Speaker 1: Imagine a patient comes into your clinic, right, their jaw
Speaker 1: is just it's swollen to the size of a grapefruit.
Speaker 1: Oh yeah, we've all seen it, right, It's inflamed, incredibly painful.
Speaker 1: So you admit them, You hook them up to an
Speaker 1: IV of the strongest, broadest spectrum antibiotics you have, and
Speaker 1: you wait for the swelling.
Speaker 2: To go down, and then it does absolutely nothing exactly.
Speaker 1: The infection just continues to rage. And why is that.
Speaker 1: It's because the most potent drug in the world is
Speaker 1: completely useless if the physical terrain like actually prevents it
Speaker 1: from reaching the bacteria.
Speaker 2: Yeah, you're hitting on honestly, one of the most frustrating
Speaker 2: realities in clinical practice. I mean, we train so hard
Speaker 2: to memorize which drug kills which.
Speaker 3: Bug, right, the classic matching gig exactly.
Speaker 2: But we often completely overlook the mechanical delivery system. We
Speaker 2: aren't treating a static, plastic model of a job. No,
Speaker 2: it's a living thing, right, It's a dynamic, highly compartmentalized
Speaker 2: biological system, and the rules of engagement they change entirely
Speaker 2: depending on the micro environment of that specific tissue, which.
Speaker 1: Is exactly why today's deep dive is custom tailored for you.
Speaker 1: So whether you're a dental student you know, prepping for clinicals,
Speaker 1: a young professional refining your habits, or just a self
Speaker 1: learner who wants to understand the why behind the protocols.
Speaker 2: Yeah, the mechanical why is so important.
Speaker 1: It really is. We are working through a massive stack
Speaker 1: of notes today from the fourteenth edition of Antibiotic.
Speaker 2: Essentials, edited by doctor Burke A. Kuna.
Speaker 1: That's the one and the mission today isn't just to
Speaker 1: like rattle off guideline lists.
Speaker 2: Yeah, that's what textbooks are for, right.
Speaker 1: We are extracting the core foundational tenets of rational antibiotic
Speaker 1: prescribing and mapping them directly onto head, neck, and oral infections.
Speaker 2: We're getting into the pharmacokinetics, the physiological barriers, and the
Speaker 2: really specific drug quirks that basically dictate success or failure
Speaker 2: in dentistry.
Speaker 1: So to understand those protocols, I mean, we really have
Speaker 1: to start with tissue penetration.
Speaker 2: Right, Yeah, absolutely. The textbook emphasizes this r and over,
Speaker 2: and antibiotics efficacy is strictly governed by its ability to
Speaker 2: literally physically achieve a therapeutic concentration at the side of
Speaker 2: the infection. It has to get there first, right, And
Speaker 2: in an acute infection like a rapidly spreading facial cellulitis,
Speaker 2: the body actually does a lot of the heavy lifting
Speaker 2: for the drug.
Speaker 1: Because the acute inflammatory response alters the vascular permeability precisely.
Speaker 2: You have this localized release of cytokine's histamines, you know,
Speaker 2: all those inflammatory mediators, and they cause vasodilation exactly, and
Speaker 2: the tight junctions between the endothelial cells that line the
Speaker 2: blood vessels they literally pull apart. Oh wow, Yeah, the
Speaker 2: vessels become leaky. And this increased microvascular permeability it allows
Speaker 2: the antibiotics circulating in the serum to just effortlessly pour
Speaker 2: into the interstitial fluid of the infected soft tissue.
Speaker 1: Okay, but the textbook draws a pretty hard line. When
Speaker 1: that acute cellulitis like organizes into a chronic, walled off abscess.
Speaker 2: Oh, it's a completely different ball game.
Speaker 1: The rules of tissue penetration completely invert.
Speaker 2: They do, because the anatomy of an abscess is fundamentally
Speaker 2: different from just inflamed tissue, and abscess is a highly
Speaker 2: organized capsule. It's full of necrotic tissue, fibrine, white blood cells,
Speaker 2: and just a massive bacterial.
Speaker 1: Load, just nasty mix.
Speaker 3: Yeah.
Speaker 2: But crucially, the interior of that capsule is a vascular
Speaker 2: meaning no blood flow exactly. There is zero capillary network
Speaker 2: feeding the center of that pus cavity.
Speaker 1: So, okay, trying to resolve a mature abscess with a
Speaker 1: systemic oral antibiotic, it's essentially like trying to deliver mail
Speaker 1: to a house in a neighborhood with no roads.
Speaker 2: That's a great way to put it.
Speaker 1: Like, it doesn't matter if you have the fastest mail
Speaker 1: truck or you know, a million letters, there's no physical
Speaker 1: path to the house. That delivery fails. You have to
Speaker 1: pave a rate first.
Speaker 2: That captures the mechanical reality perfectly. The text states definitively,
Speaker 2: and I mean definitively, that antibiotics cannot eradicate organisms from
Speaker 2: areas with impaired blood supply.
Speaker 3: This is just circulated right past it, right past the capsule.
Speaker 2: And this is why surgical intervention, you know, incision and
Speaker 2: drainage or I and D is an absolute, non negotiable
Speaker 2: prerequisite for a cure.
Speaker 1: You literally have to drain it.
Speaker 2: You must physically decompress the cavity and establish a drainage route.
Speaker 2: You have to alter the physical terrain before the systemic
Speaker 2: chemical therapy can even begin to do its job on
Speaker 2: the surrounding inflamed tissue.
Speaker 1: Okay, so that mechanical reality, it leads right into another
Speaker 1: trap the textbook highlights, which is this huge discrepancy between
Speaker 1: in vitro and in vivos susceptibility.
Speaker 2: Oh, this trips up so many people, right.
Speaker 1: Because a clinician sends a pulent sample from say, a
Speaker 1: periodontal pocket, to the microbiology lab, and the report comes
Speaker 1: back saying the bugs are susceptible to a specific.
Speaker 2: Antibiotic, and the immediate temptation is to just write the
Speaker 2: prescription exactly.
Speaker 3: You see, susceptible, You write the script.
Speaker 2: But relying surely on that lab report ignores everything we
Speaker 2: just talked about regarding tissue penetration.
Speaker 1: Because the lab isn't the human body.
Speaker 2: Right. In vitro testing, it happens in this highly controlled,
Speaker 2: standardized broth or aggar in a Petrie dish. The lab
Speaker 2: is simulating standard serum concentrations of the drug and the blood.
Speaker 2: But in vivo, you know, inside the living, breathing patient,
Speaker 2: the drug concentration in the serum almost never matches the
Speaker 2: concentration deep in the bone matrix or the cerebro spinal
Speaker 2: fluid or a necrotic periodontal pocket.
Speaker 1: So the lab just assumes a perfect delivery system it does.
Speaker 2: A drug might look like an absolute targeted missile strike
Speaker 2: in the Petrie dish, but if its molecular size, or
Speaker 2: its protein binding affinity or lipid solubility prevents it from
Speaker 2: penetrating the actual tissue you're targeting.
Speaker 1: It's going to fail.
Speaker 2: Clinically, it will completely fail. You always have to cross
Speaker 2: reference the lab susceptibility report with the known pharmacokinetic profile
Speaker 2: of the drug for that specific anatomical site.
Speaker 1: Man, that's wild. Well, let's talk about the actual mechanism
Speaker 1: of action once the drug does manage to reach the site. Sure,
Speaker 1: the text compares bactericidal drugs right, which actively induce bacterial
Speaker 1: cell death, with bacteriostatic drugs, which just inhibit replication processes
Speaker 1: like protein synthesis.
Speaker 2: Right, the killers versus the pausers.
Speaker 1: Yeah, And instinctively, as a patient or a doctor, it
Speaker 1: feels like we should always reach for the bacteriicityl you know,
Speaker 1: the actively destroying agent.
Speaker 2: Most clinicians have that exact instinct. But doctor Kuna's textbook
Speaker 2: clarifies that for the vast majority of routine infections, bactericidal
Speaker 2: and bacteriostatic antibiotics achieve clinical cure at the exact same rate.
Speaker 1: Wait, really, how does simply pausing bacterial replication achieve the
Speaker 1: same timeline as actively exploding.
Speaker 2: The cell wall Because the antibiotic isn't operating in a
Speaker 2: vacuum you know, ok, a bacteriostatic agent, it halts the
Speaker 2: exponential growth phase of the pathogen. It pins the bacteria
Speaker 2: down so they can't overwhelm the local tissue.
Speaker 3: Ah, I see, And at.
Speaker 2: That point, the host's own immune system, the neutrophils, the macrophages,
Speaker 2: they sweep through and figositize the static bacteria, clean up
Speaker 2: the mess exactly, they clear the infection. You are heavily
Speaker 2: relying on the patient's endogenous immune response, which.
Speaker 1: Means you only strictly require a bactericidal drug when the
Speaker 1: immune system, for whatever reason, cannot perform that sweep.
Speaker 2: You hit the nail on the head. The textbook lists
Speaker 2: very specific, very critical exceptions where bactericidal action is mandatory.
Speaker 2: One is endocarditis, because the heart valves actually lack a
Speaker 2: dedicated blood supply to deliver those white blood cells.
Speaker 1: Oh makes sense.
Speaker 2: Another is meningitis due to the immune privileged nature of
Speaker 2: the central nervous system. And finally, patients with profound febrel leukopenia.
Speaker 1: So patients without an immune system.
Speaker 2: Basically, yeah, if a patient doesn't have a functional white
Speaker 2: blood cell count, a bacteriostatic drug will just stall the
Speaker 2: infection until the pill bottle is empty, and then and
Speaker 2: the bacteria will simply resume replicating.
Speaker 1: For a standard dental infection in a healthy host, the
Speaker 1: distinction between cytyl and static is clinically.
Speaker 2: Irrelevant, completely irrelevant.
Speaker 1: Wow. Okay, knowing that opens up our options, which really
Speaker 1: brings us to the broader strategy of antibiotic selection and
Speaker 1: the looming threat of resistance.
Speaker 2: The big scary superbugs.
Speaker 3: Right.
Speaker 1: The text introduces this concept called resistance potential, and we
Speaker 1: tend to assume that writing any antibiotic prescription contributes equally
Speaker 1: to the global rise of superbugs.
Speaker 2: A lot of people think that, but the data actually
Speaker 2: shows that acquired resistance is highly drug specific.
Speaker 3: Oh interesting, Yeah.
Speaker 2: It's a critical distinction. Certain molecular structures inherently drive rapid
Speaker 2: resistance like which ones. Well, the book highlights a zittomycin,
Speaker 2: especially when used against Streptococcus pneumonia, as having a notoriously
Speaker 2: high resistance potential.
Speaker 3: Really, even if you don't overprescribe it.
Speaker 2: Even with conservative use, the bacteria rapidly acquire or upregulate
Speaker 2: these e flex pumps to literally just spit the drug
Speaker 2: back out of their cells, or they alter their ribosomal
Speaker 2: binding sites.
Speaker 1: So the drug just trains the bacteria to defeat it
Speaker 1: very quickly.
Speaker 3: Yes.
Speaker 1: Contrast that with something like doxycycline, which the TEFT categorizes
Speaker 1: having a low resistance potential.
Speaker 2: Right, I mean, despite decades of heavy widespread use and
Speaker 2: everything from acne to respiratory infections, bacteria really struggle to
Speaker 2: mount widespread systemic resistance to doxycycline.
Speaker 1: Why is that the.
Speaker 2: Structural hurdles required for the pathogen to bypass tenttracyclin inhibition
Speaker 2: are simply much much higher?
Speaker 1: Got it?
Speaker 2: So the clinical takeaway here is that when you're designing
Speaker 2: an empiric therapy regimen and two drugs offer equivalent coverage
Speaker 2: for your suspected bug, you always default to the one
Speaker 2: with the intrinsically lower resistance potential.
Speaker 1: Okay, that makes sense, But I want to push back
Speaker 1: on another strategic paradigm in the text.
Speaker 2: Okay, let's hear.
Speaker 1: Mono therapy versus common therapy.
Speaker 2: Ah.
Speaker 3: Yes, the book takes this.
Speaker 1: Aggressive stance that monotherapy is almost always preferred. But I mean,
Speaker 1: if we are facing a severe mixed flora oral infection,
Speaker 1: doesn't throwing two or three different mechanisms of action at
Speaker 1: the site guaranteed better coverage.
Speaker 2: It definitely seems logical, right, Yeah, but it actually creates
Speaker 2: more problems than it solves. Outside of highly specific protocol
Speaker 2: driven exceptions like tuberculosis or HIV or certain crazy pseudomonal infections.
Speaker 2: Blindly stacking antibiotics does not prevent resistance.
Speaker 1: Wait really, what does it do then?
Speaker 2: Well, first, it drastically increases the risk of medication errors,
Speaker 2: and it compounds the likelihood of adverse side effects.
Speaker 1: Double the drugs, double the side.
Speaker 2: Effects exactly, But more importantly, you risk competitive antagonism.
Speaker 1: What's up?
Speaker 2: Okay? Imagine you prescribe a bacteria static drug that halts
Speaker 2: cellular processes right right, and at the same time, you
Speaker 2: prescribe a bactericidal beta lactum that relies on active cell
Speaker 2: wall synthesis to cause the cell to lise and explode.
Speaker 1: Oh, I see where this is going.
Speaker 2: Yeah, the static drug stops the cell from building its wall,
Speaker 2: which actually prevents the sidle drug from working.
Speaker 1: Wow, so you are paying double the financial cost to
Speaker 1: create chemical interference in the patient's own body.
Speaker 3: Exactly.
Speaker 2: Monotherapy using a single, appropriately targeted, broad enough agent is cleaner,
Speaker 2: it's safer, and it's far more cost effective.
Speaker 1: Which ties perfectly into what the textbook calls the most
Speaker 1: vital cost saving strategy in hospital medicine, the ived PO switch.
Speaker 2: The intravenous to oral switch, right, and.
Speaker 1: The data shows this switch saves roughly ten dollars per
Speaker 1: dose just in administration overhead.
Speaker 2: Yeah. The IV two being the saline flushes the nursing
Speaker 2: labor It adds up fast.
Speaker 1: But again, from a patient or even a young doctor's perspective,
Speaker 1: it feels like an IV drip is delivering a superior,
Speaker 1: stronger level of care.
Speaker 2: I get that feeling.
Speaker 3: I do.
Speaker 1: Like if a patient is admitted for a huge facial swelling,
Speaker 1: stepping them down to a feels like a massive downgrade.
Speaker 1: In therapy, it.
Speaker 2: Only feels like a downgrade if you misunderstand pharmacokinetics, specifically,
Speaker 2: oral bioavailability break that down force. So bioavailability is the
Speaker 2: exact fraction of the administered drug that survives the acidic stomach,
Speaker 2: passes through the intestinal mucosa, survives first pass metabolism in
Speaker 2: the lover, and successfully enters the systemic circulation.
Speaker 1: Okay, And an IVY drug is essentially one hundred percent
Speaker 1: bioavailable by definition.
Speaker 2: Correct because you bypass the gut and the liver entirely
Speaker 2: you're mainlining it. But the textbook points out that several
Speaker 2: highly relevant antibiotics in dentistry have exceptional oral bioavailability. Which
Speaker 2: ones we are talking about clindamycin, matronodozol, amoxicillin, and doxycycline.
Speaker 1: Okay.
Speaker 2: Their chemical structures allow them to absorb so efficiently across
Speaker 2: the GI tract that the serum concentrations achieved by taking
Speaker 2: them orally are nearly indistinguishable from an IV.
Speaker 1: Push seriously indistinguishable, pretty much identical.
Speaker 2: So if a patient has a functioning gut, keeping them
Speaker 2: on a peripheral IV line is just exposing them to
Speaker 2: the risk of like phlebitis or a line infection for
Speaker 2: zero added benefit. Exactly once a patient demonstrates clinical improvement
Speaker 2: and their hemodynamically stable, usually within forty eight to seventy
Speaker 2: two hours. Maintaining IVY access for these specific drugs is
Speaker 2: basically medical.
Speaker 3: Theater, medical feed or wax.
Speaker 2: It's not medical science. The switch to oral therapy should
Speaker 2: be immediate.
Speaker 1: Okay, Let's apply that specific strategy to the actual pathogens
Speaker 1: we face in the oral cavity.
Speaker 2: Let's do it.
Speaker 1: Doctor Kuna's text breaks down impyic therapy regimens for severe
Speaker 1: dental infections, and.
Speaker 3: The usual suspects here.
Speaker 1: Are oral anaerobes which thrive in the deep oxygen depleted
Speaker 1: periodental pockets, and oral stryptococcy right.
Speaker 2: The classic dental dugs.
Speaker 1: So if that patient is hospitalized with the severe facial
Speaker 1: space infection, what is the initial IV therapy targeting those
Speaker 1: specific bugs.
Speaker 2: The standard textbook recommendation is clindamycin at six hundred milligram
Speaker 2: thavi every eight hours, or a broad spectrum combination like
Speaker 2: piper ascyllintiso buctum.
Speaker 1: Let's focus on clindamycin for a second. Why is it
Speaker 1: historically such a powerhouse for dental stuff.
Speaker 2: It really comes down to its unique tissue penetration and
Speaker 2: its mechanism of action. How so Well, clindamycin is highly.
Speaker 3: Lipophilic, meaning it likes fat.
Speaker 2: Right, it easily crosses lipid cell membranes, which allows it
Speaker 2: to penetrate deeply into bone matrix and necrotic soft tissue
Speaker 2: where vascularity is super compromise.
Speaker 1: Well, that's perfect for dental abscesses.
Speaker 2: It is, and once it's inside, it binds to the
Speaker 2: fifty s ribosomal subunit of the anaerobic bacteria, rapidly shutting
Speaker 2: down protein synthesis. It absolutely decimates the oral anaerobic populations
Speaker 2: that drive those deep fascil space infections.
Speaker 1: And when that hospitized patient stabilizes and we apply that
Speaker 1: IV to PO switch, what is the step down therapy.
Speaker 2: You utilize that near perfect bioavailability we talked about. They
Speaker 2: step down to clindamycin three hundred milligrams orly every eight
Speaker 2: hours for two weeks. Alternatively, if the initial IV therapy
Speaker 2: was a beta lactam, they switched to a maxiicellin clavulin eate.
Speaker 3: It's augmentin right at bugmenton and.
Speaker 2: A dose of eight hundred and seven hundred five one
Speaker 2: hundred and twenty five milligrams orally every twelve hours.
Speaker 1: Nice, okay, But beyond the deep tissue bacterial infections, the
Speaker 1: oral cavity is also a battleground for viral, fungal and
Speaker 1: spear shehed pathogens.
Speaker 2: So definitely it's a jungle in there.
Speaker 1: And the text differentiates treatment from mouth ulcers and vesicles
Speaker 1: based heavily on the etiology.
Speaker 2: The differential diagnosis is critical here because the mechanisms of
Speaker 2: the treatments are completely divergent. Like if the vesicles are
Speaker 2: viral specifically herpie simplex virus or HSV, the textbook points
Speaker 2: to a cyclover.
Speaker 1: I've always wondered about this. How does a cyclover specifically
Speaker 1: target the virus without destroying the host's own cellular replication?
Speaker 2: A cyclover is honestly an incredibly elegant drug.
Speaker 1: How does it work.
Speaker 2: It's a nucleoside analog, but it is administered in an
Speaker 2: inactive form.
Speaker 3: Okay, it only.
Speaker 2: Becomes activation when it encounters thymidine kinase. And that's an
Speaker 2: enzyme produced specifically by the herpes virus, not by human cells.
Speaker 1: Oh wow, So it's like a sleeper agent.
Speaker 2: Exactly once the viral enzyme activates it, the drug incorporates
Speaker 2: itself into the replicating viral DNA strand, and because it
Speaker 2: lacks a crucial chemical attachment point, it acts as a
Speaker 2: chain terminator.
Speaker 1: So it breaks the chain.
Speaker 2: The viral DNA polymerase literally cannot add the next link.
Speaker 2: Viral replication halts completely and the healthy human cells are
Speaker 2: left completely untouched.
Speaker 1: That is fascinating, but I mean, if the oral ulcers
Speaker 1: are bacterial, like the severe punched out lesions caused by
Speaker 1: spirit shates in Vincent's angina, you know, trenchmouthl cycle over
Speaker 1: does absolutely.
Speaker 2: Nothing, nothing at all. For spiro shades, the treatment of
Speaker 2: choice remains penicillin G. The classic yep spara shavs have
Speaker 2: a unique highly sensitive cell wall architecture. The beta lactum
Speaker 2: ring of penicillin G aggressively binds to the penicillin binding
Speaker 2: proteins on.
Speaker 1: The spira shape and that breaks the wall.
Speaker 2: It inhibits the cross linking of their peptidoglicin layer. The
Speaker 2: cell wall loses its structural integrity and osmotic pressure basically
Speaker 2: causes the bacteria to rise and die.
Speaker 1: Okay, So that's viral and spira shase rounding out the
Speaker 1: mucosal infections we have oropharyngeal candidiasis to rush. Right. Fungal overgrowth, yes.
Speaker 2: Driven by candida albicins. And this frequently occurs in immunocompromised
Speaker 2: patients or in patients who have recently completed a course
Speaker 2: of heavy broad spectrum antibiotics because.
Speaker 1: The antibiotics wiped out their normal bacterial.
Speaker 2: Flora exactly, eliminating a competition for the yeast. So the
Speaker 2: yeast just takes over.
Speaker 1: And the treatment options here are clotrimosoal troches which just
Speaker 1: dissolve locally in the mouth, or A nine stat and
Speaker 1: swish and swallow, or systemI fluconazole correct and these work
Speaker 1: by targeting or gostral.
Speaker 2: Right, you got it. Human cell membranes rely on cholesterol,
Speaker 2: but fungal cell membranes rely on or gostol verstability.
Speaker 1: Ah, that's the difference.
Speaker 2: Yeah. These anti fingal agents either bind directly to ergostrol
Speaker 2: or inhibit its synthesis, which tears microscopic holes in the
Speaker 2: fungal cell membrane, causing the cellular contents to just leak out.
Speaker 1: So for anyone taking notes, you basically have three main
Speaker 1: oral battlegrounds. The deep bacterial infections requiring clindamycin, the viral
Speaker 1: or spirashet ulcers, and the fungal overgrowths like thrush.
Speaker 2: That's a great way to categorize it.
Speaker 1: There's one more throat area condition we need to cover, though,
Speaker 1: because it highlights a massive prescribing trap, pharyngitis right strep throat.
Speaker 1: For true group A streptococcal pharyngitis, the textbook actually prefers
Speaker 1: a moxocillin over standard penicillin just for better GI absorption.
Speaker 2: It's much easier for the patient to tolerate.
Speaker 1: But what happens if the clinician misdiagnoses the sore throat?
Speaker 1: What if the patient actually has infectious mononucleosis caused by
Speaker 1: the epstein bar virus and the clinician prescribes a moxacillin anyway.
Speaker 2: You trigger a spectacular adverse event.
Speaker 1: It's bad, right.
Speaker 2: If you introduce a moxocillin into a system actively fighting
Speaker 2: the epstein bar virus, nearly ninety percent of those patients
Speaker 2: will erupt in a massive, intensely itchy, full body maculopopular rash.
Speaker 1: Ninety percent, And it looks exactly like a severe drug allergy. Right.
Speaker 1: The patient usually ends up in the er convinced they're
Speaker 1: going into anaphylaxis.
Speaker 2: It perfectly mimics an allergy, but it's fundamentally different. This
Speaker 2: is not a true ig mediated life threatening type one hypersensitivity.
Speaker 3: What is it? Then?
Speaker 2: It's a delayed immune complex mediated reaction. The epstein bar
Speaker 2: virus basically hyperstimulates the patient's immune system, altering how it
Speaker 2: recognizes the immoxicillin molecule, so it gets confused exactly. The
Speaker 2: immune system suddenly views the drug as a target, leading
Speaker 2: to widespread cutaneous inflammation. The patient isn't permanently allergic to ammoxicillin,
Speaker 2: They're just experiencing a transient virus induced immune confusion.
Speaker 1: Wow. That epstein bar rash perfectly illustrates the danger of
Speaker 1: treating a symptom or like a lab test rather than
Speaker 1: understanding the underlying real of the microbiome, absolutely which brings
Speaker 1: us directly to the textbook's golden rule. This is perhaps
Speaker 1: the most critical takeaway for any clinician listening.
Speaker 2: Do not use antibiotics to treat colonization.
Speaker 1: It's the bedrock of infectious disease stewardship, isn't it.
Speaker 2: It really is the human oral cavity, the gut, the skin.
Speaker 2: They are not sterile environments lilion clothes. No, they are
Speaker 2: teeming with billions of bacteria that make up your normal,
Speaker 2: healthy flora. These organisms are colonizers. They occupy physical space
Speaker 2: on the mucosal surfaces, consume local nutrients, and by their
Speaker 2: mere presence, provide colonization resistance against highly virulent outside pathogens.
Speaker 1: And a pathogen, conversely, is an organism that has breached
Speaker 1: that meucastal barrier, evaded the immune system, and is actively
Speaker 1: causing tissue destruction. Purrelens in inflammation.
Speaker 2: Precisely so, if you swab a perfectly healthy patient's throat
Speaker 2: and the lab culture's Staphylococcus aureus, that does not mean
Speaker 2: the patient has a staff infection. It simply means s
Speaker 2: ore is a transient colonizer in that specific biome. If
Speaker 2: you panic and prescribe a potent antibiotic to clear that colonizer,
Speaker 2: you aren't treating a disease.
Speaker 1: You're just doing damage.
Speaker 2: You are detonating a chemical bomb in a healthy ecosystem,
Speaker 2: wiping out the beneficial flora and basically selecting for highly
Speaker 2: resistant superbugs in the vacuum you just created.
Speaker 1: Right, you treat the clinical signs of active infection, not
Speaker 1: the piece of paper from the microbiology lab exactly. Okay,
Speaker 1: let's finish up by digging into the mechanical quirks of
Speaker 1: the specific drugs we prescribe most often in dentistry, starting
Speaker 1: with augmented.
Speaker 2: The heavy hitter.
Speaker 1: We mentioned amoxocillin clavulinate earlier as a great step down drug,
Speaker 1: but it has a pre notorious reputation for causing severe
Speaker 1: gastro intestinal distress and diarrhea.
Speaker 2: It's a very, very common complaint. The amoxiscillin component is
Speaker 2: generally well tolerated, but the clavulinate, which is added to
Speaker 2: protect the amoxicillin from being destroyed by bacterial enzymes, is
Speaker 2: highly irritating to the gut. Why is this so irritating
Speaker 2: Because clavulinate acts as a modalin receptor.
Speaker 3: Agonist O key, what does that mean?
Speaker 2: It chemically mimics the hormone modil in, which controls smooth
Speaker 2: muscle contractions in your gastri intestinal tract.
Speaker 1: Oh, so it is actively stimulating hyperactive peristolysis in the
Speaker 1: small intestine.
Speaker 3: Exactly.
Speaker 2: It forces the gut to become hypermodal, leading to intense
Speaker 2: cramping and diarrhea.
Speaker 3: So how do you stop that?
Speaker 2: To mitigate this, patients must be strictly instructed to take
Speaker 2: augmenton with a large meal, not just the snacks. A
Speaker 2: large meal. The physical presence of food buffers the mucosall
Speaker 2: lining slows gastric emptying and significantly reduces that modal in
Speaker 2: agonizing effect. It allows the patient to actually finish the
Speaker 2: prescribed course.
Speaker 1: That is such a practical tip. Oh connext quirk clinomycin.
Speaker 1: We praised its bone penetration and its affinity for anaerobes,
Speaker 1: but its ability to clear out anaerobic bacteria is exactly
Speaker 1: what triggers its dreaded black box warning right.
Speaker 2: The risk of Claustridium difficile or sea diff colitis everyone's
Speaker 2: worst truly. The lower intestine is a densely packed anaerobic ecosystem,
Speaker 2: and because clintamycin is so incredibly efficient at destroying anaerobes,
Speaker 2: it essentially clearcuts the healthy flora of the.
Speaker 1: Colon and seedf is just waiting there.
Speaker 3: Yeah.
Speaker 2: Seed dis is a spore forming bacterium that often exists
Speaker 2: in the gut in very small suppressed numbers.
Speaker 1: It's kept in check by the competition for nutrients from
Speaker 1: the good bacteria.
Speaker 3: Right.
Speaker 2: But when clintamycin wipes out that competition, the seed diff
Speaker 2: spores germinate into vegetative cells and rapidly overgrow in that
Speaker 2: newly emptied ecological niche.
Speaker 1: And then they release toxins.
Speaker 2: Yes, they begin secreting toxin A and toxin B, which
Speaker 2: actively destroy the mucosal lining of the colon, leading to
Speaker 2: severe watery, potentially life threatening pseudomembranous colitis.
Speaker 1: So any patient prescribed clindamycin must be counseled to immediately
Speaker 1: stop the drug and contact you if they experience persistent
Speaker 1: watery diarrhea.
Speaker 2: Immediate cessation is critical. Yes.
Speaker 1: Finally, let's look at doxycycling. We love it for its
Speaker 1: low resistance potential, but it has rigid, unforgiving rules regarding
Speaker 1: how it interacts with the patient's diet and physiology.
Speaker 2: Oh, very unforgiving. Doxycyclin is a safety Category D drug
Speaker 2: and pregnancy, and it is strictly contraindicated in young children.
Speaker 1: Because of the calcium affinity.
Speaker 3: Right.
Speaker 2: Yes, due to its intense molecular affinity for calcium, it
Speaker 2: actively binds to developing calcium structures, leading to permanent gray
Speaker 2: brown discoloration of erupting teeth and potentially inhibiting fetal skeletal development.
Speaker 1: But that extreme affinity for calcium doesn't just apply to
Speaker 1: teeth and bones. It applies to what the patient eats
Speaker 1: while taking the pill. Right. Absolutely, it binds with calcium, magnesium,
Speaker 1: and iron in the stomach through a chemical process called chalation.
Speaker 2: Right, the doxycycline molecule physically latches onto these divalent and
Speaker 2: trivalent metal ions in the gastrointestinal tract.
Speaker 1: So if a patient takes it with a glass of milk.
Speaker 2: Or the magnesium in an over the counter tacit, yeah,
Speaker 2: it forms a massive and soluble molecultor complex.
Speaker 1: The molecule literally becomes too large to physically cross the
Speaker 1: intestinal epithelium into the bloodstream.
Speaker 2: It neutralizes the therapy entirely. The Cholada drug complex simply
Speaker 2: passes through the digestive tract unabsorbed. You can prescribe the
Speaker 2: absolute perfect dose, but if the patient washes it down
Speaker 2: with a dairy product or takes it alongside their mourning
Speaker 2: iron supplement, their serum concentration of the antibiotic will literally
Speaker 2: be zero.
Speaker 1: So doxycycling must be taken on an empty stomach, empty.
Speaker 2: Stomach or spaced at least two to three hours apart
Speaker 2: from any interacting cass.
Speaker 1: It is wild how much of infectious disease management boils
Speaker 1: down to basic chemistry and physical plumbing.
Speaker 2: It really is plumbing.
Speaker 1: We have covered a tremendous amount of clinical ground today.
Speaker 1: Let's distill the core tenets for you, the dental professionals listening.
Speaker 2: From doctor Kuna's text. The foundational rules are pretty clear. First,
Speaker 2: surgical drainage is non negotiable and a biotics cannot reach
Speaker 2: in a vascular abscess.
Speaker 3: Pay the road first exactly.
Speaker 2: Second, favor monotherapy to avoid competitive antagonism and adverse events. Third,
Speaker 2: transition from IV to highly bioavailable oral drugs like clindamycin
Speaker 2: or amoxicillin the exact moment the patient stabilizes, and.
Speaker 1: Finally, respect the microbiome. Never prescribe antibiotics to eradicate transient colonizers.
Speaker 3: Rules. So, if you are scribbling.
Speaker 1: Notes for clinicals right now, let's test your recall on
Speaker 1: the step down protocols we covered. Here's a little review
Speaker 1: exercise for you.
Speaker 3: Let's see if they were paying attention.
Speaker 1: You are treating a patient recovering from a severe deep
Speaker 1: fascial space dental infection. They are hemodynamically stable, the swelling
Speaker 1: is reducing, and they are ready to be discharged from
Speaker 1: the hospital and switch from IV to oral therapy. According
Speaker 1: to the pharmacokinetic principles we discussed, which two highly bioavailable
Speaker 1: oral antibiotics are the preferred step down options to target
Speaker 1: the oral anaerobes and streptococ We are.
Speaker 2: Looking for the two drugs that offer in your one
Speaker 2: hundred percent absorption to maintain those therapeutic serum levels.
Speaker 3: I'll give you a second, got your answers.
Speaker 1: If you charted clindamycin or amoxilin clavulanate augmentant, you are
Speaker 1: absolutely cress.
Speaker 2: Those are the heavy hitters for oral step down therapy.
Speaker 1: To wrap up, we want to leave you with something
Speaker 1: to consider as you step back into the clinic tomorrow.
Speaker 1: We spend so much time studying how to efficiently destroy bacteria,
Speaker 1: But as our understanding of the human microbiome deepens, how
Speaker 1: might our definition of what constitutes a dangerous pathogen versus
Speaker 1: a protective colonizer shift in the coming decades.
Speaker 2: It really forces us to reconsider the entire search and
Speaker 2: destroy paradigm we were taught. Will the future of dental
Speaker 2: medicine eventually move away from broad spectrum chemical warfare? Will
Speaker 2: we one day utilized targeted bacteriophage therapy or prescribe highly
Speaker 2: engineered probiotics to actively seed the oral cavity, shaping the
Speaker 2: ecosystem through competitive exclusion rather than just trying to clear
Speaker 2: cut it with antibiotics.
Speaker 1: It is a profound shift in perspective, because an infection
Speaker 1: isn't just a static X ray, is a chaotic, living ecosystem.
Speaker 1: And the deeper our understanding of that physiological train becomes,
Speaker 1: the better equipped you are to navigate it. That's all
Speaker 1: for to day's deep dive. We'll catch it next time.