Full transcript
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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