DIP Episode 16 - Bacterial Cases B

Welcome. My name is Divine. I am a fourth year medical student. In today's episode of the Divine Intervention Podcast, we'll be talking about bacteria, primarily gram-negative organisms. So let's jump right in. So the first question says to compare and contrast the two NICERO species to discuss the general gram-staining characteristics, talk about having a capsule or not, what kinds of infections do these box cause, you see some questions about glucose and maltose and growth media, and then we'll see some things about how NICERO-MEN-GIDIDIS is detected. So let's begin. So the thing is the two NICERO species you want to be concerned about for exams, NICERO-MEN-GIDIDIS and NICERO-GONORIA. Both organisms, two certain things they have in common is that they are gram-negative, the gram-negative diplococci. Remember your gram-negative coxci, that's where you have your NICERO species and your more accelerous species. So the two NICERO species, the gram-negative, the diplococci, and they are actually oxidis-positive. So if you see diplococci, don't always jump to strep-numole. Shripp-numole is a gram-positive diplococcus. NICERO species are gram-negative diplococci. Now, if you're looking at the capsule business, NICERO-MEN-GIDIDIS does in fact have a capsule, so that's a high-yield virulence factor, NICERO-GONORIA does not.

If you're looking in terms of vaccination, we know, I mean, before you start school in the US, at least middle school, you get your NICERO-MEN-GIDIS and vaccine. But there is no such vaccine against NICERO-GONORIA. And in general, NICERO-MEN-GIDIS tends to cause respiratory infections. You can cause respiratory infections. NICERO-GONORIA tends to cause sexual infections, right? So like genital infections. Although one thing you should keep in mind is if a person, for example, gives oral sex to a person that has, like, NICERO-GONORIA arthritis, right? You can get a foreign gill infection from that. Both organisms do, in fact, ferment glucose, okay? So NICERO-MEN-GIDIDIS and NICERO-GONORIA. But it is only NICERO-MEN-GIDIDIS that has the ability to ferment mortos. So remember the MN-GIDIDIS for the MN-MATOS. And with regards to growth media, the big thing you want to remember is the Thayer-Martin-A-GAR. Both organisms grow on Thayer-Martin-A-GAR and you can actually use PCR to detect NICERO-GONORIA. Okay? You can use PCR to detect NICERO-GONORIA. So next question. So a 17-year-old college student presents with a 13-hour history of fever and severe headache. Physical exam is notable for a particular rash on the left upper extremity and no coregidity. What's your diagnosis? What's the bug? What's the demographic? How's this transmitted? What's the relationship to mucus early immunology if you make? Okay? And then I will see some things in relation to a cureless UMAP.

And then the final part of this question says, what's the diagnosis? If this patient loses consciousness, has a blood pressure of 50 over 30. Potassium of 6.1, that's super high and glucose of 45, that is super low. Okay? Now, what's the treatment? How do you treat this bug? How do you perphylaxis against this? So let's talk about this. So hopefully with all this information I've given you. So no coregidity, fever, headache, college student, I hope you're thinking about NICERO-GONORIA. I'm an engineer. Okay? So NICERO-GONORIA. Again, it's a gram-negative diplococcus. Okay? It grows on theomartina agar. Okay? Um, theomartina agar is actually chocolate agar, but you actually add some antibiotics so that no more flour does not grow. So you're selecting for NICERO species like NICERO-MEN-INGIDIDES. Okay? Now, the classic demographic, a military crew, so like college students, right? So people in dorms, so if you see mention of like college students, military crew, dorms, think about NICERO-MEN-INGIDIDES. Um, with regards to the method of transmission, this is actually transmitted by respiratory droplets. Okay? And one higher relationship to mucosyl immunologies that NICERO-MEN-INGIDIDES actually expresses Ig-PRODES. Remember, Ig-A is a dimer. It's a dimer immunoglobulin that protects the mucosol surfaces. So if you want to be any kind of pathogen that wrecks havoc on mucosol surfaces like NICERO species, you want to have Ig-PRODES to help with that.

So you cleave Ig-A, so it's ineffective. Now, the E-Q-L-U-MAP connection I'm going to, I'm talking about here is that, um, if they describe a present that tends to get recurring NICERO-MEN-INGIDES, I really hope you are thinking of a C5 through 9 deficiency, okay? Uh, remember, if you have a C5 through 9 deficiency, you have an increased risk of recurring NICERO-MEN-INGIDES. Remember that those are the constituents of the membrane attack complex. And the relationship to E-Q-L-U-MAP, remember E-Q-L-U-MAP is used to treat paroxysmal, nocturnal hemoglobinaria. Uh, that's where you have like a big age imutation, so you don't make, uh, you basically don't have GPI anchors, like CD55 and CD59. Uh, I mean, GPI anchored proteins, like CD55 and 59, on the surfaces of your red cells, right? So complement comes and explodes your red cells. So the drug of choice in the treatment of that disorder is, um, E-Q-L-U-MAP, which is a monoclonal antibody against C5, okay? So the thing is, by giving E-Q-L-U-MAP, you're inducing a pharmacological C5 deficiency. So those patients should actually be placed on NICERO vaccines. Okay. Now, um, the diagnosis, so what's the diagnosis, right? So notice this patient loses consciousness is profoundly hypotensive, has hyperkalemia, and has hypoglycemia. Um, if I add in this extra information, that this patient is bleeding from every site, what do you think about? Well, I hope you're thinking about what a house, Friedrichsens Syndrome, okay?

Uh, this is bilateral adrenal hemorrhage that you get with NICERO meningitis severe, NICERO meningitis infection, okay? It's usually like a disseminated infection. And the reason this patient has hyperkalemia, right, is because the adrenal gland is basically gone, okay? If the adrenal gland doesn't work, our dose zone is not released, and remember that our dose zone helps you dump potassium into the urine, uh, at the level of the principal cell, okay? So if you have like an out-dose-journ deficiency, if you may, with what a house, Friedrichsens Syndrome, you get a hyperkalemia. And those remember that cortisol is a de-bidogenic hormone, okay, that comes from the zona fasciculada of the adrenal cortex, okay? So if you adrenal gland, again, is not working, you're not making cortisol, so you're not increasing blood glucose levels, because remember cortisol is a pro, basically, cortisol basically increases your blood glucose levels, right? Under situations of stress, so you can deal with that stress better, let's say you need to run, or work harder for that stress to pass away, right? To increase your amount of glucose in the serum. So this patient basically has findings, consisting with adrenalins, efficiency, okay, from what a house, Friedrichsens Syndrome. So that's one thing you certainly want to keep in mind. And in general, if a kid, if a very little kid, like a neonate, has my seraminin, do this, you want to give a third-generation sephalosporin, like sephotoxin, okay?

In adults, you usually jump to sephotoxin, okay? The reason you avoid sephotoxin in neonates, right? So like the first 20 days of life, is that sephotoxin can cause a colistesis, which can precipitate, like, some liver problems in neonates, okay? So you generally go to sephotoxin where they are both third-generation sephalosporins. Now, for prophylaxis, so close contacts, right? Of a person that has my seraminin, generally you use rifampin for that, okay? But you could also use syprone, which is a fluoroquine alone, or sephotraaxop. So just something high to keep in mind with that. Okay, so let's go through the next slide. Now, 22-year-olds sexually active, ding, ding, ding, so 22-year-old sexually active, college student presents to the 3 D history of migratory joint pain and a pure lent panel discharge, okay? So what's the diagnosis? And the masking, okay, what's your diagnostic testing? What's the structural feature that increases infectious potential, especially for the urinary tract, okay? And then, common presentations in women, neonithal ophthalmology and prevention, we're gonna compare this bug with chlamydia, right? So if I'm seeing compare with chlamydia, that means the answer to this question should not be chlamydia, right? And then let's talk about how this bug is treated, right? So obviously, you know I'm talking about my serogularia.

Now, my serogularia, classically, diagnostic testing, you can take like a swab of like the pure lent discharge that this patient has. You do a smear, you do a gramsthen, you'll see gram-negative deploc oxide, okay? Gram-negative deploc oxide. But another thing you can do is PCR. In fact, PCR is probably one of the more common things that I don't right now to detect my serogularia, okay? And one thing that my serogularia has going for it, that makes it possible to attach to the urinary tract is that it has p-line, okay? It has p-line. Don't forget another high yield thin, if you're sort of drain of correlation here, is that equal light, there isn't equal light causes a lot of UT Is, is that it has a fringely that enables it to attach to urinary epithelial. Now, the common presentations of my serogularia in women, right, it can present as an infection of the cervix, sort of like serositis. It can present with PID, it can present as PID, so pelvic inflammatory disease. And if they actually describe a person, right, so sexually active, they can attach to them blah, blah, blah, and the patient has right upper quadrant pain. I really want you to think about feats here, credit syndrome, okay? That's an infection, an isereal infection of the liver capsule, okay? It's not only in a serious, that can cause that kind of infection, any bug that causes PID can also cause that kind of infection, okay?

But a liver capsule infection, right upper quadrant pain, sexually active person, think about feats here, credit syndrome, okay? And it can be a sequel of my serogularia meningitis. I mean, nicerogularia. Now, with regards to a newness of thomology, right? So if a lady has gonorrhea, and the kid passes through the birth canal, okay? Those nice cereal bugs can cause conjunctivitis in the new unit, and it's usually super, super, super purellent, okay? So that's why in general, most kids that are born in the US, they get prophylactic erythromycin ointments to prevent ophthalmianneonatura that you could get with my serogularia from passing through the birth canal, okay? And in general, if you compare nice serogularia with chlamydia, the discharge you get from the vagina or the penis in chlamydia infection, it tends to be not as purellent as what you get with nice serogularia. It's not usually purellent, it's more watery, and it's more clear, okay? So that's another high-yield thing you want to know. And if you do a gramsthine in general, you don't see anything with chlamydia. And I will just tell you this, that chlamydia is actually a much more common STI than nice serogularia, okay? So just something to keep in mind. If they give you a very non-specific question where you're just supposed to make a diagnostic prognostication with regards to STI, I think more about chlamydia. It's a lot more common than nice serogularia.

And in general, nice serogularia, you typically treat with septraaxone. Remember, septraaxone is a third generation of low sporing that covers nice sero species really well. So it gives septraaxone, but it also gives it thromicein, okay? By giving it a zithromicein, you can cover concomitant chlamydia infection. Although there are actually some nice serogularia species that are resistant to septraaxone monotherapy. So adding it is ethyromicein actually decreases that resistance. So that's just another thing to keep in mind. Another cocktail you could use is septraaxone, plus doxycycline. So it's a third generation of septraaxone, so it's a third generation of septraaxone, so it's a third generation of septraaxone, so it's a third generation of septraaxone, so it's a third generation of septraaxone, so it's a third generation of septraaxone, so it's a third generation of septraaxone, so it's a third generation of septraaxone, so it's a third generation of septraaxone, so it's a third generation of septraaxone, so it's a third generation of septraaxone, so it's a third generation of septraaxone, so it's a third generation of septraaxone, so it's a third generation of septraaxone, it has been tugging his ear and wins in and pain for the past two days. Orozcopic exam is notable for herethema, and decreased mobility of the tympanic membrane, right? So this kid obviously has otitis media. A grumstein of purulent material around the eardrum reveals gram-negative circular organisms.

Okay, what's the bog? And what are your treatment strategies? So this kid clearly has nice otitis media. Okay? And there are certain bogs that commonly cause otitis media, right? So like strep pneumocommonly causes otitis media, viruses are probably one of the most common overall causes of otitis media. More acceleratoralis also causes otitis media. Okay, remember that's a gram-negative caucus. And non-type people each flew also causes otitis media. In fact, the most common cause, very high you to know that's the most common cause of otitis media, the most common bacterial cause of otitis media is non-typable, hemophilus influenza. Now, this question says, you do a grumstein, and you see gram-negative circular organisms, right? So gram-negative coxide. Okay? If you see gram-negative coxide, that should help you roll out strep pneumo, and that should also help you roll out h-flu. H-flu is not a caucus, okay? So this leaves us with a more acceleratoralis. Okay? Our acceleratoralis is actually a fairly common cause of otitis media. And the way you treat this infection is with the same drug you use to treat most kinds of otitis media. Okay? Here's a combination of amoxicillin and a beta-lactamine inhibitor, like clavolanic acid. Okay? So amoxicillin and clavolanic acid, right? You're augmenting the activity of amoxicillin with clavolanic acid. That's why the drug is called a augmenting.

I'm just making that up, but amoxicillin and clavolanic acid is actually, in fact, a augmenting. So short question there. So let's jump up to the next one. Question five. 23-year-old cystic fibrosis patient is brought to the ED by his mom. His temperature is 105, that's super high. He has had significant respiratory difficulty for the past three days, that is worse than his normal baseline. What's the bug? What are its special characteristics, right? So let's just sort of take this step by step, right? So this bug obviously is pseudomonas. Okay? So cystic fibrosis patient with pneumonia, one big thing you definitely want to think about on your exam is pseudomonas. Okay? And in general, on exams, the most common cause of pneumonia in a CF patient that is less than 21 years old is staphores. But when that CF patient becomes greater than 21 years old, then you're thinking about pseudomonas. Okay? And when the CF patient is like about to die, like when, like the infect, like their diseases like terminal, you also want to begin to think about some exotic organisms, like Bocoderia sepicia. Okay? Bocoderia sepicia. Now, so this patient has pseudomonas ergenosa infection. Okay? A few characteristics with pseudomonas is it's a gram-negative rod. Okay? It's a gram-negative rod. It's oxidized positive. And it's actually catalyst positive as well, right? So if a person has chronic redolomatous disease, right?

So any deep-heat oxidized deficiency, they can get recurrent pseudomonal infections, right? Because again, pseudomonas is a catalyst positive organism, right? That's what the last part of this question is talking about, where I say, why would a patient with a negative NBT test get recurrent pseudomonal infections? Okay? Now, all the virulence factors that pseudomonas has going for it is that it is an encapsulated organism. Okay? So if a person has a splinear, right? So like a sickle cell patient, again, they can have life threatening pseudomonas infections. In addition, pseudomonas has an exotoxin. It's called exotoxin A. Exotoxin A actually ADP ribosilates, elongation factor, too. Okay? So that decreases protein synthesis. So hopefully you can make the correlation between the exotoxin A of pseudomonas and your protein synthesis inhibitors, right? Like your amino glycosides, your tetracycline, your chloramphenicol, your macrolids, your linesolid, and your streptogramming. Okay? So you decrease protein synthesis with the exotoxin A that comes from pseudomonas. Now, all the higher things with pseudomonas, you want to know is that it produces certain pigments. The most commonly tested one on exams is pioscianin. Okay? It's a blue, it gives it a blue-green color. Okay? In fact, that's why if you see like burnt patients and you see like pus from the oons, and it has like this blue-ish green color, you really want to think about pseudomonas, right?

So the monos is a fairly common infection in burnt patients. And... So the monos usually smells like grapes, right? So if they describe a burnt patient and they say like, oh, this patient person has like serolitis or whatever. And the... POSS or whatever. Like has like this gripe-like smell or they describe a hospital, like a burn unit in a hospital that has like a gripe-like smell. You want to think about pseudomonal infections. So the monos, the classic demographics, right? So it has an association with water, okay? So it can cause hot-top folliculitis, right? So if they describe a skin infection in the person that is an avid swimmer, think about hot-top folliculitis or pseudomonas. Although the most common cause of folliculitis, I will say like an unknown swimmer, you probably want to think more about staff workers with that. And please do not confuse hot-top folliculitis with hot-top lung. Hot-top lung is very severe, respiratory slash lung infection. That's associated with mycobacterium, avial intercellularity, right? So remember that bug that is supposed to be prolax with easy thromice in a HIV patient when the acidity for count drops below 50. Now, another classic demographic for pseudomonas is a burn, again, a burnt patient. In fact, one classic presentation on exams could be a burnt patient having like an acrotic ulcer on the skin. That's something known as a femagangrenosum. It's a very high-yod association, for exams with pseudomonas, okay?

So it can present as a blood eschar, okay? So a blood eschar is not something that is only specific to bacilos and thresus, okay? A blood eschar is also a finding you could get with cutaneous pseudomonas infections. Now, pseudomonas, right? If they describe a person that has like bone pain or osteomyelitis from having stepped on a nail that went through like sneakers or like a workout gear, again, also think about a pseudomonas, okay? Sodomonas leaves in, there's a lot of pseudomonas in shoes and in sneakers. Now, again, also think about your cystic fibrosis patients with pseudomonas, that's another thing you want to think about. And I was in general, those are the people that classically get pseudomonas on exams, although also don't forget your CGD relationship with any DPH oxidase deficiency. And the drugs that covers pseudomonas are super, super, super, super high-yod for exams, okay? The classic drugs you want to be aware of for exams include drugs like paparacillin and teizobactem, okay? Remember, pipteizo, that's like what's called zosin in hospitals or vitamin Z, if you may. Pipteizo, teizobactem is a bit of lactemiz inhibitor, piparacillin is a kind of penicillin, okay? It's an anti-sodomono penicillin. You are a minor glycosides, right? So, like drugs like gentamysin, you're mysin, amicacin, streptomycin, and if you're talking about like the cystic fibrosis patients in heel-tobromycin, those drugs all cover pseudomonas.

Your fluoroquinolones like syprophloxacin, liver-floxacin, moxifloxacin, gadi-floxacin, they all cover pseudomonas. And then certain cephalosporins also cover pseudomonas. I'll say like the third generation cephalosporins have tazedin, those cover pseudomonas. And then the fourth generation cephalosporin like cephepin also covers pseudomonas. So, those are high-yod things you want to know in relation to pseudomonas. So, let's go to the next question. So, 59-year-old smoker presents to the ED with a 3 D history of diarrhea and shortness of breath. Temperature is 101, that's high. He recently visited a resort in the Bahamas that had an artificial waterfall. Ding, ding, ding. So, what's the bug with other special characteristics or a means of transmission? What's the classic presentation? And what's the classic exam symptomatology, if you may? How do you diagnose this infection and how do you treat this bug? Okay? So, if you see a waterfall, you see pneumonia. And for example, let's assume they give you a chest extra where you see interstitial infiltrates. You really want to think about legionella nomofella. Okay? Legionella nomofella. So, this is legionear disease. Okay? So, what are some special characteristics of legionella? Okay? Legionella, it's a gram-negative organism, although it doesn't gram stain very well because it has like some branching fatty acids in its cell wall. Legionella does actually stain pretty well with silver. Okay?

So, while we're on the topic of silver stains, please don't forget that pneumocystis gerovetia and H-pilory also stain pretty well with silver. And legionella, the thing is, it's an interstellar pathogen in general and it grows very well on chocolate yeast, like sorry, chocolate yeast extract that you enrich with iron and cysteine. So, that's another thing you want to know. And here's one way you'll try to trip you up on exams with regards to the means of transmission. Okay? Legionella is not transmitted through person to person contact. Even if it's a respiratory infection, right? It is actually not transmitted through person to person contact. It's actually transmitted through inhalation of aerosolized fluids. Okay? That's why it has an association with air conditioning or with water faults or with like mist. Okay? So, those are high-yield things you want to think about with legionella. Now, the classic presentation, okay? I think of legionella as being pneumonia plus. Okay? So, the person will present with like high-feevers, walk in pneumonia. You get a chestache, you see like a intestinal infiltrate. And these patients tend to have diarrhea. Okay? And they also classically have the BMP anomaly of hyponitremia. Okay? So, if you see a person that has pneumonia, okay? It was recently exposed to like air conditioning or business conference or waterfall. And they have hyponitremia and they have respiratory problems. And you see like intestinal infiltrates on a chest x-ray.

Think about legionella, nomofella. Okay? Think about legionella, nomofella. And the way the diagnosis is made is with a urinary antigenase. Okay? And treatment of legionella like all other causes of atypical pneumonia is with a macrolead. Okay? Like a rhithromycin, clarithromycin is rhithromycin if you may. Now, I guess with that we can jump up to the next question. So, a med student presents to the ED with a temperature of 104 and a painful or straightening lesion on the left upper extremity. Physical exam is notable for significant left axillary lymphatic anapathy. Okay? He took a year off to study thugarette therapy in rabbit models of the brain of the brain malignancy glioblastoma multiformy. So, let's assume this is a mess reading the ones too much into neurology or neurosurgery or ENTO or whatever. So, studying thugarette therapy in rabbit models of GBM. Okay? So, rabbits. So, what's the book? Okay? What are the special characteristics? So, means of transmission of this book. And what's the classic presentation? Okay? So, if you see a rabbit, some you examine. Okay? You want to think about a francicella. Okay? Francicella to larences. Okay? Causes to larynia. It's a GBM negative rod. Okay? And it's actually a zoonotic infection. Now, there are certain ways you can get francicella on exams. Okay? One way you could get francicella is to just to inhale like the aerosolized secretions of rabbits. Okay?

Or, let's assume you directly come into contact with secretions of a rabbit. You could get to larynia with that. Alternatively, tick that bites a rabbit, like a GBM centric, for example, that bites a rabbit. And then goes on to bite the human being could also transmit to larynia that way. Okay? So, very high yield to remember that. If you inhale the aerosolized secretions of francicella to larences, or you're bit by a tick, okay? Like the dremacentoteck that bites a rabbit, you could get to larynia from that. And the classic presentation is the part of your skin that is inoculated with that's like beating by the tick or comes in contact with like your skin is abraced by the fingers or nails of the rabbit or whatever. That site of inoculation, you tend to get an ulcer at that site. And then you also get lymphadenopathy. So, the lymph nodes that drain that ulcer, you tend to get lymphadenopathy with that. Okay? But the big thing you want to keep in mind is that you will give you a person that you will give you, like if you see rabbits in an MBME question, and the person has fever and there is an ulcer, okay? Like on the skin. And you see like lymphadenopathy, that's very proximal to the ulcer. Think about a to larynia, okay, from francicella to larences. A francicella is actually a gram negative rod. So, that's all you need to know with that buck. Next question. A four year old female in California is rushed to the 80 by a constant parent, okay?

She has had a severe cough for the past seven days. These episodes have occasionally been associated with vomiting. That's a very high yield association to know. A fondoscopic exam is positive for subconjuring table hemorrhage. That's another high yield association to know. The white count is 60,000 with a lymphocytic predominance. And now the super high yield association to know. Basically, with this clinical presentation, I've given you the details that will almost certainly make its way to any exam question you'll see that test this buck. Okay? Now, what's the bug? What's the diagnosis? What are the stages of disease? What are the virulence factors? Any special characteristic, so growth media for this buck? How do you prevent this buck? How do you treat and how do you profile acts? Okay? So with all these questions you're seeing, you can probably tell that this is something high yield you want to know for tests. Okay? So this patient clearly has open cough. Okay? Open cough. Okay, remember, open cough is caused by borethela protosis. This is actually a vaccine preventable illness. Okay? So you could get the toxoid vaccine, the T-dap vaccine, or you could get the D-tap vaccine. Okay? Although you generally get boosters of those vaccines because immunity wins after like eight to ten years. If you're receiving your initial vaccine. So it's actually preventable.

And I'll just talk about the tripe right now so I don't forget you generally treat borethela protosis with a macrolead like a rhithromycin. And it's also good to know that because that's also the way you treat close contacts, right? That's profile access so that you don't get the infection. Now, certain high yield things you want to know about a telaportosis is that it's a bacterial infection. Or to, unlike most bacterial infections where you get a predominance of neutrophils as a reaction to that infection. You can really get a predominance of lymphocytes. So if you see bacterial infection with a lymphocytic pleocytosis, think about borethela on exams. That's one thing. Second thing is that these patients tend to get a very nasty cough. And that cough is classically associated either with on exams, either with vomiting or difficulty breathing or a subconjunctival hemorrhage. Those are like three very classic exam presentations like this. You'll see all this percent coughs and the alpha breath. I will encourage you to look up a You Tube video or something of whooping cough. It's actually pretty striking. Now, another thing you want to know with borethela pertosis is that is that is a gram negative rod. Okay. And one high yield virulence factor with B pertosis is the pertosis toxin. That's a very imaginative thing. The thing is the toxin has a relatively high yield mechanism of action because it's unusual. Okay. So the way the toxin works is that it in activates GI.

So an inhibitory G protein coupled receptor. And when you inhibit GI, you actually increase the activity of adenylate cyclists. And if adenylate cyclists activity is increased, you have an increase in cyclic A and B. That's why you get many problems with borethela pertosis. Another virulence factor is a protein that it expresses hemagglutin. Hemagglutin, you may remember that I talked about this with the influenza virus. But the thing is the hemagglutin that's expressed by borethela pertosis actually binds to the cilia. Now you find on the sudos-tranified columnopithelium of the respiratory tract. Okay. And when he binds, he basically grinds those cilia to a halt. And remember that cilia necessary for the clearance of respiratory pathogens and mucus. Okay. So if those cilia are non-functional, you then basically open up your respiratory tract for infection. That's one. And two, because you cannot whip away noxious substances, you'll always become hypersensitive to anything you inhale. Okay. Again, you get a lot of whooping cough with borethela pertosis. And while we're on the topic of cilia, please do not forget Cartagena syndrome. Okay. Primary, it's another Bosworth name is primary cilia dyskinesia. Okay. Remember these people tend to get a recurrent respiratory infections. Basically, anywhere you have cilia in the body, they will get problems in that system. So like the respiratory tract, remember the sudos-tranified columnopithelium that has cilia. Okay.

So they get tend to get recurrent respiratory infections. They get infertility. Because remember the phallopian tubes have cilia. They tend to get here in loss. Okay. Because remember you have a cilia as part of your hearing apparatus. Okay. So don't forget that cilia association. I just decided to talk about that here. And one of the virulence factors, hemagrotinium with borethela pertosis, basically grants the cilia just in a respiratory tract. So the cilia in a respiratory tract to a halt. And the way you actually acquire borethela pertosis is through respiratory droplets. So just something to keep in mind there. Okay. Now, the stages of disease with borethela pertosis, I remember that with the mnemonic CPC. So the first C stands for the cataractyl phase. Okay. Where you basically just feel like crap. You have like runny nose. You have like mouth fevers. And then there's the paroxysymal stage where again you get the nasty cough. It's usually worse at night with respiratory whoops. Okay. So like, right. And again, if they describe a kid that has like really nasty cough for like weeks and weeks on end. Where the kid has a subconjunctable hemorrhage or vomiting or is out of breath at the end of each coughing episode. Think about borethela pertosis. And borethela pertosis. So you have the catoral phase, the paroxysymal phase. And then you have the convalescent phase where you're recovering. Okay.

And if you want to isolate borethosis, you can use the bordeji-jinjul media or you can use the Regan-Lew media. Those are two things that definitely examine testable. And treatment is with a microlitre like a rhithromycin. Okay. With a microlitre like a rhithromycin. Although, don't be an anti-vaxer. Vaccineally, your kids so they don't run into these kinds of problems. Okay. Next question. A second to the last. So a Kentucky family that resides on a goat breeding farm brings the a six-year-old daughter to the ED with complaints of high fever for the past seven days. Okay. These fevers, right? So goat breeding, that's one key buzzword. High fevers, that's another key buzzword. These fevers are worse at night. That's another key buzzword. So imagine that these fevers are better during the day. So it's like a waxing and a waning fever. Now, the child's clothes are drained from profused sweating even with outside temperatures of 50. Okay. That's another key buzzword. So what's the bug? Okay. What are its special characteristics? And what is the classic association? What are the classic associations, slasher, presentation with this bug? Okay. So if you ever see farming, right, like exposure to like sheep or cattle or goats, and then they describe a person that has fevers that wax and win. Classicly, the fevers are worse in the evening and better during the day, right? So like picket fence fevers if you may. Okay. And the land fevers if you may.

I really hope you're thinking about brucellosis. Okay. Brucella from a brucella species. Okay. So this is brucella. Brucella is a gram negative rod. It's a zoonotic infection. Okay. It's zoonotic because you again, you're classically get it from cattle or from sheep or from pigs or from goats. Okay. So if they give you an example question that describes a person that works in a slaughterhouse or a person that lives on a farm or a person that consumes on pasteurized goat milk. Okay. And then they present with like fevers and very severe sweating. That's a high-yield association. And they say that, oh, this person has fevers that are worse at night and better during the day, right? So, Anduland fevers think about brucellosis. Okay. Think about brucellosis. And the last part of this question that says, Megaloblastic anemia in an infant with a strict goat milk diet. This is one of those questions for it's more step two like, but it's one of those things that could potentially show up on step one and most people will get rubbed. Okay. So hopefully you won't get it wrong because you're listening to this podcast. But the thing is, infants that take a strict goat milk diet actually tend to get a full-lit deficiency. Okay. Which can present again as a Megaloblastic anemia where the MCV is greater than 100. Okay. You see hypersegmented neutrophils on a blood smear. So just something high you'll keep in mind. Keep in mind there. Okay.

So again, brucellosis, profuse sweating, Anduland fevers, exposure to cattle, sheep, goats, pigs, slaughterhouse, on pasteurized goat milk consumption, things like that. That should tip you towards the diagnosis. Okay. So next and the last question, a 26 year old female is intubated in the ICU three days after presenting it by lateral low extremity weakness. She had a four day episode of bloody diarrhea that resolved without treatment two weeks ago. Lombard puncture is notable for a marked increase in CSF protein. White cell count is within normal limits, right? So hopefully you're already making a link here. Increase in CSF protein with a normal white cell count. Okay. That is finding known as a Buminocyteologic dissociation. Okay. So what's the bug? What's the special, what are the special characteristics of this bug? Okay. What's the means of transmission? What's the classic presentation? And how is this infection treated? Okay. So this patient clearly has Guillembury syndrome. Okay. Remember, Guillembury syndrome. You do a CSF study on exams. You see an increase in protein. CSF protein, but new increase in cells. Okay. That's known as Albuminocyteologic dissociation. There is a dissociation between the protein count as the Albuminopart and your white cell count because, classically, if you have a high white count, you have a high protein count. Okay. So having a high protein amount in your CSF with a normal white cell count, that's discordant. Okay.

That's what's known as Albuminocyteologic dissociation. Okay. This person has Guillembury syndrome. Okay. And they tell you that, oh, two weeks ago, this person had a bloody diarrhea that resolved without treatment. Okay. So hopefully you're thinking about Campylobacter, Gegro 9. Okay. Cegro 9. It's a gram-negative organism. It's a gram-negative curved rod. It's oxidized positive. And it actually grows at 42 degrees Celsius. Okay. Because at 37, many things grow. But at 42, many things do not grow. I can imagine as a human being yourself, you will feel extremely uncomfortable at 42 degrees Celsius. Okay. But Campylobacter, Gegro 9, does grow really well at 42 degrees Celsius. So that's a very unique characteristic. Remember, Campylobacter can fire 42 degrees Celsius. That's another way to keep that string in your head. Now, the classic association with Cegro 9 is the consumption of contaminated poultry. Okay. So the person consumes hamburger or meat or chicken or whatever. And then they present a bloody diarrhea. Okay. Think about Campylobacter, Gegro 9. In fact, it's probably the most common cause, very high you to notice, is probably the most common cause of bacterial bloody diarrhea in the United States. Okay. So that's something you definitely want to keep in mind. Now, why do you get Gegro 9 with Campylobacter infection? I mean, it's not everyone that gets Cegro 9 infection that gets Gegro 9. But it's a principle that the occasionally test on exams.

It's the principle of molecular mimicry. Okay. The thing that happens here is that the antibodies that your body makes against Cegro 9 cross react with proteins and myelons. Okay. So you can have a peripheral dimylunit in neuropathy in the setting of Cegro 9 infection. Okay. And that's how the person gets a guiomeric syndrome. If they don't, if they want to mess with your head on exams. Instead of putting GBS or Guiomeric syndrome, they can put acute inflammatory dimylunit in poly neuropathy as the answer choice. Okay. AIDP. That's just code word for GBS on exams. Okay. So just another thing to keep in mind there. And the way you treat GBS, I mean, the way you treat Cegro 9 is with a fluoroquinoleon, okay. Like Cepro or liver floxasin or with a microlitre like erythromycin. Okay. So I think with this, we are done for today. I would have a dedicated podcast where I just go through trigger lists that are very useful for microbiology. I'll talk about like, basically, just be where I give you like a one-liner and you supply the name of a bug. And the one-liners, I'll group them by disease condition like diarrhea, for example, on pneumonia or STI or drugs and stuff like that. And I think there'll be a very good global micro review down the line. So I wish you all the best. If you have any questions or you spot any errors, please don't forget to send the comment.

And if you have any questions, just shoot me a message at Divine Intervention Podcasts at gmail.com or you can use the contact button in the website. I mean, the contact page in the website to send me a message. I'll be sure to get back to you as quickly as possible. Have a wonderful week ahead and remain blessed. Thank you.

Both are gram-negative diplococci, but N. meningitidis has a capsule (virulence factor) and causes respiratory infections; N. gonorrhoeae does not have a capsule and causes sexual infections.

Recurrent pneumonia, especially when the patient ages past 21 years old.

Inhalation of aerosolized fluids (e.g., from air conditioning units or water fountains), not person-to-person contact.

Severe cough, subconjunctival hemorrhage, and vomiting/difficulty breathing at the end of coughing episodes.

Brucella species (brucellosis).

Molecular mimicry, where antibodies cross-react with proteins found in myelin.

Neisseria meningitidis (MN-MATOS).

Pyocyanin (blue-green color).

Urinary antigen testing.

Severe cough, subconjunctival hemorrhage, and vomiting/difficulty breathing at coughing fits (mnemonic CPC).

Molecular mimicry.

Deficiency in NADPH oxidase (DPH) activity, as Pseudomonas is catalase positive.

Macrolides (e.g., azithromycin/rhithromycin).

Neisseria meningitidis (MN-MATOS).

Pyocyanin (blue-green color).

Urinary antigen testing.

Severe cough, subconjunctival hemorrhage, and vomiting/difficulty breathing at coughing fits (mnemonic CPC).

Molecular mimicry.

Deficiency in NADPH oxidase (DPH) activity, as Pseudomonas is catalase positive.

Macrolides (e.g., azithromycin/rhithromycin).