DIP Episode 7 - Viral Cases C and Fungal Cases

Welcome, my name is Devine. I am a fourth year medical student. Welcome to episode seven of the Divine intervention podcasts. Today we're going to be finishing up our viruses, right? So we've had two episodes on viruses. We're going to have this last episode and I'm also going to cover the highly highly commonly tested information relating to the fungi on the exam. Okay. Congratulations to all the fourth years that matched yesterday. If you did not match, it's not the end of the world. There are just many options you can take. Try to speak with the Dean at your med school or speak with someone that's knowledgeable with the residency process. There's many options available. Try to explore those options and I wish you the best going forward. Okay, so let's begin. So discussion of the hepatitis viruses, right? So A through E and we're going to discuss some key factors relating to all the viruses and then we'll discuss the HB serologies, right? So clearly there are five kinds of hepatitis viruses, right? There's HB A through E. Okay? And in previous podcasts, we've talked about how A and E on the end of the hepatitis alphabet, just like your mouth and your anus at the two orifices of your body. Okay? So they are transmitted in a fecal oral fashion. Okay? So HB and E, fecal oral transmission, they have no envelope. Okay? The other viruses, the other like HBC and GV are actually all envelope viruses. Okay? And remember that hep A and E both cause acute infection. Okay?

They do not cause chronic infection for hep E, right? So E as an egg, you want to remember that it's extra virulent in pregnant women, right? Remember in pregnancy, then a relatively immunosuppressed state. Okay? So you have an increased risk of getting more virulent infections. That's why obstetricians are usually super, super, super on top of the game with regards to treating any infections in a pregnant female. Okay? And again, if they give you a question about a person that had a John Dis and they had a right-up accords and pain and they were pregnant and they passed away, think about hep E. Okay? Think about hep E. Now for hep C, right? The classic association will be a person getting like an IV drug user or a person that got a transfusion and then they present with with John Dis and they have like right-up accords and pain and they say, oh, you obtain serologies and you'll find antibodies against hep C or you have a positive hep C RNA. And if you see that, again, think about hep C, right? So, classically on exams, it's associated with transfusions and stuff like that. And remember that on like hep B where like 90 to 95% of people recover from an acute hep B infection and do not go into chronic infection. People that have hep C, about 80% of them that have an acute hep C infection, actually progress to having a chronic infection.

It so happens that there is now treatment for hep C, it just costs a lot of money and I will discuss that from ecology in a separate podcast when we go over the drugs used in microbiology. Okay? Now for hep D, think of hep D as being the dependent virus. Okay? It basically needs the hep B surface antigen from hep B. Okay? So if a person gets a hep D infection and they don't have hep B, they're totally fine. Okay? But if you have a hep B infection and a super infection with hep D, you're like super screwed. Okay? So basically the big thing you want to remember here is that if a person has vaccine vaccination against hep B, they cannot get hep D. Okay? So just something to keep in mind. Now for hep B, right? So like I've said, most people that get the infection on 90 to 95% of them recover. Okay? But there is one exception to that and those are infants. Infants that get hep B infection, about 90% of them progress to getting a chronic, chronic infection. Okay? And one thing you want to keep in mind is if they give you an exam question about a lady that has like poor prenatal care blah blah blah. And then she delivers a kid and then they tell you that oh, the mom's hep B surface antigen is positive and a hep B core IgM is positive blah blah blah. And then they ask about the next step in management for the kid. Okay? You want to make sure you give that kid the hep B vaccine. Okay?

And then you also want to go ahead and give them the hep B immunoglobulin to give them some kind of passive vaccination. That's a very common exam question. Okay? So let's sort of talk about some of these hep B serologies. But before going to the serologies, let's just talk about what these what the markers mean. If you really understand what the markers stand for, it's super easy to answer many of these exam questions. You really should not be missing these exam questions if you've studied this stuff. So the hep B surface antigen. Basically, whenever it's positive, you have disease. Okay? There is one exception to that the window period will talk about in a bit. But if your hep B surface antigen is positive, you certainly have disease. Okay? And if that hep B surface antigen is presenting your blood, it's detectable for more than six months. And you do have chronic hep B infection. Okay? If the surface antibody is positive, it could mean one of many things. Right? It could mean you've got in the vaccine or you've recovered from a past infection. And we'll talk about what that what that means in a bit. Okay? If you have the quarantine body positive, it tells you that you've been exposed to actual hep B. Right? So you could be well or so you could have like a past resolved hep B infection. It could also mean your currently infected. Okay? And if you have a hep B core IGM, it shows that you have acute infection or you're in the window period. Okay?

But if it's IGG, it shows you have a chronic infection or again, you've been exposed in the past, you're recovered from it. Okay? Remember, IGG is more of a long term marker that, oh, okay, this person did not get this infection over the past like one to two months. If your hep B and TGM is positive, it means you have very high infectivity. Okay? And the window period is just one of those high yield things you want to know. That's basically where the hep B surface antigen sort of counterbalances, the hep B surface antibody pretty well. Okay? The only thing that is positive in the window period is the hep B core antibody. Okay? Classically on exams, it's IGM. So let's discuss the different phases and talk about what will be positive and to be honest, it really doesn't make much sense to discuss what's negative. If you know what's positive and that's the only positive thing in the child you get on your board exams, you should be able to reason this out. So for acute hep B infection, right? So obviously if you infect it, the thing that's always positive is the hep B surface antigen. Okay? And your hep B core antibody will also be positive. Classically, it's IGM. Okay? Lower yield of seromarker you want to know is the E-antigen. The E-antigen will be positive in an acute infection, especially if you have very high infectivity. Now, if you have a chronic infection, again, if it's not resolved, your surface antigen will be positive. Okay?

Your core antibody, IGG this time, would also be positive. Okay? If you have a chronic infection and you're not very infective, your hep B-antigen will be negative. If you have high infectivity, your hep B-antigen will be positive. And then like I discussed earlier on, the window period, the only thing that will be positive is the hep B core antibody. Okay? The IGM. And if you've had a prior infection and you recovered from it, your surface antigen would not be positive because you don't have disease. Okay? The things that will be positive will be your hep B surface antibody, okay? And your hep B core, IGG. Okay? Those will be the only things that are positive if you had a prior infection. And then if you've been immunized, the only thing that will be positive is your hep B surface antibody. There's nothing else that is positive. Okay? The vaccine does not include the core antigen. So you do not make antibodies against that. Okay? If you know these serologies, you should always, like these are one of those questions where you can always get the answer right because they just usually make it relatively straightforward. If you're doing the material, you get it right. Okay? So let's move on to the next slide. Bilateral facial erythema in a child, steel-borne fetus, which generalizes the dima. Okay? So hopefully you're thinking of the slapped-cheek rash. This is classically caused by Parvobi 19. Okay?

Remember, it's the only single stranded DNA virus you do need to know for your exam. Okay? And just a quick word on the DNA viruses, right? Because we've discussed them in previous podcasts. But remember that all the DNA viruses they replicate in the nucleus, the only exception to that is the Pox virus. Okay? And all the DNA viruses are icosahedra. Okay? They have an icosahedra shape. Okay? Just one of those things you want to know because your friends at the NBME will classically give you questions you're like, oh, slap-cheek rash. I know the answer. It's Parvobi 19. And then you're looking for Parvobi 19 as an answer to listen. It's conspicuously missing. And all you see is like, oh, icosahedra, single stranded DNA blah, blah, blah. And you're like, oh, seriously? So just things to keep in mind. Okay? These viral morphologies and their genomic structure, those are generally high yield for the exams. Okay? So Parvobi 19, okay? It's a single stranded DNA virus causes in adults. It can cause like thritis and myologies and all that stuff. But it really tests that the thing they classically test is the congenital Parvobi 19 infection. Okay? Because it so happens that Parvobi 19 loves to infect a rethroid progenitors. And when you infect those progenitors, you do not make it itself. Okay? So the kid in utero can get like this very severe aplastic anemia. And when a kid has anemia, the kid can go into high output heart failure, which we discussed in a previous podcast.

And that high output heart failure can, if the heart fails, you can basically have like edema everywhere. Because the heart is not pumping blood forward. Okay? And there's also some problems with like extra like like hematopoetis in like other organs and all that stuff. But the big thing one remember is hydrops fetalis with congenital Parvobi 19 infection. Okay? And if they also describe a kid with hemoglobin apathy right? So like sickle cell disease or beta thalassemia major or whatever. And they tell you that this kid has a severe anemia. And they tell you about the slap-cheek crash, right? Again, you want to think about Parvobi 19. Okay? Okay. So I think that's all I'm going to say about that. Let's go ahead and move on to the next slide. So 33-year-old female presents with a one-month history of post-coidoblidin. That's not good. Well post-coidoblidin may be normal, but we need to push it down. We need to push further. So, coposcopy with biopsy reveals cells with a large nuclei and perinuclear vacuolution at the basal third of the cervix. So what's the bug? Okay? So we're potentially worried about a cervical intrepithylianneoplasia with this. Okay? So the thing I'm getting at here is HPV. Okay? It's HPV. And HPV, there are certain high yield things you want to know. I mean first things first it's a DNA virus. Okay? So double stranded DNA virus. But you definitely want to know the stereotypes. Okay? So there is like HPV1 that tends to cause a planter what? Okay?

There is HPV 6 and 11 that tends to cause a genital warts. The 5 word is Condiloma Acuminata. Please do not confuse the Condiloma Acuminata of HPV 6 and 11 with the Condiloma Lada that you get in secondary sytholus. Okay? Those words sound similar enough for people to confuse them on exams. Do not be one of those people. And then, HPV 16 and in team and the HP Vs in the 30s all cause cervical cancer. Okay? They can cause cervical malignancies, so that's something to keep in mind. So, classically any female that's between the ages of 9 to 26 should get the HPV vaccine. Okay? And I'll just as a sidebar here, I'll highly encourage you for women every year. Just go for your well-woman visit. There are so many things that are preventable in the land of woobie guy if you just get checked out regularly. Okay? So that's just my public service announcement. Probably when we discuss some male stuff, I'll discuss how I'll also have my sidebar for the guys. Okay? So, it's vaccine preventable, right? So, there's like the Gardasil vaccine that covers the really nasty HPV serotypes, like 6, 11, 16 and 18. That's the Gardasil vaccine. And another way they can present HPV on your exam is to basically tell you about a person where they say, oh, this person has like these raised lesions, like varicose lesions on the... Like in the perennial area, or they describe the cervical lesions I mentioned.

And then they say, oh, my crosscopy, you see these in large nuclei with perennial clear vacuolation. This is basically a description of the coilo sites you find in HPV. Remember, they look like fried eggs just like we observe in an oligodendroglioma. So that's just something to keep in mind. The thing is your friends at the MBME, they may not necessarily give you the fried egg appearance in a Q stem. They may describe what you see. Okay? That's one common MBME exam strategy. So, what do you know? I'm just putting a different language. So, the classic example I cite with students when I'm teaching is I talk about how they describe some of my buddies as laminated calcifications. So, just sort of things to keep in mind with that. Okay, so how does HPV cause problems? Well, the big problem with HPV is it produces certain proteins, E6 and E7. In fact, E6 is sort of involved in the ubiquitination pathway. So, that's a very nice cell biology tie-in. And another nice cell biology tie-in is that these two proteins, they basically inhibit the RB gene and P53. Okay? And when you inhibit those tumor suppressor genes, you have propensity to have on-control cell proliferation. Because cells can go from like the G1 to S phase willingly and you can get into trouble with that. So, that's certainly something to keep in mind, very nice cell biology tie-in with HPV. Okay, next slide.

So, a 10-year-old male who recently swam in a pool at a business retreat for all the executives, that is that's firm. With other kids, presents with a 40-histrov diarrhea and a radiory. He has a soft throat and bilateral watery exudation from his eyes. So, what is the bug? For this question, I basically gave you all the exam hooks. Okay? So, this is clearly adenovirus. Okay? So, you describe a kid with like gastroenteritis that has pink eye and they talk about like having a soft throat, right? So, like, firing gitis, think about adenovirus. Okay? Adenovirus is the virus that classically causes pink eye. Okay? And because it's a viral cause of conjunctiveitis, you want to think of it. You want to think of the persons I have in more of a watery exudate. Okay? It's not usually like thick or pure-length, like you observe in bacterial conjunctiveitis. And you also thought like, hmm, what if could this be strep pyogenes, right? So, like, group-based strep firing gitis, group-based strep firing gitis on exams does not present with conjunctiveitis. Okay? So, that's something to definitely keep in mind. So, the buzz word for adenovirus is firing go conjunctiveitis. Firing go conjunctiveitis, so soft throat plus pink eye. Okay? And occasionally these kids can also present with a gastroenteritis. Okay? Another thing they can present with is hemorrhagicistitis.

So, if they describe a kid that has already urine and he recently had an upper respiratory infection and maybe like conjunctiveitis, you really want to think about adenovirus. Okay? So, read the cue stem carefully, because they may try to trick you with post-streptococcal glomerulone fritis, which, as you know, has an association group-based strep infection. Okay? And also has an association with red urine. Okay? So, you need to read the question carefully, see the different books they give you. If they give you conjunctiveitis, you probably want to think more of hemorrhagicistitis. Okay? And other associations, basically the big things I wanted to discuss here, are other causes of hemorrhagicistitis. Right? So, remember that schistosomahematobia can also cause a hemorrhagicistitis. They can classically describe this in an exam question relating to Egypt. So, if you see Egypt in an exam question and a guy has already urine, like blood in his urine, think about a schistosomahesis. Okay? Schistosomahematobia. And remember the drug cyclophosphamant also causes a hemorrhagicistitis, because of its nasty metabolite acrolym. You can prevent that by giving mesna. You could also actually give an acidosystem to prevent that. Okay? Now, so I think that's all I'm going to say about adenovirus. Oh, I forgot. Most common cause of viral gastroenteritis is the no-walk virus. Remember, it's a calisi virus. So, just something to keep in mind. Okay?

So, vomiting and diarrhea and a cruise ship, C-diff preventive strategies. Right? So, cruise ship gastroenteritis, I hope you're thinking about the no-walk virus. Okay? It's passed along through the fecal oral route. So, again, vomiting and diarrhea cruise ship think about the no-walk virus. It's also called the neurovirus. Okay? And the way you prevent the spread of these virus is actually with hand washing. Okay? A classic in the exam question is a person that has a post antibiotic watery false million diarrhea. You know that C-diff, okay? And they ask about how the spread of this infection could be limited in a hospital. Okay? You want to go ahead and explore hand washing. They will try to give you an answer choice that says to use alcohol sanitizers. Don't do that. Alcohol sanitizers do not take care of C-diff. It is only washing your hands with soap and water that takes care of C-diff. Okay? Next slide. Pharma worker presents with a mix of hyper and hypopicmented skin lesions on the trunk and back in the summer. So, what is the bug? Okay? What is the bug? So, hopefully you're thinking about a malacisia fervor. Okay? I should probably have put a picture of this. Maybe I'll try to finnigo and put it in the final slide. Let me connote to myself. So, malacisia fervor. Okay. So, malacisia fervor causes tiniya vesicle. Okay? And the way you make the diagnosis is with a kill-heach prep.

And, classically, when you get a kill-heach prep, you'll see something described as a spaghetti and meatball appearance. Okay? And really treating malacisia fervor, you just need to take a topical selenium sulfide, just rub it over the skin, wash it away for like a week and boom, it goes away. Okay? So, malacisia fervor, tiniya vesicular, spaghetti and meatballs, selenium sulfide for treatment, those are the big things you want to remember. Okay? Next slide. Now, 10-year-old male presents with a paritic lesion on the left or parachstremity. The lesion appears coin-shaped with central clearing. The lesion for recess on the wood's lamb. What's your diagnosis and what's the bug? Okay? So, this is ring war. Okay? Class of medical term for ring war is tiniacoperas. And basically, tiniac, the tiniac caused by a group of fungi known as the Dermado-phidic fungi. Okay? Don't confuse Dermado-phidic fungi with dimorphic fungi. We'll talk about dimorphic fungi in a little slide. Okay? Dermado-phidic fungi. And the bug I'm actually going after with this question is micro sporo. Micro sporo. There are three kinds of Dermado-phidic fungi, at least that you need to know for your test. There is tricophyton. Okay? There is micro sporo and there is epidermal phytin. In general, tricophyton, they tested on exams in the context of tiniacaperas. Okay? It causes a lot of like, if you look at a picture of tiniacaperas, it's pretty striking when you see it online. But it causes tiniacaperas.

Ring war can be caused by any of the Dermado-phidic infections. Okay? But if they give you the qualifier that the bug on the fluorescence on the wood's lamb, think about micro sporo. We even add a dog association to the question. Think about micro sporo. Okay? Now, just other discussions with the Dermado-phidic fungi. So we've talked about the causes, micro sporo, epidermal phytin and tricophyton. Tiniacaperas is like the thing you get on the head. Tiniac and guayum. That's the thing you get on the nails. Okay? So like tiniacaperas, that's tiniac and guayum. It's also called onychomicosis. And one thing I will say with all these things is that in general, these Dermado-phidic phongolin infections, you treat them with topical antifongals and they go away. But on your exam, if they describe a person that has tiniacaperas, the person has tiniacaperas, they will give you answer choices that say like some kind of topical antifongal. And then they will give you an answer choice that talks about some oral antifongal, pick the oral antifongal. Classically on exams, it's either terbina fin or grizzio fulve. Okay? You need the oral stuff to treat the Dermado-phidic infections that involve the hair and involve the nail. I mean the head and the nails. Okay? So tiniacaperas and tiniac and guayum. You treat those with oral grizzio fulve or tribenophen. Remember that tribenophen is the thing that I believe in habits. I believe it's squelinypoxidase.

We'll talk about that when we get to the antimicrobiala pharmacology. Remember that grizzio fulve is an inhibitor of cytochromp 450. Okay? Whoops. Thank God. Grizzio fulve is actually an inducer. Sorry, I take that back. It's an inducer of cytochromp 450. Sorry about that. Okay. So, next slide. This patient was priked by a thorn while taking a walk in his friend's garden. This person should not have taken a walk in his friend's garden, but now I'm just kidding. But basically this person has a spurtricosis. Okay? This is one of the dimorphic fungi. So this is spurtthrics shenkiai. It's classically described as a ruse gardener's disease. Okay? So if you get a question about a person priked by a thorn and then they have these lesions that sort of appear in a single file on an extremity with lymphadenopathy that may or may not be painful, think about spurtthrics shenkiai. Okay? And really the way you treat spurtthricosis is with etroconozol for months. You classically need to give etroconozol for like six to nine months to get complete healing of the infection. And if they also describe that, oh, they did a kill each prep and they found a cigar shaped yeast. Okay? Also think about spurtthrics shenkiai. Next slide. 19 year old college student presents with dysmia and a mild fever. One week after returning from a field trip to the mammoth caves in Kentucky. So one week after returning from a field trip to the mammoth caves in Kentucky.

So if you notice and beginning to give you questions with pictures, believe me when I say that these pictures are not here for sure. They are actually important. I will say that these dimorphic fungi I am about to talk about. A lot of them are classically tested on exams with the pictures in the Q-stem. So it's just something you want to keep in mind. Although I will say this. Most of the pictures on the NVME exams are not very useful for answering questions. But if you could recognize the picture, a question could turn to an auto-click question. Okay? We'll explain like ten seconds and you'll move on. Okay? So this person has histoplasmosis. So histoplasma capsulata. This picture you've seen, you've basically seen macrophages. And they have these intracellular easts. So that's the biggest solution you want to know. You definitely want to know your geography with this one. So the Ohio Mississippi River Valley. And if they describe a person that went spalonkin. So that's the buzzword. Like a person went exploring a cave. And they were exposed to like bad or better poop. Think about H-capsulata. Okay? Basically what happens is you walk into a cave. Just like every other human being bats and birds, they also have to poop. And when they poop, if you inhale those things, you can basically contract H-capsulata. Okay? And H-capsulata, it classically causes an intestine pneumonia. And one unusual question. So here's one thing. So it causes an intestine pneumonia.

You do perform a chest x-ray. You'll find the intestine shell lesions like ground glass opacities and all that stuff. But one unusual question they could ask on exams is a patient that has HIV that lives in like Ohio or Kentucky or the Mississippi River Valley. And their CD4 count is less than 150. And they ask for the next best step in management. They could basically present a person that's totally symptomatic, but CD4 count less than 150 lives in Kentucky, next best step in management. Your next step in management for that person is to potentially prescribe prophylactic atroconozone. Okay? It's one of the guidelines. If a person has his stone and they live in a susceptible area, so not every HIV person that has his stone. H-cav person that, sorry, not every HIV person that lives in the US or in the world. But a HIV person that lives in a susceptible area, right? So like Kentucky or Ohio, Mississippi River Valley and the CD4 count drops below 150. Next step in management, classicly on exams, is to give them it to a connozzon. The magic number, you want to remember is 150. And while we're doing that, let's just quickly run through some other CD4 numbers for HIV patients. So if the CD4 count drops below 200, you want to prophylax against the homocystis, your vetsi. You can use TMPSMX, so trimethoprim, sofymethoxazol. You could use the app zone, you could use aerosolide, spentamidine, that should work.

Now, if the CD4 count drops below 250, you want to go ahead and the person lives in a susceptible area, right? So like Arizona or Texas or New Mexico, Nevada or California. And the CD4 count drops below 250. You want to prophylax against the oxidities imites, also the troconnozzon. Now, if a person CD4 count drops below 50, you want to prophylax against mycobacterium avium intercellularity. Remember, it's an acid fast bug. And your prophylaxis is with z-thromycin. Remember, z-thromycin is a macrolid. So just sort of a quick review there for you. So I believe we're done with this slide. So let's go ahead and move on to the next one. So it's like 10, a 19-year-old college student presents with a non-productive calf, mouth fever, and painful erythematous lesions on the shins bilaterally. The roof of his home in California was recently blown away by a county-wide typhoon. Okay. So hopefully with this picture, you can see this well-placed spherial in the center. This person has coxidium eye causes, right? So, classically caused by coxidiodes imides. Okay. So again, if you see the buzzword spherial in a sputum culture, again, think about coxidiodes imides. Remember your geography? Arizona. So the southwestern United States. So like Arizona, New Mexico, Texas, California, Nevada. Okay. Thanks to keep in mind. And on an exam question, they could also describe like some kind of natural disaster that disrupts the earth. Right.

So like an earthquake or typhoon or a really bad storm or whatever. Okay. And the person lives in visa susceptible areas and begins to present with pulmonary symptoms. And they say, oh, chest x-ray shows interstitial infiltrates. Think about a coxidiodes imides. Okay. And one of the high-yield clone exams is the presence of something known as erythematosum as a dermatologic finding. Okay. So the thing is erythematosum classically presents on the low extremities and they classically describe it as a painful red lesion. Painful red, well circumscribillage, low extremities. Think about erythematosum. It has a very strong association with coxidiodes imides. Okay. In fact, coxidiodes imides, they call it like desert rheumatism. Basically the findings are like, you have these pulmonary symptoms, you have erythematosum, and then you have like very severe arthritis. Okay. And if you're told about an African-American female that has erythematosum, what does the very first thing you want to think about? Well, I'm hoping you're saying sarcoidosis. Okay. That's a very big association as well in sarcoidosis. Sarcoidosis is one of those diseases that classically affects African-Americans, females, has erythematosum as a dermatologic finding, and has anterior uviitis as an ocular finding. So those are just very nice times you want to see with sarcoidosis. We'll probably talk about it in the leader podcast. Okay.

And I've said that if a person has HIV, delivery and susceptible area, CD4 count is less than 250 prophylaxis or tetraconozone. Okay. Now, next slide. So this slide says a resident of Missouri presents with a two-week history of a non-productive cough and multiple osuoritin skin lesions on the upper and lower extremity. This is sort of a non-specific question, so they almost always give you the picture on exams. Okay. You can see these broad-based body needs. So this is Blasto-Maisis. Okay. The geographic association again is like the Ohio Mississippi River Valley area. And I mean, if you look at the phoneme of the bug, Blasto-Maisis dermatitis. So derm tells you cause a lot of skin problems. The skin problems it causes classically are osuoritins. Okay. So something to keep in mind. Now, so I guess we can go ahead and move on to the next slide. So patient with a past history of active TB presents with hemoptysis. Operate chest x-ray is notable for an upper lobe lesion that changes position when a de-cubitus film is obtained. Okay. So operate chest x-ray is notable for an upper lobe lesion that changes position when a de-cubitus film is obtained. So I hope you're thinking of some kind of fungus ball with this question. So if I say fungus ball, what do you see back to me? Aspergillus fumigatus. Okay. So this is an aspergillus infection. If you also look at the picture, you can see the angles. So these are bugs. You basically see high fee. They grow at 45 degree angles. Okay.

And these high fee have septa. Okay. So septate 45 degree angle high fee. Think about aspergillosis. Okay. And aspergillus can present in many ways on your exam. Right. So it can present as allergic bronchopomonear aspergillosis. Right. So if they describe a farmer, okay, that may be as inhaled like some animal stuff or some, some like barley stuff, whatever. And they describe all these pulmonary symptoms. And they say, oh, you do a blood culture or you do like a sputum culture. And you see the high fee, septate high fee, 45 degree angles. You really want to think about aspergillosis with that. Okay. Just one weird, bizarre association that you may never see on step one. What if you saw it? You'll be grateful that you listen to the spot castes. If they describe a farmer that has or a person that plays with birds, whatever, that has pulmonary symptoms. And they say like, oh, you're not necessarily seeing any bugs. And the question is like very non-specific. One thing you want to think about is something known as a thermophilic actinomycetes. Okay. So if you don't see like aspergillosis, for example, also think about a thermophilic actinomycetes. I will look that up if I read you on Wikipedia. It's just one of those bizarre things that every now and then, for whatever odd reason, shows up on exams. Okay. So that's just something you want to keep in mind. Now, another presentation of aspergillosis, like I mentioned, is the fungus ball. Right.

So classically, a patient with a history of TB, those calcifications like the upper lobe, calcifications, you get with TB. Aspergillosis can invade those fins. Okay. And classically, that will present as hemoptysis. Okay. So that's something you definitely want to keep in mind. Now, another patient population, where aspergillosis may be tested, with regards to your exam, is a patient that is neutropenic. Okay. So a patient with severe neutropenia, another patient population could be someone that has a history of CGD. Okay. So chronic radiolomatos disease. Remember, that's an NADP, oxidase deficiency. And remember, the testing for that is the nitro-blue tetrozoleum test. Right. Those people have a negative NBT test. Right. And one thing you want to keep in mind is, why does a patient with a history of CGD get aspergillosis infections? Well, the thing is that aspergillosis is catellase positive. Okay. So remember, people that have CGD tend to have recurrent infections with catellase positive organisms. Okay. So that's a very high-yield tyrant. You want to keep in mind with that. And the way you treat aspergillosis is you can give or iconosol, or you can give an amphoterable, right? So an amphotericin B. I'll talk about all those drugs and a little podcast. Okay. Next slide. So 32-year-old female who was recently treated for low-bar pneumonia presents with severe vaginal and perinolarythema. A cottage cheese discharge is seen on vaginal exam. Right.

So if you look at these pictures, these things look like germ tubes. Okay. So classicly on exams, these talk about like pseudo-high-fee, showing up as germ tubes at 37 degrees Celsius. You really want to think about candida albecanes. Okay. So candidaeases. So candidae can cause many kinds of infections, right? So classically, like a female without risk factors, and they just say, oh, she recently had some kind of antibiotic treatment for some infection. And then she presents with like a cottage cheese vaginal discharge and a lot of itching and erythema around the perinol area. Think about candidaeases. Okay. I remember that candidae albecanes also causes throsh and esophageitis in an eight-spacian, right? So you treat that with like the niestadine swish and suano, all swish and spit, whatever float your boat. Remember that candidae classically does not cause a specific shape of ulcers in esophageitis in an eight-spacian, right? So remember CMV is the one that causes the linear ulcers, and HSV is the one that causes the punched-out ulcers. Okay. There's no classic ulcer description for esophageitis with candida. So the classicly on exams have to give you like some kind of throsh association or the describe what you see on KOH prep. Okay. The drum tubes, the seven-degree Celsius. Okay. And again, cottage cheese vaginal discharge in a female. I think about candidae. Classically, the vaginal pH is less than 4.5. That's something you definitely want to know. Okay.

Because if you contrast it that with garnereda vaginalis that causes bacterial vaginosis and tricomona vaginalis that causes like the strawberry cervix with a frothy, greenish discharge in a female, those infections associated with a vaginal pH greater than 4.5. Okay. But for candida albicans, the pH on exams is usually less than 4.5. So that's a very high-yield association you want to keep in mind. Okay. And in patients that are obese or have like diabetes, if they describe like red lesions on their skin folds, you want to think about candida as well. Like itchy red lesions on the skin folds, you could get that from staff warriors, but you could also get that from candidae assess. Okay. And then if a person has like invasive candida infections, think about a patient that probably has like the George syndrome. Okay. Basically any T cell disorder, like a T cell deficiency disorder, would increase your risk of getting invasive candidae assess. Okay. So like skid, severe combined immune deficiency, where you have an adenosine diaminase problem or a problem with the interlooking two receptor, think about invasive candidae assesses in those people. Okay. So next slide. Fever, no corrigidity and papillodema in a patient with a CD4 count of 93, who runs a pejan farm. Okay. This patient has AIDS. It probably should not have been running a pejan farm, okay, because they have a cryptococosis. Okay. So this is caused by cryptococcus neiformis, classic exam picture.

You have that on the slide. And remember this is a yeast. Okay. It's an encapsulated organism, right. So it's one of those high yield organisms that has a capsule. Okay. So it would potentially give you like a positive reaction on a quite long test. So that's one thing to keep in mind. And this bug has an association with pejan droppings. Okay. So remember I said bad and bird droppings. Think about histoplasmosis. Pejan droppings think about cryptococosis. Okay. In fact, this is the most common cause. Very high you to know that it's the most common cause of meningitis in an AIDS patient. And classically you, on exam, they talk about the India inxane. That's not super sensitive. The thing most people do now is the latex particle like glutination acid. Okay. So that's something you want to keep in mind with cryptococcus. And how do you treat cryptocococosis, right. So you give them for teresin B and you give a drug known as a five-fluosidosing. Okay. Remember, five-fluosidosing, it can be activated by adenosine, I mean, a cytosine, the aminage to five FU, which goes ahead to inhibit thymitylatesin phase in the bug. Okay. That's actually how a five-fluosidosing works. We'll talk about a five-fluosidosing and other antifungals in a later podcast. Okay. So next slide. 33 old male has been in the ICU for the past seven days. He was rushed to the hospital by ambulance after he was found up tunded by a close friend at home.

CBC slash BMP on admission showed a blood glucose of 300 pH of 7.13 and a bicarb of 13. Oops. He has been recovering from over the last three days but begins to complain of severe facial pain in a maxillary nerve distribution. Okay. That's cranial nerve five. Okay. The second branch. Over the next few hours, he begins to drain black, false million material from his nostrils. Okay. If you ever see a patient that has this presentation, you really shouldn't spend too much time on these questions. Also look at this picture. Right. This is these are 90 degree angles and we do not see any septa. Okay. So this is muachromycosis. Right. So, classically on exams, the bug the test is rhizopus. Okay. So this is muachromycosis. Has a very strong association with like rhino cerebral infections. Right. So like necrotic sinusitis with infections in the brain in a patient that has diabetes. Okay. In fact, I will say you can almost guarantee that on exams the only people that will ever get muachromycosis are patients that have elevated hemoglobin in your one sense. Okay. It's a very high yield association you want to keep in mind. Okay. So this is muachromycosis. The only thing you can do for these people is one, give them an footericin B and two, give them a chronic tissue. Most people die. Okay. But the only people that have ever survived, the people that got unforet terrible. Okay. So that's all I'm going to say about that. So let's go into the last slide.

We've talked about this bug many, many times. But I'm just going to hit it home again to round this up. Okay. So patient with a city for counter 45 presents with a one week history of shotness of breath and a non-productive cough. Temperature is 100.9. Chest extra is notable for bilateral, intestinal infiltrates with a ground glass morphology. LDH is markedly elevated. What's your diagnosis? And what are the other associations with this bug? Okay. So this picture should be something you're used to. Okay. I will tell you that this is something that was derived from an induced sputum sample, right? So like by Brunkova, viola la va, for example. And these organisms are silver, stained positive. You know, HIV patient with pneumonia. Intesticially infiltrates chest x-ray. What are you thinking about? Emocesis gerovetsi. Okay. So PCP. Okay. Remember PCP is silver, stained positive. That's definitely something you want to know. On almost every exam question you'll see this on. They will talk about the LDH being elevated. Okay. The people that get these infections on exams are classically HIV positive patients. But if they want to mess with your brain a little, they can give you a person that has a history of like some autoimmune disease or transplant and they need to be on chronic immunosuppression. Those people can also get PCP pneumonia, although that's usually more of a step too thin. Okay.

And remember on a chest x-ray you'll see an intestinal infiltrate ground glass appearance. Okay. Ground glass appearance. And the magic number you want to remember with PCP pneumonia is a cd 4 count less than 200. Okay. Once a patient has HIV cd 4 count less than 200, you want to profile acts with trimethoprimsulfomethoxazone or dapsone or aerosolisementamid. Okay. To prevent PCP pneumonia. Okay. And again, if they describe a HIV patient has a pneumonia and the auto-sats are like in the 80s, you should have a very good reason for not picking neomosistis gerovetsi on the exam. But I'll sound a warning to that. If a person has HIV and they present with a productive cough, a very high fever, okay. And they tell you that chest x-ray shows a low bar consolidation. They will try to trick you on the exam to pick neomosistis gerovetsi, do not be one of those people. Go ahead and pick triptococcus pneumonia. Okay. So PCP does not cause a low bar consolidation on exams. Okay. It causes an intestinal infield trick on exams. Okay. And again, the way you treat PCP pneumonia is you give trimethoprimsulfomethoxazone. If the person is severely hypoxic and they are going into respiratory failure, you'll classically also go ahead and add IV corticosteroids to the atreatment regimen. Okay. So I hope you've gotten something from this. If you understand this podcast and the other podcast on viruses, you should be able to answer most viral questions you will find on your board exams.

And if you also went through these cases, you should also be able to answer with confidence. Most of the fungi questions you'll see on your board exams. I am going to make a few podcasts that are dedicated to the antimicrobials. So we'll talk about those drugs and the later podcast. So I wish you all the best congratulations again to the awesome fourth years that matched. And I hope to see you guys on the wards in the future. Thank you.

Hepatitis A and E.

Pregnancy (due to relative immunosuppression).

Parvovirus B19.

H BsAg positive, anti-H Bc IgM positive, and potentially E-antigen positive.

Malassezia furfur.

Trichophyton, Microsporum, and Epidermophytum.

Less than 200 cells/mm³.

Erythema nodosum and fever.

Hepatitis D Virus (needs Hep B).

Aspergillus and other catalase-positive organisms.

Cottage cheese discharge.

Voriconazole or Amphotericin B.

Upper lobe calcification that changes position when a de-cubitus film is obtained.

Erythema nodosum and fever.

Hepatitis D Virus (needs Hep B).

Aspergillus and other catalase-positive organisms.

Cottage cheese discharge.

Voriconazole or Amphotericin B.

Upper lobe calcification that changes position when a de-cubitus film is obtained.