DIP Episode 201 - Comprehensive USMLE Step 1 Microbiology Review Part 1

Okay, good morning. My name is Divine, I'm a resident. This is episode 201 of the Divine Intervention Podcasts. This podcast will, I'll begin a comprehensive review for microbiology in relation to the US Emily Step 1. I'm going to release the audio version of this podcast on the website. I'm also going to upload these slides on the website. But if you want to watch a video and you know, have it a little more interactive. You'll welcome to subscribe to the You Tube channel. You'll welcome to watch the video again. All these things I make are free. And then let me go ahead and jump right into it. So if you notice from this, you may see that the title is Q&A Comprehensive Microbiology Review 1. So there is my call to the Q&A review. I plan to use this talk more in terms of clinical vignettes because for me, I don't feel it's very useful from my own perspective to give you all these things to memorize, memorize, memorize, memorize. Of course, micro is memorization heavy. But I feel that being able to recognize the bug that they're testing on the exam is the most useful. So that is what I'm going to spend the bulk of my time on today. Yes, I'll have some teaching slides, but they'll be very few and far between. So let's jump right into it. So my objectives, right, and I guess my suggested study strategy for micro.

So the thing is, as we go through these videos and these audio podcasts, if you're listening to the audio version, I will talk about some high-yield lists that you're also going to find in the pop, like in the slides that I'm going to post for this. I'll encourage you like just before your USM list upon exam. Go ahead and go through those. And the thing is, there's actually some redundancy in the slides. So there's some things I repeat over and over again. I don't do it for show. I do it because they're actually very important and very high-yield to know for exams. And then really the major goal of this slide set is just again to highlight how these bugs are tested on these tests. And to be honest with you, if I'm in a position as yourself, you know, studying for step one, well, thank God, I'm done with that. No, with that process. I would, you know, suggest at least doing like one full-throw pass through like these different reviews. And then by then you should feel super, super comfortable, right? And you should feel good with like a very large chunk of this of this information. And one other thing is I like teaching people things in slightly different ways, right? So say, for example, you watch these series of videos that I'm going to post on microbiology. And then you say, okay, I want like in a fair shot period of time, boom, let me just go and review a lot of this high-yield information.

In addition to reviewing the lists, you can actually go through my microbiology rapid reviews. I actually have some rapid review podcasts that I made back in the day. They're actually super, super high-yield. And you're welcome to go through those. They're on the website, divineinterventionpodcasts.com, right? And again, if you keep click on the exam topic lists when you get there, you'll lead you to Google.com and you'll tell you the exact episode numbers for everything that I have pretty much by subject for step one, step two, CK and step three. So let's jump into this. I guess I still have some advice for it. So again, micros super high-yield for step one. I mean, micros like 10% of the entire first day book. So that tells you how important it is to know. And the thing is, I think of micros one of two things, depending on the kind of person you are. Micro can be the gift that keeps on giving, but on the flip side, it could actually be the thief that keeps on haunting you if you don't learn it well. You're going to need to know micro for step one for your clinical words for step two, CK for step three, right? And the thing is, most board exams, especially if you're in a specialty that involves patient interaction, you are going to need to know your microbiologist. So it's just one of those things. You just want to go ahead and get it down right now.

And unfortunately, the micro is, again, it relies a lot on memorization, but I'll try to minimize that and give you like clinical hooks that can help you remember the classic presentations of many of these books, right? And micro form is important. Well, thankfully, I already have podcasts on micro form. They are very comprehensive. They cover essentially all the drugs that you will see in first state for the US and the list of one. Basically, go ahead and look at episodes 27 and 28 on the website. And also episodes 33, 34 and 35. I go through all the anti-bacterials, all the antivirals, all the antifongals, all the antipyroacetics. Now, again, like I said, know the key buzzwords and associations. There are a lot of things I highlight in these slides. Make sure you commit those to memory. If you want to make flashcards on those that's absolutely fine. And then I have some slides that I call info cluster slides. Basically, they're slides where I cluster high your bits of information relating to a bug. And then on the next slide, I ask you which bug is it, right? So again, this is designed to be interactive. Now, welcome to pause the video at each point. Think about info cluster. So play an answer and then go to the next slide and you'll get directly immediate feedback. And the thing is, there's again, you don't necessarily need to know how to treat every single bug, right? But the thing is there are some high-yield bugs that you want to know how to treat.

Like, you want to know all the drugs that cover that bug, right? For example, like Sudo Monas, right? Sudo Monas is covered by your amino glycosides, right? So like Gentamysin, Neomysin, Amicasein, Tombramysin, Structomycin. It's also covered by your flu or quinolones. It's covered by the third generation cephalosporin, cephtazidin, the fourth generation cephalosporin, cephepine, right? It's covered by your carbapenem, it's covered by papyracidin, antiso-bacter, right? It's also covered by astrayon, right? Those are all things you need to know, right? And then your Mercer drugs, right? Those are things like, like, Venkulmysin, the fifth generation cephalosporin, cephtariline, right? Doccycycline also covers Mercer, clandomycin, also covers Mercer. I've talked about, I think I've mentioned that to Mercer already. Yeah, those are kind of like the big drugs, Linesolid, also covers Mercer. Remember, Linesolid is one of those protein synthesis inhibitors. It actually covers Mercer pretty well, right? And then, Tiguscycline, it's like one of the new generation tetracycline also covers Mercer as well, right? So those are all important things to know. And the thing is, the slice, they're sort of organized, but they also sort of disorganized, right? Again, I want you to get into them because your exam is not going to be like, oh, the first five questions on bacteria. Next five questions are on viruses. No, they're not going to do that weird.

So I want you to be able to quickly make connections, so I kind of jump all over the place, but I talk about all the bacteria first and then I jump into the viruses and stuff like that, right? So, and again, this will be in parts and they'll be, they'll be in parts in rapid succession. I essentially have most of the material I want to make in my mind and slides me already, right? I just need to have time to go ahead and record them. So this first slide is just giving you some quick and dirty anti-microbial coverage, right? So for example, right? So like, again, like, stuff-oreus, remember, there's MSSA, so the methecylin-sensitive stuff-oreus, you can cover those with drugs like oxacillin, like oxacillin, naphthalin, and then for MRSA, as I've mentioned earlier, right? Vancomycin, ductile, right? Remember, vancomycin is nephrotoxic and auto-toxic and it also causes that red man syndrome and then you have ductile mitin, right? That can cause my allergies, right? Remember the other drugs that can cause my allergies are like your statins and your fibrates, right? Those are more cardiac anti-hyperlipidemic medications. Remember, linesolid, remember linesolid, right? It can cover vancomycin, resistant and terracoccus, it can cover MRSA, right? And remember that linesolid, right? It also has this problem with serotonin syndrome because it also has the ability to inhibit monamine oxidies, so it has, like, per serotonergic properties.

And then the newer generations tetracyclins, like take a cyclin, also covers stuff-oreus, covers MRSA, and then they have taroline, that's the only fifth generation sephalus sporing you need to know for the purposes of the US-70s step one. It also covers MRSA as well. And then your anaerides, right? You want to think in terms of drugs like clindamycin and drugs like metronidazole, right? So if you see, like, oh, anaerides above the diaphragm, although that rule really, it's kind of like a, it's essentially a force. You can pretty much cover most anaerides with clindamycin and you can pretty much cover most anaerides with metronidazole. When metronidazole is usually used more for, like, parasitic infections and for intra-bdominal-like infections. And then clindamycin is used more for, like, skin infections and things of that nature. And then to the monasaur, we're already reeled out the drugs. I'm going to move on from that. And then syphilis, right? Remember penicillin, right? Remember syphilis is triaponema paladum, right? Syphilis penicillin is good for that polystyrene. You won't go ahead with ampicillin. Do not pick any other drug for listeria in your exams. If you do that, you're going to go ahead and you're going to get that question wrong pretty much, right? And then for C-DeF, before back in the day metronidazole was first lined, that's nearly the case. The first line medication for clostridium difficile is now vancomycin. Okay, it's now vancomycin.

You can still use metronidazole, but look if vancomycin is an answer choice on your test, go with that first over metronidazole. And then for nimosistis, your vetsy perphylaxis, you want to think about trimethyparem sophymethoxysol, right? Remember TMPS? Remember the magic number for that, right? It's a cd 4 count below 200. You can also use TMPSMX to perphylax against toxoplasma-gongea, right? And that's when your cd 4 count drops below 100, right? So if you're doing the right thing at a cd 4 of 200, you'll automatically cover yourself against toxoplasmosis as well. Remember, you can also use like DAPSON, you can use aerosolized pentamagin and you can use that tovacone and all that stuff. And then for microbacterium, avium, intercellularity, right? You can also perphylax against that with zythromycin, right? You can use zythromycin. zythromycin is a macrelid. And the magic number for that is 50, right? A cd 4 count of less than 50. So let's jump straight to the first question, right? So two days after being a visit to a dentist, Mr. X begins to experience mild facial pain. Ten days later, he presents to the ER with a moderately expanded right jaw. Physical examination reveals an abscess with draining possible of a yellow consistency. Which of the following best describes the organism responsible for this man's symptoms, right? So the first option says a gram positive obligate arop dipococcus. Option B says a gram negative obligate anerobe cocus.

Option C says a gram positive filamentous rod working cartilage and super upside transmutates. Option D says a filamentous gram positive obligate arop and then option E says a gram positive cocus isilus, right? So you know, this is the classic question you see on your USMEL exams. Instead of telling you something directly, right, you'll just describe it and then expect you to kind of make that backtrack leap from, oh, okay, this is what this bog is. This is what it actually is. So this should be the right answer, right? So you can go ahead and pause the video now, but the right answer here is option is option C, right? It's option C. So this person, right? You can see like these granules of a like a yellow consistency, right? Those are the classically described software granules that we find in people that have that have like, actinomyces is really I, right? Remember, it's a gram positive, right? And it's a filamentous rod and it tends to cause like cervical facial infections, right? So like infections of like the face and the neck, right? Again, that's a classic thing. I want to know for purposes of the exams, right? And if you notice what I did there, instead of using the term anerope, right? All I said was, oh, this bog lacks catalyst and superoxide dismutives. That is just one nice fancy way that your friends at the NBME can try to mess with your head on these exams, right?

So instead of saying anerope, you can just say, oh, organism that lacks catalyst and superoxide dismutives because the thing is, if you're an anerope, right? Then that means oxygen is toxic to that organism, right? So the thing is, why would oxygen be toxic to you? Well, it would be toxic if you don't have the enzymes that are necessary for the metabolism or you can say the breakdown of oxygen like catalys and superoxide dismutives, right? So that's a unique way your NBME friends can test that. So the NBME they love to do this. I essentially think of many NBME questions as derivative questions. So if you're financially inclined person like myself, let's just say sometimes in my past life I used to be an investment manager and basically derivatives are things that depend on other things, right? So like if you think about the financial crisis like the credit default swaps and all those things, those are all examples of derivatives, right? We can have that discussion some other time. But basically, instead of saying the word anerope, right? I just use the derivative, something that, sounds a lot like an anerope but is not the straight up anerope word, right? That's what the NBME does all the time, right? Like you've probably heard me say this, I've not seen many of my podcasts where I talked about how they can refer to some of my buddies as laminated calcifications, right? So again, these are just all classic tricks the NBME uses from from time to time.

So again, the key buzzwords for actually, you know, my thesis is really I saw for granulums, draining abscesses that look yellow, right? They look like gold, cervical, facial infections, so infections of the head and neck, right? And then infections that are caught in across tissue planes. Those are classic boss phrases you want to try to recognize for purposes of the USM list, step one, exact. Now the next question, a met 23 student presents to the divine clinic with a fever of 103 degrees, facial palsy, headache and malaise. A circular maculopopolar rash was identified on his shoulder, which of the following routes best describes the method of infection acquisition in this unfortunate met 23 student, right? So let's assume this one that goes to Harvard, I don't know. That's a hit, right? So option A is a consumption of contaminated food. Option B is athropod vector. Option C is sexual contact. Option D is angular transmission. And option E is respiratory secretions, right? So what are you thinking about with this? So pause the video. So I hope you're thinking about line disease from Borrelia Borgdophry, right? So the answer is should be B, right? So this is an athropod vector, right? So remember, line disease, right? It's carried by Borrelia Borgdophry. And Borrelia Borgdophry itself is carried by the xidistic, right? That xidistic remember that it actually carries some other stuff. It carries a babisia microtate, right?

Remember that causes like a hemoliric anemia and it has the multis cross pattern on histology, right? And then it also carries an aplasma, right? So anaplasmosis, right? And don't forget that Borrelia Borgdophry is a spirochete, right? The key spirochete, you want to make sure you know for your exams, you want to know treponema pallidum, that's a spirochete, you want to know Borrelia Borgdophry, that's a spirochete. And you also want to know, there's one more. So think about Hawaii, right? So like leptospiro interrogens, right? That's a high olspirochete, you want to know for the purposes of the USMELIS step one exam. And again, this infection is Lyme disease, right? So they'll tell you that, oh, this person has a mucleopuular rash. I have a picture coming up. It has like central claring and then the person may have like fever, they may have like migratory arthritis and all that stuff, right? And one other thing that I think is kind of high olsinoise that Lyme disease can also affect like elementary school teachers, right? So you can occur in adults on exams, right? And again, it has three stages, right? There's like stage one where you have like the airy-fema migratory arthritis, right? And then you have like stage two where you have like the cardiac problems, the facial problems, you can have like a bell spalsy, right? So if you see like a bilateral bell spalsy, think about Lyme disease. And remember that bell spalsy is a low motor neuron, cranial seven deficits.

Excuse me, not an upper motor neuron defect, right? So I'll talk about that in my neuro, in my neuro podcast or videos, depending on the format I intend to use, right? And then stage three Lyme disease can cause CNS problems, right? And for the most part Lyme disease, you should have a doxycycline, right? You should have Lyme disease with doxycycline. I remember doxycycline, right? It is one of those protein synthesis inhibitors. If one of you a little more specific, it's a thirtieth inhibitor, right? So it prevents like amino acid, acyl, tyranine from attaching to the ribosome, right? And it's bacterostatic, unlike your amino, glycosides that are thirtieth inhibitors and a bacterosidol, right? And some other key things with Lyme disease that are actually not on this slide just kind of popped in my memory, right? So don't forget, if a person has Lyme disease, right? And they're less than like eight years old, you cannot give them doxycycline. You need to give those people a moxicillin. A moxicillin will be the drug of choice on other circumstances. But if the person is less than is greater than eight years old, you can go ahead and give doxycycline. And then if a woman has Lyme disease and she's pregnant, so antibodies that the body makes against that Lyme disease can actually cross the placenta and cause like a third degree heart block in the in the in the fetus, right? So that's actually something that's kind of weird, but also kind of high yield to know.

And then if a person has Lyme disease and involves the CNS for that, you go after you go with a septic acid, right? Now, this less than eight year old rule applies pretty much all the time with doxycycline or any tetracycline for that matter. You don't give them to kids that are less than eight years old. But that rule does not obtain for a particular bug, rickety rickety slide. That's the bug that causes Rocky Mountain spotted fever. Rocky Mountain spotted fever, everyone that has Rocky Mountain spotted fever regardless of your age gets doxycycline. The thing is the harmful side effects from the doxycycline far out with almost certain death that happens when people get Rocky Mountain spotted fever. So that's one thing you want to keep at the back of your mind for example. The only exception to that rule is if you have a pregnant woman with Rocky Mountain spotted fever, the drug of choice is quorum fenycom. That's essentially the only reason why you should ever pick quorum fenycom on your exam as the treatment as an antibacterial treatment for any kind of bug. And the key buzzwords want to remember Lyme disease, right? So erythema, chronic migraines, right? So that's like the bullseye rash. Again, if a person goes to Boston, so I'm looking at you, Harvard folk or Connecticut and looking at you, you, you, people, right, New Hampshire. And then Maryland, right? So my Hopkins folks and then Pennsylvania, right? So like you pen or whatever, right?

Basically the North, the North Eastern United States. And then again, don't forget your bells palsy by lateral bells palsy. Don't forget the exodestic. Don't forget Barriola, Bokdoferi. Don't forget the migratory arthritis. Don't forget your elementary school teachers. Don't forget the treatment strategies and don't forget the Babesia and an aplasma, right? And again, these words are very similar. So don't mix them up. Erythema, chronic migraines with Lyme disease is not the same thing as erythema, marginata with group A-strip, stripyogen, right? So don't mix those up. And again, the stages of Lyme disease, right? So you have the erythema migraines, you know, you kind of feel like crap for a while. You have the bullseye rash, right? And the thing is for you to get Lyme disease, the tick must have been on your skin for like 36 to 48 hours. You may say, oh, the fine. Who cares about that? I promise you you should care. That's something very high you that tends to pop up actually on the US-Semilistepone exam. And then stage two Lyme disease again, mostly like joint symptoms, right? Joint symptoms, balspalsy, AV blocks, things of that nature, right? And then stage three, you can have the migratory polyethylene, you can have the neurological problems. I remember when you have the neurological Lyme disease, you're going after that with sephetraaxop. And again, this is a picture that shows the erythema chronic on migraines, right? You can see it kind of looks like a bullseye.

Now, next question, a four-year-old child of an Eastern European immigrant family is brought to the divine free clinic. The child is a febrile, but we can exhaust it from a week of relentless coffin with inspiratory whoops that put him out of breath. A blood sample drawn for analysis indicates a wide blood cell count of 75,000 with a predominance of lymphocytes. The symptoms present in this child would most likely have been prevented by which of the following interventions. Option A says administration of an acetylula vaccine as a component of a triple vaccine regimen. Option B says oral administration of a 30-year-old ribosome inhibitor two days after delivery. Option C says administration of a live attenuated vaccine on a yearly basis during the winter months. Option D says administration of a monoclonal antibody that protects against viral infections, so you can pause the video of the audio recording. What do you think this is? I hope you think it boarded teleportosis. The right answer here should be A. The other answer is a bogus option C is like the influenza vaccine. Let me be a little more specific, the intranasal influenza vaccine. Remember there's an intranasal influenza vaccine. It's live attenuated, so you don't want to give it to a pregnant woman or a child that's less than a year old. Then the other answer is a bogus. Let me just go to the next slide because again I don't want this to take too long. I want to keep this relatively short. The answer is A.

The answer is essentially I'm referring to the D-tap vaccine. The thing is this kid has border teleportosis. You need to treat the patient, and you need to treat the close contacts with a microlead, like erythromycin or easy-thromycin. Then the bog, again, like I said, be pertosis, whooping cough. The thing is they may not be nice like I am and put the respiratory whoops in the chest. What do you mean? The person has a cough, and the cough cough cough cough so much. Then as they cough, they'll have like MSS, so the vomit after the cough, or they have a subconjunctival, hemorrhage after the cough, or they have apnic episodes after the cough. If you see that think about border teleportosis. The cough is pretty classic. They cough, they're like, it's kind of nasty. This thing happens for weeks on end. It's a terrible, terrible thing for a person to have. Really, there are three stages of infection. There's the catorole stage, the protégens and whatever. Catorole stage, they have malflu-like symptoms, and then there's the pyrusesumostige where they have the whooping cough, and then there's the convalescent phase. That's the recovery phase where they have a milder cough and then they get better. Really, the way you transmit this is virus-preterated droplets. This idea just dropped in my mind, so let me just go ahead and see it now. Methods of preventing transmission of infection, a very high yield to know for the year 7th step one exam.

The key ones I feel like come up all the time. C-diff, hand washing can prevent the spread of that. Rotavirus, hand washing can also prevent the spread of that. Those are all high yield things you want to know for exams. So again, what are the buzzwords with border teleportosis? Again, history of immigration, or someone from, I don't know, some anti-vaxxer part of the country. I mean, you know what those regions of the country are. I'm not going to mention those, so I don't get into trouble with anyone. Then, again, for prison coughs for a long time, like weeks, chronic cough, respiratory whoops, subconjunctival hemorrhage, acne episodes, post-tosive MSS. And again, don't confuse this whooping cough with the barking, seal-like cough. I'm going to find it with a group. Remember, a group causes like strider. That's caused by the parian friends of virus. And then, border tele is kind of unique. So it's a bug, it's a bacteria. And whenever you see bacterial infections, when you have a lychocytosis from a bacterial infection, you'd usually think that you have that associated with like neutrophilic pleocyteosis. That's actually not the case with border tele. border tele is unique in the sense that it's a bacterial infection, but it's accompanied by a lymphocytic pleocyteosis. And these people's white blood cell counts can approach like in same levels, like the really, really high margins.

So if you see that, don't think of, oh, this person has a blood malignancy, like leukemia, lymphoma, whatever, it can actually be caused by border teleportosis. So again, the context of the question is what will lead you towards the answer? Now, let's kind of delineate between gram positives and gram negatives. So the thing is, both gram positives and gram negatives, they have plasma membranes. That's what's called the inner membrane. Remember, this has like a lipid bilayer. And then, right above the inner membrane, we have like, if you look at the gram positives, they have like a very thick peptidoglycanal ear, right? Contrast this with the gram negatives that we have peptidoglycan as well, but it's very thin, right? It's very thin, right? And because the gram negatives have the thin peptidoglycanal ear, they're not able to retain your original steam that we use during the gram steam procedure. That's why they are steamed with a contrasting, that's why they look pink under like microscopy. And the thing is, the gram positive cell walls, they contain something called like, we take quake acid, you can contrast this with the gram negatives that have something called LPS, right? Like we take quake acid, LPS, they can trigger like the release of a good phycytochine, so like, if you're looking one, TNF alpha, interlooking six.

And one key difference to recognize between gram negatives and gram positives is that gram negatives are both that thin peptidoglycanal ear, they then have an outer membrane, right? So they have an inner membrane, thin peptidoglycanal ear, outer membrane versus gram positives that have the inner membrane and a thick peptidoglycanal ear, right? So the thing is, it's that outer membrane of the gram negatives that actually contains the LPS, the lipopolis apricot, right? And between that inner and outer membrane in the gram negatives, again, there's something called the periplasmic space where you tend to find some Keyentant like beta-lactamesis, that's why we have drugs like clavolanica said, we have drugs like Tizobakhtam, we have drugs like, soakakhtam that are all beta-lactamese inhibitors to deal with those things that we find in the periplasmic space. So your friends at the USML Es, they can ask you a question about, like, where's the site of action of a beta-lactamese inhibitor, and that'll be in the periplasmic space, that's a very unique way for them to test that. And then let's just rock with run through some structure bacterial components, you probably know most of these already, so like the fembrae, right? I remember they can also be called like an attachment pylos on an exam, right? They let bugs attach to surfaces, right? Like equalize the poster shell for this, this is why it can colonize the urinary tract, right? But the teleportosis also has fembrae, right?

And then sex pyline, right? Sometimes they're called like epyline, you essentially use it to transfer DNA between bacteria, I'll talk about some of those mechanisms in a second, and then the flagella, right? That we have with bacteria, right? They're kind of like wavy structures, they have usually bigger than the fembrae, and the pylite, they help those bacteria move, right? So they're for motility, and then there's capsules, so this is one region where you want to pay attention, right? So the thing is, there's this thing called like ocelex, right? That's bacteria used to cover themselves. If you have those like ocelex and it's super well arranged, that's a capsule. If it's not super well arranged, that's like biofilm, that's like slime, right? And the big thing you want to keep in mind with these capsules is for the most part they're made of police occurrence, but they are really effective at preventing phagocyteosis. They are super, super effective at preventing phagocyteosis, right? And the thing is, if you don't have a spleen, because remember your spleen is like your blood filter versus your lymphatic system that is your tissue filter, right? So your spleen is your blood filter, so the thing is we have these planing microfeatures that help with dealing with these encapsulated organisms.

If you lack a spleen, aka maybe your sickle cell disease person, or you know, you have mono, the physician says, oh, you know, no contact sports for three weeks, like, yeah, screw the physician, and then you want your rupture or spleen, or you're in an accident, and you get like a spleenic rupture, those can all increase your risk of getting infected within encapsulated organisms, right? So look out for sepsis, in patients without spines, usually it's from strep pneumo, because strep pneumo is an encapsulated organism. And then there's this quellon reaction that you see in some audio-similar resources, just to be complete, I just say through that in here. Basically it's a way you can detect like a capsule organism, essentially no one does this anymore, but basically you take some serum that has like antibodies against the capsule, and then if the serum swells, then you're like, oh, that's a positive quellon reaction, who I have an encapsulated organism on my hands. And the thing is, the encapsulated organisms, there's a ton of those, but the big ones I'll say to know, strep pneumo, hemophilus influenza, and I serum and ingyritus, and then cryptococcus pneumo, those are the big ones. Have another slide that kind of details like some other high-ovalents to know, but I'll say those are the four you probably want to really commit to memory before you take you, except.

And then biofilm, again, like any bug that loves to attach to like indwelling urinary catheters or prosthetic valves tends to have biofilm. And again, like I said, these things are made of polysaccharides. There is a bug that is unique in the sense that it's capsule is not made of polysaccharide, it's a few minutes of protein polygluedamides, that's a bacillus and thresis, that's a high-oval factoid to know for example. And then we also have ribosome, we use those for proteins, infecence, right. So like bacteria, which are prokaryotes, right, 50s, 30s, that's like the 70s ribosome, and then 60s, 40s is people like us, right, like youkaryotes, we have the one we have the 80s ribosome, so that's something I'll have to correct. I have 100s in this, it's not 100s, it is 80s because the numbers never add up because they are sedimentation units. Now the DNA transfer mechanisms in that are pretty in bacteria, right. So we have plasmids, I think of plasmids as just like crumos DNA that is not part of the regular crumosome, right. So they're like extra crumosome DNA, they tend to quote for like exotic stuff, you know, like virulence factors, toxins and all that stuff. And you can actually transfer these plasmids through conjugation, right. Cognition is again where you'd use that sex pillus to transfer information from one bacteria to the other, right. Now what are some other mechanisms that we can use for DNA transferring bacteria?

And again, these are high you to know for step one, right. There's this thing called transformation, basically what happens in transformation. One bacterial cell dies, when a cell dies, right, the sodium potassium ATP is pump will stop working, sodium flow down is great into the cell, the cell will swell and then it will explode. When it explodes, some of its DNA existing environment, if a living bacterium goes and takes up that DNA and then throws it into its own genome, right. That'll be an example of transformation, okay. And again, it's common in those bugs that encapsulated like strepnumol, immofluos influenza and niacereminucididis. And then there's transposons, right. Transposons, I think of these as like they can self-excuse themselves from a chromosome and then they can transfer to another piece of the chromosome or they can transfer to another chromosome altogether or they can transfer to like a plasmid, right. So that's another mechanism of DNA transfer because again, if you're on a plasmid, then that process of conjugation or if a bacterial cell dies, you can kind of use that to get that new genome to like a different kind of organism. And then one of the key one is like the bacteria features, right. Sometimes they're called like phage. Essentially a phage is a virus that infects bacteria, right. And it can clear a role. Essentially what happens is you have a phage that infects a bacteria, you know.

And viruses they take over the genetic machinery of the host, right. Like the bacteria to, you know, make their own thing. So you know, you make all these variants, you put them in capsids and those things explode, right. The thing is, well, the virus, because viruses, they're not, they're not super smart. Let's just put it that way. So basically the thing viruses can do is while they are replicating with the genetic machinery of the host, they can actually take like some of the bacterial genome with them and incorporate it into the DNA. Right. So you can already imagine that if the phage then goes and infects a new bacteria, it's essentially introducing new genome, like it's introducing both its viral genome and some bacterial genome from some other bacteria made as infected back in the day, right. So genetic material has been transferred that way. Now at the bottom of this slide, you see me say that the gram positive gram negative algorithms and first of all, you need to commit those to memory code. Those are high yield things to know for the exam, right. So again, what are the big encapsulated organisms, again, like I said, stripping more H Flu and Icerin and Gidetis, Cryptococcus new forms, those are the big ones, right. But some other ones you want to know, E. coli, right. So let me just read this list, right. So Cryptococcus new forms, E. coli, pseudomonas aerogenosa, right, N.I. C. C. C. C. C. C. E. L. A. N. E. Strapnimo, H Flu-Tiby.

I remember H Flu-Tiby does not cause the flu. It's the influenza virus that causes the flu and just go ahead and throw that out there. You don't want to make that kind of mistake when I'm exam, so you don't go home crying. And then some vanilla typhee, right. And then group B strepica lacte is also an encapsulated organism, right. And again, if you have no spleen, you will have trouble with encapsulated bugs for reasons I already explained earlier. And one nice way your friends at the Mbimic and Testes is they can make you, they can write a question way they try to get you to make a vaccine, like predict a vaccine regimen for a person that has like spleen injury, like a sickle cell disease patient. And actually, I'm going to go ahead and throw out here right now. It's a high-year factoid to know the most common cause of sepsis in patients with sickle cell disease is streptococcus pneumonia, right. That's something you need to come into memory. So now the next question, right. So supply the name of the organism that best meets the following descriptions, right. So there are multiple correct answers here, right. So gram positive coxine pairs, what are you thinking about? Well, I hope you're thinking about streptococcus species, like streptiniumal. Gram positive coxine clusters, what are you thinking about? Well, I hope you're thinking about streptococcus species, right. And then gram negative coxine pairs, right.

Those are your nice serospecies, most likely like nice serum and ingenious, right. Basically again, if you see the word pairs, that's the blococci, right. So again, those are the answers on the next slide. So let's go on. Now what is the bug that best? So this is one of my info cluster slides, right. So this bug causes acute endocratitis. It is the most common cause of osteomyelitis, it causes toxic shock syndrome, it causes scalded skin syndrome, and it also causes like gastroenteritis like two hours after you consume like potato salad or mayonnaise. What is that? Well, I hope you're seeing stuff for this, right. I hope you're seeing stuff for this. Again, these matching slides, like these info cluster slides, they essentially give you like the key high points. I need to commit to memory with regards to these bugs. And again, I'll talk about stuff for us in multiple. That's the thing. That's why again, I said that this slide set is redundant, and it's also integrated in a sense. So I'll talk about stuff for you seeing different contexts throughout this presentation. So that basically if you go through this whole video series, you'll become a micro master, right. You just actually have to go through the video series. Okay, now the next question, right. So what is the bug that you know is a blood culture contaminant? It's part of normal skin flora. It loves to cause prosthetic valve endocratitis, and it can cause uti as in individuals with like indwelling catheters.

Well, I hope you're thinking about stuff for determinants, right. Stuff for determinants. I remember stuff for determinants, right. You know, it's catalys positive, it's quaggolys negative. I remember the quaggolys positive stuff species you want to think about for purposes of your exam is stuff for us, right. It's stuff for us. And remember, people that have CGD, so chronic redolomatosis disease, where you have like an NADPH oxidist deficiency, those we would tend to get like recurring stuff for us abscesses. That's the classic presentation on the USMN exams, right. And remember that stuff epidermis is novel biosensitiv, contrast this with stuff, so it's a prophetical that is novel biosin resistant. Okay. And again, because it forms like biofilm, it loves to attach to plastic, right. So you can cause like a prosthetic valve endocratitis. And here's one weird thing you may not find in many resources, but it's very high yield to know for purposes of the USMN list upon exam. If a person has a prosthetic valve inserted and they have endocratitis less than 60 days after the prosthetic valve was inserted, that's something called early prosthetic valve endocratitis. That is classically caused by by stuff epidermidis, right. But if it's more than 60 days after that is lead prosthetic valve endocratitis, you want to go after stuff with that, right. If it's super, super, like 12 months after the prosthetic valve was inserted, they want to think more along the lines of shavviri dents.

Okay. Shavviri dents. Now next question, right. So what's the bug that is described by the following four cluster, right. So UTI in a sexually active young female, right. This bug is actually the second most common cause of UT Is. What bug are you thinking about here? Well, I hope you're telling me stuff's a propheticus, right. And I guess as an addendum, what is the most common cause of UT Is in this country? It's equal, I write, equal I cause it's like 80% of all UT Is. Okay. And again, stuff's a propheticus. Again, I said it's novel biosene resistant. Contrast that with stuff epidermidis that is novel biosene sensitive, right. What stuff, sub-profitical stuff epidermidis, they are both catalysts positive, but they are both quadrullis negative, right. Remember, it's stuff where it's that is cut is catalysts positive and quadrullis positive. Now the next question, what is the bug that is best described by the following info cluster, right. So it's part of your normal vaginal flora. It can cause like neonatal, like meningitis, neonatal pneumonia, neonatal sepsis. It's a bit of hemolytic bog and it's basitricin resistant. What bog am I referring to here? Well, I hope you tell me group B strap, right. It's trapegalactic, right. So remember, it's a catalysts negative organism, right. And usually, right, they can make this an OB-GYN style question or pediatric question on your exam.

Usually if woman is pregnant, when she hits like 35 to 37 weeks of gestation, you check out group B strap status, right. Because if she's group B strap positive, then you need to go ahead and treat it, right. You need to give like anti-botic prophylaxis so that a newborn doesn't get into all these problems because about 25% of women actually have their vaginas. Excuse me, already colonized with group B strap. And really, I'll just tell you this trick. If you see any notable infection in the first 20 days of life, the question is you ask yourself, is why should I not speak group B strap or strap equal acteal? So let's jump over to the next question. Now, what is the bug that again, best described by the following info cluster, right. So it's the most common cause of an ingythest pneumonia. And same you say, this one is easier, right. This is strapping them up, right. So remember strapping them up is a catalyst negative organism, right. And it's a member catalyst positive, you're thinking along the lines of your staff species, right. I mean, essentially using a backhand means to go over the gram positive algorithm here, right. So it's a gram positive diplococcus. It's catalyst negative, right. So people that have CGD will not get this problem. And remember that people that get CGD, right, it's going to be a boy on your example. So I'm going to be a girl, because CGD is inherited in an ex-linked recessive fascia, right. And the thing is strapping them all.

It's alpha hemolytic and it has a capsule and it's optochina sensitive, okay. It's optochina sensitive. Those are just things unfortunately you need to come into memory. Remember, it was one of those shinoxisms that I talked about earlier, right. And whenever you see like an Asian friend of yours and they're name is shin, thank them for, you know, gifting you this nomonic that helps you remember the high-yielding capsule, lethal box, right. Again, like strapping you more, Hian fluenza and I see I'm in jitter this. And really the literature keeps changing, but for now, the most common cause, at least from what I read in some literature, the most common cause of acutotitis media is now strapping you more, because it always vastly leads between strapping you more non-typable H flow more, etc. Catarralis, right. But from the late, like the most recent literature, right. It actually tells me it's strapping you more, but again, maybe by the time I'm maybe who knows, like a week from night's gonna be different, right. So just check that out with your professor or whatever. Find out what is most recent before you take your example. For now, it is strapping you more. And if a person has acutotitis media, your first line is a classic MME question. The first line medication is a moxicillin. If a moxicillin doesn't work for that person, go ahead and go to the second line medication, which is actually the combination of a moxicillin and the bitter lactamines inhibitor, clavolanic acid.

Now, what is the bog that matches this information cluster, right. So this bog causes firing chitis, causes in betygo, causes erycipulas, right. And this bog also causes like acetylitis, and it can cause like an acrotizing fasciitis, and it can cause rheumatic fever, it can cause glomerular nephritis. If you see this, what are you thinking about? Well, I hope you're telling me group A strap, right. So like strap biogenes, right. So remember strap biogenes is also called group A strap. Remember, it is beta-hymolytic, it is not alpha-hymolytic. You may notice, I'm sure you'll be be like, why is the vine drawing his ears as he's seeing some thinness. The thinness is some Nigerian, right. Although I'm also American, but call me a Nigerian American. Okay, you know, let's am Nigerian, right. So the thing is, when parenting Nigerian, I want to tell you something that's important, and they want you to listen and keep that in mind, they will draw their ears, right. So whenever you see me draw my ears, just happy to, I mean, I've done this pretty much all my life. So it's just a habit that probably will never be able to kick that habit. So, okay. Now, so strap biogenes, right. Again, it's group A strap. It's beta-hymolytic strap. Remember, the fact that it's group A strap does not mean it's alpha-hymolytic, right. Again, don't make that mistake on your exam. Remember that it is basic tracing and sensitive, right. And the thing is group A strap, you can cause cardiac problems, right.

Like, dramatic fever for the most part. And that dramatic fever, you can actually prevent that by giving the person that has group A strap, faring gyitis, by giving them antibiotics, right. And remember that dramatic fever actually can go on to cause mitro stenosis. In fact, this is floorily high yields to know for purposes of the USMLE exams. The biggest risk factor, very high yield, the biggest risk factor for mitro stenosis is rheumatic fever. And then mitro stenosis in turn is the biggest risk factor for AFIP. So AFIP has mitro stenosis as its biggest risk factor. And then mitro stenosis has rheumatic fever as its biggest risk factor. And again, like I said, again, ribachia strap faring gyitis, it can cause cardiac problems, it can cause renal problems. The renal problem right is the nephritic syndrome, post-infectious glomerular nephritis that you get like two to six weeks after an operator's respiratory infection, right. But I want you to note a key difference here. So group A strap faring gyitis, as I said, can cause cardiac and renal problems. But if a person has a skin infection from group A strap, it can actually only cause the renal problem, right. You cannot get dramatic fever from a group A strap skin infection like in betygo or aerocephalus, okay. That's a very key critical difference to keep in mind. And the thing is in general, these group A strap skin infections tend to be associated with antibodies against DNA's B.

That's a high yield antibody to commit to memory for these exams. Now, I know in this slide, I said that, oh, aerocephalus in betygo can both be caused by group A strap, which is true. But on an NBM exam, so I'm telling you this from an NBM perspective, the most common cause of in betygo on an NBM exam is staphorius. So the honey colored cross that whatever's that you can treat with lactopicolum, you purer sin, right. The most common cause of aerocephalus on the other hand on NBM exams is group A strap. So, classically on NBM exams, they'll give you an in betygo patient, they'll post staphorius as an answer, they'll post group A strap as an answer, pick staphorius, right. If they make it an aerocephalus question, pick group A strap as your answer over those between the two bugs. But if you don't see one, then pick the other, okay. But remember, what is first, in betygo staphorius aerocephalus group A strap, okay. And the easy way to remember that is group A strap has an aim to be. So you should have an earlier letter in the alphabet, aerocephalus, right. Staphorius, right. Staph S is like a letter letter in the alphabet, right. So, staph, right. You should take the letter letter, right, in betygo. Okay, so let's keep strolling, right. So what is the bug that is best described by the following info cluster, right. So it causes subacute material in Nucranides, recent down to a procedure, what are you thinking about? Well, this one is easy, right.

This is strap veridense, right. This strap veridense. Again, remember, it's alpha hemolytic, it's optusino resistant, it has no capsule, unlike strep pneumo, and it's actually part of your oral flora, right. That's why you can get it after having after getting like a dental procedure, like a root canal or something like that. Now, in Nucranides, just again, quick bourbon, this, I have very few teaching slides. Most of my teaching goes in the context of the questions that I wrote for this presentation, right. So, Nucranides is basically where you have like an inflammation of like the inner lining of the heart, right. Remember, the inner lining of your heart is endothelial, endothelial, and endocarditis, again, is super high up to know for exams. The classic presentation is a person having fever and a new murmur, okay. Remember that. Fever plus a new murmur equals endocraditis onto proven otherwise on any USMAD exam, okay. And the thing is, you can classify endocarditis as being acute or subacute. So what is acute endocarditis? Acute endocarditis is basically, if you see acute endocarditis, things stuff, that's the big one you want to keep at the back of your mind, right. The thing is, it's called acute endocarditis because from onset of symptoms to like the person's like symptomatic progression is usually pretty rapid, right. And these patients seem to have like pretty severe symptoms.

These are people that are coming to the emergency room and say, dog have been feeling like crub for a while, right. And the thing is acute endocarditis, this is a critical difference from subacute. It tends to affect valves that were previously normal. I mean, it can affect bad valves, but a previously normal valve can be torched by acute endocarditis, right. Contrast this with subacute endocarditis, the big, most common cause is severe events. And the classic association, again, like I said earlier, is dental procedures. Now, the thing is on like people, on like the people with acute endocarditis that have like a rapid onset, rapid progression of symptoms, very severe symptoms. People that have subacute endocarditis, they usually have minimal symptoms. It has a more endoline course like weeks to months before they come, maybe to like the family practice doctor to get to get a diagnosis that treated. Now, I said that if a person has acute endocarditis, it tends to torture previously normal valve. The thing is subacute endocarditis, almost as a requirement, needs a valve that is abnormal in some way, shape or form, right. And then please don't forget lupus, right. SLE can cause like libman sacs endocarditis. That's like a sterile endocarditis in a sense, right. And then don't forget like your genuilisions, rough spots, osler nodes. I've talked about this in my cardiology podcast. Okay, so let's do some quick endocarditis clinical scenarios, right.

So what's the bug that best fits the following clinical scenarios, right. So if you have like a neon set membrane, an IV drug user, what is that? That's stuff for you, right. Remember, stuff for you, if you're an IV drug user, right, you mean because you may say, oh, divine. Yeah, people that have like was the most common valve affected by endocarditis. It's actually the the micro valve, right. But IV drug users and an exception, right. And again, you may say, okay, divine, why? Well, it's not a surprise. I mean, literally look at the name IV drug user, right. So you inject the drugs into a vein. If you inject those drugs into a vein, where do veins drain into the right side of the heart, right. So they can torch the right side of the heart and usually they cause like a tricospid regurgitation. Now, the next question says low grade fever weeks after a dental procedure. Again, that's very dense. Again, I repeated that like three times. It's probably something you want to know for all the USM Ls, right. And then heart membrane and individual at a prosthetic valve, right. Again, stuff of the dermatitis is the poster child there. And then murmur after a recent operator infection, right. That's traumatic fever from group A strap, okay. Romantic fever from group A strap. And again, most cases of endocarditis left side of the heart, micro valve. But IV drug users tend to get like a right side of a valve endocarditis.

Now, this is not necessarily endocarditis, but I just felt I should throw this in here. So I'm talking about like sides of the heart. If you see like a right-sided heart problem like tricospid regurgitation or monics denosis, think about cross-noid syndrome on your exam. Think about cross-noid syndrome on your exam. Because remember, cross-noid is also broken down in the lungs, right. Broken down in the lungs, right. So because it's broken down in the lungs, those people will not have left-sided heart problems. And again, dramatic fever, it can prevent it by giving antibiotics, but the post-infections go better in the Fridays. Ticking antibiotics does not decrease the incidence of PSGN. Now, next question. So what is the bug that is best described by the following info cluster, right. So pinless black S-shar hemorrhagic indies the 90s. They can even make this a widened indies time on question on your exam. But the answer will not be aortic dissection, right. And this bug forms spores. And this can be found like in an FBI person or a rule disorder or a post-toe worker. Well, I hope you know this to be bacillus and thresus, right. This is anthrax. Remember the capsule, like I said, is made of like glutamate, right. It's like a polymer of glutamate, again, it's unusual because most of almost every other capsule you find in bunks is made of a polysaccharide, right. Well, this is made of protein, right. And remember that anthrax has three virulence factors, right.

It has a dima factor. A dima factor is a toxin that essentially is an adenylate cyclase, right. So it will increase the activity of cyclic AMP, et al. cause a dima. And then there's lethal factor. So lethal factor is a metalloproteinis. It essentially degrades like map kinese. And if you degrade map kinese, then that will trigger cell death, right. So it's called lethal factor, right. I mean, lethal, right. The name is very descriptive, right. And then there's also protective antigen, but the function of that is not something that is frequently tested on the USML Is. So I'm going to skip that. And again, remember it's a grand positive bug. It's an arrow, right. And you treat it with a fluoroquino loan. So like moxifloxacin, cyprophloxacin, gadi-floxacin, libo-floxacin, right. Or you can also use noxicicin. You can actually prevent anthrax, believe it or not, with a vaccine. There is a vaccine for anthrax, but it's not part of like the regular vaccine regimen. You know, if you're like, I don't know, like you're traveling to a country that uses biological terrorism or something like that, right. And you know, if the US government is sending you overseas, you'll probably imagine, again, I have no knowledge. I'm not in the military, but I will imagine that it give you some kind of anthrax vaccine, right. It will seem like a smart thing to do. And this is a picture of the anthrax of bacillus anthracis. There are some pictures I'll tell you to memorize. This is one of them.

This is a classic picture that tends to show up on the USML Is exams. Now, the next question, right. So what is the bug that is best described by the following info so it has a gray, cause is a gray pseudomembring, right. The toxin is encoded by a beta profeach. And you can get this problem in an unimmunized child that has a bull's neck appearance on physical exam. This is easy, right. This is coragny bacteria of the theory, right. This is the theory. Remember, again, the theory is vaccine preventable, right. And remember, the theory can cause CNS problems and cardiac problems if you don't treat it. It can cause like myocarditis. And again, it's a gram positive error. Again, please memorize that gram positive slash gram negative algorithm infested. It is super, super high to know that algorithm. Now, the next question, what is the bug that is best described by the following info cluster, right. So spontaneous abortion, mom consumed unpasturized milk slash dairy products while she was pregnant. Mom consumed meats at a daily while she was pregnant. Just from this question, if your mom out there, maybe don't do any of these two things while you're pregnant, it's probably not a great idea, right. And then this bug has tumbling motility. It's an intracellular organism. And it uses a projectile mechanism to go from cell to cell, like actin rockets to avoid immune system. And I can even throw in something that's not on this slide.

This bug is the third most common cause of meningitis in neonates. And it's also one of the most common causes of meningitis in the elderly. What do you think this is? This is listeria, right. This is listeria monosyctogenous, right. Again, it's a gram positive, but cellus. And again, the drug of choice, very high. The drug of choice for trillion listeriosis is an picellin. It's an picellin. Remember, in picellin is an IV medication versus a moxicillin. A moxicillin that is oral. You say, oh, do I remember that? Well, here's a trick. And picellin has a lot of eyes in it, right. So it's IV. A moxicillin has an o in it. So it's oral, right. I guess that's a nice trick there. Okay. Next one. What is the bug that is best described by the following info cluster? So it has a capsule. It can cause bilateral adrenal hemorrhage. It can cause nocorrigidity. And there is a vaccine available against this bug. This one is easy. It's my sermine ingitis, right. Now, the thing is your friends at the MDM if you're getting more, should I say, prevent or more exotic with the wavy test my sermine ingitis, right. So you're probably not going to put the nocorrigidity, right. And I know like the bilateral adrenal hemorrhage, you're like, oh, divine. What are house ferozics and syndrome? The thing is they've got in a little more crafty with the wavy test test. So they can actually make, you know, they'll give you a question about a person that has a nice sermine ingitis, right.

And then they'll test the water house ferozics and syndrome in like a renal context or like an endocrine context where you have to like they'll give you all the, they'll see which of the following labs will be expected in this individual. And then they'll give you all these hours flying along with the place. Well, here's the deal. If you have a water house ferozics and syndrome, that will cause a primary adrenal insufficiency, right. So you no longer have cortisol and you no longer have outdooster, right. So if that happens, you, because you are outdooster low, right. Your sodium will be low, you have a hyponitremia, your potassium will be high, you have a hyperchilemia, and you have a metabolic acidosis. And if you want to be a little more specific, you have a normal anion gap, metabolic acidosis. And if you want to be even more specific than that, you have a type 4 RTA, right. That's an RTA that's associated with a hypo-outdoosterone state, okay. And again, remember that the reason you get the hypo-neutrhymen and the hyperchilemia is that our dose to relaxivates that inek channel that we find at the level of the principle cell of the collecting that. So it activates that inek channel, you reabsorb sodium and then you don't potassium in the urine. Well, if that doesn't happen, then you become hypo-neutremic and you retain potassium, you become hyperchilemia and again, like I said, you develop a metabolic acidosis.

And then you'll also have an eosynophilia in your bloodstream because remember, if you don't have cortisol, cortisol causes a poptosis of eosynophilus. So if you have low levels of cortisol, aka like it's almost like a pseudo-adolescent disease, but in this case, it's caused by waterhouse phrygixin, right. Then you'll have very high levels of eosynophilus, right. So again, something to keep in mind. And really for the most part, again, remember, my seramine genitis has a capsule, but my seragonaria does not have a capsule. Okay, my seramine genitis has a capsule, my seragonaria does not have a capsule. That is why we do not have a vaccine against my seragonaria because there's no capsule that we can make antibodies against. And really, the way you treat my any my seroleinfection, you give sephiraxone. Usually if it's like an STI, if it's like my seragonaria, you give like sephiraxone and doxycycline or sephiraxone plus esythromycin, right. And if you're close contact with a person who may enjoy this, you need to get it out of your fan pin, sephiraxone or sephiraxone. So what are some key questions you can ask with that? The preferred agent is actually right fan pin, okay. But if you're pregnant, you obviously cannot take right fan pin, you obviously cannot take sephiraxone because those things are both heterogeneous. So in those circumstances, you get sephiraxone. You get sephiraxone.

Okay, now, meningitis by age group, I've kind of talked about this already, but for newborns, think about the moneg gel, so G, E, L, right. So G for group B strep, strep E, E for E, L for the stereo, right. If you're old, think about cell, but drop the last L, right. So the S is strep pneumo, the E is equal, L, and then the L is the stereo. Like really, if you think about newborns and old people, just the second and third, like number two, number three, have the same equal, L is stereo, right. But for for newborns, it's group B strep for old people is strep pneumo, that's number one, right. And again, G comes before S in the alphabet, right. And newborns come before old people, right. So that's a nice way to keep that straight. And then for every other person, every other age group strep pneumo is number one. NICR, meningitis is number two, and the environment is number three. Okay, now the next question, what is the bog that is best described by the following information cluster, right. So ophthalmian, neonadrom, and arthritis, and a young individual, right. This is going to talk us, right. This is nicer, going to reapp. Again, remember, it's a gram negative caucus, right. Has no capsule. There's no vaccine for this, right. And there are many things going to react and cause, right. It can cause like your arthritis, it can cause serviceitis, it can cause pelvic inflammatory disease, or you have like the cervical motion tenderness and the bilateral and exo tenderness.

In fact, if you see arthritis in like a young person that's like sexually active and you know, maybe doesn't use condoms consistently, think about my sergonoreal, my sergonoreal and those circumstances. And then one way, how you think that tends to pop up on the USML disease, this thing called the FITSU Critic Syndrome. I'll say it again, the FITSU Critic Syndrome, the FITSU Critic Syndrome, it's an extension of the gonococcal infection to the capsule of the liver, to the hepatic capsule. That's something you just want to commit to memory. And really, in a sergon, in jitter, it is again, as I've kind of mentioned already. Think about it in a place with like a lot of people, like you know, like military recruits, college dorms, stuff like that. Now, next question, what is the bog best described by the following four cluster? So this bog causes bloodied area, causes the symmetric ascending paralysis. I hope you think about Camp LeBacter, you join with this. This is Guillembury Syndrome. Really, for the most part, you treat Guillembury Syndrome with plasma freces, that's the preferred method. You can also use IVIG as a temporizing measure before you get to plasma freces. Don't give steroids for Guillembury Syndrome. What's the classic CSF finding in a person with Guillembury Syndrome? Well, I hope you're telling me I'll be a minocyteological dissociation, right? So what does that term mean?

Well, the thing is normally, if you have a high protein count in your CSF, there's usually a high white blood cell count as well. But if you notice that that is not the case, then that is something called up. There's like a dissociation between our biumin, right, which is the primary protein in your bloodstream and the number of cells, right, a dissociation between that amount, like you're like, oh, this person's CSF studied the protein count super, super high. We only find in like five white blood cells, that's an example of Arbiminocytology dissociation that's pathodomonic for Guillembury Syndrome on MBM exams, right? And again, Camp L'Obaté de Gignonire, it's grand negative, it's a curved rod, it's oxidized positive, right? It's associated with beef consumption, causes like bloodied area, if I use one of the most common causes of bloodied area in the US. And it's high yield to remember that it grows at 42 degrees, right? So think of like a campfire, 42 degrees, that's, you know, that temperature is relatively elevated. And that's in decreased Celsius, not in decreased Fahrenheit, I guess which people use in the US. Back in Nigeria, where it comes from, people use decreased Celsius. I was so confused when I moved to this country, but you know, nah, I'm kind of familiar with the temperatures. Okay, now what is the bug that is best described by the following info cluster, right? So bloodied area special, hemolytic uremic syndrome, right?

So that's the trend of like hemolytic anemia, thrombocytopenia, acuteroenophilia. And then you can also see like travelers diarrhea, want to zoomers, revenge, watery diarrhea. And then this bug is a lactose fermenter. Well, these are all your equalized species, right? So the bloodied area one will be the O157 H7, right? So like, enterohymoragica, E coli, H2 S will also be E-HEC again, O157 H7, travelers diarrhea that's going to be E-TEC, right? Enterotoxigenic, E coli. And all the equalized species are lactose fermenters. And I guess I have some other questions on the answer to his slide, right? So what are the two classic toxins for E-TEC? Well, the two classic toxins, right? We have like the heat stable toxin that activates one-lil cyclase, and then the heat libel toxin that activates adenyl cyclase, right? The way I remember that is like Los Angeles, like the city, right? Like LA, right? So heat libel activates adenyl cyclase, right? So, and then the other one is the other one, right? So, you know, heat stable toxin activates a cyclic GMP, right? So the thing with E-TEC, right? The thing with E-TEC is, you know, it activates these things, and obviously you have the secretion of like water, of like sodium chloride, electrolytes, and all that stuff. And that will cause like a secretory diarrhea, right? Now, the thing is because it's a secretory diarrhea, this will be associated with an elevated, no, not an elevated, low stool or smaller gap.

So this is a smaller gap concept, it's not something you find in many resources, but it's something your friends at the MBM are beginning to care about, and your stool or small gap is basically like 290 minus 2 times your the sum of your stool, sodium, and your stool potassium, right? So the thing is if you have a secretory diarrhea, that means that that diarrhea is electrolyte rich, right? So you have a ton of like sodium and potassium. So if you have more sodium and potassium, and you're subtracting those from 290, then whatever you get from that, it will be a smaller number, right? Contrast that with like an osmotic diarrhea, so let's say a person has like lactase deficiency, they have like malabsorption or something, those people will have the the things in their stool, like their stool have a greater proportion of other stuff that's not sodium and potassium, right? So osmotic diarrhea is malabsorption based diarrhea, they tend to be associated with a high stool or smaller gap. Okay, so again, high yield points with diarrhea, I've talked about secretory diarrhea, again, E-Tech is a classic one, Vibrocaler is another classic one, right? And then your osmotic diarrhea is, I think about like an inflammatory process or like malabsorption, or if you have like a non-absorbable sugar, like these are sugar-free candy, the thing can cause chronic diarrhea, like I tell people in general, sugar-free candy is probably not the greatest idea in the world. And then C-Diff, right?

Think of it again, it can cause like a nasty nasty diarrhea, it can cause both a secretory diarrhea, but it can also cause an inflammatory diarrhea as well, right? Especially if you see a person have like diarrhea after a course of one type, it's a vein in sorts, because the endemic is now shining away quite a bit from clean domestic medicine, think about C-Diff, okay? And remember if you're in chronic PPI therapy, that can also cause C-Diff, because PPI is right, the inhibit, so the proton pump inhibitors, the inhibit the production of, they give you the production of acid, right? So if you're not making acid, you, you cannot keep like your GI flowing check, right? So that's what can happen with that. Remember if you also take chronic PPI's, that can cause osteoporosis, and that can also cause like a B-tov deficiency, you can raise your risk of aspiration pneumonia. I'll talk about the mechanisms behind this in the future if I've not already in some old podcast, but this is already more than an hour so I want to wrap this up. And then enteropathogenic equal, it's actually very low yield, right? But if you see like a nasty nasty diarrhea, like a nasty diarrhea in a pediatric population, think about EPEC, but the first thing I want you to think about the way you see diarrhea in a piz patient, go with a rotovirus, go to rotovirus. Okay, so let's do some of these diarrhea clinical scenarios. I mean, not get to all of them.

I'll just kind of hit on the high point so that I can wrap up this podcast, slash video. So what are your diarrhea after you come from a trip, right? That's Travellers Diary, that's ETAQ. What are your diarrhea with rice water stools? That's a vibrocolor, right? What are you diarrhea in a Hancker camper, right? Especially some of the drinks from a stream, fast-melting diarrhea, that's a GRD in Lamblia. Remember, that's also common in people that have IG deficiency. What are you diarrhea in a cruise ship, right? That's that's that's neurovirus, right? It's also called the no walk virus. What are you diarrhea in an infant that's rotovirus, right? That's high up to now. And then what are you diarrhea in an each patient, right? That's crypto-spiridium. Don't pick crypto caucus. The NV Me can do like a plea on words on the exam with you, so don't don't don't fall for that. So what are you diarrhea in an each patient, that's that's crypto-spiridium parvin. You can treat that with like a neither socks or nine, if I'm not mistaken. And then bloody diarrhea after consuming beef that can be like, you know, Camp Luba, Tragicinai, bloody diarrhea from poultry eggs, that's more like salmonella, right? Bloody diarrhea in the city of Alatos, fermenta, that's like equalio 1577, right? Most common cause of bloody diarrhea in the U.S. if I'm not mistaken is Camp Luba, Tragicinai, diarrhea and ascending paralysis, right? That's a Guillembrace syndrome, right?

That's Camp Luba, Tragicinai, although again, these days the NV Me can give you questions on Guillembrace syndrome after having like an upper respiratory infection, a GI infection, a urinary tract infection, as long as you have like a mucuso surface infection and then you have a symmetric ascending paralysis afterwards, that's Guillembrace syndrome. And then, um, diarrhea after treatment for an anaerobic infection, right? So this is diarrhea after you get an antibiotic, that's going to be C-dif. Um, diarrhea that feels like a appendicitis, right? So like pseudo appendicitis, especially after you take pork, think about your senior enterocolerica, it usually causes a bloody diarrhea and then the protozoal cause of bloody diarrhea, think about entamiba, histolytica, um, and then I usually that can also cause like liver abscesses and liver problems. And then bloody diarrhea with a small inoculum, right? That's shigella, shigella you need as just little as you as like 10 shigella bugs and they are in trouble. And then bloody diarrhea and HUS, right? Again, that can be shigella, that can be ehec, so O157 H7.

And then diarrhea after consuming like oysters, slush seafood, uh, think about like vibrato parachymolyticus or vibrato voneficus, although like just kind of jumping to the next one, vibrato voneficus tends to have this association with, um, people that have like liver disease, like people that have liver disease, they tend to have like worsened morbidity and mortality when they get infection from vibrato voneficus. And then, thereafter, so many fresh water, uh, that can be like, uh, um, can be many things, it can be like aromones. And then, um, diarrhea with massive amounts of fluid electrolyte loss, right? This is like the, you're losing 18 liters of fluid a day, um, this is cholera. And we treat it with like oral rehydration therapy, right? Remember oral rehydration therapy is a salt sugar solution because you're essentially thinking, uh, advantage of the SGLT1 transporter that we find in the GI tract. And then, thereafter, consuming reheated rice, right? I've, I've actually had this diarrhea before. Ah, it was, it was pretty bad. This thing is awful. It is awful, awful, awful. Um, so if you see like Chinese fried rice, uh, association or Korean barbecue or something like that, uh, again, I'm not being a racist. That's just the association, believe it or not. And again, these associations actually show up on the exams. Think about, um, think about, um, basilos serious after that, uh, with that, there are two as after continuing potato salad. This one is easy.

This is a, this is a, this is a, um, um, stuff for you, right? Stuff for you. And those are the answers on the phasing slide. So my reference is the Lyme disease photo I use is from medicinenet.com. The basilos and three six photo uses from infectious landscapes.org. So, um, as I do at the end of every podcast, I offer one on one, two during an large group, two during for a ton of exams. Step one, two CK, two CS, step three pre clinical medical exams, 30th shelf exams. If you're medicine resident, I tutor for the injury exam. If you're a college student, I tutor like physics, Genkame, Okam, biochem, astrology, physiology, I tutor for many of the MCAT subjects as well. And then if you need like coaching for, um, like if you're medicine, if you're a resident, if you're a medicine or a plant to residency, so like an era, so our college student are planning to med school, so like an MCAT staff, I offer like one on one coaching for those, right? So like personal statement, editing, application editing, rec letters, mock interviews. And, um, and then I offer these booster courses for the USMN Es, right? It's like 10 hours for step two, again, step three. It's 20 hours for step one. Um, if you're interested in those, they're like, the accost is that essentially review like the most to nose for these tests in like a clinical vignette, rapid fire fashion.

If you're interested in any of those, either reach out to me through the website or you can send me an email at divine intervention, podcasts with an S.S.D.N. at gmail.com. So please, um, subscribe to the You Tube channel. I want to hear the thousand our subscribers hopefully before the end of the month. And please share this at your MCAT school, anywhere, and then please also subscribe to the podcast. I have this and please leave like, you know, like, uh, like, uh, like a recommendation or comment, it helps any little bit helps. You can actually find these podcasts on Apple podcasts, on Spotify and on Google Play. And there's also the website where I'm going to actually post the slides. So the slides will only be posted on the website, divine intervention podcasts, so you can download them from there. So have a wonderful rest of your day. I'll see you next time. Thank you. God bless you.

Draining abscesses containing yellow, granular material (sulfur granules).

Borrelia burgdorferi; transmitted by ticks.

Fever, new heart murmur, and systemic infection evidence (e.g., rash, emboli).

Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitidis, and Cryptococcus neoformans.

Gram-positives have a thick peptidoglycan layer; Gram-negatives have a thin peptidoglycan layer protected by an outer membrane containing LPS.

Escherichia coli; it is typically uropathogenic (UPEC) and often possesses adhesins/virulence factors.

S. pneumoniae, H. influenzae, N. meningitidis.

Inhibits cell wall synthesis by binding to D-Ala-D-Ala termini (a peptidoglycan precursor).

Encapsulated organisms, such as S. pneumoniae or H. influenzae.

Fever, new heart murmur, and signs of systemic embolization/infection.

Bordetella pertussis (whooping cough).

Rheumatic fever following Group A Streptococcus pharyngitis.

Fluoroquinolones (e.g., Moxifloxacin); also Ciprofloxacin or Novobiocin.

S. pneumoniae, H. influenzae, N. meningitidis.

Inhibits cell wall synthesis by binding to D-Ala-D-Ala termini (a peptidoglycan precursor).

Encapsulated organisms, such as S. pneumoniae or H. influenzae.

Fever, new heart murmur, and signs of systemic embolization/infection.

Bordetella pertussis (whooping cough).

Rheumatic fever following Group A Streptococcus pharyngitis.

Fluoroquinolones (e.g., Moxifloxacin); also Ciprofloxacin or Novobiocin.