DIP Episode 77 - Gram Positive Rapid Review

Welcome, my name is Divine. This is a current episode of the Divine Intervention Podcast. In today's podcast, I'm going to be doing something called a rapid review of Grand Positives. Okay, so this is a micro podcast. This is tuned specifically to a person that's taking like a micro quiz or a micro exam in your first two years of med school or if you're preparing for step one, and you want to very quickly review the Grand Positives. This will be a very nice way to do that. And basically, the one we're going to make this podcast is I'm going to stare at the Grand Positives algorithm in first date and then just seal the high-year fins that are classically tested with the different bugs. So we know obviously right that, I mean, we're dealing with bacteria here. It's just that with the Grand Sting, right? And we know that there's, you could have organisms that are Grand Positives or Grand Negative, right? And I mean, sort of key things you want to know, right? So Grand Positives organisms are at least in purple, right? That's easy enough versus the Grand Negative's that's Sting pink, right? And the thing is, if you're comparing your Grand Positives and Grand Negative's, you know that your Grand Positives in general, they have a thicker, peptidoglycan cell layer. So because they have that thicker, peptidoglycan cell layer, right? They're steamed purple with the Grand Sting, right?

But they do not have an outer membrane in contrast with your Grand Negative's that have both an inner membrane and an outer membrane. And inner membrane is found in both Grand Positives and Grand Negative's. But an outer membrane is found specifically in Grand Negative's, right? And the thing is between that inner and outer membrane, if you're comparing, if you're talking about Grand Negative's, right? There is this space. It's sort of think of it as like a storage warehouse. It's called a periodplasmic space. And that periodplasmic space is very high yield because it contains this enzyme known as beta-lactamics, right? And beta-lactamines super high yield enzyme, it breaks down beta-lactamantibiotics. And I'll talk about that at the end when I give a very quick brief spiel on antibiotics. Now, your Grand Positives, right? You want to sort of know, okay, why are they bad, right? The reason Grand Positives are bad is that they have something called a lipoteque acid, right? In their cell membranes. And those things can sort of trigger your immune system, right? You can release all these acute fees reactants and get into a lot of trouble. And Grand Positives in general, right? They have a exotoxin, exotoxin. Yes, I know there's Grand Negative's that makes exotoxin, but whenever you see exotoxin, think more about Grand Positives. Versus Grand Negative's that tend to make endotoxin. The big one you probably want to know is LTS, right? Lipopolisaccharide.

Lipopolisaccharide, it's, it has like something known as lipid A, and that thing sort of triggers your immune system. In fact, I'll say that lipopolisaccharide, if you're thinking in terms of immunology, it's an example of a PAMP, right? So PAMP, I don't mean PAMP, don't think of wrong things. PAMP, PAMP is like a pathogen associated molecular pattern, okay? So PAMP's, they're basically things that you can see, your body, your inid immune system can say, oh wait, this thing is a bacteria, right? So lipopolisaccharide is an example of a PAMP, and it binds to CD14, right? On micro features, and it can basically trigger signaling cascade that can operate NF-CAPB. And then through NF-CAPB, you can begin to make some higher acute phase cytokines like IL-1 and IL-6, right? And also through that signaling cascade, you break down something known as ICAPB. ICAPB is something that actually degrades and sort of shuts down NF-CAPB. So if you degrade ICAPB, NF-CAPB can run wild and you make all those acute phase cytokines. So LPS is an endotoxin. So think about endotoxin with regards to gram negatives, think about exotoxin with regards to gram positives. So if you're talking about gram positives, the first thing you want to do is you want to break them up as being like the C-line, so basically your rods, right? Or coxite, those are basically your circles, right? And then you can also have the branching filaments, and we'll talk about those in a bit, right?

So if you're talking about coxite, right? The next test you go through is your catalyst, test, remember, catalyst is part of your respiratory burst pathway, right? It breaks down hydrogen peroxide to water and oxygen. And hopefully you remember that if a patient has an NEDPH oxidized efficiency, right? They will have no ability to make hydrogen peroxide. And if they can only make hydrogen peroxide, they become susceptible to organisms that are catalyst positive, right? So organisms like staphorius, for example, right? Like E. coli, like Candida, like Aspergillus, like Clapsilla, right? Those people can get very severe infections. Pichens that have a chronic agronolomatosa disease. Now, so back to Ashpio, right? So if you're talking about the gram positive coxite, right? Your circles, right? You can say, okay, the catalyst positive or negative, right? If you say the catalyst positive, that means you're dealing with staphorius, right? You're dealing with staphorius. I mean, you're dealing with staph species in general, right? And then if you say, okay, let's break down the staph species. Let's make a more granular representation, right? Because there are multiple staph species. There's like staphorius, there's staph epidermidis, there is staph staphophidicus. Staphorius has the added property of being coagulese positive. You may see divine, cares about coagulese. Why do any coagulese? Well, the thing is coagulese. It actually binds to factor two.

So like thrombin, it sort of forms a complex with it. And then you learn about that when you study him on, I'll talk about that when I do the himonca podcast. But basically, coagulese, right? He binds to thrombin and basically converts fibrenogen to fibrin, right? That complex that it forms with thrombin converts fibrenogen, which is factor one to fibrin, right? Which is the activated form of factor one. And by having that fibrin around the staphorius, it basically sort of hides it from the immune system. It makes it very difficult for your immune systems to gain immune system to gain access to the bug. So staphorius is catalyst positive and coagulese positive, right? So what are some high yield things you want to know for your exam with regards to staphorius? One high yield thing you want to know is that staphorius has something known as protein A, right? And that protein A is kind of high yield in the sense that it is very good at binding to the constant region of IgG. And when it binds to that constant region of IgG, you cannot have phagocyteosis, right? Because remember, that constant region is usually bound by the phagocytic cell like a macrophage or something that then goes up and gobbles up that the organism that has been bound by the variable region, right? So if you have protein A, you bind to that constant region of IgG, you're basically preventing phagocytosis in a sense. Now, if other high yield things you want to know about staphorius, right?

So staphorius can cause a lot of problems, right? So it can cause certain skin infections. The classic one is a impetigo, right? So impetigo, the classic presentation on exams will be like the, it'll be like an infection on the face, usually in kids on exams. And you see like those are honey, color, cross-edulations. Right? If you ever see that, think about impetigo. And impetigo is classically caused by staphorius. Yes, I know some of you may say, oh, come on, divine. In petigo can also be caused by a group A strep, right? So strep pyogenes. That is true, but on exams, if you're presented with both possibilities, go with staphorius. Staphorius is probably a more common cause of impetigo compared with group A strep. Contrast that with airsipulas, right? So airsipulas, they are not the honey, color, cross-edged business that you find with impetigo. Airsipulas are more like very painful, acute onset, red lesions, they are very well demarcated, and they are usually elevated relative to the surrounding skin. Those can be caused by staphorius and group A strep, but on exams, if you're presented with both possibilities, go with group A strep. Okay, group A strep more common on exams causes airsipulas. So what are some other high-ealth things about staphorius? So staphorius can cause, it can produce a super antige, right? The classic one on exam is on exams is a TSS-T1, right? So you may say, oh, divide what you're throwing out all these immunology terms, right?

So what is a super antigen? The thing is basically a super antigen is something that sort of binds to MHC2 and a specific portion of the TSS receptor, it's called the V-beta region. So you bind those two things and non-specifically it causes like a massive, massive, massive release of cytokines. When you release all those cytokines, well, guess what? You're going to shock, right? So like your liver enzymes will go up, the patient will be profoundly hypotensive and all that stuff is a bad situation, right? So in general, staphorius can cause that also strep pyogenes, can also cause a toxic shock syndrome. And the classic way toxic shock syndrome will present on exams, they'll talk about a lady, right? That has been having a period and then she has had tampons inserted for like a long period of time, or it can be a person that had like, you know, like very bad nasal infection, bleeding from their nose and then they've been using like a lot of like nasal packing. You sort of like grow staphorius in those areas and then you make those super antigenes and then you get into trouble. And then staphorius, right? Classically, classically. In fact, I will say it's very high you to know this. Staphorius is the most common cause, very high you know, it's the most common cause of acute endocraditis, right? Acute endocraditis. And I mean, the classic patient, population there are the IV drug users, right?

And I mean, like what valve would if you were to hazard a guest like, oh, what's the valve? They'll be affected by staphorius, right? On an exam, right? I hope you're thinking about the tricospid valve, right? Remember the tricospid valve is between the righty trim and the right ventricle. And you may see it divine. Come on. Why is it another micro valve? Why is it just the tricospid? I mean, obviously staphorius can affect any valve. But think about it if you're an IV, IV drug user, right? Where are you injecting all those IV drugs into into a vein, right? Indravenous, right? And where do veins drink to? Right? Vins drink to the right side of the heart, right? And the right side of the heart is what contains the tricospid valve. So that is why, classically, staphorius tricospid valve endocraditis, okay? Acute endocraditis. Staphorius is the most common cause of acute endocraditis. And the thing is staphorius can damage a valve that is a-okay from the beginning. So you have like a good pristine valve. Staphorius can damage that contrast that with subacute endocraditis where usually you have like some valve problem either you have like a prosthetic valve in place or you have a valve that is already not working very well. That is where you can get into trouble. And subacute endocraditis is most commonly caused by strep viridants. I'll talk about that when we get to the catalyst negative part of this coxia algorithm. So staphorius acute endocraditis, right?

And let's see, what are the other high yield things we should probably know about staphorius? Staphorius can cause osteomyelitis. In fact, it's the most common cause of osteomyelitis, right? Staphorius is the most common cause of osteomyelitis. And then some other things you want to think about, right? If they give you a question, see for example, about a patient, about a person that has really bad watery diarrhea and vomiting, right? And they tell you that all the person recently, they say like two to six hours ago, recently eat like chameleonase or custard or salads that were left out for long, right? Like unrefigeritha just left out in the open. Usually it's at a picnic on exams. Think about staphorius as your fending organism, right? So staphorius can sort of make a certain staphorius can make like a preform toxin, right? That preform toxin actually hits the so you can make a preform toxin sort of settles out in that for you, eat that for you, and then you get into trouble very, very quickly, right? And the thing is, I just said that the most common cause of osteomyelitis is staphorius, right? But what if they give you a question about a patient that has sickle cell disease and they have osteomyelitis? What's the bug you're thinking about? I really, really hope you're not thinking about staphorius. I really hope you're thinking more along the lines of a salmonella, okay? Salmonella is the most common cause of osteomyelitis, especially in the sickle cell population.

Now, other high-ealth things about staphorius, right? So I already said it's caterlase positive, it's caterlase positive, another weird thing I guess you can keep in mind is that it ferment manateau, okay? And it's also a bit of hemolytic, just like a group A and a group B-strep, okay? Just one of those other weird things you sort of want to keep at the back of your mind. And thinking more along the lines of step one, the thing is staphorius is actually the most common cause of pneumonia, in patients with cystic fibrosis up until the age of 18. You see, divine. Everywhere I've heard it's like, oh, most common cause of pneumonia, cystic fibrosis patients is pseudomona, that is not true. The most common cause, this is very high out for example, the most common cause of pneumonia, in cystic fibrosis patients, prior to the age of 18, staphorius. But past the age of 18, it then becomes pseudomonas, right? And then one of the bulk, I guess you may hear of one example, that may cause a pneumonia in cystic fibrosis patients is a bognon as a bocodaria, B-U-R-K, H-O-L-D, E-R-I-E, bocodaria, sepicia. It's also a really, it's a less common cause of pneumonia in CF patients, compared with staphorius and pseudomonas. So again, those are weird things you want to keep at the back of your mind, right?

And then don't forget that you can also, there's this exfoliative toxin that is made by staphorius that can also cause something called like the triple S syndrome, if you may, a scalded skin syndrome. Now, how do we treat staph, right? So the thinnest staph on your exam, you probably want to keep certain things at the back of your mind, right? So the thinnest staph, there's MSSE, well see the two big groups you want to know, you exams, there's MSSE, and there's MRSE, right? So MSSE stands for methecylene sensitive staphorius, and then MRSE stands for methecylene resistant staphorius. The thinnest to avoid jumbling things together, I'll talk about the antibiotics at the end, but I'll just tell you in general, right? If you want to cover MSSE, you want to use drugs like naphthalene or oxacilene or dichloxacilene, don't choose methecylene on your exam. So no one uses methecylene anymore because it causes something called acute interstitial nephritis, something you will learn about in an immunology block or in a reno block. So learn about in an immunology block because that is one cause of eosynophilia, right? So classically right here IN will present that's like, patient that has like a fever, recently they will recently have started some kind of antibiotic, they may have started like oxacilene for like mastitis, for example. Actually, I guess I'll just throw this in there, staphorius is the most common cause of mastitis. Mastitis is just a breast infection.

So they probably just took like oxacilene or dichloxacilene for mastitis and then the study having high fever and then you have like a rash and then you find like elevated levels of eosynophiles in their blood and in their urine. If you see that, think about acute interstitial nephritis, that's a classic side effect associated with anti-staph locococon penicillins, especially the ones that are the MSSA covering penicillins, right? So again like naphthalene, dichloxacilene and oxacilene. Those drugs, classic leonic exams, they were trying to trick you by saying, oh, what is the like naphthalene, for example, is it how can a person go from MSSA to MRRC? So what's like the mechanism of resistance that basically makes staphorius methecylene resistant? The thing is, it is very high you to know that it is an alteration in the penicillin binding protein. And again, I will see more things about this down the line. But basically you have an altered structure of transpeptidys, that is what makes staphorius MRSA, not MSSA. And it's very high you to know that the MSSA covering medications like naphthalene, oxacilene and whatnot, they actually resistant to beta lactamase. So those drugs are not broken down by beta lactamase, very high you to know that for exams. And then if you talk about MRSA, right, you want to know the drugs that cover MRSA, right? So classically you want to know drugs like vancomycin, vancomycin covers MRSA.

Tigacycline, Tigacycline is a kind of, it's a kind of tetracycline, but it's like a super new, very advanced tetracycline. In fact, it belongs to a drug class known as the glycicycline. Those are very good at covering MRSA. There is a syphilosporing, a fifth-generation syphilosporing, known as septaroline. It's very good at covering MRSA. There is a drug known as a naphthalmysin. Naphthalmysin is one of those weird drugs that sort of inserts holes in the, in the walls of bacteria, a gram positives to be more specific. I'm naphthalmysin covers MRSA. Linesolid, Linesolid is a 50s inhibitor. It's a bacterostatic 50s inhibitor. It's also very good at covering MRSA, and also I guess a vancomycin resistant enterococcus. And then there is one other drug I'm forgetting right now, vancomycin, obviously, right, covers MRSA. Okay, so I think that's all I'm going to say about the stuff, or yes, if we're sort of jumping to the other stuff species, right, so we have like stuff epidermidus, right, stuff epidermidus. The big thing I want to know about it, for exams, is that if a patient has like plastic, right, so say like, I don't know, like, let's see, they have like a prosthetic valve or a fully catheter, and let's say they have like a UTI from a fully catheter, or they have like prosthetic valve in Ducraditis. Think about stuff epidermidus.

Stuff epidermidus, it's actually a normal part of your skin flora, but it's a fairly common contaminant in blood cultures, right, so if you grow stuff epidermidus from blood, it's probably a contaminant. And stuff epidermidus, one test that you could use to identify it is that it is a novel biosena sensitive. That's just one weird thing you want to know about stuff epidermidus. And the reason stuff epidermidus loves plastic is because it makes kind of like a lusy-gusy capsule. The boss phrase you want to know for example is a biofilm, right, so because it makes that biofilm it sticks to plastic really well, right, and because it sticks to plastic really well, it's just very hard to get, it just loves, loves, loves, loves, loves plastic, right, so that's why it can cause infections, especially when a person has like plastic somewhere in their bodies. Now, contrast stuff epidermidus with stuff sub-profiticus. Staphs-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s staphs-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s-s for some bizarre reason, Yuri's producing organisms are high yield to know for many exams, especially step one, right?

So, steps that prophetic us is your responsive, and other classic one, probably the highest yield of them all is a H by Laurie, right? H by Laurie's your responsive, that's why you can sort of survive in the acidic environment of the stomach. Another high yield one is your plasma, your elitica, that one also causes UT Is, and then another weird one is produce, produce merabilis, produce, it causes a lot of UT Is, right? And especially if a person has a UTI, and the urine has like a super high pH, think about produce merabilis, classically, it's that thing that grows with a swarming motility on E-GAR, it's just one of those weird things you want to keep at the back of your mind. So, I think that is all I'm going to say about the staff species, so I'm going to go down the strep pathway, the strep pathway. So, for the strep pathway, right? So, all strep species are cut at least negative, right? So, the next thing you want to be next is to want to order his ball, what's the hemolytic pattern, right? So, it's the alpha hemolysis, it's a beta hemolysis, it's a gamma hemolysis, right? So, the thing is, let's start with the alpha hemolytic strep, again, I'm just again looking at this first table of grand positives, and I'm just again literally like I said, I'm just going to be reading off the high yield information for each bug on the algorithm, so you can sort of listen to this podcast as like a very quick rapid review before an exam.

So, if we're talking about alpha hemolysis, right? So, alpha hemolysis is basically partial hemolysis, and that partial hemolysis refers to blood eager, right? So, like, you're partially hemolyzing blood eager, that is what a scribe's strep species is being alpha hemolytic. And the thing is, under the alpha hemolytic streps, there's two big ones you want to know, right? So, you want to know strep viridense and strep pneumo, right? So, strep pneumo and strep viridense. Now, there's this test, right? Actually, I guess, well, we're on this topic. Let's sort of talk about key differences between strep viridense and strep pneumo, right? So, the thing is between these two, it's very high yield to know that strep pneumo has a capsule, right? And the thing is strep pneumo, right? So, this is why strep pneumo is not a big constituent of your GI floor, right? The thing is strep pneumo is especially basically excluded by bile, right? So, it's soluble in bile, it does not grow in bile, okay? And then, optochin, strep pneumo is also sensitive to optochin. That's very low yield test, really if ever shows upon exams, but I'll just throw that in there, just for completeness sake. But the big thing you want to know about strep pneumo is, it is soluble in bile, so you cannot grow in bile and it has a capsule, right? Contrast that with strep viridense, strep viridense can grow very nicely in bile, okay? Strep viridense actually has no capsule, first of strep pneumo that actually has a capsule.

And strep viridense is resistant to is resistant to optochin. And I guess since I'm making this big fuss about capsules, right, it's very high yield to know the organisms that are in capsule, right? So, let me try to introduce these organisms with veneants, right? So, let's assume you get a question about a patient that has pneumonia and that pneumonia contains rust-colored sputum, right? I hope you're thinking about strep pneumo, strep pneumo is in capsule, what if you get a question about a patient that recently came back from Mexico, right? And they have very bad, bad, bad, like 3, 4 days, watery diarrhea. I hope you're thinking about travelers diarrhea, right? It's caused by e-tech and terotoxygenic e-coli. Another name for that is like Montezuma's revenge, right? That's e-coli, e-tech, right? E-tech. Remember, it has two toxins, right? It has like the heat stable toxin that activates a cyclic GMP and a heat libal toxin that activates a cyclic GMP. There's like a pneumonia, libal has the air, stable has the ground, bloody, bloody, blood. Like, would you remember that? But basically, e-tech, right? Like, olicolized species has a capsule. What if you get a question about a patient that has a pneumonia and their spudum is corangelli, like? If you see that, I hope you're thinking about Klepsiela, pneumonia, classically, that's an alcoholics. Klepsiela species are also encapsulated. Remember, another high-yield disease causing Klepsiela species is what is it called?

Klepsiela granolomatis. It causes granoloma in Guenali. It's like a pinless ulcer around the genitals. It's not a weird thing to keep in mind, for example. Let me give you another one. What if you get a question about a patient, right? That has like their pinnacle, like the pin of their external ears heard a lot. And let's say they're from California and the swimmer tongue, right? Hopefully, that gets you thinking of pseudomonas. pseudomonas, erudinosa, also produces a capsule. Now, what if you get a question about a college student that has like a 12-hour history of super high fever and no-corrigidity and has a severe headache? Hopefully, you're thinking about my cereal meningitis. Remember, that's a gram negative diplococcus. My cereal meningitis does have a capsule. Please don't confuse that one. My cereal conoria does not have a capsule. My cereal meningitis does. I remember you treat that with a seftraaxle. Let's see. What if you get a question about a patient that has... All right, that... Let's just put it this way. Okay, what if you get a question about a patient and they have a... It's like a kid, like a five-year-old and they have a really bad upper respiratory infection and they sort of try to point in and they're sort of taking like this dog sniffing position in like a dog sniffing position. And then let's assume you do like a like a lateral neck x-ray, right? And you see something known as the... What is it called? The Thump sign.

And let's assume this person has not gotten the vaccine. Let's assume they're like an anti-vaxxer child. Hopefully you're thinking about HFLEU and epiglotitis. HFLEU used to be the most common cause of epiglotitis back in the day when there was no vaccine for it. But now, HFLEU now has a conjugate vaccine. Very high auto-nude. It has a conjugate vaccine. And because of that, in fact, the incidence of epiglotitis has gone down quite significantly just because of that. HFLEU is an encapsulated bug. Let's see. What if you get a question about a child that is 14-dys old and has meningitis, right? Hopefully you're thinking about where we're be strapped, right? Strepic Galactic. Strepic Galactic is another encapsulated organism. Okay, let's sort of get back into things here. But those are the high-yield encapsulated organisms to know, right? So like E. coli, strep pneumoclepsiala, pseudomonas, HFLEU, my serum and angiitis, group B strep. Very high-yield ones to know for tests. And encapsulated for my guest fungus that you probably want to know is, what does it mean? Well, this thing that causes meningitis in its patients, cryptococcus, new formants, right? That's another encapsulated organism. Okay, remember the India-inx thing with that or the Lidex particle like glutination, asi. Okay, back to this. So we're still under the purview of alpha-hemolosis, right? And we're talking about strep pneumons revered, that's right. So let's talk about strep pneumo first.

It's probably the highest yield one to know, for example, right? So we know that strep pneumo, right? It's the most common cause of pneumonia, right? It's the most common cause of sinusitis, it's the most common cause of meningitis, it's the most common cause of otitis media. So initially it was strep pneumo and then it became non-typable heat flu. But last I checked, the most common cause of otitis media these days is it's kind of like a tussle between strep pneumo and more acetylocaduralis, but if I were you on exams, probably go ahead and go with strep pneumo, right? And the classic we'll present on exams is like an erythematos bulging, tympanic membrane in a kid. If you see that, think about a tightness media, right? No. So strep pneumo, right? So we know that strep pneumo, loves, loves, loves to cause an operator infection, right? So you see divine. Why does strep pneumo love to cause operator infection? Well, the thing is it can survive very nicely in your respiratory tract, right? So let's sort of take a step back to immunology to understand why this may be the case, right? So in your immunology course, right? You probably learned about particularly immunoglobulin that has a secretory component that helps sort of protect it against the rough neighborhood of mucosa, but it's like the guardian of your mucosa. What's the immunoglobulin I'm talking about? I hope you're seeing IGA, right?

The thing is if you want to be any kind of north worthy respiratory tract bug, you need to have something that can destroy that IGA, so that you can sort of leave free in the respiratory tract. And the thing that destroys that IGA is easier and often known as IGA proteins. IGA proteins is made by strep pneumo and it helps it destroy IGA. Another high you thing you want to know about strep, I guess another bug you want to know that actually has that IGA proteins is also my serum and ingested, it's nice serum and ingested is remember it's actually the route of spread is through like respiratory droplets. It actually does have IGA proteins as well. And as far as I know, H Flu also has IGA proteins and just please, this misconception that many people get wrong on the exams for some reason, H Flu does not cause the flu, okay? The flu is caused by the influenza virus, okay? H Flu does not cause the flu. H Flu, like I said, commonly causes like otitis media, what you can also, especially the non-type of food form. And there's a particular H Flu species that can also cause general infections, like painful ulcers in the genitals, hemophlos ducry. I think there's like a nice and funny for that that hemophlos ducry makes you cry. To help you remember that it causes a painful ulcers on the genitals. So back to the real world, right? So strep pneumo, right? So strep pneumo has IGA proteins, right? And again, it's kind of least negative, right?

So if you have CGD, you will not have issues with strep pneumo. But some other high-yield things you want to know about strep pneumo, right? So strep pneumo, it can cause a lot of problems in people that don't have splints. So guess what? Who are the people that don't have splints on exams? Those are patients with sickle cells. Remember, those sickle cells can basically like kill their splints from like auto-infarction of their splints. So strep pneumo can cause like very bad sepsis in patients with sickle cell disease. In fact, if a patient has sickle cell disease, you'll classically have to place them on like penicillin perphylaxis for like the first five or seven years of life so that they don't get into trouble, okay? Now, strep pneumo, right? Like I said, it's breath through respiratory droplets and it's the most common cause of pneumonia, right? So it causes like a low bar pneumonia. So if you see like consolidation, chest x-ray, think about strep pneumo versus the more etypical causes of pneumonia like mycoplasma or chlamydia or legionella, those tend to cause more along the lines of intestinal pneumonia, those intestinal pneumonia, you tend to have like more like intestinal spread on chest x-ray versus like a low bar consolidation. And again, strep pneumo has a capsule, right? So again, if you don't have a spleen, you have a lot of trouble dealing with encapsulated organisms.

So I can envision a very good USML step one question where they basically describe a person that has, let's see, basically describe a person, he's from sickle cell disease, they see they have like a very severe infection, and then they give you a list of bugs as answer choices as like the potential causes of that infection. And there'll be one encapsulated bug and there'll be like five or six unincapsulated bugs, right? So that's why you want to know the bugs that encapsulate it, for example. And strep pneumo, right? Causes pneumonia classically with the rust color, with the rust color, the speedum, right? And the thing is, if you get a question about a patient that has strep pneumo, and they have meningitis as a result of that, just for purposes of the future, especially for step one, in addition to treating those people with antibiotics, you need to add steroids, right? Because strep pneumo meningitis can ultimately cause hearing loss and just some other like just bad, bad, bad problems. So you want to sort of give steroids to decrease the inflammation, really helps if a person has a strep pneumo meningitis. And again, because strep pneumo has a capsule, right? There is a particular test you may be able to use to detect encapsulated organisms like strep pneumo. Well, I hope you're thinking about the quellon reaction. The quellon reaction is a very nice test to detect encapsulated organisms. So, during the real world, no one really does that anymore.

And in general, how do you treat strep pneumo? You can give like a sephalosporine, like seph traaxone. You generally do not give like straight-up penicillin for strep pneumo, because there's almost like a hundred percent resistance these days. If it's so tight this media, you want to give your amino penicillins, right? So like a moxicillin, or you can give a moxicillin combined with clavolanic acid, right? So like augmentin. I'll talk about those as we proceed to as we proceed down the line with antibiotics, although I already described these in like excursiating detail in my antibiotic podcasts. So, what else I want to say about strep pneumo? They're actually vaccines to strep pneumo, and they're kind of high, you'll to know for example, right? So, there's like the PCV13, and then there is the PPSV23, right? So, the thing is the PCV13 vaccine is the one you usually give to like kids, right? And it's actually a conjugate vaccine, kind of like the hemofluos influenza type B vaccine. The PCV13, it's a conjugate vaccine, it's usually conjugated to like the the deuteria toxoid, okay? And it's a pretty good vaccine. Contrast it with the PPSV23. So, this one contains like 23 capsula, like serotypes, and this one is usually given to adults, right? So like adults over the age of 65. And classically, right? If you're a person that has chronic disease like AIDS, like HIV, or you have diabetes, or you have kidney disease, that makes your candidate for strep pneumo vaccination.

So, just again, where things you want to keep at the back of your mind with strep pneumo? And let's see, I think that's all I'm going to say about strep pneumo. Now, let's jump to strep veridense. So, strep veridense, the big bugs you want to know here, there's like strep mites, there's strep mutants, there's unknown as a strep sanguineus. I remember I said earlier on, right? That your veridense strep docoxy, they are optochin resistant, and you can grow in bile, okay? But they don't have capsules. And remember, the most common cause very high yield is the most common cause of subacurian ducarditis, right? And the thing is in general, you only get strep veridense in ducarditis. If you have like a damaged valve, if you have like a damaged heart valve, we have like a prosthetic valve, right? You can get problems with strep veridense. Usually if you have like a completely normal valve, you usually don't get endocarditis from strep veridense with that. The only thing that can torch a normal valve is a staph orius. And the thing is strep veridense, right? So classically, the will present on exams is a patient that has like endocarditis after like a recent dental procedure, right? The reasoning, excuse me, say why does strep veridense have this big association with oral cavity? The reasoning is that kind of like staph epidermitis, strep veridense makes it so biofilm, classically on exams, that biofilm, the bus-freeze is like dextran.

So that dextran binds very well to teeth, right? So that's why if you have like a dental procedure, you can get into trouble with strep veridense endocarditis. So usually if a person has like a bad heart valve, and the about to get a dental procedure like a root canal or whatever, and usually place them on some kind of prophylactic antibiotic so that they don't get endocarditis from strep veridense. And to be honest, I think that's all I'm going to say about strep veridense. So let's go ahead and jump to the beta-hemolitic strep topoccus. Real quick, just as a review, is there any other beta-hemolitic bug already talked about? I hope you're telling me staph orius. Remember staph orius is beta-hemolitic. So the beta-hemolitic strep topoccus, right? So these ones are easy, group A strep and group B strep. Let's talk about the easy one first, group B strep, right? So group B strep topoccus. Now group B strep topoccus, right? It's beta-hemolitic, so you have like complete hemolysis on blood eager. And there is this thin, this antibiotic known as basitricin. group B strep or strep Egalacty is resistant to basitricin. Basitricin does not destroy group B strep. And then there is this thin, this enzyme that is expressed by certain strep species. It's known as PYR. I think the phoneme is like pyrolydenial arylamides. Pyrolydenial arylamides is not expressed by group B strep, okay? So contrast is with group B strep. group B strep is actually sensitive to basitricin.

So the antibiotic basitricin destroys group A strep. And then group B strep is actually positive for this pyrolydenial arylamides enzyme, okay? It's just one of those weird things to keep at the back of your mind. And then what are the higher things you want to know about group B strep, right? So group B strep can cause a lot of problems in neonates. In fact, here's what I will tell you. If you get an example question that details a neonate, right? So by neonate, I mean the first 20 days of life, if you get a question about a neonate that has any kind of like major infection like sepsis or meningitis or pneumonia or anything of that sort, you really want to think about group B strep, strepigalactia as the incitin bug, okay? Basically, group B strep is what you need to protect against in the first 20 days of life. Most common cause meningitis, first 20 days of life group B strep, easy question. Actually, another question I have for you, what is the second most common cause of meningitis in the neonatal period? I hope you're seeing equal, I remember that's a gram negative. Another question for you, what is the third most common cause of meningitis in the neonatal period? I hope you're thinking about Listeria, right? So the numonic to remember those is gel G-E-L. So group B strep is the G, equalize the E, and Listeria is the L. Those are the top three most common causes of meningitis in that order.

So group B strep number one, equalize number two, Listeria number three, in the neonatal period. And then there are some other weird tests you may see on exams for group B strep like the ability to hydrolyze, hepirate, that's a property of group B strep. And then there is this test known as the Cump test. Please don't think of Cump as a cyclic AMP. It's just like a weird name that deals with like the blue that sort of meet up the test. But basically the Cump test, it's like it's a test where remember I said that Staphoreus is better at him, or let it correct. The thing is you can essentially increase the area of himolysis surrounding Staphoreus if group B strep is around. And the reasoning behind that is the Cump test, it takes like something called a Cump factor. That Cump factor, I sort of think of it as like a co-factor for Sphingo Mylinis. Sphingo Mylinis is the thing that's expressed by Staphoreus that helps it with that better hemolytic process. So the Cump factor that's expressed by group B strep is kind of like a co-factor for that Sphingo Mylinis. So it increases the area of hemolysis around Staphoreus. And again group B strep, your little period, bad, bad infections, that's why usually if you're between like 35 to 37 weeks as a female, where you see your OB-GYN doctor, they sort of do a swab of your vagina to see if your group B strep positive if you are, they put you on like a penicillin, like a picellin or a moxacillin, right?

Because the classic means of transmission is the vagina, right? The vagina is how group B strep is transmitted from like moms to to neonates. Remember that group B strep is encapsulated, I already mentioned that, I already mentioned that earlier. And yeah, I think that's all I'm going to say about I'm going to say about group B strep. So now let's talk about group A strep, right? So group A strep is strep pyogenes, right? So strep pyogenes, again, super high-yield moxanol about. Don't say, many people make this mistake on the example, right? So group B strep is beta hemolytic. So many people say, oh, if group B strep is beta hemolytic, that means group A strep is alpha hemolytic. No, no, no, no, no, no, no, that is not a good, it's not a good knowledge transfer. Don't make for examples. Group B strep is beta hemolytic. Group A strep is alpha hemolytic, okay? So again, so I just said the wrong thing, I'm sorry. Group B strep is beta hemolytic. Group A strep pyogenes is also beta hemolytic, okay? Very, very, very high-yield. To know that for example. Now group B strep is a mega high-yield box to lower test rate. So it's beta hemolytic, already talked about it being basitricin sensitive and being positive for that pyrolidonyl arylamidesinzyme, right? And the thing is group B strep. Classically you get it through like respiratory droplets, right? You can also get it through direct contact, I guess, at all limits, that extent.

Now, there are many high-yield things you want to know about group B strep, right? So group B strep makes certain toxins, right? So it makes like strep to lysine O, right? Strep to lysine O is oxygenal libel. Strep to lysine S is oxygen stable, right? Those are two high-yield toxins made by group B strep. Now, it is very high-yield to know that of those two if you're comparing ESO, so I mean if you're comparing strep to lysine O to strep to lysine S, I say that strep to lysine O is oxygen libel, strep to lysine S is oxygen stable. And it's also high-yield to know that between those two it is strep to lysine O that is immunogenic so you can make antibodies against strep to lysine O. That's why you can measure things like ESO titers in the setting of romantic fever. It's very high-yield to know that strep to lysine S is not immunogenic, okay? It's just one of those bizarre things that you see on exams and like 99% of people get wrong. There's no something as an ASS-TITER, okay? It's ESO titers. Strep to lysine O is the only immunogenic thing in that bunch, right? Now, what are high-yield things that group B strep makes, right? So it makes like a higher-yielding these, basically that sort of cost-thro collagen and like ground substance that surrounds a connective tissue. And then there's like M protein. The M protein actually prevents a phagocyteosis.

The thing is there are actually some, that M protein is kind of unique in the sense that it's actually used by certain like microbiologists to predict the person's risk of getting something called a glomerulone fritis. I'll talk about that in a bit. But basically the M protein is anti-phagocytic, but there are certain M proteins, there are certain group A strep organisms, right? That makes certain M proteins and those M proteins as they're higher than no more risk of posting factors or post-striptococcal or glomerulone fritis. Especially like if you want to memorize one, for example, like the M12, the M12, like basically any group A strep that makes the M12 strain of the M protein, high, high, high strong association with glomerulone fritis. Now, group A strep can also make like a pyrogenic toxin that can cause like a scarlet fever. Right? So scarlet fever, right? Usually they'll have like a sun-piper rash on their trunk, right? And those kids could also have like a strawberry tongue and it is floridly high yield to know that on exams. The rash of scarlet fever spares the palms and soaps. Okay? The rash of scarlet fever spares the palms and soaps. If you see a rash on the palms and soaps on exams, right? You want to think about some other bugs instead of group A strep. You want to think about things like the coxacchi e-virus, right? So causes a rash and I mean that's why it's called like hand-foot-mouth disease, right?

So coxacchi e-virus, ricketsia, ricketsia, that causes a rocky mountain-spotted fever. And then syphilis, right? Like secondary syphilis is associated with a rash that affects the palms and soaps. And then there is this rheumatologic disease. It's a vasculitis. Kawasaki's disease is also associated with the rash on the palms and soaps. In fact, there's this numaniq me here that you drive a Kawasaki cars with your hands and feet to remember situations where you can have a rash that involves the palms and soaps, right? So the Kawasaki cars, Kawasaki is for Kawasaki's disease. And then the cars, the CA is for coxacchi e-virus. And then the R is for ricketsia, ricketsia, and then the S is for secondary syphilis. Let's just want again, those rare things you want to keep at the back of your mind for, for example. And remember, replace strap. It can cause carlet fever. It makes super antigens, right? So again, they'll bind to the T cell receptor and MHC class too. And then cause like a non-specific release of cytokines that can put a patient in trouble. I mean, the mortality days are super, super high. Remember, replace strap, right? Can cause a strap throat, right? So like fire angitis. It's like you see like a just whiteish badness in the back of the throat. It can cause some air sypulas.

Air sypulas are classically, remember I told you that classically air sypulas are caused by group e-strip versus in petago that is classically caused by by staph-porias, especially like bullos in petago that's classically caused by staph-porias. Now, other high-yield things you want to know about group e-strip, right? So the thing is, group e-strip can be associated with something known as a first thing's first. I said strap throat. One weird thing I want to keep at the back of your mind with strap throat is that there's certain criteria, they're known as the center criteria. You can actually use those clinical decision tools to sort of determine who has group e-strip or who has a high probability of group e-strip infection versus a person that has a lower probability of group e-strip infection. So the big disease I want to talk about is rheumatic fever. Right? So rheumatic fever, basically it's like a body infection that can happen with a group e-strip, right? Usually it will affect like a heart valve, classically it affects like the mytro valve, and then it can cause other problems, right? So it can cause like fevers, it can cause like jumping, it can cause like a myocarditis, it can cause like an endocarditis, it can cause like a rash, like a red rash on the skin, it's called like a arithema marginatum, it can cause, it can cause just many problems, it can cause like a query form movement.

In fact, it's called like Sidenham's Korea, that's a classic thing that's a rheumatic fever. In fact, there are some criteria, they're known as like the Jones criteria for rheumatic fever, and the thing is rheumatic fever can only arise after a strep pyogenes, upper respiratory infection. If you have a strep pyogeneskin infection, you cannot get rheumatic fever after that. Contrast this with post-infectious or post-striptococcal glomerulone fritis. You can actually get this after strep pyroinjitis or like a strep, like upper respiratory infection or strep skin infection, you can get it after any of those. Versus rheumatic fever that you can only get after strep pyogenes, upper respiratory infection. And then another thing to know is that given antibiotics actually decreases the incidence of rheumatic fever after a strep, upper respiratory infection, but given antibiotics actually does not decrease the incidence of post-striptococcal glomerulone fritis. After, yeah, after like a strep upper respiratory infection, and remember that again, if you want to sort of bring some immunology times here, remember that rheumatic fever. So that arises in the setting of molecular mimicry. I'm just like a classic cell physiology boss phrase to remember for USMELIS. Usually rheumatic fever is an example of a type 2 hypersensitivity reaction. You sort of want to be able to contrast that with post-striptococcal glomerulone fritis that is more of a type 3 hypersensitivity reaction.

So it arises from the position of immunocomplexes. And, classically, on USMELIS, you'll be like two to six weeks after an upper respiratory infection. You see a kid with T-colored, or T-or-coccal colored urine. Think about a post-infectious glomerulone fritis. And I guess just to sort of help you out here. There's some of these Latin words that sort of sound very similar. And then they screw people up on exams. So I just said that erythema margenadum is a classic finding in rheumatic fever. Please do not confuse erythema margenadum with erythema chronicom migrates. Erythema chronicom migrates is something that is observed with Lyme disease. Remember Lyme disease caused by a bornea, bocdofree and carried by the x-edistic. And then another Latin sounding word that sort of message people of is ectema gangrenosum. So EC, THYMA and then gangrenosum. That's classically caused by pseudomonas eryginosa. That's like where you have like a black escar. Caused by pseudomonas. Again, remember, pseudomonas is not the only thing that causes black escar. Basilos and thresus can also cause a black escar. So again, just weird things you want to keep at the back of your mind. If you like I've said a lot of stuff about group A strap. So let's go ahead and move to gamma hemolysis. So gamma hemolytic strap. These ones are lower here for exams. Much fewer things to know about each. Again, like this first leaf page says that the anterior coccus species are growing 6.5% sodium chloride.

And again, the anterior coccus species are positive for that pyrolydenial arylamides enzyme versus your non-interococcus gamma hemolytic strap that cannot grow in 6.5% sodium chloride. And they are not positive for that pyro enzyme. The big things I'll just see here is that anterior coccus species. The big things you want to know is if a person has like endocraditis and they have like a recent like they have like a recent like GI. So like a gastrointestinal or like genitorial urinary procedure and they have endocraditis. Think about interococcus species as the inciting agents. And the thing is interococcus in general, right? You can have like vancomycin resistant interococcal bugs. VRE you'll definitely want to know for example that those are covered by lignisolid. Remember, lignisolid is a bacterostatic 50s inhibitor. And then strep bovis is like a non-interococcal gamma hemolytic strap. Remember gamma hemolysis just basically means no hemolysis. So the big thing you want to know about strep bovis is that if you find in a person's blood you need to work that patient for colon cancer. Because like 20 to 30% of patients that have strep bovis in their blood actually end up having colon cancer. So again one of those bizarre things at the back of your mind you want to know for tests. So now that we've talked about that strep and stuff and all that and again you may see you divine well. Spent a lot of time. This podcast should hopefully be over in the next few minutes.

But let me just see some quick things about the other grand positives and then that'll be it. So and I guess I may actually not have that time to talk about the antibiotics in this podcast. Just go back and listen if you just scroll on my website, divineinterventionpodcast.com. I have podcasts that are dedicated to the antibiotics. So I think you can get like a very full discussion with those. If I maybe have like three minutes at the end of this podcast I can just see like high old things about every other like big like the cell wall synthesis inhibitors and protein synthesis inhibitors but I probably will not because I mean this is I'm already at almost 50 minutes right now. Okay so let's go to the basil. So we've talked about the coxine. So let's go to the basil. So basically like the upper part of this is a grand positive algorithm. So the basil line. So these are your rods. Your grand positive rods easy way to divide those things up is the aerobic or the an aerobic right aerobic or an aerobic. So let's talk about those that are aerobic first right. So let's see how do I how do I give these things up. In fact you know what let me I think to make this easy. I will see some high old identification things related to these grand positive rods. Then I'll talk about each each of them one by one right. So first thing you probably want to keep in mind with these grand positive rods are which ones make spores right.

The ones that make spores just remember your B and C in the alphabet right. So like your bacillus species and your close tridium species. Those are spore formats. Remember bacillus species are aerobic your close tridium species are an aerobic. Okay it's just again one of those things you want to keep at the back of your mind. And then just real quick one of the high old spore forming organism you want to know for examples is a coxelia coxielaboneriae it causes some q fever. It's another spore forming organism. And I said that again your bacillus species are aerobic your posterior species are also aerobic your corainy bacterium species right. So the bugs that cause the dystheiria they are also aerobic no cardio. No cardio. Remember it's like weekly acid fast it is also aerobic and your micro bacterium species right. So like TB basically is also aerobic. And then the high old ones here that make exotoxin that you want to keep at the back of your mind right. So like obviously your bacillus species with like bacillus and threesis and all that stuff those are make exotoxin. Remember grand positives make exotoxin right. So like your bacillus species your close tridium species right. So like tetanus pasmin. So like the tetanus toxin and all that stuff. Those are all exotoxin. Listeria right. Listeria does make exotoxin. Remember I love to grow in the cold. And then your corainy bacterium right.

Your corainy bacterium like the theory the the the theory of toxin about the the the the theory of causing bug also makes the exotoxin. Remember like the exotoxin A that causes an adp ribosylation. It's like a pros-translational modification of elongation factor two. And then the ones that are like facultative intercellular that you want to know. Listeria is a big big big big one. You want to keep in mind for exams. Your micro bacterium species actually facultative intercellular as well. And then like the big big one you want to know that is acid fast right. In case you can see it's like partially acid fast is no cardio. For the purposes of micro there are three organisms in general that are acid fast that you want to know for tests. The first one is no cardio. Especially acid fast it's an aerob. The second one are your micro bacterial species. Remember the acid fasting is like the zel-nelson stain. Your micro bacterial species like leprosy or TB those are all acid fast. And then when you get to the purview of the parasites especially like AIDS think about water diarrhea in an eat-specient that's like cryptosporidium, cryptosporidium, parvin. That's another acid fast organism you want to keep in mind for exams. And then I guess if you're talking about like branching rods you want to think about like your acetinomyces and nocardia. Remember acetinomyces is not acet fast and it's an anerobe. Nocardia is partially acet fast and it's an aerobe. In fact you know what?

Let me give you a nice no-monic. Think of it as devine ABC no-monic for bugs that are anaerobic. Okay? So the A, think of A for anaerobic or A for acetinomyces. And then think of the B as standing for bacterial disease like bacterial disease fragilis. And then think of the C as standing for clostridium. Okay? Those are your anaerobic bugs. How you're anaerobic bugs for exams. So let's just go ahead and talk about the bacillus species first. So the two big bacillus species you want to know for exams. There's a bacillus and threesis. And then there's bacillus serious. So B serious. So bacillus and threesis. So what are the high-of-things you want to know about bacillus and threesis? You want to know that again the sport formula is it's it's an aerobe, right? And remember that it can cause like a classic disease such as a post-ohm worker or like an FBI agent or like a patient that's sort of a person that sort of handles animals like animal hide. If that's why it's called like whoresorters disease. Think about bacillus and threesis with that. And bacillus and threesis, right? The capsule is actually kind of unique, right? Because you remember I don't know if I said this earlier, but most capsules. In fact, I'll see pretty much every capsule of bacteria is made up from polysaccharides. But for bacillus and threesis it's very different actually. bacillus and threesis, it's capsule is made of polypeptide, made of like protein. I think it's known as like polyglutamide. Okay?

So you're just one of those again where things you want to keep at the back of your mind because it's unique. And the thing is when you inhale the spores, right? So you have like contact with like infected animals. That's how you can get bacillus and threesis. Now, the thing is bacillus and threesis, the key things you want to know are that it can cause like a black escar on the skin. It can also cause like a hemorrhagic pulmonary infection. In fact, classically on exams, they mean talk about like a post-au worker and the CD do a chest x-ray and you see like a wide incline, and the patient has been like coughing or blood. Think about hemorrhagic mediasthenitis, classically caused by a bacillus and threesis. And I mean, you want to know the toxins, right? That are associated with bacillus and threesis. There's three of them, right? So one is known as edema factor. Edema factor is actually like a legit adenylid cyclase. So it increases your levels of cyclic AMP. The other one is known as a little factor in a sort of self-descriptive, right? Like a little factor, little factor. I mean, it's not a good sounding imadol. So little factor literally is little to cells. And then there's something known as protective antigen. It's the third sort of like member of the triad for the bacillus and threesis exotoxins. The protective antigen, I sort of think of it as like a vehicle, like a bus or car, something that sort of brings a dimma factor or lethal factor into like your human cells.

Okay? Anthrox is very, very, very bad. And I mean, how do we treat anthrax? You can give like a fluke and a long like superflexicin or you can give a tetracycline like a doxycycline. Those cover anthrax are very nicely. And there's actually a vaccine, but it's not widely available. It's probably used mostly like in the military because anthrax could potentially be wet one night, right? As for like bioterrorism or something like that. And then the other bacillus species you want to know about is like B-serious, bacillus serious, big, big thing you want to know here again. Sport for me, all that stuff already talked about that. But remember, Chinese fried rice, watery diorama ton of vomiting, think about bacillus serious, right? I mean, the reasoning here is that one of the exotoxins it makes is known as like an emetic toxin. So MSS means vomiting, right? Because there's a lot of vomiting. I mean, actually, I'm pretty sure I've had this problem before. It wasn't Chinese fried rice. We was like fried rice that I cooked at home and then I ate it and then I was just throwing up for a day. So it's then it really sucks B-serious. It's like a self-limiting watery diorama and vomiting but it's pretty bad. It's pretty bad. And it's again, it's from a pre-form toxin. Kind of similar to like this pre-form toxin, the stuff where you're mixed to cause a gastroenteritis. And again, yeah, it can cause the area that there is watery.

And that's pretty much I think all I'll say about bacillus serious. And then I can talk about the Clostridium species. So remember, Clostridium is anaerobic. Remember ABC, it's the C-N-E-B-C, Formsports, it's a rod. And there is actually a bunch of Clostridium species we want to know about for example. So there's like Clostridium Tep 9, there's Clostridium Botolina, there's like Clostridium fringes, the causes, gask and green. And then there is C-Diff, right? Clostridium difficile. Now Clostridium Tep 9, right? It's the classic thing you want to keep in mind for example is like a person having like a puncture wound right from like a nail or something, right? You have that and the person has like spastic paralysis. Think about Tepnus with that. And I mean, this is something that is vaccine preventable, right? So if you take like the T-Dab vaccine or the the D-Tab vaccine, you can prevent Tepnus. So how does the Tepnus toxin work? It's an exotoxin because it's grand positive. The way it works is that it basically binds to like certain receptors on some intern neurons you find in the central nervous system. I don't know it's like ganglocyte receptors. When the toxin binds to those receptors, it basically prevents those internal cells, they're called like rinsals cells. It makes them not release gaban glycine.

Hopefully you know that gaban is the primary neurotransmitter in the primary inhibitory neurotransmitter in the brain versus glycine that is the primary inhibitory neurotransmitter in the spinal cord. So when you bind to those ganglocyte receptors with the Tepnus toxin, you prevent the release of gaban glycine. And if you don't have those inhibitory neurotransmitters, guess what? Your skeletal muscle just keeps firing, keeps firing, keeps firing. So you get a spastic paralysis with that. Key thing you want to keep at the back of your mind is like some boss freezes for like the expressions you may see in individuals that have Tepnus. So you may see the words like RISUS or DONICUS. Just look up pictures of these terms. You'll get the just like RISUS DONICUS. They're like the arched back. I think it's called like opistopherners. They have to just bad bad bad bad spasms. I mean these people usually like you can give them like a benzodiazepine to sort of try to calm them down and relieve their like spastic paralysis. It's a pretty bad pretty bad infection. And really the way you treat this is you give like a Tepnus immune globuline to sort of bind up the toxin. And again you can give like a benzodiazepine to sort of calm relieve like those are release those are spasms. Let me know, obviously you should try to tell these people to you know get vaccinated at some point. So I guess that's all I'll say about Closurium Tepnus. So let's talk about Closurium Botulinus.

So the big things you want to know here again anaerobic right it's form spores. In fact I'm gonna stop repeating like the anaerobic. That's why me that's somewhere at the beginning. But basically this bug it's very high you to know that the method of transmission is different between adults versus kids right especially kids less than a year or it's like infants. The thing is infants do not have a robust TGI flour. So if they consume spores of Closurium Botulinum those spores can germinate in the GI tracks like on a post make toxin and then recover from that infant. Whereas as an adult if an adult consumes Closurium Botulinum spores they won't get any problems because those spores cannot germinate in the rough neighborhood of the robust TGI track of an adult. As an adult you need to consume like a preformed toxin of Closurium Botulinum to get into trouble. And that preformed toxin comes from like home kind veggies versus the spores in infants that comes from like honey. That's why if a kid is less than a year old you should not give them honey that's like a very bad idea. So how does that botulinum toxin work right? So the way the botulinum toxin works is it basically cleans like snare proteins. You probably remember this from like a self-hesiology block like v-snares and t-snares. So you basically do not send vesicles to the membranes of neurons right to release a Masidokolid right. So if you're not releasing a Masidokolid guess what?

Your skeletal muscle is not going to work right because you need a Masidokolid for those things to work right. In fact if they want them to be very evil on an exam they can basically give you a question that talks about other like anticholinergic symptoms you get in the setting of Closurium Botulinum a toxicity right. So you could get things like like tummy upsets right because your GI tract basically grains to a halt. If a classical in kids on exams botulinum presents with um presents with um what I want to see. Classically presents with um with like like abdominal pain right so like tummy upsets and stuff like that. Again I apologize for the omens and ars and pretty much giving this lecture from memory. I'm just looking at the first data chart of our grand positives. I mean if you also have like anticholinergic toxicity or Closurium Botulinum right. Remember that um your birth and pathetic system causes my dry asses so those people could have uh sorry your birth and pathetic system causes meiosis. So these people have like my dry asses right. Your salivary glands are stimulated by your brothers and pathetic nervous system. So if you're not releasing acetylcholine right um you'll have you have like a tongue dryness right. And then these people already will have a flaccid paralysis and the flaccid paralysis is really descending right. So symmetric descending paralysis that may ultimately require like endotrykyl intubation.

Think of that with Closurium Botulinum versus um Guillembris syndrome that emesias an antecedent of um Campylobacter gijunai infection that causes like a symmetric ascending paralysis okay. Symmetric ascending flaccid paralysis. Think about Guillembris syndrome from Campylobacter gijunai versus Closurium Botulinum that you see a symmetric descending flaccid paralysis. And then contrast this with Closuridium tetanide that causes uh spastic paralysis. Flaccid paralysis is Closuridium Botulinum. Okay so I think that is all I should say about um um Closuridium Botulinum. Let's talk about Closuridium perfringing right. Basically the big thing I want to know about this is that it makes a toxin known as alpha toxin. That alpha toxin basically breaks down forceful like BC right. Um in fact sometimes you may see the alpha toxin referred to as elicinics. It basically disrupts acting so your cytoskeleton is gone right. Um and you just get like massive hemolysis so like your riblocells just explode. You get like a lot of tissue destruction um uh causes gas can grimray so they usually should like a nasty looking lower extremity that's like blue with like gas bubbles. Think about those tridium perfringents. And one test you can actually do for Closuridium perfringents is something known as the niggler reactions like N-A-G-L-E-R. It's just one of those things that will show up on step one highly unlikely but if it does show up you'll probably be like the lone person that gets it correct.

And the thing is at the end of the day if you're looking at those two 65 or higher score ranges on the USML Es these low yield details then become high yield. If you're in for like the 250's, probably not a huge issue but stuff like this can sort of put you in those very nice score ranges if you sort of commit them to memory. And then super fringents it can also cause uh you know it can cause like a gastroenteritis it can cause like a watery diarrhea. Um usually results pretty quickly. And then I guess the association you may wonder like define how do people get um super fringents like diarrhea right like if you think of about like a reheated meat like let's say like a person has had like meat in their refrigerator for a long time and then they keep like reheating it and reheating it, reheating it that it can get super fringents with uh with that. And I mean usually you want to debride like tissue extensively if you see guys can grit right uh spread that's pretty bad. I guess one thing I neglected to talk about with group A strep is that uh strep pyroginics can actually cause like a chronic disease. And then we have a lot of different types of um like um uh like um uh strep pyroginics can cause like a chronic disease. And then we have like a one of the most important things that we can do is to make sure that we have a lot of strep pyroginics that we can do is to make sure that we have a lot of strep pyroginics that we can identify.

Identification properties with other close-stream species um you know causes a watery false-melting diarrhea um and classically it's associated with like recent antibiotic exposure right. So the patient has like recent antibiotic exposure and then you have like a watery false-melting diarrhea think about C-diff and the treatment so this is actually one place you want to pay attention before the first line treatment for C-diff was metronideousel that is no longer first like the first line treatment for C-diff these days is vancomycin. Vancomycin is the drug of choice for the treatment of C-diff. If that doesn't work you can give metronideousel okay if that doesn't work you can give this drug is known as a fidaxomycin. Fidaxomycin okay um guess what are some weird things you want not all C-diff you can sort of prevent the transmission of C-diff by hand that's a classic question that shows up on the USM Ls and I guess if you're going some more basic science here um you may wonder divine C-diff like what's the toxin um it's actually like uh two toxins right there's like a toxin A and a toxin B.

The thing is I sort of think of the toxin B as the thing that binds to your cells for C-diff to sort of make its grand entrance and then I think of toxin A as the thin that damages like your G-I mucosa right so classically with C-diff they see that it causes like a pseudo-membranos colitis um and it can actually cause like a toxic mega colon right so if you see like severe abdominal pain and then you get like an abdominal x-ray and you see like like usually on USM Ls they'll show you like the transverse colonia will like super super wide think about a pseudo-membranos colitis I mean think about toxic mega colon those people need to be taking to the operating room pronto if not the die relatively quickly um and again so if you see antibiotic and in a few days after studying antibiotic watery false million diarrhea think about C-diff okay and usually on exams that inciting antibiotic is clean the mice in but the thing is your friends at the MBA me are realizing that everyone has memorized that so clean the mice in is almost never the inciting antibiotic for C-diff anymore so um yeah that's all I'm gonna say about C-diff um Listeria um so I'm known that Plustridial species Listeria big things you want to know have like a tumbling motility um it's like an intracellular bug it's like fuck-ultitively intracellular and it can cause problems especially in moms that consume like daily meats or like on paste rice cheese uh think and then they deliver like a steel-born infant I mean a steel-born kid think about um Listerios uh congenital Listerios is with that in fact there's a there's a think like a Latin term for that I think it's called um granuloma tosis in phanticeptical that's classically classically classically associated with Listeria and remember Listeria is the third most common cause of meningitis in the neonatal period and it is floridae high yield to know that the dr

ug of choice in the treatment of Listeria is ampicillin do not forget that basically like fuse that into your brain forever it's a classic classic classic thing that shows up on exams Listeria and piscillin okay um and again it loves to grow in like cold environments right so that's why like daily meats you'll find Listeria in those a lot and Listeria another high thing to know for example is that it loves to spread from cell to cell um through like they call them like actin rockets if you may um just one of those weird things you want to keep at the back now this is a low yield factoid but it may show up on the usmally this is like a 270 kind of question basically if they give you a question about a patient that recently had like a kidney transplant or let's say it's a patient with like cancer and they have meningitis you really want to think about Listeria as the inciting agent under those circumstances like renal like kidney transplant patients cancer patients with meningitis Listeria is probably the most common cause of meningitis in that patient population again where things you want to keep at the back of your mind for tests now um corany bacteria this is what causes the phtoria remember your corany bacterium species again they are rods right they are eropes and they don't form spores remember spores are bacillus, clostridium and coxialaboneidiate right so corany bacterium species they don't form spores they are eropes these are vaccine preventable so don't be an anti-vaxer it's a terrible idea you just kill your kids for no reason look at what is happening i think in the Washington state or something like that a smart idea just give you kids those vaccines vaccines don't cause autism uh that's a lie that has just been propagated in the world of the world of science and basically cost many kids lives unfortunately um so what are the big things you want to know a

bout uh cdiv theory right so you want to know about its toxin right exotoxin A um basically kills elongation factor two through post-translational modification that post-translational modification is um like a adp ribosylation and remember right it can cause pseudonymembranos firing gytus right so they may describe like like pseudonymembranes in the back of the throat like a bull's neck there's the classic example presentation usually it's like an immigrant right that does not have the oc has like an unknown vaccination history if you see that you really want to think about a dithyria right and the thing is the toxin that uh this is a weird thing you want to know for the usml is the toxin the dithyria toxin is actually not made by the theory itself it's actually made by a virus that infects the theory it's made by your profitech okay again weird thing you want to keep at the back of your mind and the theory uh some i guess weird things you want to keep at the back of your mind is that um there's this test known as the elect test ELEK it's a test that is actually used to detect the theory and the thing is the deuteria infection when it makes that toxin that toxic and actually spread to the heart and disrupt it basically cause like a myocarditis and it can also spread to the brain and cause very serious um cns infections right so this is not something to mess around with this is why you need to this is why you need to um vaccinate your kids and to be honest i think that's all i'm going to say about a dithyria i mean you can treat it with a macrolid like erythrolyce something like that okay um last things i'll talk about atino maces let me see is any of the bugs i want to mention here um talked about listeria bacillus cornee bacterium talked about clostridium propione bacterium i guess the acolyne Qt bacterium these days causes acne bad bad bad infection i remember that

cornee propione bacterium or Qt bacterium i guess is this unique is covered by uh geotecher cyclins geotecher cyclins like doxycyclic amino cyclin also clin damai sin remember that's a 50s inhibitor covers uh the propione bacterium acne that causes acne i guess now it's called Qt bacterium um actinomyces remember it's an anero it's not acid fast um usually causes like infections usually like in the face um like the buzzword on exams are like cervical facial infections and we talk about like some sulfur granules it's not like legit sulfur it's just basically like did add dithyneomyces and like natrophilts um one weird scenario though you may see on exempt with actinomyces is that it can cause infections in females using iud's okay like if you see like sulfur granules iud female birth control think about actinomyces as well and then uh the close cousin of actinomyces nocardia um nocardia um let's see nocardia nocardia right so it's it's weekly acid fast it's an erode um there's really not much to know about nocardia i mean you want to know that it is covered you can treat it with uh bacteria so like trimethoprima sulfur methoxazone um i think sulfonamides if yeah sulfonamides can also treat um uh nocardia but yeah i mean it can cause like pneumonia usually with like cavitary lesions sometimes it can cause like abscesses in the brain but to be honest i think that is probably much too much to know about nocardia and that's i think all i'm gonna say about nocardia uh there's also like micro bacteria uh but uh i will talk i'll probably talk about that in the gram negative podcast um because micro bacterial species i mean i mean the gram negative there's not many bugs there um and usually for those there's like just one or two things you need to know um but basically i'll see i'm done with the gram positives um i guess i'm one minute 86 let me just see some quick things abou

t the antibiotics uh you know what this will make this going for too long um yeah i think i'll stop here i think i'll stop here i have the related antibiotic podcasts you can listen to so i'm gonna stop here so just think of this as the rapid review of gram positives if you're listening to this podcast and you digest it uh me good notes um you should know pretty much all the high-ealth things that could show up on exams in addition to gram positives so i wish all the best on your test and as i'm rounding up i just want to say out loud like i say at the end of every podcast um that i offer one on one tutoring for uh met school exams basically every met met school exam i offered tutoring for i also offered tutoring for the usml exams so step one step two ck step two cs step three and then i um also prepare applications so if you have a like if you're an undergrad that is applying to met school or you know someone in that position please send them my way um i do mocking reviews i prepare amcas applications i help with personal statements and stuff like that and um i guess another high-ealth thing is i also prepare residency applications so ira's applications mocking reviews and all that stuff recommendation letters um personal statements i i have tutoring or prepared people for all those uh situations um i mean i've been on an admissions committee before so i have a lot of experience in visa matters so um i wish all the best hopefully you find this podcast to be helpful please share with your friends and if you have any questions or reach out to me through the website divine intervention podcasts.com podcast with an s or you can send me an email um divine intervention podcasts with an s at gmail.com so have a wonderful day i enjoy your Sunday and god bless i'll see you in the next podcast.

Gram-positives have a thicker peptidoglycan layer, lack an outer membrane, and tend to produce exotoxins. Gram-negatives have both an inner and outer membrane, possess a periplasmic space containing beta-lactamase, and tend to produce endotoxins (LPS).

Impetigo presents with honey-colored crusting on the face. Erysipelas presents as very painful, acute onset, red, well-demarcated lesions.

Listeria monocytogenes. It is a high-yield pathogen for meningitis in this population and is also the third most common cause of neonatal meningitis.

Edema factor, Lethal factor, and Protective antigen. These toxins contribute to its virulence and ability to cause anthrax.

Group B Streptococcus (Streptococcus agalactiae). This is a key differentiating biochemical test from other strep species.

1. Group B Streptococcus (GBS); 2. E. coli; 3. Listeria monocytogenes.

E. coli (traveler's diarrhea), Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, and Listeria monocytogenes.

Gram-positives generally produce exotoxins (toxins secreted by the organism), while Gram-negatives generally cause septic shock via endotoxins (LPS released upon cell death).

Strep pyogenes causes scarlet fever, rheumatic fever, and toxic shock syndrome. Key complications include post-streptococcal glomerulonephritis (Type III hypersensitivity) and acute rheumatic fever (Type II hypersensitivity).

Both are neurotoxins that cause flaccid paralysis by interfering with neurotransmitter release. Tetanus toxin causes spastic paralysis, while Botulism toxin causes flaccid paralysis.

Ampicillin (or penicillin). This is a classic pairing that must be memorized due to its importance in treating infections caused by Listeria monocytogenes.

Vancomycin. The resistance mechanism involves an alteration in the penicillin-binding protein (PBP), preventing binding by beta-lactam antibiotics.

E. coli (traveler's diarrhea), Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae, and Listeria monocytogenes.

Gram-positives generally produce exotoxins (toxins secreted by the organism), while Gram-negatives generally cause septic shock via endotoxins (LPS released upon cell death).

Strep pyogenes causes scarlet fever, rheumatic fever, and toxic shock syndrome. Key complications include post-streptococcal glomerulonephritis (Type III hypersensitivity) and acute rheumatic fever (Type II hypersensitivity).

Both are neurotoxins that cause flaccid paralysis by interfering with neurotransmitter release. Tetanus toxin causes spastic paralysis, while Botulism toxin causes flaccid paralysis.

Ampicillin (or penicillin). This is a classic pairing that must be memorized due to its importance in treating infections caused by Listeria monocytogenes.

Vancomycin. The resistance mechanism involves an alteration in the penicillin-binding protein (PBP), preventing binding by beta-lactam antibiotics.