think i've ever seen them utilize i

6:26don't know what happened to these dang

6:28things but your second gen are going to

6:29be something like cephaclor

6:32sufoxetin

6:35cephotin but again

6:38not too commonly utilized to be honest

6:40with you

6:41third generation cephalosporin are the

6:42workhorse of antibiotics to be honest

6:44with you these are utilized pretty

6:46heavily with the big one being

6:48ceftriaxone it's a pretty solid agent

6:50cefotaxine

6:52and to be honest with they don't see

6:53this one too commonly utilized but

6:54ceftriax on a big one and then another

6:56one that's also commonly utilized is

6:57called ceftazidime

6:59so it's ceftazadine so again first gen

7:02cephalexin and cephazolam pretty

7:04commonly utilized drugs second

7:06generation cephalus of oxatin cephotene

7:08not too commonly utilized third gen big

7:10workhorses especially ceftriaxone and

7:12ceftasidine your fourth generation is

7:15primarily going to be with something

7:16called cephepeme

7:18and your fifth generation if you've got

7:20heavy pockets because this is extremely

7:22expensive drug is called cephtaryline

7:26okay so again that covers the

7:28cephalosporins for the beta active so we

7:29got our natural penicillins

7:31anti-staphylococcal amino and

7:32anti-pseudomonal and then we got our

7:34first through fifth generation

7:35cephalosporins all a part of this

7:37beta-lactam group which reduces the

7:39cross-linking of peptidoglycans the one

7:40that reduced the synthesis is vanco and

7:43phospho there's two more categories here

7:45these are called your carbapenems these

7:47antibiotics they're like taking a

7:49grenade and just throwing it into a pool

7:50back here they'll kill anything but

7:51these are really broad agents and so you

7:53can remember these by the mnemonic dime

7:55so you have what's called dory penum

8:00you have what's called emmy penum

8:03you have something called marrow

8:06penum

8:07and then you have something called urtra

8:10penum these are beast agents the last

8:13one is a monobactin and this is actually

8:15called astrinum and really the claim to

8:18fame for this antibiotic is really just

8:20if you have those penicillin allergic

8:21patients but it's also a super broad

8:23agent gram negative coverage and

8:25sometimes pseudomonas as well but this

8:27would be a lot of your beta-lactams and

8:28again remember your beta-lactams they're

8:30pretty intense drugs your natural

8:32penicillins anti-staphylococcal amino

8:34anti-pseudomonas penicillins is a good

8:36way to categorize these

8:38your first through fifth generation

8:39cephalosporins your carbapenums and your

8:41monobactums now

8:43vancophospho out of these i would

8:45remember vanco vanco's a really good

8:47glycopeptide and again it inhibits the

8:49pipettor glycogen synthesis

8:51for the last thing here before we

8:53actually go through all the other

8:54antibiotics is we have to talk about

8:55this thing called beta-lactamase

8:57innovators so some bacteria very nasty

9:00bacteria have the ability to produce a

9:02very interesting enzyme so naturally we

9:05have a protein called a penicillin

9:08binding protein

9:10and this is the one that actually

9:11synthesizes the peptidoglycan layer

9:14right it helps to be able to take the

9:16names and the nags that make up the

9:17peptidoglycan layer and cross link them

9:19via the tetrapeptide connections

9:21we can utilize antibiotics

9:24and what these antibiotics do let's

9:25imagine here is your antibiotic what

9:27it'll do is it'll bind to the penicillin

9:29binding protein and inhibit it so it

9:31can't synthesize the cell wall or cross

9:33link them

9:34what happened is we actually developed

9:36these bacteria these nasty little

9:38bacteria they actually produced an

9:40enzyme they developed a resistance

9:41mechanism where they produce something

9:43called a beta

9:44lactamase and what this beta-lactamase

9:46does is it takes the beta-lactam

9:48antibiotics and inhibits them

9:51now these are actually they actually

9:53break the brady beta-lactam ring if they

9:55break the beta-lactam ring they no

9:56longer combine to the penicillin binding

9:58proteins they're no longer able to

10:00inhibit the penicillin binding proteins

10:02they don't inhibit the peptidoglycan

10:03synthesis and cross-linking and now the

10:06bacteria can continue to survive so what

10:08we need is we need drugs that can

10:10actually break the beta-lactamase

10:12a particular enzyme and that way these

10:15beta-lactams can actually still bind to

10:17the penicillin binding protein so what

10:18are the drugs

10:20that are going to work to inhibit this

10:22beta lactamase what are those drugs

10:25these are the ones that we add on so we

10:27can remember them by clavulanate so

10:30clavillonate is a really interesting one

10:32we add this to amoxicillin you remember

10:34which one that was for the beta lactose

10:36it was your amino penicillin the other

10:39one is we can utilize something called

10:40sulbactim

10:42and sulbactin we add on to ampicillin do

10:45you remember that one that's another

10:46amino penicillin this actually becomes

10:48augmentin this actually becomes unison

10:51the other one is pepercillin do you

10:53remember we added with that tazobactum

10:56so tazobactum and again we add the

10:58tasobactum onto

11:00pippericillin

11:03and the last one here not too commonly

11:06thought about but it's a newer one it's

11:08called avibactum and avibactum is added

11:11on to ceftazidime do you remember which

11:14of the actual cephalosporins

11:16cephtazidine was

11:18it was a third generation cephalosporin

11:21so when we talk about the beta-lactamase

11:23inhibitors what they're doing is they're

11:25inhibiting the beta-lactamase so that

11:27the beta-lactaman antibiotic can inhibit

11:28the penicillin binding protein so that

11:30it can reduce the cross-linking of the

11:32peptidoglycan layer allowing for the

11:34bacteria to still be able to die so

11:36that's a pretty cool mechanism for these

11:38antibiotics all right so we covered the

11:40cell wall synthesis inhibitors with the

11:42beta-lactams like glycopeptide like

11:44vancomycin and we talked about the

11:46beta-lactamase inhibitors let's keep

11:47going through all the other antibiotics

11:49and their mechanism of action all right

11:50knows a lot we're going to cover a lot i

11:52really urge you guys use our table of

11:54contents in the video we have all the

11:55different chapters that i urge you guys

11:57to go through maybe go through mechanism

11:59of action take a little break get a

12:01snack review it and then go on to the

12:03next part which will be the bacterial

12:04coverage or the antibiotic spectrum of

12:06specific antibiotics so let's talk about

12:09the next type of antibiotics which alter

12:11the cell membrane so if you remember if

12:13your cell wall which is the

12:14peptidoglycan layer with the

12:15tetrapeptides cross-linking them we

12:17talked about the drugs that work on that

12:19we now have drugs that can actually

12:20alter the cell membrane the inner cell

12:22membrane the integrity of it can be

12:23thrown off

12:25there are certain drugs here

12:27we don't commonly utilize them

12:29but one of them would be daptomycin so

12:32daptomycin is an interesting drug

12:34and what it does is it actually creates

12:37these little pumps if you will so it

12:38creates these little efflux pumps in the

12:40cell membrane so imagine it kind of

12:42plugs in these little efflux pumps which

12:44allows for things like potassium to move

12:46out of the cell and maybe other types of

12:48ions and water to move into the cell and

12:50this can actually produce bacterial like

12:51cell lysis so adaptomycin may be one of

12:54those and it creates these little efflux

12:55pumps which inhibits the membrane

12:57integrity makes it a little bit more

12:59porous and it increases the permeability

13:01of the bacteria so that's one particular

13:03thing

13:04the other one

13:05lord have mercy if you ever have to

13:07utilize this drug but it's called

13:09polymixins these are intense drugs you

13:12really don't ever want to have to

13:13utilize these but these are good for

13:16multi-drug resistant types of bacteria

13:19as a salvage therapy like you have no

13:21other antibiotic that's going to treat

13:22these patients they're resistant to

13:23everything this is kind of like the one

13:25last resort that you can throw in there

13:27now how polymixin's work is it's a very

13:30interesting type of drug it's like a

13:31cationic like detergent if you will and

13:34so what it does is it actually increases

13:36the permeability of the cell membrane as

13:38well but again it kind of acts like this

13:40like very interesting types of cationic

13:43detergent molecule which will bind with

13:45the actual cell membrane and increase

13:47the permeability of the cell membrane

13:49allowing for things to be able to move

13:50in or out of the bacteria increasing the

13:52risk of bacterial cell lysis so a pretty

13:55interesting type of drug all right so we

13:56got our cell membrane integrity

13:58inhibitors remember daptomycin creates

13:59efflux pumps for potassium and then

14:02polymixins are your really interesting

14:04cationic detergents that bind to the

14:06cell membrane and increase the

14:07permeability of the cell membrane

14:09all right the next drugs

14:11work particularly not on the cell wall

14:13not on the cell membrane but they work

14:15on these little metabolic pathways

14:17inside the cell that are crucial for dna

14:19and rna synthesis and this is your folic

14:22acid pathway you know folic acid you

14:25start off bacteria use something called

14:27para aminobenzoic acid and then they get

14:30taken inside of the bacteria and then

14:32they get converted via specific enzymes

14:34into something called

14:36dihydrofolate

14:38and then through more mechanisms they

14:39get converted to something called

14:40tetrahydrofolate

14:43and then from this this tetrahydrofolate

14:45can be utilized to can be put into mrna

14:48or rna and it can also be utilized to

14:51make dna so it's very important for

14:53nucleotide synthesis

14:55so what if we utilize drugs to inhibit

14:58the synthesis of dihydrofolate or

15:00tetrahydrofolate and we have those drugs

15:03that can inhibit these particular

15:05mechanisms and if you inhibit this you

15:07reduce the synthesis of tetrahydrofolate

15:09and reduce the synthesis of dna and rna

15:12and now the bacteria can't divide so you

15:14know there's very interesting

15:15terminology that sometimes you have to

15:17utilize

15:18these cell wall synthesis inhibitors

15:20they kill

15:22bacteria they blow these suckers up so

15:25when we use the term kill

15:28these are called bacteriocidal agents

15:31they kill bacteria they blow them up

15:33the cell membrane integrity they alter

15:35the permeability and increase the risk

15:36of blowing the bacteria up so they kill

15:39bacteria

15:41but this one it doesn't really do

15:43anything to kill the bacteria it just

15:46reduces the growth or the division of

15:49the bacteria that's called

15:51bacteriostatic

15:53so this one it actually reduces the

15:55actual growth

15:58and so we refer to this one as a

15:59bacteriostatic agent now there's two

16:02drugs we actually utilize them in combo

16:05so this is called your sulfonamides and

16:07so we usually use like so your

16:09sulfonamides the most commonly utilized

16:10one is called sulfur methoxazole we

16:12commonly use the abbreviation smx

16:15this one will particularly inhibit the

16:17conversion of paraminal benzoic acid

16:19into dihydrofolate okay so you can

16:22remember this one's the for that first

16:23step

16:25then from there the second step which is

16:27inhibiting the conversion of

16:28dihydrofolate to tetrahydrofoil which

16:30reduces the synthesis of nucleotides is

16:33the other drug called trimethoprim

16:36and this inhibits that second step we

16:38commonly give these in combo

16:40trimethoprim and sulfur methoxazole this

16:43is also known as bactrum and so this is

16:45a very commonly utilized drug as well so

16:48these ones will inhibit the folic acid

16:50synthesis pathway but we know which ones

16:51kill kill

16:53and then reduce growth okay

16:56the next one's your dna integrity so

16:58they alter the dna integrity these are

17:00really like interesting agents so one of

17:03these

17:04is actually called metronidazole so

17:07metronidazole is a pretty interesting

17:09agent can kill a lot of anaerobes some

17:11like really like weird types of

17:13pathogens as well but metronidazole

17:15works to be able to create a lot of

17:16what's called reactive oxygen species so

17:18it increases the formation of something

17:20called your reactive oxygen species like

17:22free radicals and that can actually

17:24produce damage to the bacteria can

17:26actually produce like breaks within the

17:27dna strands and if you produce breaks

17:30within the dna strain it can actually

17:31lead to complete like destruction of the

17:32dna and then now the bacteria doesn't

17:34have the ability to completely like

17:36survive and so this can actually kill

17:38bacteria the other one is called

17:40nitropharantoid

17:41and nitropharantone

17:44is also another one that can actually

17:46increase the formation of reactive

17:47oxygen species of free radicals which

17:49again can produce damage to dna they can

17:52actually damage your rna and they can

17:53even inhibit some of the protein

17:54synthesis pathways as well

17:56so when we talk about dna integrity

17:59metronidazole nitropharantoid again

18:01these are the ones that are really

18:02particularly producing a lot of reactive

18:04oxygen species free radicals which are

18:06producing damage to dna rna and proteins

18:09okay

18:10the next group we're not going to really

18:12talk about it too much in this video

18:14we'll talk about it in another

18:16video on

18:18anti-mycobacterial drugs so drugs that

18:20work against tuberculosis but there's

18:22drugs that actually inhibit the rna

18:23polymerase you see this cute little red

18:25little blue enzyme they inhibit what's

18:27called the rna

18:29polymerase enzyme and this is called

18:31your rifampin so this is one of the

18:33commonly utilized drugs that we give in

18:36patients who have tuberculosis so we're

18:38not going to talk too much about that

18:39one let's move on to the next one that

18:40we do utilize a lot unfortunately and

18:42this developed a lot of resistance

18:45so there's another one that inhibits

18:46this enzyme here this pink enzyme so we

18:48already have how this one inhibits this

18:50particular process and we have how the

18:53mrna synthesis rifampin inhibits this

18:56process

18:57and then we talked about how the dna

18:58integrity metronidazole nitrofrancoin

19:00inhibit the actual

19:02they destroy the dna they destroy the

19:04actual rna and some of the proteins but

19:06the next one is we can utilize drugs

19:07that inhibit the dna gyrase or

19:09topoisomerase type 4 enzyme

19:11and what this drug does is so

19:13topoisomerases they could actually help

19:15to be able to maintain the topology of

19:18the the dna so what they do is they

19:20produce little nicks within the dna

19:22allow for it to unwind whenever there's

19:24a lot of like super coils and then they

19:26allow for it to unwind and then they

19:27link it back up together once you

19:28relieve the super coils

19:29what if we activated the actual cutting

19:32part of this enzyme and it just chops

19:33and chops and chops and never re-ligates

19:36it then you just chop the actual dna up

19:39into pieces and this is a terrible

19:41situation but it's good whenever we want

19:43to get rid of bacteria so this types of

19:45drugs that i want you to remember here

19:46are what's called your fluoroquinolones

19:49so these are called jor

19:50fluro

19:53quinolones and there's a bunch of that

19:55actually part of this category so

19:57there's our first generations and the

19:59primary commonly utilized one for the

20:00first gens

20:02is going to be ciprofloxacin

20:06and then you have your second gens also

20:09known as your respiratory

20:10fluoroquinolones and this is your

20:12levofloxacin

20:14your gemifloxacin

20:18and then the last one is moxifloxacin

20:23so these are going to be the

20:24fluoroquinolones and they inhibit the

20:26dna gyrus they inhibit the actual

20:28topoisomerase enzyme and so it produces

20:31a multiple well particularly they

20:33inhibit the the actual ligating the

20:35annealing portion of it and then they

20:37increase the activity of the cutting

20:38portion the nucleus portion and it just

20:40fragments and fragments and fragments

20:42the dna into pieces so now you don't

20:44have any dna to be able to allow for the

20:45bacteria to survive so again this one

20:47will

20:49kill

20:51all right so it's a bacteriocyte agent

20:54all right we come on to the ones that

20:56inhibit the protein synthesis so you

20:57know that dna we utilize rna polymerases

21:00to make rna particularly mrna mrna binds

21:03with the ribosomes particularly which

21:04types of ribosomes and bacteria your 50s

21:07and your 30s ribosomal subunits

21:09and then from the mrna we make proteins

21:12well what if we utilize particular

21:15antibiotics that inhibit the protein

21:17synthesis so particularly some will act

21:19on the 50s ribosomal subunit and some

21:21will inhibit at the 30s ribosomal

21:23subunit what are those drugs glad you

21:26asked

21:26all right so for the 50s ribosomal

21:29subunit the big one is your macrolides

21:31so your macrolides this actually is

21:34going to be particularly

21:36it'll be

21:37your

21:38something called a zythromycin

21:42you have something called erythro

21:45mycin

21:47and you have chlorithro

21:50mycin

21:53so these are your macrolides pretty good

21:55one is the azithromycin which will be

21:56the more commonly utilized ones the

21:58other ones that are kind of like

21:59scattered there's no like very specific

22:01like category for these well there is

22:03but i think it's easier just remember

22:04the name of these for these ones you

22:06have something called clindamycin

22:10the other one is called chloramphenicol

22:16now chloramphenicol is not superly

22:18commonly utilized

22:20it's more in the low-income countries

22:24and then the last one is lynasolid

22:27now what's important to remember for

22:29these drugs is all of them inhibit the

22:3150s ribosomal subunit which inhibits

22:33protein synthesis which proteins are

22:35important for being able to allow for

22:36certain replication functions and growth

22:38of the cell so these do not kill they

22:41actually reduce growth so they are

22:43called

22:43bacteriostatic agents so these reduce

22:47growth

22:48they don't blow the bacteria up they

22:49just reduce them from being able to grow

22:51all right so the next one is your 30s

22:52ribosomal subunits again these are

22:54inhibiting the actual 30s ribosomal

22:56subunit inhibiting protein synthesis

22:58will they kill will they reduce growth a

23:00little bit of both and i'll talk about

23:01which ones do that and which ones don't

23:03so for these your aminoglycosides and

23:05tetracyclines for the aminoglycosides i

23:06want you to remember primarily three so

23:08tobramycin

23:10is a is a good one amy casein is a

23:13pretty good one and

23:15gentomycin is a pretty good one as well

23:19okay for the tetracyclines there is

23:22doxycycline and tetracycline that's

23:24really it you can consider minocycline

23:25but we don't really use that too often

23:27maybe for like acne for the propriano

23:29bacterium but really i would just

23:31primarily remember doxycycline and if

23:33you want to add another one in there you

23:35can remember tetracycline but primarily

23:38the one that is worth remembering is

23:39your doxycycline

23:41now

23:42we can't just consider this whole group

23:44to kill or blow up cells and then some

23:46to be able to reduce growth one of them

23:48actually reduces growth and one of them

23:50kills so the ones that actually kill

23:53is going to be your amino glycosides

23:55where's my maroon marker here this one's

23:57good here all right so this one this

23:59group will

24:01kill

24:02and this one will reduce

24:05the growth so the tetracyclines are the

24:07bacteriostatic

24:09and then your aminoglycosides will kill

24:11okay

24:12now that we covered the mechanism of

24:13action which took forever now we're

24:15going to cover the bacterial coverage of

24:17the spectrum of these antibiotics

Bacterial Coverage

24:18alright guys so now we're going to move

24:19into the next chapter which is going to

24:20be the bacterial coverage of these

24:22antibiotics now there's a lot of ways of

24:24looking at this i personally think this

24:27is the easiest way to remember

24:29which antibiotics cover which types of

24:31bacteria

24:32and i also think it's more clinically

24:34like representative because a lot of the

24:37times you learn in school here's the

24:39antibiotic here's the bacteria that that

24:40antibiotic covers

24:42oftentimes in the clinical world and i

24:44think an easier way to remember is you

24:46either start patients on empiric

24:48antibiotic therapy and we'll talk about

24:49that for common infections and you base

24:51it upon what the most likely pathogen is

24:53and then what you do is you get cultures

24:56and from those cultures once the

24:57cultures come back they tell you which

24:59type of bacteria

25:00was showed up in the culture and then

25:02you utilize the actual bacteria that

25:05covers that pathogen very specifically

25:07and so i think it's a little bit easier

25:09to remember and it's more clinically

25:10applicable

25:11so what i'm going to do first is i'm

25:13going to talk about here's the pathogen

25:15here's the gram-positive gram-negative

25:17anaerobe atypical bacteria that came

25:19back from the culture what's the best

25:21antibiotics that cover this without

25:23being too broad and then after that

25:25we'll talk about what are the empiric

25:27antibiotic therapy the common regimens

25:29for very common infections and then how

25:31we tailor back based upon what the

25:32actual culture shows us okay

25:35so the first thing is gram-positive

25:36bacteria there's a lot of different

25:37types of gram-positive bacteria but the

25:39most common ones that you'll see on your

25:40exam or in the clinical world is going

25:42to be these so misa is what's called

25:44your methicillin sensitive

25:46staphylococcus aureus there's a couple

25:48antibiotics that work relatively well

25:50against this without being too broad and

25:53so the ones that i would want you guys

25:54to remember is think about first

25:56your your beta lactams if you will

25:59okay so the first ones that i want you

26:01guys to remember within the betalactin

26:02but your penicillin category is the

26:05anti-staphylococcal penicillins right so

26:07those ones will be very very good so i

26:09want you to remember your anti

26:11staphylococcal

26:15penicillins so do you guys remember what

26:17these were

26:18your naphcillin your oxacillin and your

26:20dicloxacillin these are going to be good

26:22against your methicillin sensitive

26:24staphylococcus aureus then you go into

26:26your cephalus more so keep going through

26:28the mechanism of action in your head so

26:29the next one is is there any other types

26:31of penicillins no is there any

26:33cephalosporins oh yeah the first

26:35generation cephalosporin is a really

26:37good one so your first gen

26:39cephalosporins

26:41are going to be very very good against

26:44your misa so this is your cephalexin

26:46keflex cephalexin or cefazolin these are

26:49very very good against these

26:51and then the other one that you can add

26:52into this category as well

26:55if you continue to keep going through in

26:56your head you can go through all the

26:58other ones and think about okay what

26:59else is there in the cephalosporins

27:00nothing else is really good against it

27:02do bactrim no bactrim not really what

27:04about your fluoroquinolones

27:05fluorquinolones are actually decent

27:07against misa so you can also add in your

27:09fluoroquinolones as well to cover some

27:11of the misses species

27:13if you go down to the other ones

27:14doxycycline no tetracyclines macrolides

27:17no so this would be the big ones that i

27:19would remember for your misa is going to

27:20be your anti-staphylococcal penicillins

27:22your first gen cephalosporins and your

27:24fluoroquinolones

27:26okay for your mrsa these are nasty like

27:28bugs these are usually your nosocomial

27:30infections so these are the ones that

27:31you get from like multi-drug resistant

27:33types of situations like in the hospital

27:35and so mrsa methicillin-resistant

27:37staphylococcus aureus there's only a

27:39specific types of antibiotics that cover

27:42these so again go through it in your

27:42head any of the penicillins

27:45no

27:46any of the actual generation

27:47cephalosporins actually the fifth

27:49generation cephalosporin it's called

27:51ceftaryline this one will actually cover

27:54your mrsa all right what about the um

27:56vanco or fossilmycin vanco is actually a

27:59really good agent that covers it so then

28:00we have vancomycin okay what about your

28:03full gasoline inhibitors like your

28:04trimethylamine sulfate oxal this one

28:06actually does cover mrsa so your

28:07trimethoprim sulfamethoxazole will cover

28:10it

28:11metronidazole nitrofarantoin no

28:13fluoroquinolones no what else can i go

28:16on to my next one which are going to be

28:17like my macrolides macrolides won't

28:19cover it we'll clean to cover it clinda

28:20covers it so clindamycin will cover it

28:23chloramphenicol will not cover it

28:25lynasalid will cover it

28:28and then if we continue to keep going on

28:30here then we go on to the next part

28:31which is your amino glycosides none of

28:33the aminoglycosides cover tetracyclines

28:35the only one is doxycycline

28:37now there is one other one that i want

28:39to talk about but it's a very

28:41interesting one it was going back to the

28:43cell membrane integrity inhibitors that

28:44was your daptomycin daptomycin does

28:48cover mrsa but you have to be very

28:50careful it only covers it on the skin or

28:53right-sided endocarditis

28:57it will not cover any type of lung

28:59infection due to mrsa because it gets

29:01inactivated by the surfactant in the

29:02lungs so daptomycin really the only mrsa

29:05coverage you'll get is some skin soft

29:07tissue infections and some right sided

29:09infective endocarditis due to mrsa so

29:11that would be your mrsa so your misa

29:13anti-staphylococcal so your naphthalene

29:14oxacillin and in your diet clocks first

29:16gen and cephalozone cephalexin and then

29:19fluoroquinolones but these would

29:20definitely be the best

29:22mrsa all of these and again go in that

29:24order all right so for the strep

29:26pneumonia there's a bunch of different

29:27antibiotics that we can utilize for

29:29these ones so think about your

29:30penicillins let's put them in a group

29:32here just i think it's easier so your

29:33penicillins penicillin itself penicillin

29:36g

29:37this would actually cover this one so

29:38you can cover this one with penicillin

29:41and then another type of beta-lactam

29:42that i want you guys to remember is your

29:44aminopenicillins you remember those

29:45amoxicillin and ampicillin plus the

29:49beta-lactamase inhibitors gives you a

29:50little bit of coverage against those

29:51with the resistance so the other one

29:53here will actually just continue on

29:54penicillin you can also consider your

29:56amino penicillins your amino penicillins

29:59are actually pretty good here

30:00your anti-staphylococcal not too much

30:03and then if we go into the

30:04cephalosporins i would actually consider

30:07really more of like your third gen

30:09cephalosporins will actually be pretty

30:10good i wouldn't actually forget those

30:12and again that's your your cef triaxone

30:15so cephalosporins for this one

30:18if you continue to go down here carpet

30:19venoms that's way too broad

30:21monobactine's way too broad the other

30:22ones that i would actually consider and

30:24if you go into dapto no

30:26you know polymixon's heck no

30:28bactrum bactrim's not too good at

30:30covering strep pneumonia

30:31fluoroquinolones will cover strep dumo

30:34so you can actually consider your

30:35fluoroquinolones as well

30:37so moxifloxus and levofloxacin

30:39if we were to go into the next ones and

30:41you actually consider some of the

30:42macrolides macrolides have some benefit

30:44i think there's becoming a lot of

30:45resistance out there against it but you

30:47can consider macrolides

30:48and then the other one

30:50is clindamycin so clindamycin will also

30:53cover these um not so much so for the

30:56nasality not so much for for the

30:57chloramphenicol and then your

30:59aminoglycosides not really and then

31:01again on top of that your tetracycline's

31:02not really as well so these would be the

31:03primary ones for strep pneumo if you had

31:06out of all of these which ones would you

31:07pick to be the best ones i would say

31:09your penicillin your amino penicils and

31:10your third gen cephalosporins would be

31:12the best ones these ones down here

31:14fluoroquinolones are okay mackerel is a

31:15lot of resistance cleaned up becoming a

31:16lot of resistance as well

31:18all right for the strep a and b so this

31:21is your group a strep so this is your

31:23streptococcus pyogenes and then your

31:24streptococcus agueleciae which is your

31:26strep b

31:27these ones again some of the similar

31:29agents here so penicillin will also

31:31cover this one

31:33your amino penicillins will also cover

31:35this one

31:36now for the cephalosporins not really

31:38the third gin it'd be more of your first

31:40gen cephalosporins so your first gen

31:42cephalosporins especially cephalexin

31:45that one will also cover this one as

31:46well

31:48and then again if you continue to keep

31:49going through carbopenum is way too

31:51broad monobacter's way too broad

31:54if you go into bacterium bactrim will

31:56actually cover these so you can add in

31:58trimethoprim sulfur methoxazole

32:01dapto way too

32:02way not to specifically for mrsa

32:05polymixins heck no

32:07if you go on to fluoroquinolones

32:08fluoroquinolones not too great against

32:10the strep a and b so i wouldn't really

32:12like consider those if you go on to your

32:14macrolides macrolides somewhat

32:16beneficial again there is becoming a lot

32:18of resistance against these and then

32:20again if you go into clindamycin

32:21clindamycin's not too bad as well so

32:23these would be the primary ones that i

32:24would consider for the patients who have

32:27strep a and b

32:29all right your enterococcus species your

32:31enterococcus you have enterococcus

32:33ficalis fecium there's a lot of these

32:35suckers here the amino penicillins tend

32:37to be the best for this one so i'd

32:39primarily remember you can consider

32:41penicillin

32:42so if you really wanted to you can

32:43consider penicillin you can consider

32:45your amino penicillins i would really

32:47consider these first

32:48okay and then the other one that you can

32:51consider as an add-on because it

32:53concentrates well particularly within

32:55the urine so it's good against utis due

32:57to enterococcus i'll add a little side

32:59note on to that is your nitropharantoid

33:03so nitropharantome will cover those in

33:05terracocca species but primarily because

33:07it concentrates well in the urine that

33:09would be the primary area you wouldn't

33:10use this for any other infections except

33:12for urinary tract infections due to

33:14enterococcus

33:15the last one here is listeria

33:17monocytogenes this is a heck of a

33:19pathogen and to be honest with you amino

33:21penicillins would be the best one

33:22ampicillin amoxicillin plus clavilani so

33:25you can cover your amino penicillins and

33:27again i would really consider whenever

33:28you add on these amino penicillins

33:30consider the resistance so sometimes if

33:33we add on amino penicillins it might not

33:36be enough to just have amoxicillin or

33:37ampicillin by itself sometimes you may

33:39have to add on their beta-lactamase

33:41inhibitor same thing for the

33:42enterococcus and listeria you may have

33:44to add on the beta-lactamase inhibitor

33:46and the last one of the listeria is

33:47bactrim trimethoprim sulfamethoxazole

33:51okay

33:52the last thing that i want to talk about

33:54is vancomycin so let's say that you have

33:55a patient who you think you've treated

33:59for

34:00any of these gram-positive infections

34:02they either are penicillin allergic or

34:04they're super resistant to all of these

34:06pathogens vancomycin will be the best

34:09one for that agent okay so if i have a

34:10patient who is penicillin allergic

34:15and on top of that they have resistance

34:20to

34:21the above gram-positive pathogens

34:23vancomycin will be your best agent it'll

34:25cover any one of these with the

34:27exception

34:29of vancomycin resistant staphylococcus

34:31aureus you'll have to use other agents

34:33for that one or vancomycin resistant

34:35enterococcus so sometimes certain these

34:37two bacteria enterococcus and

34:39staphylococcus aureus can become

34:41resistant we call that vre for

34:43vancomycin-resistant enterococcus and

34:45vancomycin resistant staphylococcus

34:47aureus as well but that's going to be

34:49the gram positive coverage so if you had

34:51a patient had an infection you treated

34:52them with broad spectrum it was from the

34:54lungs and it came back oh their

34:56infection was very specifically

34:58streptococcus pneumonia you can utilize

35:01one of these agents and peel back on the

35:02other ones oh their skin infection came

35:04back as missa and not mrsa start them on

35:07one of these agents okay so that's how

35:08you peel them back

35:10the next one is the monsters which is

35:12your gram negative coverage so now we

35:13move on to our gram negative coverage so

35:16when we talk about gram negative i think

35:17the easiest way to remember these we're

35:19going to do them in groups just like we

35:20did with the misa the mrsa strep the

35:23enterococcus and listeria

35:25so for the gram negative coverage

35:26there's a big group of bacteria i

35:28couldn't fit them all out i tried to

35:29come up with the easiest kind of

35:30mnemonic they actually used this in the

35:32first aid book for the usmle step one

35:35but it's hens peck so you can remember

35:37this by homophilus influenza

35:40enterobacter neseria gonorrhea and

35:43meningitidis

35:44seratia proteus like mirabilis e coli

35:49for the ec and klebsiella okay so

35:52haemophilus influenza enterobacter

35:54neseria seratia proteus e coli and

35:57klebsiella what types of antibiotics

35:59will cover these this is a huge one

36:02because it's a pretty common like type

36:03of infection for certain types of

36:05common infections that we'll talk about

36:07later but for the first one here is go

36:09through again your penicillins any of

36:11those penicillins not the first like

36:12natural penicillins aminopenicillins not

36:14too bad they can cover some of these so

36:17if you add on here amino penicillins

36:21they will cover all of these with the

36:23exception that they will not cover the

36:25enterobacter

36:26they will not cover serratia

36:29for these ones and they will not cover

36:31nessaria so in this case they will not

36:34cover the uh enterobacter and the

36:35necessary and they will not cover

36:36serratia for the amino penicillins so

36:38this would be again your amoxicillin

36:40plus clavilani or your ampicillin plus

36:42the sulbactum

36:44then you go into the other one so then

36:45continue down the penicillins

36:46anti-staphylococcal no anti-pseudomonal

36:48penicillins those ones are actually

36:50pretty good they have a very very

36:51significant broad coverage so if you

36:54considered your anti-pseudomonal

36:56penicillin

36:57this would definitely be a good one so

36:59this would be your pipracillin

37:00tazobactum

37:02all right go to the next ones your car

37:03your generally your cephalosporins so

37:05any of the cephalosporins first

37:07generation heck no

37:08well actually that's not necessarily

37:10true your first generation

37:11cephalosporins they actually can cover

37:14some of these

37:15they will only cover the peck

37:17portion so they'll only cover the

37:20proteus they'll cover the e coli and

37:22they'll cover the klebsiella

37:25the second generation third generation

37:27and fourth generation will cover all of

37:29these so you can actually consider your

37:32second

37:33through fourth gen these will actually

37:35cover all of them

37:37the next one is you move on to your

37:38carbopenums again carbohydrate boom that

37:41blow up everything so carbohydrates you

37:43can always put down to pretty much cover

37:44every single type of bacteria

37:46okay do you guys remember this the dime

37:48dory penum imma penemeropenum and

37:50urjapenum

37:51monobactums will cover these as well

37:54the monobactums

37:56will also cover these

37:58now the monobactums on in this situation

38:01here are pretty good the next one is if

38:03we continue to go through so keep keep

38:05moving through you got your adapto no

38:06vanco no poly mix and poly mexicans will

38:09cover everything so if you had to add

38:11this one on for the last one yes poly

38:12mixins will also cover it

38:14if you continue to move on into the

38:16fluoroquinolones fluoroquinolones will

38:18also cover this pretty well as well so

38:19you can definitely add in your

38:20fluoroquinolones

38:23and then if you move into your

38:24macrolides no clinda no chloramphenicol

38:27no lynasalidno aminoglycosides

38:29aminoglycosides will also cover these as

38:31well

38:32the one thing i would try to remember

38:34though is for your fluoroquinolones and

38:35your aminoglycosides

38:37these don't cover

38:39the nesaria as well so this one will not

38:41cover the nasseria and this one will not

38:43cover necessarily as well

38:45so these would be the primary agents to

38:47remember here for these and then again

38:49if you add on doxycycline or your

38:50tetracyclines they don't cover as much

38:52of these as well so this would be the

38:54primary antibiotics that would cover the

38:56hemophilus influenza enterobacter

38:58neseria seratia proteus e coli and

39:00klebsiella amino penicillins with the

39:02exception of anterobacter serratia and

39:05nyseria your anti-pseudomonal

39:07penicillins like percentage of bacterium

39:08first gens they only cover the pec

39:10portion second to fourth gen they'll

39:12cover all of them carbopenums

39:15particularly if you had to remember any

39:16of these the third gen will be the best

39:18one because that will specifically cover

39:20necessarily meningitis

39:22your carbopenes will cover these your

39:23monobactins will cover these your

39:24fluoroquinolone glycosides they will

39:26just not cover the nasseria species okay

39:29so we got the hens peck ones now we move

39:31on to the really nasty organisms

39:33remember how we had mrsa that was a type

39:35of nosocomial infection well your

39:38pseudomonas and acetate needle bacter

39:40are also some really nasty

39:42nosocomial types of gram-negative

39:44bacteria so pseudomonas originosa

39:47this is probably one of the big big big

39:49ones so let's keep going down that list

39:51any of the penicillins penicillin no

39:53aminopenicillin aminopenicillin will

39:55only cover the asynetobacter so if you

39:57put in these the aminopenicillins just

39:59realize it will not cover the

40:01pseudomonas it only

40:03covers the acetobacter

40:06if you continue to go down

40:07anti-staphylococcus no anti-pseudomonas

40:09penicillins heck yes

40:11peppercilantazobactum so you can

40:12consider the anti-pseudomonal

40:16penicillins like your

40:17pipercylentazobactum

40:20cephalosporins any of the first heck no

40:22second no third only one of the third

40:25generation cephalosporins will cover

40:26pseudomonas do you guys know so only one

40:29of the third gen and this is the

40:31ceftazidine

40:33so ceftazidime the fourth gen will

40:36definitely cover it and your fourth gen

40:38is going to be cephepine

40:42okay move through carbipenems do they

40:44cover pseudomonas yes monobactums do

40:46they cover it yes they just don't cover

40:48acetobacter so your carbapenems will

40:50cover all of these

40:53and your monobactums will cover all of

40:55these except for

40:57no

40:58acetobacter

41:02okay continue to go on

41:04trimethylsulfoxazole no fluoroquinolones

41:07here's the thing for fluoroquinolones

41:10they actually do consider these to cover

41:12the pseudomonas specifically your cipro

41:16and your levo but this is mainly for

41:19something called double coverage

41:22of pseudo and it's not really backed by

41:24a lot of evidence so they say that you

41:26can take one of these other agents that

41:27covers pseudomonas and add on a

41:28fluoroquinolone like ciproflox and

41:30levofloxacin for double coverage but

41:32it's not really heavy

41:33you know balanced inside of the actual

41:34evidence so they're not really good for

41:36monotherapy against uh pseudomonas but

41:38they can be somewhat considered as an

41:40add-on for double coverage of

41:41pseudomonas if you're considering it but

41:42there's not a lot of evidence to back

41:43that up

41:44okay then we continue to go down any of

41:46the macrolides any of the clinda any of

41:48the chloramphenicol

41:50um any of the other ones particularly

41:52no not really so then the last one here

41:55would be your aminoglycosides and your

41:56tetracyclines do any of those

41:57aminoglycosides will cover the

41:59pseudomonas so you can consider

42:00aminoglycosides

42:03one of the things to consider though for

42:04the aminoglycosides is they're not super

42:06good at covering the asynetobacter

42:08though so they will not cover the acid

42:10needle bacter as well

42:12but they will cover the pseudomonas and

42:14the last one is that like last one where

42:17you ain't got no other agent and like

42:18the patients like near death and they

42:20have no other antibiotic you can cover

42:21these you can add on the poly mixins so

42:23poly mixins is kind of like that last

42:25resort it's that salvage therapy so yes

42:27you could also consider this one to

42:28cover your pseudomonas and ace needle

42:30bacter all right so we got our hens pec

42:32hemophilus your enterobacter neseria

42:34seratia proteus e coli cleb and now we

42:37got the pseudomonas and acetobacter

42:39let's come down and talk about two other

42:41gram negatives that i need you guys to

42:42remember that being espl species and

42:44then the last one is called

42:45stenotrophomonas all right so let's talk

42:47about espls so what types of antibiotics

42:49will cover the espl well what the heck

42:51is an espl so it's an extended spectrum

42:53beta-lactamase

42:54bacteria so these are bacteria that have

42:57beta-lactamases that are so broad they

42:59can actually make a lot of antibiotics

43:01that we've just talked about for gram

43:02negatives not work so pretty much a lot

43:05of your beta-lactase so if you think

43:06about it think about for example the

43:08hens peck and then the pseudomonas a lot

43:09of similarities right amino penicillins

43:11won't work anti pseudomonas penicillins

43:13won't work thirds gens won't work fourth

43:15gens won't work carbopenems actually are

43:17remember boom that'll blow up everything

43:20fluoroquinolones these aren't even good

43:21at the extended spectrum aminoglycosides

43:24is not a beta-lactam so we can add that

43:25one on and remember i told you poly

43:27mixins will blow up everything so

43:29because of that we're really only left

43:30with carbapenems aminoglycosides and

43:33polymixins and then one last thing which

43:34there has been some literature to

43:36support so for these i remember

43:37karmapenums

43:41i'd remember your aminoglycosides

43:44i'd remember your polymixins

43:47now here's the one thing that there's

43:49actually been some research against you

43:51can take a

43:52third generation cephalosporin

43:54like ceftazidine

43:57and you can add on a beta-lactamase

44:00inhibitor like avibactum

44:02and this may have enough coverage to

44:06break down some of these extended

44:07spectrum beta-lactamase bacteria now the

44:10question is what are some of these

44:11bacteria it's a lot of the ones that we

44:13talked about really so i would really

44:15remember your enterobacters so you're in

44:17pterobactericie this is some big ones

44:19that have some extended spectrum your e

44:21coli

44:23your klebsiella is a huge one my friends

44:26so don't forget these these are really

44:28some of those bacteria that have

44:29developed a lot of resistance via these

44:31extended spectrum betalactamases that we

44:33need very specific antibiotics to cover

44:36okay

44:37the last one here is the

44:38stenotrophomonas so stenotrophomonas i

44:40really want you guys to remember for

44:42specifically for this one your ant so go

44:44through your penicillins do any of the

44:45penicillins cover this one the only

44:47penicillin to cover this one is the

44:48anti-pseudomonas penicillin which one's

44:50that one piparcillin plus you have to

44:53add the taseobactin to that one so your

44:54anti

44:56pseudomonal

44:58penicillins

45:01the other one to remember here for this

45:02guy is if you go through um is your

45:06polymixins polymixons cover everything

45:08this is a really nasty pathogen so

45:10polymixons would kind of be a big one to

45:12add on here and then believe it or not

45:14it's just a random one bactrim so

45:17trimethoprim sulfamethoxazole will also

45:18cover your

45:20stenotrophomonas so this will be a lot

45:22of your gram negative coverage i know

45:24there is a lot there again i encourage

45:26you to sit down write them all out with

45:28me write them out on your own and keep

45:30doing it it's a lot of work but we're

45:31gonna get there let's move on to the uh

45:33atypicals and anaerobes so the next one

45:35is your anaerobic coverage so i like to

45:37help to remember this is can't breathe

45:39perfectly fresh air so for the can't

45:42breathe perfectly fresh air

45:44you can remember this by claustridium so

45:46the clostridium species clostridium

45:48perfringens clostridium difficile

45:51clostridium uh botulinum clostridium uh

45:55tetani so there's a lot of different

45:57clostridial species the next one is

45:59bacterioides so bacterioides for jealous

46:03p for pepto streptococcus f for fuso

46:06bacterium and a for actinomyces so again

46:10these are your anaerobic bacteria again

46:12clostridium bacteroides

46:14peptostreptococcus fusibacterium and

46:16actinomycetes what are the antibiotics

46:18that will cover your anaerobes so the

46:21ways i like to remember this is first

46:22off i like to remember above the

46:24diaphragm there's a very specific set of

46:26antibiotics that cover these and then

46:28the ones below the diaphragm and then

46:29we'll cover the ones that just hit

46:31everything and again those obviously you

46:33know carbohydrates are going to be a

46:34part of it so let's cover these so if

46:36it's above the diaphragm clindamycin has

46:40been shown to be the primary one that

46:42will cover some of the anaerobes that

46:44are above the diaphragm

46:48now for the ones below the diaphragm so

46:50your gi infection so this would be above

46:52the diaphragm and the skin so any parts

46:54of the skin and above the diaphragm so

46:56here we'll put diaphragm and

46:58skin metronidazole is not really good

47:00against the skin infections

47:01that are anaerobic so like your

47:02decubitus ulcers from diabetics that

47:04have like um so decubitus ulcers or like

47:06the diabetic foot ulcers that are

47:07polymicrobial that have probably some

47:09gram positive and anaerobes in them then

47:12clintomics will be the better one for

47:13that one but for the ones that are below

47:15the diaphragm so your git infections

47:17some of the pelvic infections that's

47:19going to be your metronidazole so let's

47:20put that down here

47:23metronidazole so this will be for the

47:25actual pathogens that are below

47:28the diaphragm okay so git infections

47:32the ones that if you're not trying to be

47:34specific and you just want to hit

47:36everything gram negatives and anaerobes

47:38it'll just hit everything it's

47:40karbapenums and your anti-pseudomonal

47:42penicillins like pepperocidal

47:43taseobactin those are again they're

47:44bombs you just throw them in they kill

47:46everything so this will be your

47:47carbapenems

47:51and then last but not least is your

47:54anti-pseudomonal penicillins now i'm

47:56going to add in just a little kind of

47:58thing here there is a questionable

48:00effect of fluoroquinolones being

48:02effective against some types of

48:03anaerobics there is some literature that

48:05is suggesting that there's a lot of

48:07resistance so i'd be very careful it is

48:09mentioned in the textbooks as a

48:10potential coverage for anaerobics

48:12especially like cipro that's the primary

48:15one so ciprofloxacin but there is some

48:18question if it's actually good enough to

48:19be able to cover that

48:21okay the seed differs so when you're

48:23peeing out your butthole what is the

48:25bacteria that's causing that that's the

48:27clostridium difficile it's one of the

48:30types of clostridium for the anaerobes

48:32but the types of antibiotics that we

48:34utilize to cover this one is very

48:36specific we already talked about one of

48:37them so c diff it's affecting the git so

48:40the colon right so you get pseudomonas

48:42colitis so which one is below the

48:44diaphragm to cover that one

48:45metronidazole so metronidazole will

48:47actually cover the c diff but there's

48:49one other one which is just like you're

48:50like what the heck

48:51where'd this one come from

48:53it's vancomycin but not the iv form

48:56the po form so vancomycin the po form

49:00will actually cover c diff so those are

49:02the two options that i want you to

49:03remember for that specific and rope

49:05all right let's come down and talk about

49:07the atypical coverage so they don't

49:08really fit well within the gram positive

49:10the gram negative the anaerobe they're

49:12just some random wonky ones that may be

49:15possibly get tested on so i want you

49:16guys to know these

49:17so this is mcl mycoplasma chlamydia

49:22lesionella these are very specific types

49:24of atypical bacteria that there's very

49:27specific antibiotics that cover

49:29all right so go through the list again

49:31any of the penicillins cover this one

49:33not really your bactrim cover this one

49:35or dapto or phospho or polymixins no

49:40fluoroquinolones cover this one the

49:41fluoroquinolones actually do cover these

49:43especially if it's lesionell it's

49:45actually the preferred agent so for the

49:47fluoroquinolones i would actually

49:49remember that these are actually

49:50preferred especially

49:53if lesionella is the type it's preferred

49:56okay then go on to the next part go into

49:58your macrolides

50:00macrolides do cover these pretty well

50:02actually so macrolides will definitely

50:04be one to consider

50:06the other thing here is chloramphenicol

50:08does that one cover it yes it does

50:11except for

50:12the last one so chlor

50:16and phenical this will not

50:19cover the legionella so if you have

50:21legionella not preferred but again this

50:23is more of like the low-income countries

50:24that will be utilized and then the next

50:26thing is what about your linasalidno

50:28what about clinda no what about your

50:30aminoglycosides no what about your

50:31tetracyclines yes doxycycline preferred

50:36so doxycycline is really good one

50:37because it'll cover all of these really

50:39well so these will be the agents that

50:41will cover your atypical types of

50:43bacteria mycoplasma chlamydia and

50:45lesionella okay

50:47the other ones are your tick-borne

50:49bacteria so this covers all of them

50:52except for babesiosis do you guys

50:53remember all of these sons of guns here

50:56borrelia burgdorferi rickettsia ricatzia

50:59erlickia anaplasma all of these guys

51:03cover multiple types of these tick-borne

51:06illnesses so again berylia causes lymes

51:08rickettsia rickettsia causes rocky

51:10mountain spot of fever earlykia causes

51:12erlichiosis and anaplasma causes

51:14anaplasmosis

51:15these can be covered very well

51:18okay so if you go through here some of

51:20these are similar so the big one here

51:21that i want you guys to remember is

51:23going to be doxycycline so doxycycline

51:26is the preferred

51:27agent for all of your tick-borne

51:29illnesses and here we'll just put them

51:30as abbreviations borrelia burgdorferi

51:33rickettsia rickettsia likiosis and

51:36anaplasmosis except for babesiosis

51:38that's not the treatment for these ones

51:40so doxycycline is one chlorine finical

51:44will be the one for like those

51:45low-income countries and then a little

51:48side note to remember here especially

51:50for borrelia burgdorferi if it becomes

51:53disseminated so it actually causes like

51:56meningitis it causes bilateral facial

51:58nerve palsy it causes like an av block

52:00the preferred agent for that is

52:03cephtriaxone

52:04especially if it's cns because

52:06ceftriaxone has good cns penetration so

52:09it's the preferred agent for cns

52:11infections especially for beryllium or

52:13dorphy so it might be a little add-on

52:14that they throw at you okay

52:16the last thing to remember here is

52:18treponema politum this is a spirochete

52:20so this is actually the thing that

52:21causes syphilis

52:23so in this disease which ones do we

52:25utilize

52:26penicillin is actually the preferred

52:28it's a penicillin g

52:30and then if that's not an option or they

52:32have an allergy you can consider

52:33doxycycline so to be honest with you if

52:36you don't know which one to pick for the

52:38atypicals

52:39you notice a common trend among all

52:41these doxycycline tends to be the best

52:42for your atypicals okay that covers the

52:45anaerobe that covers the atypical

52:46coverage and that covers the bacterial

52:48coverage of all these antibiotics now

52:49what we have to move on to in the next

52:51chapter here is we have to talk about

52:54what are the actual empiric antibiotic

52:56therapies for common infections so i

52:58have no idea what the actual bacteria is

53:01i just have a suspicion of what it is

53:03based upon the infection that they have

53:05what are the antibiotics i'm going to

53:06throw at them then when the cultures

53:08come back and they tell me which type of

53:10bacteria it is i know which antibiotic

53:12to pick that's best suited for the

53:14bacteria now let's talk about that now

Empiric Antibiotics for Common Infections

53:16all right guys so now let's talk about

53:18the empiric antibiotics for common

53:19infection so you have a patient who

53:21comes in they have pneumonia right you

53:23diagnose it based upon the clinical

53:25features of pneumonia and the

53:26radiographic evidence of pneumonia so

53:28you have

53:29concern for pneumonia you have to

53:31discern if it's a community acquired

53:32versus a hospital acquired pneumonia

53:34right and based upon that that kind of

53:36gives you an idea of which kind of

53:36pathogens are the most likely cause of

53:39their pneumonia so for a community

53:40acquired pneumonia you usually think

53:41about strep pneumo as the big one

53:43hemophilus influenza

53:45maybe morex celicate or alice right so

53:47you can think about again i remember

53:49strep pneumo haemophilus influenza morex

53:52electoralis and then i think about my

53:54atypicals right so i think about

53:55lesionella mycoplasma chlamydia ammonia

53:58right

53:59in those situations i need to think

54:00about which types of antibiotics will

54:01cover my strep pneuma primarily and my

54:04atypicals

54:05so one of those that covers both of them

54:08that cover strep pneumo is my

54:09fluoroquinolones and then the other

54:11thing is that fluoroquinolones also

54:12cover all the types of atypicals

54:14especially preferred for lesionella so

54:16if i wanted to with one antibiotic and

54:18done fluoroquinolones would kind of be

54:19the ideal one to go here so i would pick

54:21like a fluoroquinolone the respiratory

54:23fluoroquinolones okay

54:25the other thing here is if i wanted a

54:28little bit of a better coverage maybe to

54:29give me some of the coverage of strep

54:31pneumo as well as hemophilus influenza

54:33morexella and then i have another agent

54:35that's really more targeted to the

54:37atypicals like doxycycline or a

54:39macrolide then i could use that plus

54:42something that would give me the strep

54:43pneumo and some of the gram negative

54:44coverage what's that ceftriaxone a very

54:47specific beta-lactam so i would pick

54:49something like a beta-lactam and the

54:50preferred agent as the betalactim is

54:53going to be ceftriaxone so i remember

54:55ceftriaxone

54:57again you're going to see

54:58out of all these antibiotics that we

55:00have there's very specific ones that are

55:01most commonly utilized

55:03and then add on to that either a

55:05macrolide

55:08plus or sorry or doxycycline

55:11or doxycycline these would be the agents

55:14that i would pick so for cap community

55:15acquired pneumonia monotherapy

55:17fluoroquinolone or a beta-lactam plus

55:20a doxy or a macrolide

55:22for the hospital acquired pneumonia now

55:24on the other hand you're thinking about

55:25nasty multi-drug resistant type of

55:27pathogens you're talking about the

55:28pseudomonas you're talking about mrsa so

55:30for this situation here you're talking

55:32about mrsa so you need to have coverage

55:33for mrsa

55:34and you're talking about pseudomonas

55:37so you need to think about all the

55:38antibiotics that'll cover mrsa and the

55:40ones that will cover pseudomonas

55:41remember all those that's the preferred

55:43one for for mrsa vancomycin so that'll

55:46be the first one for your for your mrsa

55:47coverage so vancomycin and then for your

55:50peppers sorry for your pseudomonas i

55:51already gave you the answer but you

55:53could have a bunch of drugs here so you

55:55could pick your anti

55:57pseudomonal penicillins which is your

55:58pipper cylinder tazobactin

56:01you could also pick ceftazity

56:04you could pick cefepime

56:06you could even pick an aminoglycoside

56:10right so these are the options that you

56:11could add here so it would be a

56:12vancomycin plus one of these to give you

56:14your pseudomonas coverage the more

56:16commonly utilized one is going to be

56:17anti-pseudomonopenizing and cefapine

56:19okay that'll cover your pneumonia so

56:21once you have them come in you treat

56:23them with these particular antibiotics

56:24for your cat do these

56:26get some cultures and then once you get

56:28the cultures and they come back oh it

56:29was only strapped pneumo then you can

56:31peel back some of the other antibiotics

56:32and only utilize the ones that will

56:34cover your atypicals or your strep

56:36pneumo if you end up getting a hap

56:38you end up starting them on the worst

56:40case bacteria mrsa pseudomonas

56:43then you get the cultures back and then

56:45they come back and they say oh it wasn't

56:46even merc it was misa oh then i can get

56:48rid of vanco i can get rid of the

56:50pseudomonal coverage and i can only

56:52target the missus species which i can

56:54use something like

56:56naphthalene oxacil oxacyline

56:57dicloxacillin or cefazolins cephalaxin

57:00something like that or even potentially

57:02like a fluoroquinolone so in those

57:04situations that's how i would go about

57:06targeting these

57:07now the next thing is your git infection

57:09so this includes like cholecystitis

57:12cholangitis appendicitis diverticulitis

57:15pancreatic walled off necrosis

57:17peritonitis and intra-abdominal abscess

57:19anything that you can think of git wise

57:22there's a lot of things that we have to

57:23cover but most specifically for the git

57:26you think about your gram negative rods

57:29the hens peck

57:31so with particular emphasis

57:33on

57:34enterobactericie

57:36e coli klebsiella

57:39and then for the other thing you have to

57:41consider is your anaerobic infections so

57:44all those anaerobes so the clostridium

57:46species the bacteroides the

57:47fusibacterium the peptostreptococcus and

57:50the actinomycetes you have to cover

57:51those so i need gram negative and

57:53anaerobe coverage now to think about

57:56this which one is the

57:58boom blows up everything we'll cover

58:00every gram negative and every anaerobe

58:01there's the

58:03karba pendums and then your

58:04anti-pseudomonal penicillins are also

58:05pretty good there because they'll cover

58:06anaerobes and gram negatives by

58:08themselves so

58:09the ones i would consider for these is

58:11going to be your

58:13carbapenems that would be a monotherapy

58:15there

58:16or your anti-pseudomonal

58:20penicillins because they'll cover you

58:21all your gram negatives

58:25and your anaerobes now if you're trying

58:28to do double coverage like you actually

58:29have two agents where you want to be a

58:31little bit less intense with these nasty

58:32agents because they're really intense

58:34they're great drugs but they're super

58:36broad

58:37you can consider something like a double

58:38coverage where you add on metronidazole

58:40which is for anaerobic infections below

58:42the diaphragm and then you have

58:43something that covers a gram negative

58:45so i would cover let's put metronidazole

58:48plus metronidazole plus metronidazole

58:52plus so metronidazole plus a

58:54fluoroquinolone like cipro would

58:55actually be not a bad idea because that

58:57also gives a little bit anaerobic

58:58coverage metronidazole plus ceftriaxone

59:01which gives a good gram-negative

59:03coverage against collab e coli and

59:05enterobacter and metronide is all

59:07placefein because that also gives a good

59:09coverage and even gives you some

59:11pseudomonas coverage as well so those

59:13would be the types of antibiotics that i

59:14would cover for a gram-negative and

59:15anaerobic infection okay so commonly

59:18it's usually you'll see

59:19the the third option here or the fourth

59:22option and if you really want to carbon

59:23pendulums will cover it all

59:25okay

59:26the next thing is your skin and soft

59:27tissue infections for the skin and soft

59:30tissue infections there's two types of

59:31pathogens that i want you to remember

59:32you're going to see staphylococcus

59:34aureus and strep a as the streptococcus

59:36pyogenes but there's two types there's

59:38the misa and the mrsa for the staph

59:40aureus so for misa and strep a i want

59:43you to know the po and iv version so if

59:45you have someone with a cellulitis or

59:46they have an abscess or they have some

59:48type of like nasty like skin infection

59:50soft tissue infection what do i cover

59:51them with

59:52well the first thing is if they have

59:54miss and strep a and i want to cover

59:56them with po versions then i would

59:58consider which one was the coverage for

1:00:00the missa

1:00:01it was

1:00:02the anti-staphylococcal so diclox so

1:00:05diclox was the only like really po one

1:00:08um that would cover the misa and the

1:00:10strep a okay what are some other agents

1:00:12that i could utilize it was the first

1:00:14generation cephalosporins which one was

1:00:15those cephas nolan is pretty much iv so

1:00:18cephalexin would be the other one or

1:00:21cephalexin

1:00:23okay if i want to cover more of an iv

1:00:26form then i could use all the other ones

1:00:28so nafcillin

1:00:30or

1:00:31oxicillin

1:00:34or i could utilize which one for the

1:00:36first generation cephalosporins

1:00:37cefazolin

1:00:39another cool thing about cefazolin which

1:00:40is actually interesting since we just

1:00:41talked about anaerobes is there's

1:00:43actually some literature that suggests

1:00:44that these can be used as a

1:00:45post-surgical prophylaxis so if somebody

1:00:48has like their abdomen open they get a

1:00:49surgery of any kind um any kind of like

1:00:51post-surgical process you can give them

1:00:53a couple doses of cefazolin and it's

1:00:55actually been shown to be pretty good at

1:00:56post-exposure like treatment of a

1:00:58prevention of bacterial infections and

1:01:00it actually has anaerobic coverage

1:01:01cefazolin but anyway

1:01:03the next thing is your mrsa infection so

1:01:05mrsa

1:01:06so these won't work for mrsa so i need

1:01:07to know what things will cover mrsa but

1:01:09let's know the po versions and then

1:01:10what's the iv versions so the po

1:01:13versions is going to be things like

1:01:15particularly if you had for these i

1:01:17would actually consider something like

1:01:18bactrim like trimethoprim

1:01:20sulfamethoxazole

1:01:22the other one that i would consider

1:01:23something like doxycycline or

1:01:25clindamycin because these will cover

1:01:27both

1:01:28your mrsa and your strep a if you're

1:01:30going po form for the iv form the

1:01:33preferred agents are going to be your

1:01:34vancomycin

1:01:36okay the vancomycin will be the

1:01:37preferred agent for this and if you've

1:01:39got heavy pockets and you can consider

1:01:41like ceftaroline but

1:01:42vancomycin be the primary one

1:01:44okay so the next thing is if we have the

1:01:46urinary tract infection so the utis we

1:01:48have to think about what if it's

1:01:49actually due to a pilo what if it's due

1:01:51to an acute cystitis so the most common

1:01:53pathogens particularly for a pilot or

1:01:55for an acute cystitis are particularly

1:01:57going to be

1:01:59those pec

1:02:00organisms so again you're going to think

1:02:02about the proteus mirabilis your e coli

1:02:05your klebsiella

1:02:07and then don't forget your enterobacter

1:02:09so your enterobacter are going to be

1:02:10some of those as well

1:02:12so same thing pec

1:02:14and enterobacter

1:02:17okay so for these i want to know which

1:02:20kinds of

1:02:21antibiotics are going to cover me for

1:02:22pyelonephritis especially against the

1:02:24pec and the enterobacter well the big

1:02:26one that i would think about is

1:02:28ceftriaxone the third generation

1:02:29cephalosporin is an obvious one here

1:02:31definitely can't go wrong with this one

1:02:33so ceftriaxone is a pretty good one here

1:02:36the other one that i would also consider

1:02:38here is going to be a fluoroquinolone

1:02:40particularly ciprofloxacin this one's

1:02:42also pretty good can i also give you

1:02:43some coverage against these organisms as

1:02:46well

1:02:47the other one that you could potentially

1:02:49consider against these is something

1:02:51in the lines of like a amino penicillin

1:02:54amino penicillins may not be too bad

1:02:56they don't cover your enterobacter

1:02:58very well

1:03:00but they would cover some of the proteus

1:03:02the e coli and the klebsiella so you can

1:03:03consider something like an amino

1:03:05penicillin

1:03:06particularly

1:03:08ampicillin

1:03:09but these would be some of the agents

1:03:10that you can consider for the

1:03:12pyelonephritis for the acute cystitis so

1:03:15this is primarily of the bladder

1:03:17this would be particularly in your pec

1:03:18in your enterobacter but there's a very

1:03:20subset of antibiotics very specific to

1:03:22these so trimethoprim sulfamethoxazole

1:03:25would be one if they're like not

1:03:26pregnant

1:03:27nitropharan tone is usually good for

1:03:29also known as macro bit is good for like

1:03:31post

1:03:32coital prophylaxis against certain types

1:03:34of utis

1:03:36another one that you can consider here

1:03:38is phosphomycin

1:03:40and then lastly is if a second lyden

1:03:42agent it would be like ciprofloxacin so

1:03:44this would be more of your second line

1:03:45agent because there is a lot of

1:03:46resistance out there to get this drug so

1:03:48these would be the agents that you would

1:03:49consider for a patient

1:03:51for acute societies now the last

1:03:53situation is what if the patient has a

1:03:54complicated uti so it's a complicated

1:03:57uti meaning that they got some nasty

1:03:59pathogens in this bad boy they got

1:04:01something like pseudomonas

1:04:04they got something like mrsa

1:04:07or they have something like enterococcus

1:04:10and these situations now we have to

1:04:12broaden up our coverage a little bit so

1:04:13i have to think primarily about the

1:04:14pseudomonas what's going to cover that

1:04:16pseudomonas really well so the pseudo i

1:04:18got to think about any kind of

1:04:20anti-pseudomonal drug so this would be

1:04:22again think about your

1:04:24piperacillin so we'll put piptazo that's

1:04:26your anti-suitable penicillin you can

1:04:28think about cefepime

1:04:31you can think about an aminoglycoside

1:04:33maybe even ceftazidim something of that

1:04:34nature

1:04:36um

1:04:37the other thing that you can consider

1:04:38here is what else for the complicated

1:04:39utis especially for the mrsa if you're

1:04:42definitely concerned about mrsa and

1:04:43enterococcus

1:04:45because they have like their chronic

1:04:46foley so they have like a chronic and

1:04:47dwelling foley then you can consider

1:04:49something like vancomycin

1:04:53and then again for some of these you can

1:04:54even potentially consider like an amino

1:04:56penicillin but amino penicillins

1:04:57wouldn't really um actually amino

1:04:59penicillins would particularly be

1:05:00against the enterococcus so amino

1:05:02penicillins would really be primarily

1:05:05against the enterococcus if it came back

1:05:07it was definitely enterococcus the amino

1:05:09penicillins would actually be beneficial

1:05:10against this one you can even consider

1:05:12carbapenems but that's way too broad i

1:05:14wouldn't go ahead with a carbohydrate

1:05:16okay that's our uti so we covered

1:05:18pneumonia git infections skin soft

1:05:20tissue urinary tracts what about bone

1:05:23and joint particularly like septic

1:05:24arthritis or maybe even like an

1:05:25osteomyelitis

1:05:27in those situations you want to think

1:05:29primarily about mrsa because it's off

1:05:31the skin right so it spreads from the

1:05:33skin into the actual boner joint so if

1:05:35you want to think about mrsa coverage

1:05:36what's the best antibiotic for mrsa

1:05:38especially iv which you're going to need

1:05:39vancomycin

1:05:41if you also have to think about this one

1:05:43here add this one into the list it's a

1:05:45tricky one so nesarius this okay so

1:05:47naserio gonorrhea especially in this

1:05:50situation sometimes

1:05:52patients can get some nasty like

1:05:54sexually transmitted infections and it

1:05:56can actually spread to the actual joint

1:05:58so for this one you want to consider

1:06:00something like a ceftriaxone if you have

1:06:04concern for this okay and the last thing

1:06:07is pseudomonas pseudomonas is a pretty

1:06:08nasty one especially like diabetics um

1:06:10so you want to think about any kind of

1:06:12pseudomonal penicillin a pseudomonal

1:06:13drug so specifically for these

1:06:16cefepime

1:06:19and ceftaz are a little bit better

1:06:22in comparison to your

1:06:23pipercellontesobactum

1:06:25okay that would cover our bone joint uti

1:06:28skin soft tissue our pneumonias and git

1:06:30infections let's now come down here and

1:06:32talk about meningitis and then some

1:06:33bloodstream infections like uh

1:06:35clabsis and sepsis all right my friends

1:06:38now let's move on to cns infection so

1:06:39now we're talking about like meningitis

1:06:40a really nasty meningitis if a patient

1:06:42comes in they've got symptoms of

1:06:43energized photophobia headache they got

1:06:45neck stiffness they got fevers all the

1:06:46above

1:06:47and you're considering is this a

1:06:49community acquired meningitis so they

1:06:51actually developed what types of

1:06:52pathogens here likely

1:06:54you want to think about strep pneumo you

1:06:56want to think about homophilus influenza

1:06:57and you want to think about nesaria

1:06:59meningitidis okay these are the primary

1:07:01community acquired meningitis infections

1:07:03so you have to think about what kind of

1:07:04things are going to cover your strep

1:07:05pneumonia your hemophilus and uranus

1:07:07area so the best things to consider in

1:07:09these situations here is actually going

1:07:11to be vancomycin

1:07:13because that'll cover a lot of your

1:07:14strep pneumo okay

1:07:15especially if there's any resistance

1:07:17situations here and then ceftriaxone

1:07:20because that'll also be a really good

1:07:22one because it has the best cns

1:07:23penetration remember good cns

1:07:26penetration for ceftriaxone

1:07:28now the other thing that's a benefit to

1:07:30this one

1:07:32is that you also get coverage of the

1:07:34hemophilus influenza and the necessary

1:07:35meningitis

1:07:37the last thing that you can consider is

1:07:39ampicillin and the only reason i would

1:07:41add this one on is the concern for

1:07:43listeria

1:07:44so if you're concerned for listeria the

1:07:47patient is greater than 60 years of age

1:07:48or 50 years of age actually some

1:07:50literature says they're

1:07:50immunocompromised like they have hiv the

1:07:52transplant something like that or their

1:07:54little baby

1:07:55then you can consider the addition of

1:07:56ampicillin because you're trying to

1:07:58cover for listeria if not if they don't

1:07:59have a lot of those risk factors you

1:08:00don't really need to add on ampicillin

1:08:03okay so that your community acquired

1:08:05meningitis now hospital acquired they

1:08:08had a neurosurgical procedure they had a

1:08:09hemicraniactomy they had a evd they had

1:08:12some type of thing where we opened up

1:08:14the skull or we did some type of surgery

1:08:16mucked around near the meninges and we

1:08:19introduced a pathogen that's in the

1:08:21hospital nasty stuff

1:08:23into the actual meninges that's mrsa and

1:08:26pseudomonas

1:08:27so what do we give for those infections

1:08:29that we're concerned about if we think

1:08:31it's mrsa my friends

1:08:33we give vanco

1:08:36and sometimes even linaselli is actually

1:08:38a decent one as well

1:08:40for the other one we're concerned about

1:08:42pseudomonas because this is a a

1:08:44nosocomial infection

1:08:46episode taser bacterium not too good at

1:08:48penetrating into the actual meninges

1:08:50cefepime is and unfortunately can

1:08:52actually cause encephalopathy and

1:08:53seizures too but cephepim is a pretty

1:08:56good one that i would actually consider

1:08:57here and if you really need another one

1:08:59that penetrates well but it also can

1:09:00cause neurotoxicity and seizures

1:09:01carbopenes as well but i would go with

1:09:03cephepene primarily for this one

1:09:05okay

1:09:06now we move on to the bloodstream

1:09:07infections you have a patient who's

1:09:09coming in they're coding you have to

1:09:10throw in an emergent crash line and you

1:09:12don't do it sterily or you do do it

1:09:14sterily whatever it may be sometimes you

1:09:16actually do a sterile procedure you put

1:09:17in an ig you put in a subclavian line

1:09:19whatever it is and you perform it

1:09:20sterile what are the pathogens that are

1:09:22on the skin that actually may move along

1:09:24the actual length of the catheter or the

1:09:26actual needle and get into the

1:09:27bloodstream along that catheter what's

1:09:29the big one to think about mrsa

1:09:31staphylococcus aureus you can get things

1:09:33like um staphylococcus epidermidis but

1:09:36that's more like not a concerning one i

1:09:38wouldn't be too worried about that one

1:09:39i'd be worried about mrsa okay so if i'm

1:09:41concerned about that definitely think

1:09:43about that one so in a patient who has a

1:09:45bloodstream infection they got fever

1:09:46they got hypotension they got

1:09:48a leukocytosis in those situations and

1:09:51you're thinking about oh they got a line

1:09:53in

1:09:53think about that as a potential source

1:09:55of their infection and so i got to cover

1:09:56the possibility if this is mrsa which is

1:09:59the most likely one because of where the

1:10:01actual pathogens would have a route into

1:10:03then i would consider something like

1:10:06vancomycin now the times where i would

1:10:08add on a plus or minus

1:10:11for the actual gram negatives so any

1:10:14kind of gram negative that you can think

1:10:16about why i would think about this with

1:10:19the femme lines so if you have a femoral

1:10:21central line what's that right near

1:10:23right near the booty hole so a lot of

1:10:25opportunity for gram-negative bacteria

1:10:27to hop onto that area if they're pooping

1:10:29if they're having like incontinence and

1:10:31moving along the length of that catheter

1:10:32into the actual bloodstream so in those

1:10:35situations like you have like a a

1:10:37non-sterile line

1:10:39or a crash femme line or fem line in

1:10:42general think about this as a potential

1:10:44opportunity and then you'll add on the

1:10:46things that will give you the gram

1:10:47negative coverage what's the best one

1:10:49really that'll cover your gram negatives

1:10:50your pseudomonas

1:10:52i'd say peppercilantazobactum okay so

1:10:54for this one you want to consider

1:10:55piptazo

1:10:57okay and that's your anti-pseudomonal

1:10:58penicillin i just don't want to write it

1:10:59out my arms are getting weak okay the

1:11:01next one is sepsis you have a

1:11:04bloodstream infection and you actually

1:11:06are concerned a patient comes in you

1:11:08have no idea what's going on to them

1:11:10they are tachycardic they're hypotensive

1:11:12they're fibra they've got a blasting

1:11:14white count you have them on pressers

1:11:16you have them on fluids you have them

1:11:17intubated you're doing everything to be

1:11:18able to keep this patient alive but they

1:11:19have a sepsis of unknown etiology

1:11:21there's always the classic antibiotics

1:11:23that you start them on and that's

1:11:24vancomycin to cover mrsa

1:11:26and any other kind of gram-positive

1:11:28infection and then the other one is your

1:11:30pipercelantazobactum to cover any kind

1:11:32of gram-negative pseudomonas

1:11:33acetynobacteria extended spectrum

1:11:34beta-lactamases anaerobes because it's

1:11:36just a broad agent if you don't want to

1:11:37use that one what was the other one boom

1:11:40carbopenums so those are the agents that

1:11:42i would think about if for any gram

1:11:44positive that you're trying to cover for

1:11:46especially mrsa is vanco and then if

1:11:49it's the other ones for your gram negs

1:11:51or

1:11:52anaerobes and i'm talking any of them

1:11:55what was the ones that covered almost

1:11:57every dang gram negative in almost every

1:11:58anaerobe possible pseudomonas per the

1:12:01anticipated penicillin like piptazo

1:12:05and

1:12:06the carbopenums

1:12:10okay i know this was a lot take the time

1:12:13now to go back review it keep writing it

1:12:16down and trying to go through this stuff

1:12:17a couple times let's now take a break do

1:12:20that and move on to the next big beast

1:12:22to tackle and that is the adverse

1:12:24effects and contraindications lots to

1:12:26talk about let's get there all right

Adverse Drug Reactions & Contraindications

1:12:27guys so we have covered so far up to

1:12:29this point the mechanism of action we

1:12:31covered the bacterial coverage we

1:12:32covered empiric antibiotic particularly

1:12:34for common infections

1:12:36now we move on to the next chapter which

1:12:38is the adverse effects and

1:12:39contraindications as if it wasn't enough

1:12:42to remember all the actual bacterial

1:12:44coverage of these antibiotics now we got

1:12:45to remember their adverse effects and

1:12:47there is a lot of them i think the best

1:12:49way to do this is to take the

1:12:51big common adverse effects and then

1:12:54group which antibiotics particularly

1:12:56cause these adverse effects and then

1:12:58we'll talk about some of the other types

1:13:00of random ones that don't really fit

1:13:02within these categories super well and

1:13:04we'll get into those a little bit all

1:13:05right so first things first

1:13:06neurotoxicity so this can look a couple

1:13:09different ways it can look like seizures

1:13:10it can look like myoclonus it can look

1:13:11like encephalopathy it can even cause

1:13:14some really weird situations here we'll

1:13:15talk about

1:13:16another one called serotonin syndrome

1:13:19but

1:13:20what are some of these actual types of

1:13:21antibiotics that cause neurotoxic

1:13:23effects in other words they penetrate

1:13:24into the actual central nervous system

1:13:26and cause adverse effects big ones to

1:13:28remember are your penicillins

1:13:30your cephalosporins are also going to be

1:13:32really good ones

1:13:34okay the other one is your carbipenums

1:13:37these are are really big offenders

1:13:39especially at high dosages

1:13:41the other ones that i want to remember

1:13:42is your polymixins so

1:13:45mixins are also another one

1:13:47and then last but not least is your

1:13:49lenasa lid now linaselid i have to add a

1:13:51little side note here it actually

1:13:53produces something called serotonin

1:13:56syndrome and it can also cause

1:13:57peripheral neuropathy now the reason why

1:14:00this isn't important was because

1:14:02linaselid can actually and work against

1:14:04those monoamine oxidase inhibitors and

1:14:06help to increase the level of serotonin

1:14:08with inside of the synapses which can

1:14:10produce a serotonin syndrome so for

1:14:12penicillins cephalosporins carbipenums

1:14:15really you can just remember all your

1:14:16beta-lactams really and then after that

1:14:18polymixins and linasa litter for the

1:14:20neurotoxic drugs for your pancytopenia

1:14:23same thing penicillins tend to be a big

1:14:25one they can work particularly by maybe

1:14:27causing pancytopenia and on top of that

1:14:29they also may induce a little bit of a

1:14:31hemolytic anemia to talk about a little

1:14:32bit later but penicillins can be one

1:14:35cephalosporins are one

1:14:39now your carbapenel is not so much so

1:14:41the other ones that i want you guys to

1:14:43remember here is going to be if you

1:14:44continue to kind of go down through the

1:14:46wheel of all these antibiotics that

1:14:47we've been going through any of the

1:14:48other beta-lactams

1:14:50carbophenomenas no monobactins no vanco

1:14:53no phosphomycin no dapto no polymixins

1:14:57um not too much maybe a little bit of uh

1:14:59the actual kind of effect there but not

1:15:01too much not worth mentioning bactrim

1:15:03yes bactrim actually can produce um some

1:15:06panzero penis so trimethoprim

1:15:07sulfamethoxazole then you go into the

1:15:09next one's metronidazole nitrofarantoin

1:15:11no you go into your fluoroquinolones no

1:15:14you move into your macrolides

1:15:17no you move into your clinda

1:15:19chloramphenicol chloramphenicol can

1:15:21actually cause some pancytopenia so i'd

1:15:23remember that one as well

1:15:24chloramphenicol

1:15:27and then lynasolid linaseali can also

1:15:29suppress your bone marrow as well

1:15:31so these are the ones that i would

1:15:32remember penicillin cephalosporin

1:15:34bactrum chloramphenicol and linaselid

1:15:37now the respiratory failure is an

1:15:38interesting one

1:15:40for respiratory failure what you want to

1:15:42remember here is going to be polymixin

1:15:44so polymixins can actually cause

1:15:46respiratory failure

1:15:47and then the other one here is going to

1:15:50be pulmonary fibrosis due to

1:15:52nitrofarantone so nitroforantone that we

1:15:55use pretty much for a lot of those

1:15:56urinary tract infections can actually

1:15:58cause pulmonary fibrosis so it actually

1:16:01cause fibrosis which can lead to

1:16:03respiratory failure okay let's come down

1:16:06now and talk about these other kind of

1:16:07ones here nephrotoxic ototoxics and

1:16:09things that can actually exacerbate

1:16:11myasthenia gravis all right so now the

1:16:12next thing is nephrotoxic agents so

1:16:14these things that actually cause kidney

1:16:16injury so ones that actually cause

1:16:18direct kidney injury that we'll talk

1:16:19about those last but the ones that

1:16:20actually work through an indirect

1:16:21mechanism they produce kind of something

1:16:23called acute interstitial arthritis by a

1:16:25kind of like a hypersensitivity reaction

1:16:27so we'll talk about a little bit later

1:16:28but basically you exposed to the drug

1:16:29your immune system cells produce

1:16:31antibodies like ige and igg antibodies

1:16:33and these kind of molecules actually

1:16:35lead to inflammation around the kidney

1:16:37tubules and cause acute interstitial

1:16:38nephritis which can cause an acute

1:16:40kidney injury the ones that i want you

1:16:42to remember for that one is your

1:16:43penicillins

1:16:44your cephalosporins

1:16:48and then the last one here is your

1:16:49bactrum

1:16:50so your trimethoprim sulfamethoxazole

1:16:53all of these is a category can cause

1:16:54acute interstitial nephritis the ones

1:16:57that cause direct nephrotoxic

1:16:59destruction though are going to be your

1:17:01aminoglycosides

1:17:03and don't forget this one vancomycin

1:17:06these ones will actually cause direct

1:17:08nephrotoxic effects

1:17:10so big big ones to monitor in these

1:17:12patients ototoxic just take the two ones

1:17:14that we just talked about

1:17:14aminoglycosides and vancomycin bring

1:17:16them down so aminoglycosides can cause

1:17:19ototoxic effect and

1:17:21vancomycin can cause

1:17:23ototoxic effects especially if combined

1:17:25with aminoglycosides

1:17:27myasthenia gravis so myasthenia gravis

1:17:29is basically again it's that whenever

1:17:31patients produce antibodies that are

1:17:33against like the nicotinic receptors

1:17:34that are present on the muscle cells the

1:17:36skeletal muscles right where we can

1:17:38actually have particular drugs that can

1:17:39worsen the myostinia gravis and put them

1:17:41into a crisis and so the big ones to

1:17:43remember for this one is going to be

1:17:45your fluoroquinolones

1:17:47your

1:17:48aminoglycosides your macrolides

1:17:52and then last but not least your

1:17:53clindamycin

1:17:57so these ones would probably stay away

1:17:58from if a patient has myasthenia gravis

1:18:00and you don't want to put them into a

1:18:01mycenaean crisis all right so that's the

1:18:03ones for again nephrotoxic ototoxic and

1:18:05then worsening the mystery graphics

1:18:07let's go back up and talk about the

1:18:09other ones particularly the teratogenic

1:18:10medications all right so the next thing

1:18:12is teratogenic medications meaning that

1:18:13you should not give these to patients

1:18:14because they have the risk of causing

1:18:16particular types of destructive effects

1:18:18to the baby during the actual

1:18:19gestational period so avoid these

1:18:20medications and so the big ones that i

1:18:22definitely think are worth remembering

1:18:24here

1:18:25are going to be a couple different drugs

1:18:26so if we go through all the penicillins

1:18:28they're all safe the beta lactams are

1:18:29safe vancomycin's safe bactrim i would

1:18:31actually kind of avoid that one the

1:18:33reason why is bactrim

1:18:34trimethoprim sulfamethoxazole has been

1:18:37shown to be able to produce

1:18:39something called kernicterus so it can

1:18:41actually cause a lot of um

1:18:44unconjugated types of bilirubin to

1:18:45accumulate within like the cerebellum

1:18:47the brain stem and then like the uh

1:18:49particularly some of the actual basal

1:18:50ganglia structures which can cause a lot

1:18:52of like neurotoxic effects so that's one

1:18:53particular one that i would stay away

1:18:54from

1:18:56um if you go through the other ones like

1:18:57metronidazole nitrofarantone not so much

1:19:00then if you go into your

1:19:01fluoroquinolones fluoroquinolones there

1:19:03actually is particularly like

1:19:04contraindications against those less

1:19:06than 18 years of age because it can

1:19:07produce a lot of cartilaginous damage

1:19:09and arthropathies so that's one

1:19:10particular drug that i would also

1:19:11consider like fluoroquinolones to kind

1:19:12of just stay away from

1:19:14um

1:19:15then if you move on from there you move

1:19:16into um your

1:19:1850s ribosomal inhibitors so macrolives

1:19:21are pretty safe

1:19:22clinda is relatively safe

1:19:24chloramphenicol i would actually kind of

1:19:25avoid as well especially in certain

1:19:27situations so chloramphenicol one of the

1:19:30problems with this drug is it can

1:19:32produce something called gray

1:19:34baby syndrome and you're like what the

1:19:36heck so this is important in like the

1:19:38glucoronate reaction so you know there's

1:19:40an enzyme called udp glucose

1:19:41glucuronasal transferase and what it

1:19:43does it produces puts a glucaronic

1:19:45molecule on certain types of drugs

1:19:46during the biotransformation process if

1:19:48they have a deficiency in that enzyme

1:19:49then they don't glucoroni uh put a

1:19:51glucoronidal on chloramphenicol and so

1:19:52we have lots of these metabolites of

1:19:54chloramphenicol which can produce kind

1:19:55of a gray ash and appearance of the baby

1:19:57and also cause significant hypotension

1:19:59tachyarrhythmias and produce

1:20:00cardiovascular collapse and even

1:20:02respiratory failure in these babies so

1:20:04avoid chloramphenicol

1:20:06the nasal lid is actually relatively

1:20:07okay

1:20:08if you go into your aminoglycosides

1:20:10those are not too bad

1:20:12and then the other one that i would also

1:20:13consider is your tetracyclines like

1:20:14doxycycline that's a big one as well so

1:20:16i would also consider doxycycline

1:20:19maybe avoid that one as well just

1:20:21because of the risk particularly for

1:20:22this one um this one can also

1:20:24potentially cause a lot of teratogenic

1:20:26effects as well

1:20:27so these are some of the big ones that i

1:20:28would actually say to avoid in a patient

1:20:30who has again who is pregnant and uh you

1:20:33don't want to actually cause some type

1:20:34of teratogenic effect the next thing is

1:20:36your disulfiram reaction so disulfiram

1:20:38reactions are basically whenever someone

1:20:39takes a medication and combines with

1:20:40alcohol they can actually develop like

1:20:42nasty like nausea vomiting like exorcist

1:20:45level vomiting like flushing hypotension

1:20:47tachycardia a lot of problematic issues

1:20:49with this and the big one to remember

1:20:51for the disulfiram reaction i'm actually

1:20:52gonna get rid of the other one because i

1:20:53think this one's the more important one

1:20:54remember i don't want you guys get too

1:20:55confused is metronidazole so do not

1:20:58forget metronidazole

1:21:00the other one if you really want to

1:21:01remember it it's the third generation

1:21:02cephalosporin ceftriaxis has been shown

1:21:04to be able to produce this as well but

1:21:06again i focus more particularly on

1:21:08disulfiram reaction metronidazole the

1:21:10other one is qt prolongation with the

1:21:12increased risk of producing something

1:21:14called torso's deployment so you know if

1:21:16you actually increase your qt interval

1:21:18you increase the risk of something

1:21:19called torsades to points which is a

1:21:21nasty type of polymorphic ventricular

1:21:22tachycardia that can quickly

1:21:23defibrillate break down into ventricular

1:21:26fibrillation so i would also be careful

1:21:28for this one the two particular drugs

1:21:29that you want to remember for this one

1:21:30is your fluoroquinolones and your

1:21:32macrolides so fluoroquinolones

1:21:35and your macrolides

1:21:37are going to be the big ones for this

1:21:38one okay

1:21:39so now that we got these let's move on

1:21:41to the next group here which is your cyp

1:21:43450 inhibitors let's talk about these

1:21:45all right so the next thing is your

1:21:46cyp-450 inhibitor so what are the

1:21:47particular drugs that can actually work

1:21:50so you know whenever you have cyp-450

1:21:51molecules these are basically particular

1:21:53enzymes that are going to work to take a

1:21:56drug and undergo a biotransformation

1:21:58process so to be able to kind of add on

1:22:00a little intermediate metabolite that

1:22:01makes this molecule a little bit more

1:22:03polar and allow for it to be able to

1:22:05exert its effects

1:22:06okay if we give particular drugs like

1:22:09cyp we give some of these other

1:22:11antibiotics they can act like inhibitors

1:22:13and if they act like inhibitors what

1:22:15happens is they actually reduce the

1:22:17metabolism of the drug and that causes

1:22:19the concentrations of the actual drug to

1:22:21be a lot higher within bloodstream

1:22:22producing more negative connotations of

1:22:24that drug and so the big ones to

1:22:26remember for this one are going to be

1:22:27your fluoroquinolones

1:22:29your macrolides

1:22:33and your trimethoprim sulfamethoxazole

1:22:35so these are the ones that can actually

1:22:36kind of increase the concentrations of

1:22:37the drug because they can inhibit the

1:22:39cyp-450 and enzyme which doesn't allow

1:22:41for it to be able to get converted into

1:22:42like this metabolite form and so because

1:22:44of that now this drug concentration is a

1:22:46lot higher and it has the ability to

1:22:47presume more

1:22:48negative effects so for example if i

1:22:50took this with like warfarin which is

1:22:51designed to be able to cause a patient

1:22:52to thin out their blood right

1:22:54anticoagulant now if i give it with

1:22:56these medications it can actually

1:22:57increase the concentration of the

1:22:58warfarin within the bloodstream and

1:23:00produce a potential increased risk of

1:23:01bleeding so that's a thing to consider

1:23:03all right the next thing is your

1:23:04hemolytic anemia so hemolytic anemia is

1:23:07uh particularly the destruction of your

1:23:09red blood cells and there's a lot of

1:23:10particular drugs that work at this level

1:23:11too the big thing to remember is if you

1:23:13remember for the thrombocytopenia there

1:23:15was penicillins and cephalosporins these

1:23:17actually cause like hypersensitivity

1:23:19reactions which can lead to kind of a a

1:23:21coombs positive coombs test which

1:23:23actually can be positive on these

1:23:25patients so they'll have anemia you can

1:23:27check their ldh you can check their

1:23:28haptoglobin there may be some evidence

1:23:29of hemolysis and then you check their

1:23:30coombs test and it's actually positive

1:23:32and so for these patients i would

1:23:33remember

1:23:34penicillin

1:23:36encephalosporins

1:23:38that these can actually produce

1:23:40a positive coombs test

1:23:43the other ones that i actually would

1:23:45remember here specifically exacerbate

1:23:47our worst in our produce a hemolytic

1:23:48crisis in patients with g6 pdh

1:23:50deficiencies and so this one's i would

1:23:52remember trimethoprim sulfamethoxazole

1:23:56fluoroquinolones

1:23:58and nitropharantone

1:24:00these can actually worsen your

1:24:04g6pdh deficiency and produce a kind of a

1:24:08hemolytic event or hemolytic crisis so i

1:24:10would remember these

1:24:11the last one here to add on is

1:24:13phototoxicity so if exposed to the sun

1:24:15it can actually cause a lot of rashes

1:24:16and kind of skin burning effect and i

1:24:17would remember for this one is

1:24:19doxycycline

1:24:22and

1:24:23trimethoprim sulfamethoxazole

1:24:26all right my friends we talked about the

1:24:28most common types of like adverse

1:24:30effects as groups based upon the type of

1:24:32problem that they have let's now come

1:24:34for some of like the little more nuanced

1:24:36types of adverse effects or

1:24:37contraindications of each individual

1:24:39kind of drug class and we'll talk about

1:24:41one more thing which is the c diff all

1:24:42right let's get in there all right so

1:24:43now let's talk about just some extra

1:24:45adverse effects that i want you guys to

1:24:46remember in case it comes up for your

1:24:47exam so penicillins are there anything

1:24:49else besides what we talked about over

1:24:51here with the neurotoxic effects the

1:24:53pancytopenia

1:24:54particularly the nephrotoxic effects we

1:24:56talked about its effects particularly

1:24:58within um

1:24:59the hemolytic anemias as well are there

1:25:01any other kind of things that we should

1:25:02talk about particularly for this one i

1:25:04would remember uh the hypersensitivity

1:25:06reaction that it can actually produce is

1:25:07anaphylactic shock so because of that

1:25:09you actually get exposed let's say at

1:25:10some point in time to penicillin right

1:25:12what happens is your immune system

1:25:14responds to that and produces like

1:25:15different types of antibodies like ige

1:25:17antibodies and then what happens that

1:25:19can get plugged into like different mast

1:25:21cells and let's say in the future you

1:25:22get exposed to penicillin again now you

1:25:24have these particular antibodies on the

1:25:26mast cells when they're exposed to them

1:25:27they can start producing massive amounts

1:25:29of histamines and bradykinins and things

1:25:31of that nature and this can hit the

1:25:32lungs this can hit the skin this can

1:25:34obviously cause particulate like nasty

1:25:36bronchial constriction bronchospasm it

1:25:38can produce respiratory failure can

1:25:39produce a lot of like rashes and heaves

1:25:41and it can even cause the point where

1:25:42you can actually become hypotensive and

1:25:43lead to anaphylactic shock so those are

1:25:45things to consider particularly for the

1:25:46penicillin is the anaphylactic shock

1:25:48effect

1:25:49for cephalosporins on the other hand the

1:25:52other things that i would actually add

1:25:53on to this one

1:25:54is particularly it's been shown by some

1:25:56type of mechanism whether it be the

1:25:57absorption whether it be destroying the

1:25:58bacteria whether it be working directly

1:26:00on the liver enzymes but it's been shown

1:26:01to potentially produce a vitamin k

1:26:03deficiency so if you can actually

1:26:05produce a vitamin k deficiency what

1:26:07happens is is it inhibits the ability to

1:26:09be able to make particular types of

1:26:10coagulation proteins procoagulants and

1:26:12so you might have a higher risk of being

1:26:14able to potentially bleed the other

1:26:15thing is that it's been shown very

1:26:16interesting especially with ceftriaxone

1:26:19is it can produce an increased risk of a

1:26:21biliary sludge you're like what the heck

1:26:24is that it can increase the risk of like

1:26:26cholecystitis especially ceftriaxone and

1:26:30the last thing is that particularly

1:26:31whenever you use cephalosporins and in

1:26:34combo with aminoglycosides this can

1:26:36really increase an acute kidney injury

1:26:38and have a very nasty nephrotoxic effect

1:26:41okay so penicillins remember big thing

1:26:43for this one is anaphylaxis

1:26:48and then for cephalosporins don't forget

1:26:49the vitamin k deficiency the biliary

1:26:51sludge especially with ceftriaxone and

1:26:53then if you combine these with

1:26:54aminoglycosides they have an increased

1:26:55net for toxic effect all right let's

1:26:57move on now talk about vanco adapto all

1:26:59right so with vancomycin there's a

1:27:00couple extra things that i want you guys

1:27:01to remember so particularly for this one

1:27:03not only does it cause net for toxic and

1:27:05ototoxic effects but the other thing is

1:27:06it can also cause like especially if you

1:27:08push a little bit too fast it can cause

1:27:10phlebitis so it can really kind of burn

1:27:11whenever you push it into the vessel's

1:27:12iv here's the other thing

1:27:14if you push it too quickly

1:27:17you can cause something called red

1:27:20man

1:27:21syndrome

1:27:22so red man syndrome is whenever you push

1:27:24it too quickly it causes like a really

1:27:27nasty redness red rash to become super

1:27:30itchy

1:27:31it can lead to muscle spasms

1:27:34and it can even precipitate precipitate

1:27:36hypotension so this is one of the big

1:27:39things to consider if you push

1:27:40vancomycin too quickly it can cause a

1:27:42phlebitis and it can also cause red man

1:27:44syndrome like redness itchiness muscle

1:27:47spasms hypotension even a little bit of

1:27:48tachycardia

1:27:50the last thing to consider is it can

1:27:52also produce something called dress so

1:27:54this is kind of a drug related

1:27:55eosinophilic kind of like systemic

1:27:57reaction

1:27:58and so the classic kind of tetrad for

1:28:00this one is the patient has fevers

1:28:03they have a rash

1:28:05they have an increase in their

1:28:06eosinophils you see the red eosin acid

1:28:08with a telephone shaped nucleus and then

1:28:10they can also have lymphadenopathy

1:28:13so this is another particular thing to

1:28:14think about especially in patients with

1:28:16vancomycin

1:28:17the next one dapto please don't forget

1:28:20this one if you're utilizing this to

1:28:21treat a patient who has some type of

1:28:23like mrsa infection of the skin or a

1:28:25right-sided infective endocarditis for

1:28:27daptomycin it's been shown to be able to

1:28:29cause destruction of the actual muscle

1:28:30cells so what is this called rhabdo

1:28:34myolysis

1:28:36okay that's a big one so don't forget

1:28:38that one consider checking like a ck

1:28:39enzyme on these these patients okay so

1:28:42we talked about our penicillin or

1:28:43cephalosporins our vanco are dapto let's

1:28:45move on to the other ones so doxycycline

1:28:48so this is part of the grip of your

1:28:48tetracyclines is there any other

1:28:50additional effects i want you guys

1:28:51remember this one especially if a

1:28:52patient is taking doxycycline they

1:28:54should take it with a good amount of

1:28:55water and they should try to stay

1:28:56upright for a little bit the reason why

1:28:57is if it gets stuck inside the esophagus

1:28:58can actually cause like destruction of

1:29:00the esophageal tissue and it can cause

1:29:02what's called pill induced esophagitis

1:29:04so a big one to think about for this one

1:29:05especially like this one and like your

1:29:06bisphosphonates and stuff like that this

1:29:08is the big ones so don't forget pill

1:29:10induced

1:29:12esophagitis the other thing is this

1:29:14sucker loves like calcium and so it can

1:29:16love to bind to the calcium in the teeth

1:29:18especially little babies that can cause

1:29:19like teeth discoloration so the other

1:29:21one to remember here is especially in

1:29:22like children is really try to avoid

1:29:24this one because it can actually cause

1:29:26like staining of the teeth like the

1:29:27teeth discoloration

1:29:29macrolides you can remember the mnemonic

1:29:31for the adverse effects by macro so m is

1:29:34for motility dysfunction so the git

1:29:36there is potentially like some git

1:29:39dysfunction so alteration within the

1:29:42motility dysfunction a for arrhythmias

1:29:44you guys remember what it did prolong

1:29:46your qt interval increase the risk of

1:29:47testosterone points and increase the

1:29:48risk of v fib

1:29:50c for cholestasis

1:29:52so it can actually increase the risk of

1:29:54stasis of biliary flow

1:29:56the other thing is it can do r so rash

1:29:59and the last thing is oh this is kind of

1:30:01a stretch eosinophilia

1:30:03so i can increase the number of your

1:30:05eosinophils

1:30:06all right so big thing here doxy pill

1:30:08induce esophagitis teeth discoloration

1:30:10for macrolides remember macro motility

1:30:12dysfunction arrhythmias

1:30:15cholestasis rash and eosinophilia all

1:30:18right let's talk about clinda and

1:30:19lynasolid all right so the next one is

1:30:21clindamycin so with clindamycin one of

1:30:23the big things for this guy is it can

1:30:24cause c diff all right so we know that

1:30:26clindamycin definitely increases the

1:30:28risk of c diff so we can add clindamycin

1:30:30into the c diff column here right so

1:30:31clinda

1:30:32is there any other drugs that have

1:30:34actually been shown to be able to have a

1:30:36high risk of clostridium difficility

1:30:37really you can consider any antibiotic

1:30:39but with the most prominent ones to

1:30:41watch out for and to consider especially

1:30:43if you put a patient on antibiotic and

1:30:44they really develop really really nasty

1:30:46diarrhea and acute leukocytosis things

1:30:48of that nature then you can consider oh

1:30:51is it c diff so clinda is a big one but

1:30:54the other one to think about is

1:30:55carbapenem so anytime you put somebody

1:30:57on this like monster of an antibiotic

1:30:59you better consider that they have an

1:31:00increased risk of c diff

1:31:02the other one is trimethoprim sulfur

1:31:05methoxazole your third and fourth

1:31:08generation cephalosporins

1:31:11and the other one to consider here is

1:31:13your fluoroquinolones

1:31:15so these are the ones that i would

1:31:16really really be concerned about if a

1:31:18patient has seed if you started them on

1:31:19one of these antibiotics and developed

1:31:21some really nasty rip roaring

1:31:23diarrhea possibility that they have c

1:31:25dip with these antibiotics

1:31:27okay the last one that i want you to

1:31:28remember as a very specific thing is

1:31:30linaselli so we know that this one also

1:31:31caused like neurotoxicity like the

1:31:33serotonin peripheral neuropathy

1:31:35pancytopenia

1:31:36the other thing for this one it's been

1:31:38shown to cause lactic acidosis

1:31:40so because of that it works through

1:31:41particular mechanisms which increases

1:31:43the productive production of lactic acid

1:31:46so if you increase the production of

1:31:47lactic acid you can cause a lactic

1:31:49acidosis especially if you stay on this

1:31:50truck for a long period of time so if

1:31:53you're approaching like 10-14 days there

1:31:55is an increased risk of lactic acidosis

1:31:57with this drug all right we covered the

1:31:59most common ones for this column let's

1:32:01finish it off with fluoroquinolones and

1:32:03bactrim all right my friends almost

1:32:06there fluoroquinolones is there any

1:32:07additional like adverse effects that we

1:32:09should remember for this one

1:32:10so another thing to remember for this

1:32:12one is it can actually affect your

1:32:13glucose levels and believe it or not it

1:32:14can do both things it can cause

1:32:16hypoglycemia or hyperglycemia but that's

1:32:18not as the significant of the importance

1:32:20that i would want you to remember the

1:32:21other thing is it's been shown

1:32:22especially in children less than 18

1:32:24years of age is to potentially cause

1:32:26destruction of cartilage so it can kind

1:32:28of cause like an arthropathy and so

1:32:29that's another big thing that's why i

1:32:31should be kind of like avoided in like

1:32:32young children or patiently patients who

1:32:34are actually growing so you know

1:32:35teratogenic in that effect so i remember

1:32:37that it also can cause like an

1:32:39arthropathy

1:32:40especially in

1:32:42patients less than 18 years of age the

1:32:44other thing that it can actually do is

1:32:46it can actually increase the risk of

1:32:47tendon rupture especially the achilles

1:32:49tendon so we can actually cause an

1:32:50achilles tendon rupture now with this

1:32:53tendon rupture the big thing that i

1:32:55would consider in these is maybe trying

1:32:57to avoid this in a patient who's greater

1:32:59than 60 years of age or who is on

1:33:01steroids like prednisone because that

1:33:03also can weaken the tendon a little bit

1:33:05so you throw them on fluoroquinolones

1:33:06they're greater than 60 and on steroids

1:33:07oh boy get ready for attendant rupture

1:33:10so that's the big thing with

1:33:11fluoroquinolones hyper hypoglycemia

1:33:12arthropathy and children less than 18

1:33:14years of age and don't forget tendon

1:33:16rupture in those greater than 60 years

1:33:17of age or on steroids the last thing is

1:33:19bactrim so what can it do it can also

1:33:21cause hyperkalemia so it can also bump

1:33:24up your potassium so it can cause

1:33:25hyperkalemia

1:33:27all right we talked about the adverse

1:33:29effects the contraindications of these

1:33:30medications now the last thing is guess

1:33:32what bacteria are so intelligent they've

1:33:34tried to come up with ways that they can

1:33:36make themselves resistant to antibiotics

1:33:38let's talk about those mechanisms all

Mechanisms of Antibiotic Resistance

1:33:40right so now we're going to move on to

1:33:41the next chapter here which is talking

1:33:43about the mechanisms of antibiotic

1:33:44resistance if you haven't already take a

1:33:46little break again go review everything

1:33:48we've talked about with the mechanism of

1:33:49action the bacterial coverage the

1:33:51empiric antibiotics the adverse effects

1:33:53and contraindications now we're going to

1:33:54talk about how these tricky little

1:33:56bacteria have figured out a way to

1:33:57develop resistance against certain types

1:33:59of antibiotics and there's four

1:34:00particular mechanisms okay

1:34:02so normally when an antibiotic works it

1:34:04has to be able to get into the bacteria

1:34:07bind onto a target site and try to

1:34:09accumulate in high concentrations inside

1:34:11of the bacteria binding onto its target

1:34:13site

1:34:13and then there's particular enzymes that

1:34:16are working to be able to try to

1:34:18inactivate the actual antibiotic all

1:34:20right so those are the ways that

1:34:21antibiotics work as they try to get into

1:34:23the cell accumulate into the cell bind

1:34:25onto their target sites and exert their

1:34:27effects generally we want them to be

1:34:29able to evade the inactivation by

1:34:31enzymes that's the way that they should

1:34:33work

1:34:34what if the actual bacteria have figured

1:34:36out a way to reduce the actual

1:34:38permeability of the antibiotics so now

1:34:40antibiotics are supposed to be able to

1:34:42work to

1:34:43get into the bacterial cell

1:34:46to exert its effects by binding onto the

1:34:48target site

1:34:49what if the bacteria figured out a way

1:34:51to work against particular antibiotics

1:34:54to reduce the permeability

1:34:56of these antibiotics coming into the

1:34:59cell so now there's less of the actual

1:35:01antibiotics getting into

1:35:03the bacteria now they can't accumulate

1:35:05as well

1:35:06that's one particular mechanism the

1:35:08other mechanism is that we can reduce

1:35:10their accumulation by reducing

1:35:11permeability or causing them to get

1:35:14pushed out of the bacterial cell so now

1:35:17on top of that we figure out ways for

1:35:19these dang bacteria to push the

1:35:22antibiotic out of

1:35:25the bacterial cell reducing the amount

1:35:27of the antibiotic inside of the cell so

1:35:29if you think about it you reduce the

1:35:30permeability by letting less of them

1:35:32come in or you push them out of the cell

1:35:35via increased efflux the result of both

1:35:38of these things is that there is a

1:35:40decreased amount of the antibiotic

1:35:42accumulating with inside of the cell

1:35:44that means less of it is available to

1:35:45bind onto the target site and exert its

1:35:47effects

1:35:48which types of antibiotics target these

1:35:51i'm sorry which types of bacteria have

1:35:53actually developed in resistance to

1:35:55specific antibiotics via these

1:35:57mechanisms for decreased permeability

1:35:59this is the only way i remember these

1:36:01dang things is vat b so vat b

1:36:05is vancomycin

1:36:08amino aminoglycosides tetracyclines like

1:36:12doxy

1:36:14and then b

1:36:15is going to be for beta lactams

1:36:19okay this is the only way that i can

1:36:20remember so what happens is if certain

1:36:23bacteria have developed resistance to

1:36:25these antibiotics by reducing their

1:36:28entry into the bacterial cell

1:36:31they've also developed resistance to

1:36:33particular antibiotics by pushing them

1:36:35out of the cell what are the ones for

1:36:36this one you can remember and this is

1:36:38the only way i remember it i'm not

1:36:39trying to be mean but fat m

1:36:41okay so fluoroquinolones

1:36:45aminoglycosides tetracyclines again like

1:36:48doxy

1:36:50and then the last one here is going to

1:36:51be your macrolides

1:36:55okay

1:36:56these are the two mechanisms by which we

1:36:58reduce the amount of accumulation of the

1:36:59drug inside of the bacterial cell now

1:37:01the other ways that we can reduce the

1:37:03effectiveness of these antibiotics

1:37:04through resistance mechanisms is we can

1:37:06reduce their binding to the actual

1:37:09target site so you know some of the

1:37:10antibiotics are supposed to be able to

1:37:12bind onto dna bind onto protein like the

1:37:15ribosomal subunits supposed to bind onto

1:37:17specific proteins inside of the cell

1:37:19wall so whatever it may be they're

1:37:21supposed to bind to a particular protein

1:37:22and exert their effect on it

1:37:24now particular bacteria have reduced or

1:37:27altered their target site maybe they

1:37:29change an amino acid sequence maybe they

1:37:31change a particular structural

1:37:33morphology of a protein to where now the

1:37:35actual antibiotic can't bind to it

1:37:37anymore but they alter their ability of

1:37:39the antibiotic to bind to them and

1:37:41inhibit them

1:37:42there is many different drugs that do

1:37:44this so now you get the antibiotic

1:37:46inside now the antibiotic can't even

1:37:48bind to these dang target sites because

1:37:50they're altered in some particular way

1:37:52if you had a change in their morphology

1:37:53a chain in their amino acid sequence or

1:37:55something else that's binding to them

1:37:56preventing them from being able to be

1:37:58bound by the antibiotic what are the

1:37:59ones for this one again it's just the

1:38:01way i remember it but i remember fat bvm

1:38:04lt

1:38:05so fluoroquinolones

1:38:08aminoglycosides tetracyclines like doxy

1:38:13bvm so again i remember my beta lactams

1:38:18vancomycin

1:38:21and then

1:38:23m for macrolides

1:38:26and then lt so linaselid

1:38:30and then trimethoprim sulfamethoxazole

1:38:33so this is the ones that are going to

1:38:34reduce the actual binding of the

1:38:36antibiotic to their particular target

1:38:37sites again reducing the ability of the

1:38:39antibiotic to exert its effect now the

1:38:41bacteria is resistant it doesn't die or

1:38:43it doesn't stop growing

1:38:45the other thing is again normally the

1:38:48antibiotics are supposed to be able to

1:38:50not be broken down

1:38:52by the actual enzymes they're supposed

1:38:54to be able to evade the inactivation by

1:38:56particular enzymes

1:38:57what if

1:38:58we make these enzymes super inactivating

1:39:00enzymes we increase the production of

1:39:01carbopentaminases beta-lactamases a

1:39:04bunch of different types of enzymes that

1:39:06now can go and phosphorylate or can

1:39:08actually destroy or acetylate or

1:39:11phosphorylate all these different types

1:39:12of things that they can do to inactivate

1:39:13these antibiotics so now these

1:39:15antibiotics are going to be inactivated

1:39:18by these particular enzymes

1:39:20beta lactamases carbopenemasis other

1:39:22different types of enzymes that actually

1:39:23phosphorylate or inactivate the actual

1:39:25molecule what are these i remember bam

1:39:28so b

1:39:30for beta lactams

1:39:34okay and again this is obviously your

1:39:35beta lactamases are going to be those

1:39:37enzymes the other one is aminoglycosides

1:39:40again this is particularly via

1:39:42phosphorylation acetylation

1:39:44methylation reactions and the last one

1:39:46is your macrolides

1:39:49so these are the particular ways that

1:39:51these actual bacteria have developed

1:39:53resistance to antibiotics they either

1:39:54reduce the concentration of the drug

1:39:57inside of the bacteria by reducing its

1:39:59permeability vat b

1:40:01or pushing it out of the bacteria

1:40:04fat m

1:40:05it also reduces the binding of the

1:40:07antibiotic to the target side by

1:40:09changing the structure of the actual

1:40:10target site changing an amino acid

1:40:12having something bind to that actual

1:40:14target site and therefore inhibiting its

1:40:16ability to bind with the antibiotic

1:40:18remember fat bvm lt

1:40:21or we have particular enzymes that we

1:40:24produce that inactivate or destroy the

1:40:26actual antibiotic and render it

1:40:28ineffective the classic one is your beta

1:40:32lactamases that's why beta lactams are

1:40:34very very susceptible to this and then

1:40:36aminoglycosides via they transfer

1:40:39phosphorylate acetylate

1:40:41different types of molecules onto these

1:40:42and inactivate them or macrolides

1:40:45okay now that we've talked about this

1:40:47the mechanisms what i need to do is go

1:40:50in a little bit deeper

1:40:51so now bacteria have developed a

1:40:53resistance but how do more and more and

1:40:56more bacteria continue this transmission

1:40:59this further growth of resistance so in

1:41:01other words how does one bacteria that

1:41:03we have develop these mechanisms

1:41:05to become resistant to an antibiotic and

1:41:07then therefore pass that on to other

1:41:09bacteria let's talk about that next all

1:41:12right so what are the ways that we can

1:41:14actually see this transmission of

1:41:15antibiotic resistance in other words how

1:41:16does one bacteria that maybe becomes

1:41:18resistant to an antibiotic via reducing

1:41:21permeability pushing the antibiotic out

1:41:23changing the structure of its target

1:41:25site that actually the antibiotics

1:41:27supposed to bind to or producing enzymes

1:41:29that break down the actual antibiotic

1:41:31how does it pass it on to other bacteria

1:41:33and so it's via a vertical gene transfer

1:41:36or a horizontal gene transfer so it's

1:41:38kind of like a horizontal type of way

1:41:40that we can pass this on or a vertical

1:41:42way and we'll talk about what that means

1:41:43so the horizontal transfer of resistance

1:41:47is via three particular mechanisms so

1:41:49the horizontal transfer from one

1:41:50bacteria to another bacteria okay

1:41:53this would be something called

1:41:55transformation so let's say that you

1:41:57have a bacteria that is a really nasty

1:42:01bacteria okay and what happens is it

1:42:04gets destroyed and when it gets

1:42:05destroyed it releases out some of the

1:42:07dna or rna inside of it that's really

1:42:10really nasty and what brings about the

1:42:12opportunities to maybe change the

1:42:15permeability of the bacterial cell

1:42:17increase the efflux of the antibiotic

1:42:18out of the bacterial cell change the

1:42:20actual target of the protein

1:42:22that the antibiotics supposed to bind to

1:42:24or

1:42:25increase the activation of

1:42:26increase the formation of inactivating

1:42:28enzymes okay that's in that dna that it

1:42:30encodes those particular mechanisms

1:42:33what happens is you take a bacteria who

1:42:34doesn't have that ability to do any of

1:42:36those things it's susceptible to

1:42:37antibiotics

1:42:39it takes up

1:42:41this actual bacteria this other nasty

1:42:44dna rna from this harmful bacteria takes

1:42:46it up and now it gains the ability to be

1:42:49able to

1:42:50produce any of these mechanisms that's

1:42:52one that's called transformation

1:42:54the other mechanism is you take one

1:42:57bacteria and you connect it to another

1:42:59bacteria via a sex pilus

1:43:01and this mechanism which we can do this

1:43:03is called conjugation so what is this

1:43:05called this is called conjugation so in

1:43:08this actual bacteria here you have

1:43:11something called a plasmid and this

1:43:13plasmid may have on it a particular kind

1:43:15of dna sequence that allows for it to

1:43:18encode particular proteins or enzymes

1:43:20that then can reduce permeability

1:43:22increase efflux of the drug out change

1:43:24its target site or increase the

1:43:25formation of activating enzymes and pass

1:43:28that on to this bacteria who now has

1:43:30that

1:43:32that's called conjugation

1:43:34the other mechanism is we can have

1:43:36something where we can pass on this dna

1:43:38or rna material via something called a

1:43:41bacteriophage so via something called a

1:43:45bacteriophage so this bacteriophage

1:43:48contains in it some type of dna rna

1:43:50material that carries the ability to

1:43:52produce maybe specific protein enzymes

1:43:54that reduce permeability increase efflux

1:43:56change the target site or produce

1:43:58inactivating enzymes and we can pass

1:44:00that on

1:44:01to this person onto this bacteria here

1:44:05and what is this mechanism at which we

1:44:07pass this genetic material off to

1:44:09another bacterial cell via horizontal

1:44:10gene transfer this is called

1:44:12transduction

1:44:15so these would be some of the mechanisms

1:44:16by horizontal gene transfer conjugation

1:44:19transduction transformation the other

1:44:22way is let's say now this bacteria has

1:44:26inside of it

1:44:27this dna

1:44:28or rna or any kind of ability to produce

1:44:32resistance to particular antibiotics

1:44:35now what it can do is it can pass it

1:44:37through what's called vertical gene

1:44:38transfer in other words it goes through

1:44:40binary fission so it undergoes a binary

1:44:44fission process it actually replicates

1:44:46and it produces two daughter bacteria

1:44:49that now have within it

1:44:51the dna

1:44:53material or rna material that allow for

1:44:56it to be also resistant

1:44:59to

1:45:00particular types of antibiotics

1:45:04isn't that cool so these are the ways

1:45:05that these actual bacteria have

1:45:07developed resistance to antibiotics via

1:45:09conjugation mechanisms transduction

1:45:11mechanisms transformation mechanisms or

1:45:14once they've gathered all of this

1:45:15material they can pass it on to their

1:45:17actual daughter cells through binary

1:45:19fission or vertical transfer process

1:45:21okay now the question is

1:45:24these bacteria all have the ability to

1:45:25do this what actually increases

1:45:28these particular dna sequences rna

1:45:31sequences to undergo these particular

1:45:33mutations and produce resistance in the

1:45:35first place what triggers this what are

1:45:38the risk factors for antibiotic

1:45:40resistance and you know what it is it's

1:45:42often due to patients who get sick they

1:45:45go to the hospital in the hospital you

1:45:46have patients who are super super sick

1:45:49and in the hospital they develop some

1:45:51nasty multi-drug resistant pathogens

1:45:53there so anytime you go to the hospital

1:45:55there is always a risk of these really

1:45:57nasty multi-drug resistant pathogens

1:46:01that's one particular way so if you go

1:46:02to the hospital there's obviously an

1:46:04opportunity to catch something like mrsa

1:46:05something like pseudomonas something

1:46:07like ace needle bacter

1:46:09the other problematic issue here is that

1:46:11so again if you go to hospital you could

1:46:12be exposed to any of these and that's a

1:46:13problematic issue the other one it

1:46:15happens to be sometimes unfortunately

1:46:17for clinicians we like to over prescribe

1:46:19medications like antibiotics when it's

1:46:21not really necessary and so if we have a

1:46:22patient who has like a viral infection

1:46:24they don't really need an antibiotic and

1:46:25we put them on an enematic anyway we

1:46:27increase the opportunity for resistance

1:46:29to become available because now this

1:46:30person's been exposed to an antibiotic

1:46:31and their body can then create again

1:46:33their bacteria can create a way to

1:46:34become resistant to that antibiotic so

1:46:36trying to be able to prevent over

1:46:38prescription of antibiotics so over

1:46:42prescribing

1:46:44this is a big one

1:46:46and the last one here is a son of a gun

1:46:49the last one here is a little calo

1:46:51chicken you know we like to eat beef and

1:46:52all these other different types of

1:46:53things that we like to impregnate some

1:46:54of these things with antibiotics

1:46:56unfortunately some of the actual meats

1:46:57that we eat we're then

1:46:59ingesting those meats that now have

1:47:01particular antibiotics that were used in

1:47:02that meat

1:47:03and now we've been exposed to them and

1:47:05now our actual bacteria can develop ways

1:47:07to become resistant to it so also it can

1:47:09be via certain types of antibiotics in

1:47:12food products

1:47:14that we become exposed to and then again

1:47:16now we develop some resistance to

1:47:17antibiotics so these are a lot of the

1:47:19factors that can increase the resistance

1:47:21to antibiotics these are the mechanisms

1:47:23of which you get antibiotics and become

1:47:24resistant and this is the way we can

1:47:26take one bacteria and then pass on the

1:47:28ability from multiple other bacteria to

1:47:30develop resistance antibiotics

1:47:32it's just a terrible thing so i guess

1:47:35the question is is now we know that

1:47:36bacteria can develop a lot of resistance

1:47:38to antibiotics through many different

1:47:40mechanisms and a lot of the risk factors

1:47:42are here they have a lot of opportunity

1:47:43for transmission how do we

1:47:46as a clinician

1:47:47figure out which antibiotic is best

1:47:50particularly utilized for a very

1:47:53specific pathogen we already talked

1:47:54about that right the bacterial coverage

1:47:56of very specific pathogen

1:47:58well here's the thing some of these

1:48:00pathogens may develop resistance to the

1:48:02antibiotics that we talked about so how

1:48:04do we know what is the best antibiotic

1:48:06for this pathogen that they haven't

1:48:09developed resistance to it yet and

1:48:11that's we're going to talk about next

1:48:12there's these different methods that

1:48:13people figured out to talk about

1:48:15antibiotic susceptibility all right so

1:48:17when we talk about antibiotic

1:48:19susceptibility it's really saying okay

1:48:22we have a patient let's say that they

1:48:23come in they have an infection there's

1:48:25an obvious infection whether it be let's

1:48:27say pneumonia

1:48:28we think that it's a community-acquired

1:48:30pneumonia or acquired demonic we start

1:48:32them on the imperial antibiotics and we

1:48:33get cultures we get sputum cultures once

1:48:35we get those sputum cultures we'll

1:48:36obviously grow and see what kind of

1:48:38bacteria they grow and then which

1:48:39antibiotics would be best suited for

1:48:40them okay

1:48:42then we could do the same thing with

1:48:43skin soft tissue if the nasty skin soft

1:48:45tissue infection you have an abscess you

1:48:46take a sample from that you culture it

1:48:48send it off see what kind of bacteria

1:48:49come back what antibiotics are best

1:48:51suited for that one same thing you take

1:48:52a urinary urine culture because you have

1:48:55a patient with a uti you start treating

1:48:56them with either whether it's acute

1:48:57cystitis pyelonephritis or complicated

1:48:59uti and then again you start figuring

1:49:01out what kind of actual bacteria comes

1:49:02back from your culture

1:49:04and the last thing is you have like

1:49:05blood cultures you think somebody's

1:49:06septic or they have a concern for a

1:49:08clabsi then in those situations you can

1:49:11again take the actual blood culture

1:49:13sorry them on particular antibiotics or

1:49:14whatever you think the actual most

1:49:15common pathogen is and then from there

1:49:17once you get the actual uh

1:49:19cultures back and you figure out which

1:49:20antibiotics are best you can

1:49:21particularly target it right so the

1:49:23whole point is you're getting cultures

1:49:25you're going to be grabbing cultures

1:49:26whether this is sputum cultures whether

1:49:28this is uh skin cultures whether this is

1:49:30urine cultures whether this is blood

1:49:31cultures once you do that you take again

1:49:34treat them with the empiric antibiotic

1:49:35therapy we talked about over there

1:49:37what happens is you take the bacteria

1:49:40and you grow them right and you see

1:49:42which types of bacteria grow and then

1:49:44again once you kind of figure out oh it

1:49:45grew back

1:49:47klebsiella okay let's just say let's say

1:49:49that you had a patient with pneumonia

1:49:50the pathogen that it actually grew is

1:49:52klebsiella

1:49:54pneumonia

1:49:55okay

1:49:56from there you want to say okay

1:49:58klebsiella pneumonia was the one that

1:50:00grew so you had a gram-negative rod

1:50:01klebsiella pneumonia was the particular

1:50:02pathogen that grew on the culture from

1:50:04the sputum

1:50:05the next thing you have to figure out is

1:50:06okay which antibiotics would be best for

1:50:08this well i know any of those gram

1:50:10negative ones so part this is a part of

1:50:12the hens peck one right so i know really

1:50:14any of those would be best suited for

1:50:16that do you guys remember the hens pack

1:50:17ones they said the amino penicillins

1:50:19would be an okay one we said that the

1:50:21third generation cephalosporins would be

1:50:23good ones the fourth generation

1:50:25cephalosporins these are carbapenems

1:50:26monobactins we even went in to say like

1:50:29potentially fluoroquinolones

1:50:31aminoglycosides

1:50:32so a lot of these different ones would

1:50:34cover klebsiella

1:50:36but

1:50:36out of all of those antibiotics that we

1:50:39could pick from we want to know which

1:50:41one is the best

1:50:43and that's dependent upon what we do is

1:50:45we maybe there's a bunch of different

1:50:46methods there's what's called the broth

1:50:48micro dilution and macro dilution the

1:50:50kirby bauer method and all these

1:50:52different ways that we can do it like

1:50:53this diffusion so you know one of them i

1:50:55think is the coolest one it's the old

1:50:57school way is you would take the

1:50:58bacteria

1:51:00and what you would do is you would

1:51:01introduce antibiotics onto this let's

1:51:03say here is an antibiotic here was an

1:51:05antibiotic here's an antibiotic you

1:51:07would see how much like bacteria died

1:51:10around the antibiotic and that would

1:51:12actually determine like your minimum

1:51:13inhibitory concentration you could do

1:51:16this for a lot of different ways you

1:51:16could do with the kirby bower method you

1:51:18could do with micro dilution macro

1:51:19dilution a lot of different things but

1:51:21the whole point is is what this tells us

1:51:24is it tells us what's called the minimum

1:51:26inhibitory concentration the mic so what

1:51:30is the minimum amount of the actual drug

1:51:32that is needed to be able to kill the

1:51:34particular bacteria and it tells us

1:51:36which types of bacteria are susceptible

1:51:39to specific antibiotics that would cover

1:51:42it so again think about everything that

1:51:43would cover klebsiella there's a

1:51:45plethora of drugs right sometimes you

1:51:47have no idea which one to pick you'd

1:51:48want to prefer more of the narrow one

1:51:50not go super broad but what if the

1:51:52actual bacteria has developed resistance

1:51:54to it how do we know so what you do is

1:51:57you do these methods again the broth

1:51:58micro dilution macrolide dilution the

1:52:00kirby bower method but again the whole

1:52:02point is you expose the actual

1:52:05bacteria to multiple drugs and figure

1:52:08out which one of these had the best

1:52:10coverage which one when the actual

1:52:11bacteria was susceptible to

1:52:14or which one of these antibiotics the

1:52:16bacteria was resistant to

1:52:19or which one of these antibiotics was

1:52:20the bacteria kind of like ah it's kind

1:52:22of like in between

1:52:24that is the best way to be able to pick

1:52:26the perfect antibiotic that will cover

1:52:28the bacteria

1:52:29very well and so for example

1:52:32let's say you had a patient

1:52:34you have a sputum culture okay you have

1:52:36a patient who comes in

1:52:37they have pneumonia

1:52:38you start them on antibiotics whether

1:52:40it's a cap or a hap

1:52:42you get the sputum culture it comes back

1:52:45when the sputum culture comes back with

1:52:47klebsiella pneumonia maybe you had them

1:52:49on let's say let's say you had them on

1:52:52ceftriaxone and doxycycline

1:52:54but it comes back and they have

1:52:56klebsiella and ammonia and you weren't

1:52:57covering it particularly well

1:52:59from there you have to figure out okay

1:53:00which one of the antibiotics would be

1:53:02best well i can do anyone within the

1:53:03hens pec category

1:53:05but out of that hens pet category which

1:53:07one would the actual bacteria be very

1:53:09susceptible to resistant to or

1:53:11intermediate to and so let's say that we

1:53:13did that we took the klebsiella we grew

1:53:15it we'd found that out and then we

1:53:16actually exposed it to multiple

1:53:17antibiotics and when we did that then we

1:53:19found that ceftriaxone there was

1:53:21susceptibility to it so if you say give

1:53:23ceftriaxone it's actually pretty good

1:53:25ceftazine there was resistance to the

1:53:26klebsiella so we can't use this one

1:53:28pipercellon taste of bacterium there was

1:53:30susceptibility to it so if you want to

1:53:31you can use this one

1:53:32maripenum there was susceptibility to it

1:53:35gentamicin there was resistance to it

1:53:38levofloxacin there was resistance to it

1:53:41ampicillin soul bacterium let's just say

1:53:42for the heck of it just to have another

1:53:43one there was intermediate coverage

1:53:46out of all of these which ones do i not

1:53:48pick it's obvious don't give them

1:53:50ceftasidine because it's not going to

1:53:51cover it because it's resistant to it

1:53:53based upon the susceptibility testing

1:53:55which we did with microdilution macro

1:53:56dilution kirby bower method

1:53:59don't give them gentamicin because

1:54:00there's resistance to it don't give them

1:54:02levofloxane because it's resistance to

1:54:03it and i would even avoid ampicillin

1:54:05sulbactin because it's intermediate pick

1:54:07something else or if you really really

1:54:09like this drug give a higher dose than

1:54:11you usually need to to cover it but if

1:54:14that's the case i would just avoid these

1:54:16and this one and stick with either

1:54:18ceftriaxone piper cell and taser

1:54:20bacteripenum now if you're between these

1:54:22which one of these would you pick

1:54:24try to pick the one with the narrow

1:54:25coverage so you don't have too much

1:54:27broad coverage because remember pip tazo

1:54:29is a super broad agent not really

1:54:31necessary to go super broad

1:54:33meripenem not really necessary to go

1:54:34super broad i would just go with

1:54:35ceftriaxone it's not crazy crazy broad

1:54:38and i think it would be a good choice so

1:54:40again you have options here but which

1:54:42one you're going to pick and this is

1:54:43obviously

1:54:45more of a provider preference but you

1:54:46could pick ceftriaxone

1:54:48pipercellantasabactum and meropenem

1:54:50because these are the ones that the

1:54:52klebsiella pneumonia which we grew out

1:54:54from the sputum culture and we tested

1:54:56against multiple antibiotics these were

1:54:57the ones that the actual bacteria was

1:54:59susceptible to and would actually kill

1:55:01the bacteria

1:55:02that's the ones that i would pick so i

1:55:04hope that made sense now

1:55:06you would think that we're done but

1:55:08we're not

1:55:09i really want you guys to understand

1:55:10this information antibiotics is a lot

1:55:13take a little break review everything

1:55:15but get ready because now i want to test

1:55:17your knowledge to the max and i want to

1:55:19see how much of this you guys remember

1:55:20so let's do some

1:55:22practice problems some some cases and

1:55:24see if you guys can put this stuff

1:55:25together all right let's get into it all

Antibiotics Cases

1:55:26right guys let's do some cases and put

1:55:28to practice everything that we talked

1:55:29about on the whiteboard so it's gonna be

1:55:30pretty systematic all right 65 year old

1:55:32male past medical history myasthenia

1:55:34recent ons recently on steroids for that

1:55:36for an exacerbation presented to eddy

1:55:38with fever shortness of breath

1:55:39productive cough chest x-ray shows a

1:55:41nice right low bar infiltrate and a cvc

1:55:43with leukocytosis definitely seems that

1:55:45this patient has pneumonia right so the

1:55:47way that their actual clinical features

1:55:49present definitely pneumonia so the

1:55:51question is is that they have a

1:55:52pneumonia this is usually not hospital

1:55:54acquired because they weren't in the

1:55:55hospital they were coming to the

1:55:56emergency department so this is

1:55:57definitely a community acquired

1:55:58pneumonia so the pathogens that you want

1:56:00to be concerned about for community

1:56:01acquired are strep pneumone atypicals is

1:56:03the most common ones

1:56:05so that being said what kind of

1:56:07antibiotics would i start this patient

1:56:08on for a community acquired pneumonia

1:56:10empirically then i can get cultures

1:56:11figure out what the pathogen is and then

1:56:13narrow it down to that specific pathogen

1:56:15well i'm going to cover for strep new

1:56:17and atypical so i can do something like

1:56:19ceftriaxone if you guys remember that

1:56:21one which was the beta-lactam third

1:56:23generation plus a macrolide or

1:56:25doxycycline or i could do something like

1:56:27a monotherapy fluoroquinolone like moxie

1:56:29foxes and which covers strep pneumo and

1:56:31atypicals especially legionella if you

1:56:33guys remember so that would be my

1:56:34options to start off with then i would

1:56:36get cultures if i get my cultures back

1:56:38and then i say okay i'm going to give

1:56:40you a call in a couple days when your

1:56:42cultures come back and then what we'll

1:56:43do is we'll may you know modify your

1:56:45antibiotic regimen potentially

1:56:47and then you get it back and it comes

1:56:48back just strep pneumo okay well we

1:56:50don't really need that atypical coverage

1:56:51then

1:56:52so you know with this situation here

1:56:54doxycycline is not a great strep pneumo

1:56:56coverage macrolides will cover you know

1:56:58strep pneumos after action will cover

1:56:59strep pneumonia solely your first gens

1:57:01fluoroquinolones will cover you know

1:57:03your your strep pneuma as well

1:57:05aminopenicillins to some degree they're

1:57:07not too great you have to give a really

1:57:09high dose amoxicillin to hit the lungs

1:57:11but that's another option

1:57:13clindamycin's a decent one

1:57:15so these are some of the options that

1:57:16you could consider

1:57:18so these would be the ones that i

1:57:19consider so we already talked about

1:57:20amoxicillin but you have to bring a

1:57:21pretty high dose some first third gen

1:57:23cephs macrolides clinda and

1:57:25fluoroquinolones but the one thing that

1:57:26you got to be careful of is remember

1:57:27when you prescribe an antibiotic you

1:57:29have to be thinking about what are the

1:57:31adverse effects and what would be a

1:57:32contraindication and be prescribing this

1:57:34one well this basically is myasthenia

1:57:35gravis let's say that i start them off

1:57:37on just fluoroquinolone by itself

1:57:39ah do you guys remember what the adverse

1:57:41effect of fluoroquinolones are

1:57:44it is exacerbates myasthenia gravis

1:57:47that's not good so we don't want to be

1:57:48giving this medication but you know what

1:57:50else does that clindamycin does that um

1:57:52and and aminoglycosides will do that

1:57:55so i think it's important to be able to

1:57:57consider that um you probably would want

1:57:59to stay away from a fluoroquinolone

1:58:01consider something like a i'd say like

1:58:03more likely a first or third gen

1:58:04cephalosporin um you don't want to give

1:58:07clinda you wouldn't want to give

1:58:08fluoroquinolones if you give amoxicillin

1:58:10you just got to give a high dose

1:58:12macrolides even i'd be careful with that

1:58:13one too in this situation so

1:58:16it can exacerbate mycenia that's

1:58:18potentially a contraindication but guess

1:58:19what else is a contraindication tendon

1:58:20rupture with greater than 16 steroids

1:58:22this patient's greater than 60 and

1:58:23they're just on steroids so they have

1:58:25very high risk of an achilles tendon

1:58:26rupture so just things to be considering

1:58:28and again remember that they prolong the

1:58:30qt they cause the cyp450 inhibition they

1:58:32can also have a pretty high risk of c

1:58:34diff and cause hyper and hypoglycemia so

1:58:36things to consider

1:58:38i think the other thing that's important

1:58:39to think about is like what are the ways

1:58:40that bacteria develop resistance because

1:58:42a lot of the problems with

1:58:43fluoroquinolones is that they are

1:58:44becoming

1:58:45there's a lot of bacteria that are

1:58:46developing resistance to this in certain

1:58:47areas so it's important remember those

1:58:49mechanisms it was the decreased

1:58:50permeability efflux pumps altering the

1:58:52target site and then creating a lot of

1:58:54inactivating enzymes so if you guys

1:58:55remember i said it was that b

1:58:57fat m fat bvmlt and then bam

1:59:01so it's wherever the f is so fat m so e

1:59:04flux bumps and fat bv mlt

1:59:07that would be again within the altering

1:59:09the target binding size so they create

1:59:10eflux pumps and then alter the target

1:59:12binding site to be able to reduce the

1:59:15effectiveness and the efficacy of the

1:59:16fluoroquinolones

1:59:18all right

1:59:19i hope that made sense alright so the

1:59:20next one case study two we got a patient

1:59:22who presents the ed feverfang flank pain

1:59:24nausea vomiting diarrhea

1:59:26they got a cbc it shows the leukocytosis

1:59:28their ua shows white blood cell casts

1:59:30leukocyte esterase nitrates are positive

1:59:32there's more than 100 white cells per

1:59:34housefill unit on the ua

1:59:36and they have a lot of bacteria in their

1:59:37urine so this definitely seems like

1:59:38based upon their symptoms they have a

1:59:40symptomatic urinary tract infection

1:59:42particularly pilonephritis based upon

1:59:43some of the

1:59:44exam findings and the laboratory

1:59:46findings so i have a patient with an

1:59:48acute pyelonephritis

1:59:50so you guys got to remember for empiric

1:59:52antibiotic coverage of a you know a

1:59:54pyelonephritis what were the options do

1:59:55you guys remember

1:59:57one is you can consider ceftriaxone you

1:59:59can consider a fluoroquinolone and even

2:00:01aminoglycosides aren't a bad idea as

2:00:03well

2:00:04so these would be the things i would

2:00:05consider amino penicillins if you're

2:00:07going to give this you want to give

2:00:09particularly ampicillin

2:00:11just because of the imiv it would give a

2:00:14better penetration so these are options

2:00:16that i could consider a fluoroquinolone

2:00:17ceftriaxone or aminopenicils but i would

2:00:19consider ampicillin

2:00:21particularly over amoxicillin

2:00:23all right you get the urine cultures

2:00:25because you're going to start them on

2:00:26empiric antibiotics

2:00:28but you want to make sure that you're

2:00:29covering the correct bacteria so you get

2:00:30a culture when you get the culture it

2:00:32comes back with enterococcus well

2:00:34there's only a certain amount of

2:00:35antibiotics that cover this do you guys

2:00:37know which one out of all of these would

2:00:38be the best for enterococcus coverage

2:00:41because remember it was a gram-positive

2:00:43bacteria and this was amino penicillins

2:00:45so aminopenicillins would definitely be

2:00:47pretty good at covering your

2:00:48enterococcus we said nitropharantome but

2:00:50that's more particularly for in the

2:00:51bladder so cystitis would be better for

2:00:53coverage for that one and then

2:00:55vancomycin is another one especially if

2:00:57they're resistant

2:00:59but not for the vancomycin resistant

2:01:01enterococcus but again i would say amino

2:01:03penicillins are good and then vancomycin

2:01:05is another option for that one so this

2:01:07would be the the best situation for that

2:01:10okay now i guess the question is is when

2:01:12you put a patient on an immunopenicillin

2:01:14like ampicillin what are the potential

2:01:15things that you have to watch out for

2:01:17and it's very common it's always acute

2:01:19interstitial nephritis some type of like

2:01:21you know a pancytopenia

2:01:25a rash

2:01:26maybe some type of like hypersensitivity

2:01:28reaction and neurotoxicity like reducing

2:01:31threshold for seizures so these are big

2:01:33things to be considering okay

2:01:36uh again what are the mechanisms that

2:01:38bacteria have developed to become

2:01:40resistant to amino penicillins well one

2:01:42of them we already know again we'll talk

2:01:43about this if you guys remember the

2:01:44mechanism of action oh real quick what

2:01:46is the mechanism of action of amino

2:01:47penicillins do you guys remember it

2:01:48works against the cell wall uh

2:01:51particularly reducing the cross-linking

2:01:52so it's reducing cell wall synthesis by

2:01:55preventing the cross-linking of the uh

2:01:57cell wall peptidoglycans okay

2:02:00but bacteria have developed a resistance

2:02:02that so again you got to go

2:02:03again with this one it's a beta lactam

2:02:05so you go vat b

2:02:07fat m

2:02:08fat

2:02:10bvmlt and then bam so pretty much the

2:02:14when you think about that that b that

2:02:17would be one so the first thing is it

2:02:18can reduce permeability fat m doesn't

2:02:21work on the e flux pumps fat bvmlt does

2:02:25work on altering the target binding site

2:02:27bam works on um

2:02:29potentially increasing the inactivating

2:02:32enzyme so it's three of those particular

2:02:33things that it works on just not the

2:02:35efflux bumps

2:02:37okay so that would be the way now one of

2:02:38these that's the most prominent one the

2:02:40one that we think about a lot is that it

2:02:41really increases the inactivating

2:02:43enzymes

2:02:44so because of that these are your beta

2:02:46lactamases so they break down the

2:02:48beta-lactam ring in amino penicillin

2:02:50rendering it ineffective and not being

2:02:51able to bind to the penicillin binding

2:02:53protein so we need a drug that we can

2:02:56combine with ampison in the case that

2:02:58this enterococcus has developed

2:03:00resistance to the amino penicillins we

2:03:03should add something on to that to break

2:03:06to bind onto the beta lactamases so that

2:03:07the amino penicillin can continue to

2:03:09work so what are the things that i can

2:03:11add to a beta-lactamase to make it more

2:03:13effective i'm sorry add to the amino

2:03:16penicillins to make it more effective

2:03:18against the beta-lactamases that that

2:03:19bacteria produces

2:03:21and you guys remember

2:03:23there was the beta-lactamase inhibitors

2:03:24such as clavillonate which combines with

2:03:28amoxicillin to make

2:03:30augmentin um and then you have sulbactum

2:03:33that combines with ampicillin to make

2:03:35unison and then if you wanted to

2:03:37remember there's the taseobacter with

2:03:38pipper cell and to make zosin and then

2:03:41there is the combination of avibactum

2:03:44and ceftazidime and that's going to be a

2:03:46combo that you know you don't commonly

2:03:48utilize unless you're like an infectious

2:03:49disease per you know expert

2:03:51but that would be the general ones that

2:03:53we would do here so that's perfect that

2:03:54works out well to kind of understand

2:03:56that stuff all right case study three

2:03:58a 35-year-old male presents the e.d with

2:04:00red edematous and painful cellulite so

2:04:01the right forearm some induration and

2:04:04it's spreading over the the right elbow

2:04:06um now so we definitely see like some

2:04:08just like some pretty good spread of a

2:04:10really nasty looking cellulitis so with

2:04:12that being said

2:04:13what is the empiric coverage for

2:04:15cellulitis assuming that this is like

2:04:18you know an outpatient one that we can

2:04:20continue to monitor they don't really

2:04:21look septic appearing they don't need to

2:04:23be observed in the hospital it's not

2:04:25that diffuse so we can kind of prescribe

2:04:27them an antibiotic send them home but

2:04:29you know if we have to we can get

2:04:30cultures and stuff like that if but

2:04:32there's nothing really to culture

2:04:33there's no abscess or anything so with

2:04:35this i'm just going to start covering

2:04:36for missa

2:04:38as the most common misa and

2:04:40streptococcus a or strep-paya genes so

2:04:43with that being said what are the

2:04:44pathogens what are the types of

2:04:46antibiotics that would cover that very

2:04:48well the misa and the strep a

2:04:50well the first thing to remember for the

2:04:52missa was your anti-staphylococcal

2:04:54penicillins

2:04:55so naphthalene oxacillin dicloxacillin

2:04:58out of all of those the only one that's

2:04:59po is the diclox

2:05:01and then the first generation

2:05:02cephalosporins like cefazolin and sep

2:05:05kefla encephalexin and they're really

2:05:07the primary one that's po is the

2:05:08cephalexin so if i'm gonna send this

2:05:10patient home with po meds it's either

2:05:11gonna be cephalexin or dicloxacillin

2:05:14okay now if i let's say for whatever

2:05:17reason they start to get worse right

2:05:20they don't get any better the cellulitis

2:05:22isn't improving even after i start them

2:05:24on a couple days of um

2:05:26keflax or cephalexin and they're still

2:05:28getting worse it's not getting any

2:05:29better which antibiotics do i consider

2:05:31now well now i'm wondering was it misa

2:05:34or is it mrsa now because maybe the

2:05:36diclox or the catholics isn't working

2:05:39particularly against the nasty types of

2:05:41pathogen that i think it is and it's a

2:05:43mrsa type and that's

2:05:45cephalax and diclox are just not going

2:05:47to hit it so i'm thinking it's mrsa what

2:05:49kind of antibiotics cover mrsa but i

2:05:52still think that this patient doesn't

2:05:54need to be in the hospital receiving iv

2:05:56medications yet

2:05:57do you guys remember

2:05:59so start thinking through them with

2:06:00starting with your betalactams and

2:06:02working your way through the mechanism

2:06:03of action so first thing if you really

2:06:05wanted to

2:06:07you can go through cephteraline i would

2:06:09not kind of go with that one i would

2:06:10avoid that one then you go to the next

2:06:12thing

2:06:13which is going to be vancomycin that's

2:06:15iv i wouldn't go with vancomycin just

2:06:17yet then we go to trimethoprim

2:06:19sulfamethoxazole that's definitely one

2:06:21didn't go to the metronidazole

2:06:22nitrofrancoin no fluoroquinolones no

2:06:26then you go to your macrolides

2:06:28doxycycline will actually cover

2:06:29community acquired mrsa

2:06:31um linaselid will cover it

2:06:35clendamycin will cover it and then if

2:06:37you go into the next part which is the

2:06:38aminoglycosides and the uh

2:06:40there's no amino glycosides that will

2:06:42cover that as well and again macrolides

2:06:44don't cover it tetracycline is the

2:06:45doxycycline will so for these i would

2:06:47say trimethoprim sulfamethoxazole

2:06:49clindamycin uh lynnae's lid would be

2:06:52another option doxycycline would be

2:06:54another option

2:06:55so these would be some things that i

2:06:56would consider for mrsa coverage okay

2:06:59now

2:07:00let's say that you put them on

2:07:02trimethoprim sulfoxazole okay

2:07:05you put them on that and they continue

2:07:07to get worse

2:07:08so it's not enough now the infection is

2:07:10really really bad and it's just it's

2:07:12becoming more systemically involved

2:07:14because now they're starting to have

2:07:15fevers rigers and they're starting to

2:07:17kind of like look a little septic

2:07:19in that situation they're probably going

2:07:21to require iv antibiotics which

2:07:23antibiotic would be best when it comes

2:07:24to this now vancomycin that begs the

2:07:27question though if i put someone on one

2:07:29of these drugs like trimethoprim

2:07:30sulfamethoxazole or you know i put them

2:07:32on vancomycin what are some of the

2:07:34things that i got to watch out for

2:07:36so adverse effects of bactrim is

2:07:38pancytopenia that's one hemolytic anemia

2:07:41particularly because it can worsen the

2:07:42g6pdh deficiency okay

2:07:45the other thing here is acute

2:07:47interstitial nephritis teratogenic it

2:07:50can actually increase the amount of the

2:07:51unconjugated bilirubin like and that can

2:07:53lead to kernicterus in babies it's a

2:07:55cyp450 inhibitor it also has the ability

2:07:57to cause phototoxicity so if you're

2:07:59exposed in the sun it can cause some

2:08:00rashes and then it can also bump your k

2:08:02and cause hyperkalemia same concept here

2:08:04what if i put them on vancomycin what do

2:08:06i got to watch out for it can hit the

2:08:07kidneys especially if you are a little

2:08:09bit super therapeutic on that can cause

2:08:10nephrotoxicity it can cause ototoxicity

2:08:13especially if combined with an

2:08:14aminoglycoside it can really burn when

2:08:16you infuse it so it can cause some

2:08:17phlebitis and uncomfortable kind of

2:08:18feeling there and then if you infuse it

2:08:21way too quickly it can lead to something

2:08:22called red man syndrome where they have

2:08:24rash muscle spasm itching paritis they

2:08:28have hypotension tachycardia so these

2:08:30things to consider and then dress so

2:08:32they can develop fevers they can develop

2:08:33lymphadenopathy they can develop

2:08:36some really like nasty eosinophilia

2:08:39so i would watch out for that one as

2:08:40well

2:08:41all right now the question i think that

2:08:44comes is again what are the mechanisms

2:08:46the bacteria have developed as a way to

2:08:48become resistant to particular

2:08:50antibiotics such as vancomycin well

2:08:52think about it again you got to go vat b

2:08:56fat m fat bv mlt and then bam so the v

2:09:00particularly for vancomycin was in the

2:09:02first one which was going to be

2:09:04decreasing the permeability and then it

2:09:06also was going to be in the third one

2:09:08which is altering the target binding

2:09:10site

2:09:11so with that being said i only think

2:09:13that it's going to alter the target

2:09:14binding site and again it will also

2:09:17decrease permeability

2:09:18okay so those are particular ways and

2:09:20this is especially significant when you

2:09:22have

2:09:23bacteria such as

2:09:25mrsa it can become resistant to

2:09:27vancomycin so we see like a vancomycin

2:09:29resistant staphylococcus aureus and then

2:09:31you can also have enterococcus become

2:09:33resistant to vancomycin we call that

2:09:35vancomycin resistant in pterococcus and

2:09:37then that's a that's a rough situation

2:09:40all right last case here for you guys 66

2:09:42year old female in icu on the ventilator

2:09:43for the past three days develops an

2:09:45increasing speed and production hypoxia

2:09:46fevers and then nasty infiltrate on her

2:09:48chest x-ray definitely seems like

2:09:50pneumonia but she's been in the hospital

2:09:51for at least three days that's more than

2:09:53two days so this is a hospital-acquired

2:09:54pneumonia so what are the two pathogens

2:09:56i've got to think about

2:09:57i think about

2:09:59staphylococcus mursa sorry mrsa and then

2:10:02pseudomonas originosa so what are the

2:10:04actual best like commonly utilized

2:10:06antibiotic combo that you'll see most of

2:10:08the time in the hospital that covers

2:10:09mrsa that's vancomycin or lynasalid and

2:10:12then what covers the pseudo there's so

2:10:13many you could obviously go through them

2:10:14that you can give the ceftazidime the

2:10:16cephepem the pippercellentazobactum

2:10:19um there there's like a neverending

2:10:21amount of these um you can consider even

2:10:23like polymixins if you really had to

2:10:26that's more of a salvage therapy though

2:10:29um again

2:10:30trimethoprimocyloxis all know

2:10:32metronidazole nitrofanto and no

2:10:33fluoroquinolones those are more for your

2:10:35double coverage

2:10:36so those are very specific for double

2:10:38coverage it wouldn't be a monotherapy

2:10:40macrolides will not cover it clinda will

2:10:43not linnae's lid will not

2:10:44chloramphenicol will not aminoglycosides

2:10:47will cover um pseudomonas and then your

2:10:50um

2:10:51tetracyclines won't cover it as well

2:10:53so with that being said i would put them

2:10:54on i think the most commonly utilized

2:10:56one is vancomycin and

2:10:57peppercilantaseobactum

2:10:58so that would be the empiric regiment

2:11:00then i would get cultures from their

2:11:01sputum and i would see what it grows it

2:11:03grows pseudo so it would be all those

2:11:05ones that we just literally named so

2:11:07ceftasidium cifipim

2:11:10oh yeah this is going to forget about

2:11:11these carbopenums these are super broad

2:11:13remember boom it'll blow every bacteria

2:11:15up monobactins aminoglycosides

2:11:17fluoroquinolones only as a double

2:11:19coverage not as a monotherapy

2:11:21and polymixins as a salvage therapy when

2:11:23they're just resistant to everything

2:11:25okay so that would be this kind of

2:11:27process here so i'd start them on that

2:11:29and then i would get rid of the

2:11:29vancomycin once i got this pseudomonas

2:11:31back

2:11:32the next question is what are the

2:11:34adverse effects though aminoglycoside so

2:11:35we've talked about a lot of these but

2:11:36let's say that you know we decide to

2:11:39just keep them on percentages of

2:11:40bacterium but we're considering

2:11:41aminoglycosides and we just got to have

2:11:43a discussion about why would we not pick

2:11:46aminoglycosides and it's because of the

2:11:48adverse effects of it right um

2:11:50nephrotoxicity so they can really hit

2:11:51the kidneys pretty well they're ototoxic

2:11:53they can worsen myasthenia gravis and

2:11:55they are teratogenic so again things to

2:11:57consider i'm not to be honest they don't

2:11:59really ever use aminoglycosides but

2:12:01they're they're out there if you ever

2:12:02need them but one of the things that's

2:12:04interesting i think out of out of

2:12:06aminoglycosides and i think this is

2:12:07probably a really interesting reason as

2:12:09to why we don't use them that often

2:12:10they're just really

2:12:11never toxicity is a pretty rough thing

2:12:13with this one but

2:12:15when you think about this drug

2:12:16what are the mechanisms that a bacteria

2:12:18develop resistance to watch this

2:12:21it's the a in all of these right so

2:12:24you have vat b fat uh

2:12:27fat m fat bvmlt and then bam do you

2:12:30notice something

2:12:31bacteria develop all the mechanisms of

2:12:33resistance to the sucker

2:12:35so that's one of the nasty things about

2:12:37this one but

2:12:39it is a good drug if it's absolutely

2:12:40necessary in situations like infective

2:12:42endocarditis due to a prostatic valve or

2:12:44you know some of the urinary tract

2:12:46infections it's it's decent okay

2:12:48all right that would be the adverse

2:12:50effects there now we're not done

2:12:52unfortunately this patient develops a

2:12:53complication um

2:12:55all right so we have i'm sorry we have

2:12:56another patient i thought this was the

2:12:57same one my bad so you have a 46 year

2:12:59old male who's an icu status post large

2:13:01intracranial hemorrhaging on the

2:13:03ventilator develops high fevers

2:13:04hypotension tachycardia intense

2:13:05leukocytosis and is now started on

2:13:07vasopressors

2:13:09so this sounds like sepsis i mean it

2:13:11does all right so we got a patient who's

2:13:13definitely probably developed a hospital

2:13:14acquired pneumonia and then it's seeded

2:13:16into the bloodstream because now they

2:13:18have fevers they have hypotension they

2:13:19have tachycardia they have a white cell

2:13:22count

2:13:23and now they're started on vasopressors

2:13:24so now they're becoming hypotensive

2:13:26that's requiring basal pressure support

2:13:28definitely sounds like a septic shock

2:13:29patient in septic shock we assume that

2:13:32this patient is a

2:13:34septic due to two bugs one mrsa second

2:13:37pseudo what do we start them on same

2:13:39thing we just started before for the vap

2:13:42vancomycin and peppercilantase of

2:13:43bacterium those are the commonly

2:13:44utilized ones

2:13:45we get cultures in this patient we're

2:13:47going to get sputum cultures and blood

2:13:49cultures

2:13:50because they're pretty sick right so we

2:13:52get blood culture sputum cultures and it

2:13:53comes back as extended spectrum

2:13:55beta-lactamase klebsiella

2:13:59which antibiotic is best in this

2:14:01situation remember this is a nasty bug

2:14:03when you get those extended spectrum

2:14:05beta-lactamase bacteria they are really

2:14:06really nasty so which antibiotics will

2:14:08cover these there's not very many

2:14:10carbopenems blows everything up right

2:14:13what else aminoglycosides

2:14:15and polymixins would probably be about

2:14:18what you're going to get for these so

2:14:21that would pretty much be it here

2:14:23oh and then yeah i forgot about this one

2:14:25ceftazidime and avibactum that's a more

2:14:27of an infectious disease specialist who

2:14:29can

2:14:30give this one because if you remember

2:14:32extended spectrum beta-lactamase

2:14:33bacteria like e coli cleb you know some

2:14:35of the entire bactericie

2:14:37they develop such a significant extended

2:14:40spectrum beta lactamase that it's really

2:14:42hard for them to be able to respond to

2:14:44ceftasidine you remember your third your

2:14:46fourth generation cephalosporins

2:14:48and even someone like

2:14:49pippercontazobactum so you have to add

2:14:51on this thing avibactum and it might be

2:14:54enough to be able to knock out some of

2:14:55the betalactamases and allow ceftazidime

2:14:57to penetrate and kill the bacteria such

2:14:59as cleb

2:15:00so these would be your options now

2:15:02you're looking at these and you start

2:15:03considering which one you're going to

2:15:04put the patient on carbo venoms will

2:15:06probably be your best option out of all

2:15:07of these but you can consider the last

2:15:09one ceftaz and have you backed him if

2:15:11you have an infectious disease

2:15:12consultant on board

2:15:13but i think one of the things to think

2:15:14about is we haven't talked about these

2:15:16since you know carbopenums are a

2:15:17betalactim cephtazidim is a big lactone

2:15:20aminoglycosis we already talked about

2:15:21its adverse effects what will be the

2:15:22downside of polymixins one is their

2:15:25neurotoxic so they can really induce

2:15:27seizures nephrotoxic is another really

2:15:29nasty thing about these and respiratory

2:15:31failure so with this patient already

2:15:33having a likely vap i don't know i

2:15:35probably wouldn't go as far as to put

2:15:37them on this drug just because of how

2:15:39nasty it is but

2:15:41again it's an option if you have no

2:15:43nothing else to do for the patient

2:15:45so

2:15:46unfortunately the patient needed to get

2:15:48an evd their bleed was so big that their

2:15:50pressures inside their skull was

2:15:51increasing and we needed to be able to

2:15:53drain because the blood started pushing

2:15:54into their ventricles now and now they

2:15:55have some ivh and we need to put an evd

2:15:58to start sucking some of the blood out

2:15:59of those ventricles because they're

2:16:00starting to get hydro hydrocephalus when

2:16:03that happens and you get the evdn they

2:16:05end up developing a meningitis now

2:16:06because of the evd that was inserted and

2:16:09so they developed a hospital acquired

2:16:10meningitis what are the nasty types of

2:16:12bugs that you have to be thinking about

2:16:13for this one

2:16:14one is mrsa

2:16:15the other one is pseudomonas right so

2:16:17that's the primary thing so in this

2:16:18situation you start them on vancomycin

2:16:20but you need something that's going to

2:16:21penetrate the this central nervous

2:16:23system so cefepimesim seems to be a

2:16:25little bit better ceftazine is another

2:16:27option percentage of bacterium doesn't

2:16:29have this great of a central penetration

2:16:32so that one i would kind of maybe hold

2:16:34off on so i would start the vancomycin

2:16:36or lineage lid to cover the mrsa and

2:16:38then i would start them on

2:16:40something for the pseudo so cefepime or

2:16:43ceftazidim or something of that nature

2:16:45and wait till the cultures come back

2:16:46when i get the cultures back it reveals

2:16:48a really weird combo for some odd reason

2:16:52in this patient

2:16:53they have mrsa but they have nessaria

2:16:56meningitidis you're like what the heck

2:16:58all right well

2:16:59they have this i'm going to start them

2:17:01on vancolinaselid for the mrsa but i

2:17:03need something that's going to penetrate

2:17:04the central nervous system

2:17:06that's got good coverage against

2:17:07necessary do you guys remember third gen

2:17:09cephalosports ceftriaxone would be your

2:17:11best

2:17:12all right and that's what you start them

2:17:14on

2:17:15all right i know this was a lot i hope

2:17:17this lecture made sense i really hope

2:17:18that you guys enjoyed this and

2:17:19antibiotics have really become a little

2:17:20bit easier to grasp now um as always i

2:17:24love you thank you and until next time

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