DIP Episode 12 - Bacterial Cases A

Hello, welcome. My name is Divine. I am a 4-fear medical student. Today is the 12th episode of the Divine Intervention Podcasts. I am going to be going over bacterial cases. We'll try to review some high-yield information relating to bacteria. This will be the first of many podcasts relating to the bacteria. I wish everyone studying for step one of the best. If you're studying for step two, if you're with the authorities, rock in it out right now because you don't have much to do. Because you're about to start residency, I wish you guys all the best. If you have any questions or any feedback on the podcasts, feel free to reach out to Divine Intervention Podcasts at gmail.com. Let's get right into it. The first question. 26-year-old presents to the ED with a two-day history of high-fever and joint pain. He recently completed a tough mother race in Oahu. Physical exam is notable for conjunctivalary fema with no pure lane drainage discharge. ASTLT are markedly elevated. Creatin is 2.5. So, the questions I have. What's the bug? What are its special properties? What are the risk factors? And how do you treat this bug? The thing is, they generally do not give you names of places on NVME exams for sure. Those country names or state names or city names are almost always related to something that will give you a clue to answering the question. In this case, I talk about Oahu, which is in Hawaii. That's one, two.

I talk about a person going for a muddy-ish race where they probably are in contact with a lot of dirty water and things like that. Hopefully, you are thinking about leptospirosis. It's caused by leptospiral interrogants. You know this is a spirochitis. Just like Trapunima palidum, it should be visible under dark-filled microscopy. That's not very sensitive. The classic presentation is this bug has an association with exposure to bodies of water that are infected with animal urine, so like urine or rooting-turing, anything like that. You definitely want to know the classic presentation. It's classically presented with high-fever, joint pain. Usually, people have conjunctivitis, but it's a non-pure-lent conjunctivitis. The thing is, if it's left untreated, it can become very severe and create something called well-desize. That's where your liver explodes. If you ever hear me say your liver explodes, I'll just mean you have some kind of hepatitis. Your liver explodes and your kidneys explode as well. That's why the creatinine is elevated. The way you treat leptospirosis is with penicillin, or you could also use the 30th inhibitor doxysyclyrim. Doxysyclyrim is a kind of tetracycline. The biggest factor is exposure to bodies of water that have been infected with rodent urine. Next question. 23-year-old presents with left jaw pain. He recently had a root canal procedure, completed in a foreign country to reduce cost.

Physical exam is notable for a lumpy mass just below the left maxilla. Gentle palpation leads to the expression of purulent material. So what's the bug? Without special properties? What's the classic presentation? How do you treat this issue? Contrast with a closely-releafed cousin. This closely-reveafed cousin is a particular bug and going after certain sources of this infection. The bug has special properties. I'll talk about how you also treat that close cousin. This person had a dental procedure and then they have a mass that's draining pure-releafed material, a cervical facial mass. Hopefully, you're thinking of acetylomycesis, remember it's a filamentous, gram-positive rod that is anaerobic, so it doesn't use oxygen. It is not acid-fast, so it doesn't stain positive with the zionose-instein. You can already begin to think that the second part of the question is released to no cardio. The classic presentation is a person that got some kind of dental procedure done and then they have some kind of infection where the infection drains sinus tract. You see what the classically-called sulfur granules. Those sulfur granules just contain dead bacteria and a ton of neutrophils. The way you treat this bug is you give penicillin. The close cousin I was referring to here is no cardio. Unlike acetylomycesis, that's an anaerobic. No cardio is an aerobic. Unlike acetylomycesis, that is not acid-fast. No cardio is, in fact, weekly acid-fast.

In fact, it stains positive with the zionose-instein. Just like acetylomyces, no cardio is a filamentous branching gram-positive rod. The thing is, it classically presents as abscesses in many different organs of the body. The way you actually treat it is with back trim. Back trim is the treatment for trimethyl-prim-sulfome ethoxazole. Hopefully, remember that sulfur-methoxazole is an inhibitor of dihydroctorates in this, which is the enzyme that metabolizes papa to dihydrofolate. Then, trimethyl-prim is a dihydrofolate reductase inhibitor. It prevents the formation of tetrahhydrofolate from dihydrofolate. Remember, there are other drugs that work that way. Drugs like methyl-tracksate and drugs like pyramethamine. Just something to keep in mind. Now, just as an aside, just real quick as an aside, what is one high-yield enzyme that is expressed by no cardio, by H-pilory, by proteospirabilis, by ureplasma urelyticome, by clapsilla pneumonia, and also by stuff epidermidis, if I remember correctly. That's urese. Just another added treatment for you there. Just real quick, if you hear a murmur on a quotation of a person's chest and you recently had a dental procedure, what are you thinking about? I hope you are saying strawberry dance. Let's jump on to the next question.

So, a seven-year-old male who recently went through an ozology class trip to a forest in North Carolina presents with a 24-hour history of a temperature to 104-datt super-high, severe headache and shortness of breath. Physical exam is notable for a rash on the palms and soles. Ding-ding-ding-ding-ding-ding. His mom mentions that this rash initially started on the ankles and wrists and spread to his trunk. Ding-ding-ding-ding-ding-ding. So, what's the bug? How is it transmitted? What are its special properties? And how do you treat this bug? This bug is actually kind of unique in that there are different treatment strategies for different populations of individuals. So, talk about that shortly. Okay. And then I will talk about some special wear testing and the CBC electrolyte anomalies you get with this bug. So, this is a Riketsiya Riketsai. So, this is Rocky Mountain spotted fever. So, hopefully the clue for you was the rash on the palms and soles. Remember the moneq you learned as you are studying for a step one that you drive Kawasaki cars with your hands and feet. So, like Kawasaki A, Riketsiya Riketsai and secondary syphilis and Kawasaki's disease are present with a rash on the palms and soles. So, this person has Riketsiya Riketsai. That's Rocky Mountain spotted fever. It's a zoonotic infection. It's carried by the dermiscented tech. So, that's something I want to know. It's also a gram negative intracellular bug. And it's actually an obligate intracellular bug.

The reasoning behind that is that it cannot make enough ATP for its own use. And it can actually sting positive with GIMZA. It can actually sting positive with GIMZA. Other GIMZA positive organisms include bugs like Borrelia, Bodofreed, Acosis, Lyme disease and Clamidia. Now, you definitely also want to know your geographic association. Not necessarily the Rocky Mountains, but states like North Carolina, Tennessee or Oklahoma. And the rash spreads in a centripetal fashion. So, it starts on the ankles and wrists. It then goes to the trunk. So, it spreads from the outside inwards. And then it spreads back out to the palms and soles. And in general, for every patient that has Riketsai Riketsai infection, you go ahead and treat with Doxycycline. So, you've probably heard this thing, which is largely true for most other bugs, but this one specifically. You've largely heard that if kids are less than eight, instead of giving them Doxycycline for infections like Lyme disease, for example, you give them a moxicillin. That is true for Lyme disease, but that is absolutely not true for Riketsai Riketsai. For everyone, including kids that are less than eight years old, you treat Riketsai Riketsai with Doxycycline. Because usually the kids get those for like a very short period of time. So, there is a very low risk of them having the toothless coloration and the stunten of bone growth that you come to expect with the tetracycline.

But in pregnant women, in general, you give Lauren Fennecoll. Hopefully, remember that Lauren Fennecoll is a 50 years, peptidal transfer is inhibitor. Now, the way of testing that you use for Riketsai spics in general is the Will Felix test. Basically, you... The antibodies that are buddy mix against Riketsai Riketsai. For some reason, they are gluten-atorn. They are exposed to antigens from proteospicis. So, that is what constitutes the Will Felix test. It is just a good test for most of the Riketsai spics. One way they can test this in the context of another bug on your exams is with Cocciella Boneriai. Cocciella is... it is sort of related to the Riketsai spics, but it is actually Will Felix test negative. And in general, with Riketsai infections on exams, they will give you the person having low platelets, so they will have a thrombocytopenia, and the assodium concentration in the blood will also be low. So, they classically have a hyponychromia. As an aside, also remember that hyponychromia is associated with legionella, nomofelola. We will talk about that in a later question. Okay, so next question, this is actually multiple choice. So, it is a 33-year-old female who presents with a 12-hour history of severe growing pain. A past medical history is unremarkable, although she recently received sephazolem for an infection. So, sephazolem is a sephalous sparring. The patient is uncooperative during the physical exam due to severe pain.

Your analysis reveals a pH of 7.1 that is really high. Other studies are pending. CBC and CNPA within normal limits results of a non-contrast helical CT that is like the diagnostic test of choice for the Pfizer. Results of a non-conhelical CT are shown below. What is the most likely cause of this patient's symptoms? So, if you look at this x-ray pretty well, you can see that it is clearly a star corn calculus. So, you are thinking of some kind of ure-spositive bug, and the only one that fits that description here, consequently, is proteus merabilis. So, the answer here is D. So, the answer is D. So, again, urine, high pH, imaging, star corn calculus, think about a ure-spositive bug. So, like, pain merabilis, staphsaprophytic cause, glipsialis, species. And, in general, if a person ever has nephrolithiasis, the thing you generally want to do is not to get an x-ray. That will be the wrong answer on the exam. So, the thing you want to get is a helical, is a non-contrast helical CT scan. In general, on x-ray, you generally reveal kidney stones with the exception of ure-cacid stones. Remember, those are really loosened. So, those cannot be picked up on an abdominal film. Now, there are certain high-yield associations you definitely want to keep in mind, right, with kidney stones, right? So, the most common kind of kidney stone is calcium stone, okay?

But, the thing is, you will think that everyone that has calcium stones, calcium kidney stones, have high levels of calcium in the blood and high levels of calcium in the urine. That is not true, okay? In general, these people tend to have normal calcium levels and elevated levels of calcium in the urine, right? So, you may potentially be able to treat these problems with a thiozide diuretic, right? Because, remember, thiozides, they help you retain calcium in the urine, but loops actually help you dump calcium in the urine. So, you probably don't want to give a loop diuretic to a person that has a history of calcium kidney stones. Staghorn calcular, I've talked about that with the urea-spositive bugs. Urea-cassage stones, gout, I've talked about that. If you have any kind of hematologic malignancy, right, where you're overproducing an overkillin lymphoid cells or other myeloid cells. As you kill those cells, you release a lot of DNA into the surroundings, okay? So, you can imagine that you can also get a very high urea-cassage load with that. They can precipitate anaphylithiasis. That's why you generally give a lopyrinol of a boxostat, which is xanthinoxidides in habiters, to people that are getting chemotherapy for the hematologic malignancies. Okay, now, you can also get disease in the terminal helium that can cause hyperoxyluria, okay? And if you have hyperoxyluria, you can get calcium-oxelite stones, okay?

If you also try to poison yourself with antifreeze, you can also get calcium-oxelite stones. And in general, the way you treat lymphoid ethyasis is you hydrate the patient, you give them pain control, or for a big one, like the staghorn calcular, you probably need to do some kind of surgery or like super-hyper-dynamic shockwave with lithotrypsi. Well, I was in general for staghorn calcular, you're going to get a urologist to get that stuff out. There's no way you can really use some whips to break something like that up. And as an aside, don't forget the bog of the hour, right? P-mirabolis, it's gram-negative, it's oxidis-negative, okay? I'll talk about the oxidis test in a little, little slide, okay? But it's gram-negative, it's an oxidis-negative rod, okay? It does not grow in maconkey's agar, right? So it's a lactose non-fermentar. And one classic way to describe P-mirabolis in exam questions is it has swarming motility. If you see swarming motility, stop reading the question, it's almost certainly going to be P-mirabolis, okay? And again, it's your espozative, it can form ammonium magnesium phosphate stones, okay? Those are known as true-vide stones or staghorn calcular. But those are classically coffeinated shaped, okay? And again, the urine peach is almost always high, okay? And in general, if you have like a bladder infection, right? So cystitis from P-mirabolis, you're classically treated with bactrim, right? So trimethoprims are from ethoxazole or cybrofloxis.

And remember, cypris of fluoroquino-lones, work by inhibiting a DNA gyris, also known as topyl summaries, okay? But if you have like pylonofritis, you generally want to either give cypral or you want to give a septrax. And I'll say in general, on NVME exams, if a person has pylonofritis, your go-to drug is septrax. That is the most common answer choice on exams. Okay, so let's go on to the next slide. A 10-year-old kid presents with a three-day history of temperature to 104 severe headache and shortness of breath. A 4-year-old sexist-stolic murmur is heard of the apex. He lives on a farm with his parents, where they raise shape and cattle. Plytolet count is 90,000, okay? So what's the diagnosis? What's the bug? What are its special properties? What kind of diagnostic testing can be done? Then you'll have other associations, we'll talk about those. And how do you treat this bug? Okay, then we'll talk about four bugs that are carried by the exodistink. And I put on the money there for you, a-ben. I don't know how helpful that is, but we'll talk about that. So this kid plays with cattle and sheep, okay? And then this kid has very high temperatures, severe headache, shortness of breath, and thrombocytopenia. A normal pleated leg count is from 150,000 to 400,000. If you see this, I really hope you're thinking about Q-fever, okay? From Coxiella, Buonediai, okay? Remember, it's an obligated intracellular bug. It actually forms spores while we're on this topic of spores, right?

So remember, you'll high yield spore forming bugs. There's your close-tridium species, there's your bacillus species. There is crypto-coc- no, not crypto-coccus. So, close-tridium, bacillus, Coxiella, there is one more I'm forgetting for some reason. Well, hopefully we'll come before the end of the podcast. Okay, so from spores, okay? And the way you actually diagnose C-bornediai, usually it's diagnosed by clinical history, but you can also do an indirect fluorescent antibody test, okay? Now, some other associations with C-bornediai, it actually has some unusual things that your friends at the NBME love to test quite often, okay? So it's actually associated with endocarditis, right? That's why this kid has the farthest six esstolic murmur in the question stem. But the thing is, in general, the blood cultures, right? Because if a person, if you suspect the endocarditis, you get blood cultures, right? The blood cultures with C-bornediai and Ducarditis, classically, do not grain anything, okay? So that's an example of a culture-negative endocarditis. If you see culture-negative endocarditis, besides the Coxiella-bornediai, which is actually one of the most common causes of culture-negative endocarditis, you also want to think about your Hasek organisms, right? So bugs like hemophilus, attino bacillus, cardio bacterium, echinolankingela, okay? Those are the high-yield causes of culture-negative endocarditis.

And like I mentioned, in a previous question, Coxiella-bornediai is Will Felix-negative, okay? You actually treat with Doxycycline. In general, a safe answer for the treatment of tic-born eonesis is Doxycycline, okay? It's only if the kid is less than eight years old than you proceed with amoxicillin, with the exception of what bug? Recatericocyc, good. So, the exodestic, we, I put that as the last question, it carries anaplosmosis, okay? It carries Babesia-micro-d, remember the multiscross pattern in red cells on ginsesthenin? It actually carries Ehrlichia as well, okay? It carries Ehrlichia. At least 13 species of Ehrlichia. For the most part, on exams, if you see Ehrlichiosis, think of it being carried by the lone-start tick, okay? And then it also carries Borrelia-bogdophari, so that's the last big. Which, remember, Borrelia-bogdophari is a spirochite. And just as an aside, remember that Ehrlichiosis, right, presents with like headache, fever, thrombocytopenia, so it's kind of similar to Coxila-bogneri-i and Ehrlichatsia-ricat-sign. But the big thing you want to keep in mind is that you do not get a rash, and the white count is usually low with Ehrlichiosis, right? So you get the headache, you get the fever, you get the low platelets, but you also get low white cell count, and in addition, you generally do not have a rash on like Ehrlichatsia-ricat-sign, where you do get a rash. So next question.

21-year-old female presents with mild vaginal paritis, and what appears to be some vaginal discharge? A vaginal swab is obtained. pH of the obtained secretion is 5.1. With my cross-copy, revealing epithelial cells, with bacteria crowded around the edges, stinging, the addition of CoH to this sample, so potassium hydroxide, is accompanied by a fishy smell. Ding, ding, ding, right? So hopefully you're thinking about the bug and thinking about in this question. So what is the bug? What is the classic presentation? How do you treat this? Do you need to treat the partner? And I will give you a bonus for free for your OB-GYN shelf exam in the future. So this is hopefully you realized from the outset, fishy smell from the vagina. That's a bacterial vaginosis, okay? Classically caused by Gardner-Ele vaginalis, okay? So the classic presentation is a fishy thing. Vaginal discharge, usually the pH is greater than 4.5 of the vaginal secretions. Contrast that with the pH less than 4.5 with the kind of diocese, okay? Trichomonas vaginalis is also associated with a vaginal pH greater than 4.5. Although for that, you'll see like the frothy, green, nasty, guppist of coming from the vagina. And you'll see the strawberry cervix, right? So like these plantations on the cervix. Now the cells I described are clue cells, okay? That's what you see on my cross-copy. So pithelial cells that are just chock-full with a lot of Gardner-Ele vaginalis, you treat it metronidousol, okay?

Remember the get-gap on the metronomonic for the bugs that can be treated metronidousol, right? So like, giardia, remember, giardia causes the fast-milling diarrhea in a patient that drinks from a stream when they go on a hike. There's an intamiba histolirica. It's one of the protozoa causes of a bloody diarrhea. Districtomonas vaginalis, I just talked about that. There is Gardner-Ele vaginalis that causes bacterial vaginosis. There's anaeropes and there's protozoa. So, okay, so get gap on the metronomonic for the bugs that are covered by metronidousol. Now, remember if you treat it metronidousol and then they describe that this person presents with hypotension and flushing and they feel like crap, like they're hungover. Well, hopefully you're thinking about the diesopharm side effect, okay? From metronidousol inhibiting as a tauta-hide or dehydrogenic. Okay, so this is how they can link from ecology with microbiology and biochemistry very nicely in an exam question. Okay. In addition to metronidousol, you could actually potentially give clean dameisin for Gardner-Ele vaginalis. I mean, it works pretty well, but that's not the classic answer on exams. Classicly on exams, the equafter metronidousol. And remember if they describe a person that takes a clean dameisin for Gardner-Ele vaginalis and then they present with a fast-moving watered diarrhea after they took clean dameisin, okay? Hopefully you're thinking about a c-difcolitis with that, okay?

Now, in general, bacterial vaginalis is not sexually transmitted, so you usually do not need to treat the sexual partner, okay? And the OB-GYN association here is that bacterial vaginalis actually has an association with preterm labor. You'll thank me when you potentially see this on an OB-GYN shelf you will take in the future in your 30. Okay? So, let's move on to the next question. So, STI triggers. These are just statements that should trigger memories of certain common causes of ST Is, okay? So, the first statement is pinless shanker, right? Let's tip-aledom that syphilis. That's pretty easy. You'll give me a silly one for that, okay? Now, pinful genital ulcer with an erythematos bays and soft ragged edges, right? So, hopefully with this you're thinking about hemophlos ducryl, okay? Remember, the ulcer in H-ducryl is pinful, right? So, hemophlos ducryl makes you cry, okay? That's a very classic nomonic that is thought. And for H-ducryl, you can give it a zythromycin, you can give us a tetraaxyl, okay? Remember, safe drag. So, is a third generation syphilis sparring? Is it thromycin? Is it 50th inhibitor? It's a macaillin inhibits translocation. Next one, pinful vesicles, right? So, this is not an ulcer. Pinful vesicles on an erythematos base that's H-s-v, classically H-s-v2, right? So, that's genital herpes. Large intra-nuclear inclusions on zank smear, okay? This is also H-s-v2. Although, you can also find that in human herpes virus 3 or V-s-v, okay?

That's why zank smear is not very sensitive for herpes simplex virus. Now, school of fish pattern on microscopy, this is also the cause, this is also the bug that makes you cry, okay? So, it's hemophlos ducryl. And then, spyrokites, detected on dark-filled microscopy, the spyrokid you're thinking about here is triplonymapyladum, right? And then, the positive agent in syphilis. Pinless ulcer, heart-based, raised edges with lymphadenopathy. This is, again, also syphilis, cause by triplonymapyladum. And then, if you see pinless ulcer, and you see this buzzword, very hard, like these two buzzwords, very high up to no-dose. B-f-red base, irregular edges. B-f-red base, irregular edges. And usually on exams, molymphadenopathy, this is Klepsiela granulomatis, okay? So, this is the causative agent of granuloma in granuloma in granuloma. And for this, you just give it a zythromyza, okay? And you can see, like, dunovan buddies in white cells when you do microscopy, okay? So, they are usually shaped like basil, like, they're shaped like rods. So, again, pinless, think about Klepsiela granulomatis, causing granuloma in granuloma in granuloma in granuloma, and T-palidum causes syphilis painful. Vesicles, think more about H-SV2. All serves, think more about hemoflose ducry, which makes you cry. Okay, next question. Most common cause of UT Is in the US. UTI in a sexually active young female, okay? Plus special characteristics of this book, right?

So, the most common cause of UT Is in the US is equal, like, causes like 85% of UT Is. Okay, remember, it has, like, a fimbria that enables it to attach to urinary epithelium. And remember that equalizer is also a part of the normal GI flora. But UT Is sexually active young female, and you don't see equalizer as an answer choice on exams, go for staffs atrophidicus, okay? Staffs atrophidicus is actually the second most common cause of UT Is in the US, okay? And the thing is, classically on exams, you see UT Is and they say, oh, they did a urinalysis, whatever. And it was positive for nitrites, okay? The thing is, staffs atrophidicus is actually nitrite negative, so that can be a very nice clue on exams, okay? So that may be something to tip you more, tip you more in that direction. Now, because remember, nitrite positivity is usually used to detect the entire bacteria, you see, okay? Staffs atrophidicus does not belong to that group, so it's nitrite negative. And staffs atrophidicus is also UR Is positive, okay, just like Hpilory, Klebsilla species, like Klebsilla pneumonia, Hpilus, there was one of the box, Prudios Mirabilus, okay? And URI plus my URI lid become, okay? So it's UR Is positive, it's cutely positive because it's a staff species, obviously, okay? But unlike staffs for areas which is squagally positive, staffs atrophidicus is squagally negative, okay?

And unlike staff at Pydramidist, that is Nouveau biocin sensitive, staffs atrophidicus is Nouveau biocin resistant, okay? So how you to know those things? Next slide. 76 year old male presents with a three week history of shortness of breath and mouth fevers. Physical exam is notable for what appears for, sorry, for pain for red. Sorry, made a type on this slide, I'm just corrected now so I don't forget. And post-crap when I post the final thing. So physical exam is notable for pain for red lesions on the finger pads. Fundoscopic exam reveals bilateral retinohemorrhage with pale centers, okay? So pain for lesions on the finger pads, I don't know, are you thinking of something that starts with osler? Bilateral retinohemorrhage with pale centers, are you thinking of something that starts with rough? Okay, a three out of six murmurs of scothed at the apex, ding, ding, ding, ding, okay? So blood cultures here detect a gram positive, catalys negative, gamma-himolytic caucus, whose growth is inhibited by 6.5% sodium chloride. Okay? What is the next best step in management? Okay, and then I will say a few words about interococcus. So with this, I hope that I could convince you that this patient has endocraditis. Okay? And the bug I'm thinking about here is strebobus. Okay, strebobus. If you need to memorize your diagnostic trees, unfortunately for step one, for the bugs.

Okay, so if you follow the diagnostic tree that you should have learned from first state, you should realize that this is strebobus. Okay, it's a kind of group D streb. And get demonstrates a gamma-himolytic. Okay, so this is strebobus. Okay? Another closely related bug that we mentioned on your exam instead of strebobus is a strebobus. It's a streb galoleticus. Okay? So note your parameters here. It's a gram-positive bug. Okay? It's a streb species, so it's catalys negative. Okay? And because it exhibits gamma-himolysis, it shows no-himolysis on blood at a guard. Okay? And its growth is actually inhibited by 6.5% sodium chloride. Contrast that within the interococcus species that can grow on 6.5% sodium chloride. Okay? This bug, if you ever find it in a person's blood, your next step in money has been very classic exam question, is to get a colonoscopy. Okay? Because about 30% of patients that have strebobus bacteremia actually have a colon cancer. Okay? And the way you treat strebobus is you can give penicillin or you can give an comaicin. And for the interococci, which is somewhat closely related, streb species, they are gram-positive, they are catalys negative, they also exhibit gamma-himolysis. Okay? Although you may read some text to say, oh, it's a variable-himolysis, but that's not really high-yout for the exam. Okay? But unlike strebobus, okay? The interococcus species actually catalys negative, I mean, sorry, they actually grow on the 6.5% sodium chloride.

In fact, they are actually a part of the normal GI floor. And they are usually associated with subaccurendocritis, right? So something that sort of takes weeks to broover as against the acute endocritis, you get with stuff, or else, that comes on really, really quick. Okay? So if you hear about subaccurendocritis after a GI or a GI or a procedure, think about the interococcus species. Okay? And as an aside, don't forget that Vencomisin resistant enterococcus, right? So interococcus that Vencomisin doesn't work for can be treated with linesolid. Okay? With linesolid. I remember linesolid is your 50-S P-site inhibitor, so it basically kills initiation, like the amino glycosides. But remember, the amino glycosides perform that role from the 30-S side of things. Okay? I remember linesolid is bacterostatic, and it has an associational serotonin syndrome, right? Because it's actually a weak inhibitor of monoaminoxidics. And if they don't give you linesolid as an answer choice for the tributyl VRE, you could also use your streptograms. Okay? Quinopristin, daphylpristin. Remember, these are 50-S inhibitors, and the 50-S A-site inhibitors. Okay? So they basically shut down the longation step of protein synthesis. Okay? Let's go to the next question. 30-year-old female presents with a 12-hour history of severe vomiting. She has passed seven stools in the last eight hours. Oh no. She visited a Chinese restaurant. Ding, ding, ding.

Last night, when a few friends, where they had some fried rufs. Ding, ding, ding, ding. Okay? So what's the bug? What are its toxins? What's the association? And what are the special bug characteristics, right? So this is a gimmie on an MBME exam. Okay? This is bacillus serious. Okay? Be serious. Okay? So be serious. Pay attention to this podcast. Just kidding. So bacillus serious. Okay? This is actually a heat stable. It actually produces two kinds of toxins. One toxin is a serolite toxin that is heat stable. Okay? And the thing is, this toxin is actually what causes the severe nausea and vomiting. That you get with bacillus serious, direlling infection. Okay? So you may ask yourself, why would this be? Think about this. If you think about the nausea and vomiting and associated with chemotherapy, right? The classic drug used is Zofra, right? On Dancer Trum, which is a serotonin receptor antagonist. Okay? The thing is, on the flip side, it so happens that the serolite toxin that comes from B serious actually acts as a serotonin receptor agonist. Okay? So if you're something that activates serotonin receptors, it actually causes a lot of nausea and vomiting. Contrast that with the drug that's used to treat nausea and vomiting in chemotherapy. Okay? On Dancer Trum, which is a serotonin receptor antagonist. Okay? So just something nice to keep in mind.

Now, in addition to the heat stable serolite toxin, it also has a heat libel toxin that actually kind of works like a toxin that I'll mention in a later podcast. But the heat libel toxin actually activates adenylate cyclase. Okay? So if you activate adenylate cyclase, you convert more ATP to cyclic AMP. And then you overactivate the cystic fibrosis transmembrane conductance receptor. Okay? So the CFTR receptor, and by doing that, you release more and more chloride. As that chloride is going to the lumen of the GI tract, it happily walks along with water. Okay? So you get some kind of a secretory diurea. Okay? So you get a secretory diurea with a bacillus serious. Okay? The bog is aerobic. Remember, it's a bacillus species. Basilus species deforms spores, but they are aerobic. Contrast that with clostridium species that form spores, but are an aerobic. Okay? So it's an aerobic bog. It forms spores, and it is mota. Okay? It is mota. Okay? Although bacillus and thresus also has those similar properties, but B and thresus is actually non-muta. Okay? So something to keep in mind. And again, the classic assertion on exams, fried rice consumption, Chinese restaurant, watery diarrhea, and a lot of vomiting, that's bacillus serious, so 100% of the time. Okay. Next slide. A 30-year-old G1 P1 presents to Libra and the Levery at 39-weeks gestation with regular phosphol contractions. She missed her 35-week appointment. It's not a good sign.

A quick vaginal smear today reveals grand positive organisms that exhibit beta-humoluses and irresistant to bussy tracin. What is the next step in the management of this patient? Okay? And then I just put an addendum question at the end. Three drug cocktail for new needle meningitis. Right? So this is a stripy galactia, okay? Grobis strap. The next best step in management will actually be to give mom intra pardon penicillin, right? So penicillin before she delivers. Remember that Grobis strap is catalase negative, okay? It exhibits complete humoluses on blood eager, right? So it's beta-humolidic and it's hiporyth and cum test positive. Okay? It's just one of those weird things you unfortunately need to know for your step one exams. And basically if you see an exam question that talks about any kind of notable infection in the first month of life, the first 20 days, the new needle period, your first choice in general on exams should be Grobis strap, okay? It causes like new needle meningitis, pneumonia, sepsis. In fact, it's probably the most common cause for all three kinds of those infections. And in general, if a new needle is present with no corrigidity, right? So you're thinking about a Grobis strap. But the thing is, the also have to entertain the idea that E. coli, or Listeria, could also be causing the meningitis in the new needle, okay? So you cover those new needles with sephotaxin. Sephotaxin is very good at covering a Grobis strap. It can also cover E.

coli pretty well, okay? Sephotaxin is a kind of third generation sephalosporing. We generally prefer that over sephtraxone in neonates because sephtraxone can cause coli stasis and cause some biliary problems. So you give sephotaxin, that's one of the three in the drug cocktail. You give an ampicellin, remember ampicellin is the drug of choice for the coverage of Listeria. If you don't treat Listeria meningitis as like 100% fatal, and you also give a cyclover to cover HSV, okay? HSV again, in neonates. If it's not treated, it's almost 100% fatal. And the classic way HSV meningitis represent on the examinees, is they show you a lumber puncture, you see a ton of red cells. In the CSF, if you see that, stop reading the question that's HSV on the NBM exams. Okay, so let's go on to the next slide. 23 year old female presents to the ED after having three bouts of bloody diarrhea this morning. She has been having watery diarrhea for the past three days. CBC is notable for a hemoglobin of 8.1 that's low. A retic index of 5%, so the person's bone marrow is turning out a ton of red cells. A platelet count is 87,000 that's low. A normal platelet count is greater than 150,000. Okay, and a creatinine is 3.1 that's elevated. Okay, she's those sites are visualized on a blood smear. Love this question. So, what's your diagnosis? What's the bug? What's the virulence factor? What's the classic presentation? What are its special properties?

And then we'll compare the bug in this key stem to a close cousin that also causes a bloody diarrhea. Okay, so hopefully you can recognize the triad here of a microndriopatic hemolytic anemia. Thrombocide opinea and the low platelets. Okay, so this is hemolytic remixed syndrome. So this can be caused by shegala. Okay, it can also be caused by E coli o157 H7. Okay, so again, triad, microndriopatic hemolytic anemia, reticulosidosis, and the bone marrow is trying to turn out a ton of reticels. She's those sites. We tell you that it's a hemolytic microndriopatic anemia. Okay, because remember, she's those sites. You get those when you literally share reticels in the blood vessels. You also get a thrombocide opinea and then get an acute renal failure. That's why the creatinine is elevated in the question. Okay, so the way this bug almost always presents. And remember, you need like just 10 for shegala to recover car on your GI tract and cause bloody diarrhea. But in general, this infection usually presents with watery diarrhea for a few days, which then progresses to a bloody diarrhea. Okay, and the virulence factor is actually the shegatoxin. The shegatoxin damages the 60s ribosomal subunit in humans. Remember, bacteria have the 50s and 30s ribosomal subunits, but humans, we have the 60s and the 40s ribosomal subunits. So the 60s ribosomal subunits is damaged by the shegatoxin. And shegala, you definitely want to remember that it's gram-negative.

Okay, it's also oxidized negative. And it's a lactose non-fermentar. Okay, so it does not ferment, it does not turn pink on the conch is a agar. Okay, and it's non-motel. It's non-motel. It's non-motel. It doesn't produce hydrogen sulfide when you subject it to a TSI agar. Okay, so contrast this with the close cause in salmonella. Salmonella also causes a bloody diarrhea. But salmonella is motel. It produces hydrogen sulfide on TSI agar. So these are two characteristics that are not held by shegala. Okay, and just real quick, let me just sort of slow down for a moment here and talk about the oxidized test. You always hear people say oxidized positive, oxidized negative, oxidized positive, what oxidized negative? What does that stand for? The thing is being the oxidized test is usually indicative of bacteria that are aeropes. Okay, although remember that being an aerope does not mean you cannot survive without oxygen. You can be a facotidiv aerope or you can be a obligate aerope. Obligate aerope, you always need oxygen. Fagotidiv aerope, you can work with oxygen or you can also do without oxygen. Okay, but being oxidized positive generally means you an aerope. Okay, because the test basically detects the ability of the bacteria to secrets the presence of cytochrome C Oxidies in the bacteria. And remember that cytochrome C Oxidies is actually a part of the electron-transport chain.

Okay, and you only have an electron-transport chain in general if you're using oxygen as a finite electron acceptor to produce ATP. Okay, so that's what I'm going to say about this. Let's jump on to the next slide. We're almost done. So, slide 13. Child of a recent immigrant to the US. If you ever see immigrants and accuse them on MBM exams, it's almost always trying to guide you towards something. Okay, so child of a recent immigrant to the US presents with a seven-day history of difficulty breathing. Vaccination records are not available, that's not good. Physical exam is notable for what appears to be small, grayish masses in the pharynx. These lesions begin to bleed significantly when poked by the Examining Medical Student. So, what's the bug? What's the round of transmission? Classic presentation, special properties, identification, findings with identification. What's the virulence factor? What are the two classically torched organs? We'll talk about preventive strategies and then treatment strategies. Okay, so gray pseudo membrane in the neck, right? So, hopefully you're thinking about corainy bacterium, the theory. Okay, so C. The theory causes the theory. This bug is actually transmitted by respiratory droplets. And the classic exam presentation is as a gray pseudo membrane in the back of the throat, usually in the pharynx, that bleeds easily when you scrape that. That's more of a step to clue that you provide. Okay, and you can also say something like bosnick.

Okay, the bosnick just comes from having a ton of your cervical lymph nodes severely enlarged. Okay, and this bug is grand positive. It's an erup. Okay, it's a grand positive erobic rod and it does not move. I sort of think of C. The theory as a mafia boss. Doesn't go on actual like bad stuff, but he sends out his people to go and do the killings or taking money from people. That's the way C. The theory works. Okay, doesn't move anywhere. Just stays in your airway, but it shoots out toxin that's encoded by bacteria. It's very high to know that the toxin is bacteria and code it. Okay, so it sends out its toxin. Okay, to do its dirty deeds. And the toxin does a lot of bad stuff that I'll talk about shortly. But other things you want to know with regards to identification is that see the theory grows on a tellerite egar. Okay, so it grows as like black colonies on tellerite egar. And there is actually a test where you basically perform an assay, where you try to observe toxin antitoxin interactions. You can actually use that test to detect the toxin. Okay, it's known as the elect test, ELAK, the elect test. And on light microscopy, if you actually look up a picture of this, it's actually pretty striking. See the theory actually looks like Chinese letters. Now, the virulence factor is the deferior toxin. That's easy to remember. And the way the toxin works is that it causes ADP ribosylation of elongation factor 2. Okay, ADP ribosylation of elongation factor 2.

Okay, member elongation factor 2 is actually involved in translocation of stuff along the ribosome. Right, so helping you go, for example, from the a-cyth of the ribosome to the p-cyth of the ribosome. Okay, if you ADP ribosylate elongation factor 2, then elongation factor 2 doesn't work anymore. Okay, so because you've basically killed protein synthesis, that is how you get many of the badness with c-diftheria infection. Okay, so this toxin, again, remember, it's encoded by a bacteria phase, so by a virus that infects bacteria. And as an aside, remember that it is not only the deferior toxin that causes ADP ribosylation of elongation factor 2. This is also done by exotoxin A that we get with our friend Soudomona-sa-erigenosa. Okay, in fact, the MBME, they could actually tie this to a pharmacology question by just asking about drugs that could produce us cellular effects that similar to the action of this ADP ribosylating toxin. Right, so like preventing translocation if you make. So, drugs you want to think about are like your 50s inhibitors like Linda Maisen and your macroleads. Okay, those are prime target exam questions. And the organs that are classically torched by c-diftheria, especially the toxin, is your heart. Right, so you can get them in your craditis, you can get a heart block, and also your brain and your nerves. Okay, those are the things that are classically engaged by the toxin of corainy bacteria, the theory. Now, how do you prevent this infection?

Right, well, don't be an anti-vaxer. That's usually like a not smart thing to do to yourself or your kids. Okay, but you prevent it by giving the D-tap or the T-dap vaccine. They are pretty much the same, it's just like the age ranges of when you give what that is sort of different. Okay, and the treatment of c-diftheria is with the macroleadary thromicein. You could also use penicillin, but I will say in general for MDM is the big thing you want to know is the erythromycin or any other macrolead. And if a person has active disease, you can try to give anti-toxin to bind up whatever toxin that has not wreaked havoc on the presence of brain and heart. Okay, next question. Common blood culture contaminant, common cause of prosthetic valve endocraditis. This bug is grand positive, c-dilise positive and coagulise negative. Okay, so c-dilise positive, grand positive. I really hope you're thinking of some kind of staff species. Okay, so what's the bug? And why does this bug have such an easy time attaching to prosthetic valves? And how do you treat this? Okay, so this bug is staff epidermidis. Remember that it is novel biocene sensitive, unlike staffs at Propheticus, that causes uti and is novel biocene resistant. Okay, it has all the characteristics I mentioned in the slide right, so it's like grand positive, it's coagulise positive, it's coagulise negative. Remember the high yield staff species that coagulise positive is staff or is. Okay, so this bug is novel biocene.

It's novel biocene sensitive, okay, and the reason it has such an easy time attaching to prosthetic valves is that it makes biofilm. Okay, and the way you actually treat staff epidermidis is, classically, give them cumisand, okay, or you can give any other kind of anti-staff lococcal penicillin. Okay, final slide. For the five-year-old male presents with high fevers, shortness of breath and diarrhea, he recently returned from a business conference, oh now, at the unique hotel, which is known for having an indoor waterfall. CMP is notable for a sodium of 123. So what's the bug when I had special characteristics? How's this stained? How do I do this bug? How do you test for this bug? How does it classically present on how do you treat this? Okay, so this is legionella, right, so legionnaires disease. Okay, remember legionella, no muffula, it's a gram negative, right? It actually has some unusual branching fatty acids in the cell wall, so it doesn't stain very well. Okay, and the thing is, it stains positive with silver. And real quick, as an aside, what is the bug that also causes serious ish respiratory infections in its patients that also stains positive with silver? I hope you're saying, you must seriously do it. Okay, now back to legionella, right? So legionella, no muffula, it actually grows on charcoal yeast extract, and if you're iron and cysteins, just something you love to test, you definitely want to commit that to memory.

And the way you diagnose this bug is by doing a urinary antigen test. It's called the legionella urine antigen test, like the luaht, if you may. And the classic presentation on exams is in relation to business conferences. And the almost always mentions some kind of thing with like a waterfall or central air condition. That's the way they love to present this. And another presentation is as I think of legionella as like pneumonia plus, so pneumonia plus like other bad stuff like diarrhea or hyponitrimia, which is a relatively specific finding in legionella, no muffula. Okay, and you can also present with other weird stuff, but I really want to think of diarrhea and hyponitrimia. Okay, and the way you treat legionella, like every other cause of atypical pneumonia, is with a microlett, okay, with a microlett. And actually this microlett, no money, help you remember how you treat the three, I guess, help you remember how you treat and the three common causes of it. So just spell out the word microlett and capitalize the letter M, the letter C and the letter L, okay, this was actually thought to me by a person I treated back in the day. So I'll give the person credit right now. So the M stands for microplasma, okay, the capitalized C stands for chlamydia and the capitalized L stands for legionella. Okay, so these are the three bugs that are covered by microlets and these three bugs, all causes of atypical pneumonia, although the most common one is microplasma.

Okay, so that's the end of this podcast. If you have any questions or spot any errors, please don't be afraid to send out an email or try to put a comment in the comment section below the podcast. And I look forward to seeing you in the next episode, we'll definitely have some more podcasts on Batira coming up. Have a good night and God bless you.

Bacterial Vaginosis (BV), classically associated with Gardnerella vaginalis and a fishy-smelling discharge.

High-yield organisms include Haemophilus, Actinobacillus, Cardiobacterium, and Echinococcus.

Shigella causes hemorrhagic colitis, while Salmonella typically presents with watery diarrhea. Also, Shigella is often associated with dysentery/bloody stool, whereas Salmonella can be more variable.

Microangiopathic hemolytic anemia (schistocytes), thrombocytopenia (low platelets), and acute kidney injury (elevated creatinine).

Actinomyces is strictly anaerobic. Nocardia is aerobic.

It is typically nitrite-negative, even though the patient has a UTI.

Proteus mirabilis.

Microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure.

Corynebacterium diphtheriae.

Macrolides (e.g., Azithromycin), Doxycycline, and sometimes Fluoroquinolones (though macrolide/doxy is preferred).

High fever, joint pain, conjunctivitis, and potential acute kidney injury/hepatitis.

Coxiella burnetii.

Urine antigen test (LUAHT). Classic associations include business conferences and exposure to aerosols/water sources (e.g., waterfalls).

Proteus mirabilis.

Microangiopathic hemolytic anemia, thrombocytopenia, and acute renal failure.

Corynebacterium diphtheriae.

Macrolides (e.g., Azithromycin), Doxycycline, and sometimes Fluoroquinolones (though macrolide/doxy is preferred).

High fever, joint pain, conjunctivitis, and potential acute kidney injury/hepatitis.

Coxiella burnetii.

Urine antigen test (LUAHT). Classic associations include business conferences and exposure to aerosols/water sources (e.g., waterfalls).