Cram The Pance - S1E57 Bacterial Disease Review

Episode Date: February 22, 2026

High Yield Bacterial Disease Review:Cholera (Vibrio cholerae) Chlamydia (Chlamydia trachomatis) Gonorrhea (Neisseria gonorrhoeae) Bartonella henselae (Cat scratch disease) Botulism (Clostridium botulinum) Campylobacter (Campylobacter jejuni) Diphtheria (Corynebacterium diphtheriae) Acute Rheumatic fever (Group A Streptococcus) Rocky Mountain spotted fever (Rickettsia rickettsia) Tetanus (Clostridium tetani)Review for your PANCE, PANRE, Eor's, Physician Assistant exams, USMLE, NCLEX, nursing exams.►Support the channel by joining and becoming a member! (Thank you so much!)►Paypal Donation Link: https://bit.ly/3dxmTql (Thank you!)►INSTAGRAM: https://www.instagram.com/cramthepance/►YOUTUBE: https://www.youtube.com/channel/UCZCILePJ-E17txF-ObXlFKwIncluded in review: Cholera (Vibrio cholerae), Chlamydia trachomatis, Gonorrhea (Neisseria gonorrhoeae), Bartonella henselae (Cat scratch disease), Botulism (Clostridium botulinum), Campylobacter (Campylobacter jejuni) Diphtheria (Corynebacterium diphtheriae), Acute Rheumatic fever (Group A Streptococcus), Rocky Mountain spotted fever (Rickettsia rickettsia), Tetanus (Clostridium tetani), Major and Minor Jones criteria, Doxycycline, Azithromycin.Become a supporter of this podcast: https://www.spreaker.com/podcast/cram-the-pance--5520744/support.

Okay, so I've been getting a lot of requests for some more infectious disease topics. So today we're going to go over bacterial diseases. High-yo, there's lots of them, and I focused on the highest deal topics that are frequently tested on. Bartonella, botulism, chlamydia, cute rheumatic fever, campobacter J. Juni, as well as many others. Got plenty of pneumonics in here, maybe too many. So we'll get started. But as always, a quick thank you for all of the nice comments, the support, everybody who's bought a t-shirt, donated to the channel.

I really do appreciate it. So thank you so much. Let's go ahead and get started, starting first with cholera. So when you see cholera, C-H-O-L-E-R-A on an exam question, the first thing I want you to do is put a two between the H-N-E-O. You put a two between the H-N-E-O. That makes H-2-O. Why?

Because every time you see cholera, I want you to be thinking of water. As everything you need to know about this disease from the infectious organism, the mode of transmission, treatment, clinical manifestations involves water. So if you can remember H-2-O, you can likely get the question right on the exam. So cholera is a life-threatening infection caused by toxin-producing strains of an organism called Vibrio cholerae. Vibrio colorei is a comma-shaped gram-negative rod. And again, everything ties back to water, just like we talked about before. And even with Fibrio, R-I-O, Rio, if you speak Spanish, you may already see it, but Vibrio ends in Rio, which means river in Spanish. So when you see Vibrio, Rio,

think river, think water, think H-2-O. So where are people typically exposed to this organism? This will most commonly be through the fecal to oral route through consumption of contaminated water. Ingestion of Water contaminated with feces is often cited as one of the most common sources of transmission of cholera. And it's why this is more common in settings with poor sanitation and limited access to clean drinking water. Water, water, water. With that being said, contaminated food is another one.

So consumption of specific contaminated foods can also spread the disease. And while there are a number of foods that can become contaminated, contaminated shellfish is an exam favorite. And I personally got a question on this in school. And luckily for you, me and my mnemonic shellfish live in. you got it water. So for transmission, remember, contaminated water and shellfish. Next, let's talk about clinical manifestations. The main thing you need to know is this infection can cause profuse watery diarrhea. So the hallmark of this disease is profuse watery diarrhea. It will sometimes be

described as rice water stool, which is this pale and cloudy looking with little flex of mucus, basically looking like the water that's left over after you rinse or cook rice. So once fibrio gets into the small bowel, it releases a toxin, which is the main issue. As this toxin hijacks the cells lining the intestine, which can lead to massive amounts of water and electrolytes being dumped. This disease can be fatal if it's not treated, as it can lead to rapid dehydration and electrolyte loss from all of the fluid being dumped. There can be asymptomatic cases depending on the strain that's involved. There can be nausea, vomiting. And fever is actually uncommon, and the presence should prompt the search for concomitant infection.

But most importantly, know your profuse watery diarrhea and or rice water stool, water, water, water. diagnosis i won't go too deep into it as it's pretty straightforward often made clinically and confirmed via stool culture but treatment is very important and i'll give you a second to think about what the treatment might be that's right water and to be more specific iv fluids or oral rehydration solutions so fluid management is the cornerstone of cholera treatment reducing mortality in severe cases from over 10 percent to less than 0.5 percent the type and amount of fluid depends on the degree of dehydration mild dehydration can be treated with oral rehydration solutions composed of water and electrolytes. Moderate and severe cases require IV fluids often using ringers lactate, which is water electrolytes

and sodium lactate. Antibiotics can also be used as adjunctive treatment in more severe cases as well. But remember, the main state treatment for cholera is water, aka your fluid replacement. That's what you need to know. Okay, cholera, remember, add a two between the H and the O. You get H2O. Remember, transmission is often through contaminated water. Clinical manifestations are profuse watery diarrhea or rice water stool.

Treat with water, aka fluid replacement. And the organism here is Vibrio Colore, Rio, aka River, and that's cholera. Let's talk about chlamydia next. Specifically, chlamydia trachomitis, which is a gram-negative bacteria and is the most commonly reported STI in the United States. What do we need to know? Let's start with clinical manifestations. Surprisingly, a great majority of chlamydia infections are asymptomatic, but that's not

what you'll be tested on, so let's focus on the symptomatic patient. So when symptoms do occur, they most commonly involve the urogenital tract leading to classic urgenital syndromes such as urethritis with mucoid or watery urethral discharge and dysuria, cervicitis with vaginal discharge or periolent endoservical discharge and epidemitis with testicular pain and swelling. There are extra genital manifestations depending on the serotype involved, including conjunctivitis, pharyhybititis, among others. And while these are important to know, the next two complications are tested on far more often, so make sure you know them well. If chlamydia trachromatis goes untreated in females, it can lead to pelvic inflammatory

disease presenting with lower abdominal or pelvic pain and cervical motion tenderness, and ultimately can lead to infertility and chronic pain. Another high-yield dissociation is reactive arthritis. Chlamydia is actually the most common sexually transmitted pathogen linked to reactive arthritis, so this connection is absolutely worth knowing. Moving on to diagnosis next, which will be made with nucleic acid amplification testing or NAA-NAT, Nat, a test which detects the genetic material DNA or RNA of viruses or bacteria by amplifying it to detectable levels through a sample obtained.

For chlamydia samples are typically obtained via a vaginal swab in female patients or a urine sample in male patients. One other important thing to consider when conducting diagnostic testing is that Niceria gonorrhea co-infection is common. So all patients with chlamydia trachomitis infection should, also be tested for Nicere gonorrhea, as they have similar clinical manifestations and co-infection is common. Finally, let's talk about treatment. One med to commit to memory here is going to be doxycycline. Doxy is your treatment of choice in non-pregnant individuals as compared with azithromycin,

which is an alternative. Doxy has better microbial cure rates. So really you just need to remember doxy. And it's actually easy to remember. Why? Because when you hear clamidia, clamidia, what word sticks out? Clam, right? And where do you find clams and a dock by the sea, doxycycline. So anytime you hear clamidia, think about finding those clams in a dock by the sea, and you'll remember your first line med, dock Cicline. And if you want to get really fancy, remember those clams have been sitting out in the sun for a little too long, getting all nasty and they're getting swarmed with gnats. And then I'll help you remember your first line test, nucleic acid amplification or nat testing. So for clamidia, remember your clams on a dock by the sea

being swarmed by gnats, and you'll remember your first line med and diagnostic test. And that's chlamydia. Let's talk about gonorrhea next. So gonorrhea infection with gram negative bacterium, nisiria gonorrhea, which you will forever remember instead as nisiria gonorrhea. Remember it as nisiria gonorrhea. As in the joint, the knee, knee syria gonorrhea. More about that in a minute. So in the U.S. knee syria gonorrhea, it's the second most commonly reported communicable disease. There's not a whole lot to know here and there's definitely some overlap with chlamydia. Let's first start with clinical manifestations. So while there are areas, outside of the genitalia that can be infected. Genital infections are the most common

associated with this organism, and just like in chlamydia, a large number of patients may be asymptomatic. So keep that in mind. But let's talk about your symptomatic patients, that's likely what will be tested on. So in females, we'll see cervacitis. This can manifest as vaginal peritis and or mucoperulent discharge. And just like in chlamydia, this can spread and develop into pelvic inflammatory disease, which occurs in approximately 10 to 20 percent of females with cervical gonorrhea. Both males and females will see your arthritis, so dysuria, urinary urgency or frequency, perulant discharge, which is more common in males. This organism can also affect areas outside of the genitalia, gonococcal conjunctavitis, which mainly

affects infants born to untreated mothers, perihypotitis known as Fitzhucuritin syndrome, and disseminated infection can occur. And this is the highest you'll think to know about gonorrhea, as it's always tested on. So gonacoccal infection can spread from the initial site in up to 3% of patients. Disseminated infection often leads to one of two clinical synchreferral syndromes, which is a triad of tenocinovitis, dermatitis, polyarthriagis, or, and this is the one to know, periolent arthritis, which can involve the wrist or ankles, but most commonly the knee. This vignette always seems to pop up on exams time and time again. It'll be a young patient complaining of dysuria and knee pain recently engaging in unprotected

sexual intercourse, etc. I've seen this question so many times, so it's in your best interest, just remember this. And that's why instead of Niceria gonorrhea, again, remember it as knee syria gonorrhea. just to help you remember the periolent arthritis most commonly involving the knee. Don't forget it. All right, diagnosis, just as in chlamydia, you're going to use nat, again, nucleic acid amplification testing. This will be your test of choice for initial diagnosis. Treatment, one med to know, and that's going to be seftriaxone. As of the time of this recording, seftriaxone is the standard of care for treatment of gonorrhea and has the lowest rate of gonacoccal drug resistance. This may

change in the future, but as of now, no sefriaxone, which is usually administered as a single intramuscular dose. With that being said, if you're treating gonorrhea, what other presumptive treatment should likely be considered? That's right, like we talked about before, glimedia. Climedia and gonorrhea are unfortunate friends and often come together. So doxycycline likely will be added to this regimen unless it's been excluded through testing. So that's gonorrhea, servicitis, eurythoritis, possible to progress to PID. Most importantly know of the potential for purulent arthritis most commonly in the knee. Remember, knee-serie gonorrhea, diagnosed with nat, treat with septriaxone, and as co-infection with chlamydia is common,

it will likely be added to your regimen. Next, let's talk about Bartonella. And while there are a number of Bartonella species that can infect humans, when we're talking about the exam, the species you need to know is Bartonella Hensley, which is the causative organism for cat scratch disease. So Bartonella Hensley is the most common form of bartnolosis in the United States and the one you'll be tested on.

So Bartnala Hensley is a gram-negative bacteria that can spread between animals and humans, which is by definition a zoonotic disease. As far as transmission, this will most often be from a scratch. or a bite from a cat infected with Bartonella Hensley. And that's why this is called cat scratch disease, as cats serve as a natural reservoir for Bartonella Hensley, a scratch or a bite from an infected cat, as well as exposure to cat fleas infected with the species

can lead to transmission in humans. Most commonly see this in young individuals. More than 50% of cases in children younger than 18 years of age, so likely will be a child in the vignette. As far as clinical manifestations, a number of things can be seen, fever, malaise, even disseminated disease affecting the liver, spleen, bone, etc. What you need to know for the exam is lymphadenopathy.

Regional lymphadenopathy is the hallmark of this disease due to a granulomatose inflammatory response, and it's what you have to know. This will definitely be in the question. So enlarged lymph nodes that will appear proximal to the site of inoculation, so near the bite or scratch. There'll be tender erythema of the overlying skin, usually appearing around two weeks after the bite or scratch.

So remember, lymphadenopathy, that's the highest you'll thing to know for clinical medicine. manifestations. Nothing high yield for diagnosis, generally a clinical diagnosis that can be supported with serologic tests or biopsy. Treatment next, there's one man that you need to know, and that is is itramycin. So even though many patients will have resolution of symptoms without antibiotics, the whole point is to prevent serious complications, which as many as 14% of patients will have disseminated disease. So patients with mild to moderate disease with just lymphadenopathy are going to get a five-day course of azithromycin. There are alternatives, Cypro, et cetera, but focus on

Zythromycin as that's your first line. In patients with disseminated disease, you'll usually add refampin to azithromycin. Main takeaway for treatment, though, for your exam, I would just focus on azithromycin. Okay, so cat scratch disease, a few high-y-old things to know, how to remember all of those high-yield points. Well, this is cat-scratch disease. So when you think of cat-scratch disease, I want you to think of black cat-scratch disease. So think of a black cat, so B-L-A-C-K contains all of the high-yield things you need to know. Starting with B for Bartonella-Hensley, Cat Scratch Disease is an infectious disease caused by Bartonella Hensley. Next, L, which stands for lymphadenopathy.

This disease is usually characterized by self-limited regional lymphadenopathy. Got to remember that. Next, the A stands for xithromycin, which is your first line med for most patients. C, of course, stands for cats as they serve as the natural reservoir for Bartonella Hensley. And finally, K stands for kids, as this will most commonly be a disease of children and young adults. So again, cat scratch disease. Remember, black cat scratch disease, Bartnella Hensley, lymphadenopathy, azithromat. in cats and kids. Next, let's talk about botulism. What's botulism? Well, this is a rare,

but potentially life-threatening paralysis caused by a neurotoxin that's produced by Lostridium botulinum, a group of gram-positive, rod-shaped, spore-forming anaerobic bacteria. Let's hit the high-yield topics. So there's three common types of botulism. These are infant botulism, food-borne botulism, and wound botulism. And each of these are associated with high-old sources or little things that you need to know. So let's talk about the three common types in the source of infection in each. And because there's three sources that do have high-yield associations, I have a mnemonic for you to remember them. So what I want you to remember is Baby's Black Bottle. Baby's Black Bottle to help you remember the three high-yield

associations, which we're going to talk about now. Starting with baby, which helps you remember infant botulism, which happens when a baby swallows C. Botulinum spores because infants have poorly developed gut flora, these spores can actually settle, colonize, and release toxin right inside the GI tract. In the U.S., even though we have typically associated this with consumption of honey, most cases actually come from everyday environmental dust and soil that contain these spores that infants are susceptible to. So even though honey can contain spores, it's likely not the main source as even after years of warning parents to avoid honey, the rates of infant botulism haven't gone down, which tells us honey is likely only a minor source of this infection. And in just 2025,

there was an outbreak of infant botulism that was actually associated with a popular brand of powdered formula. So for babies, it's not so much a specific source as it is their susceptibility. Next is wound botulism, which I want you to remember the word black, as in baby's black bottle. So there's something known as wound botulism when C botulinum infects wounds, puncture wounds, etc. But the most important and the one that will likely be in your vignette, and the reason this one is labeled black is because wound botulism has often been associated with injection drug use, particularly with black tar heroin, which I had this exact question in school. So remember black tar heroin, it's very special.

specific, but it does come up. Last is foodborne botulism, which you'll remember as bottle because bottle helps remind you of canned or bottle foods, which often contain preformed botulinum toxin, an exam favorite. So foodborne botulism is often seen with home canned foods, vegetables, and fish. And the U.S. higher rates occur in Alaska native populations due to the consumption of aged or fermented fish. Well, in China, it's commonly linked to home fermented tofu and bean products. All right. So to tie everything together, remember Baby's Black bottle for the types of botulism in their sources, baby for infant botulism or spores colonized the gut, black for wound botulism with IV drug use, particularly with black tar heroin,

and bottle for foodborne botulism with impropered bottled or canned foods. Next clinical manifestations. So Clostridium botulinum can cause muscle weakness or flacid paralysis by blocking the release of acetylcholine at the neuromuscular junction. This happens because the toxin cuts something called a snare protein, which are what nerve cells need to release a acetylcholine into the synapse. So without that signal, the muscle can't contract. And we have the clinical presentation will go over next. So the classic presentation of botulism is acute onset of bilateral cranial neuropathies with symmetric descending weakness. So we can see things like double vision, slurred speech, and difficulty swallowing. If you want to focus on the five main clinical

manifestations, you'll most likely see on an exam question, remember the five Ds of botulism, which are dilated fixed pupils, diplopia, which is double vision, dysphasia, which is difficult swallowing, dysarthria, which is difficulty speaking, and descending muscle weakness or paralysis. So that's your clinical manifestations. Remember the key here is the muscle weakness and cranial nerve dysfunction, focus on the 5Ds. Diagnosis, this is usually going to be made on clinical findings alone. This can later be confirmed by botulinum toxin detected in serum, stool, or wound specimens. Confirmatory testing can take a while to come back, though, and generally you do not want to wait for these test results before moving on to treatment, which will be with botulinum.

antitoxin, which is the main therapeutic option for botulism. Of course, be aware of supportive treatment like nasogastric feedings to minimize aspiration risk, intubation for patients with respiratory failure, but botulinum antitoxin is the main focus here. Okay, recap for botulism, remember baby's black bottle for the types of botulism and their sources, baby for infant botulism or spores colonize the gut, black for wound botulism with ib drug use, particularly black tar heroin, and bottle for foodborne botulism with improperly bottled or canned foods. remember your 5Ds for clinical manifestations, dilated fixed pupils, diplopia, dysphasia, dysarthria, and descending muscle weakness.

Diagnosis can be made clinically and confirmed with toxin detection later. Treat with antitoxin. That's botulism. Moving on to campelobacter J.J.J.J. Which is a gram-negative, curved or comma-shaped bacteria. Campilobacter J.J.J. Or C.J. as we'll call him, is a common foodborne pathogen that can cause diarrhea in all age groups.

Let's start with transmission. So CJ can be found in a variety of domestic and wild animals. An infection may be acquired through consuming these animals, usually raw or undercooked meat. So poultry is a common one. Know this one for sure. Contamination of beef, pork, or lamb is less common, so really focus on poultry. Milk is another big one, specifically consumption of unpasteurized milk is a common source and definitely an exam favorite.

And contaminated water, nearly any natural water source can be infected. There's other routes person to person. transmission via fecal oral route, vertical transmission from mom to baby. Even domestic pets like puppies can be a source, but poultry, unpasteurized milk, that's what you got to know for the exam. All right. So clinical manifestations, as you'd expect, abdominal pain, cramping fever, diarrhea, which can be watery or bloody. So bloody diarrhea can be seen in around 15% of adults. In children, it's much more common, closer to 50%. And this is an important differentiating factor, remember, because things like cholera was typically watery, but not bloody. And that's because,

CJ invades the intestinal mucosa, causing inflammation, damaging capillaries, and allowing blood to leak into the stool. Another important thing to know is that CJ can closely mimic other conditions, most notably acute appendicitis, because sometimes abdominal pain may occur before the onset of diarrhea, which can delay recognition of an infectious cause. So someone that comes in with abdominal pain that radiates to the right iliac phassa, tenderness on exam, very similar to appendicitis, which is why this is called pseudo appendicitis, And you can, of course, use ultrasound or CT to help differentiate the two.

But remember this as it's sometimes tested on. It definitely was for me. And of course, good to know when you're out there practicing as well. As far as diagnosis, so I suspect CJ in a patient with abdominal pain and diarrhea in the context of risk factors for transmission, somebody who is drinking milk straight from the udder, for instance. And then diagnosis can be established with stool testing, usually with stool culture. Finally, treatment, it's pretty straightforward.

For most patients, this is going to be supportive care. And in patients with severe disease, antibiotics can be used, typically as if the romycin is recommended. Fluoroquinolones are an alternative. One last thing I want you to know for CJ is that CJ can cause some pretty high-yield complications that are often tested on. And the main one to know is going to be Guillain-Burray syndrome. CJ is actually the most common precipitant of Guillain-Burray syndrome. So you need to know this. Reactive arthritis, post-infectious irritable bowel syndrome are other late-onset complications of CJ.

But please focus on Guillain-Buray syndrome, as this will very likely be. tested on. All right, so there's a few high-ealed things to know for CJ. Here's a quick way to remember the important details. When you think of Camp Lobacter, Camp Elobacter, think of a camp, a summer camp, named Camp Elobacter, with a camp counselor named, you guess it's CJ. Now, CJ, our trusty camp counselor at Camp Eilobacter, is grilling up some food for the campers, and on the grill, we see a big old raw chicken. And since it's hot at Camp Eilobacter, he's drinking a cold glass of milk to cool him down. The raw chicken and milk help us to remember the undercooked meat, most commonly poultry, and unpasteurized milk, which are common methods of transmission for this pathogen.

Now, a few other things you'll notice about CJ. He's wearing a beret, which helps you remember Guillain-Barray syndrome. In his front pocket, there is a big oversized fake pen, like something from a gag store, which helps us remember the pseudo-apendicitis, commonly associated with this condition. And finally, poor CJ is wearing a diaper, which helps us remember the diarrhea, sometimes bloody seen with CJ infections. So quick recap, the raw chicken and glass of milk points to the common transmission sources. The beret C.J. is wearing helps you to remember Gian Barre syndrome.

The oversized fake pen in his pocket represents pseudo-apendicitis, and the diaper helps remind you of the diarrhea, often bloody, associated with campelobacter J. Juni. That's CJ. Next, let's talk about diphtheria. So diphtheria is an infectious disease caused by the gram-positive bacillus, Griny Bacterium Diphtheriae or C-diptheriae, and for the sake of this lecture, it will now be called C-dip-theory gray. Instead of C-dip-T theory A, remember it as C-dip- Theory gray. Gray, gray, gray, gray, remember that word.

Also, for the sake of the mnemonic, gray is spelled with three A's. So dip theory gray, G-R-A-A-A-A-Y. Remember that, it will help you get the exam question right, and I'll explain why in a minute. So C-Dip-Dy-Dy-Rae infection can lead to respiratory or cutaneous disease, Some patients may also be asymptomatic carriers. We don't see this as often since the availability of vaccination, but C-diptheri-Gray gray is reappearing in some regions. So what do you need to know?

Let's keep it simple, starting with the clinical manifestations. So with respiratory diphthery gray, you can have sore throat, malaise, cervical lymph anopathy. These patients can actually have some pretty severe swelling of the neck. They can develop what's called a bullneck where you have this massive swelling of the tonsils, uvula, cervical lymph nodes. And finally, the most important finding, and the one, one that you will not forget, and the reason you'll always call the seed with theory gray is because the hallmark finding is going to be gray pseudomebranes.

So at least a third of patients infected with this organism will have these adherent gray, what they call pseudomebranes covering the pharynx soft palate nasal membrane. These will often bleed if scraped. And the reason people with diphtheri gray develop these is because these organisms attached to the pharynx or surrounding areas. And it can release a toxin, a dT toxin, which causes, inflammation and ultimately necrosis of the tissue. This resulting necrotic epithelium mixed with inflammatory cells and cellular debris lead to the appearance of this gray leathery adherent membrane.

The pseudomebrane can also dislodge and wind up in the bronchial tree leading to respiratory compromise. There are systemic manifestations which can involve the heart, nervous system, kidneys, but the main takeaway, you do not want to forget your hallmark gray pseudal membrane. That's why you will always call this C. Diphtheri Gray. All right, less important, but no, there is cutaneous disease, which patients may develop these on healing sores or shallow gray ulcers, but again, focus on gray pseudomebranes and respiratory C. Diphtheri gray. All right, so for diagnosis, and a patient you suspect may have diphthery gray. You'll order culture and PCR testing. Diagnosis is a little bit involved. You first start with a swab of the throat,

nairs, or any cutaneous lesion that demonstrates signs of infection. Then you send them out for culture. The culture will identify the Karine bacterium species. Then we have to determine if the species identified is, dun-d-done-doxogenic. And the PCR testing helps with that. It will help detect the presence of the toxin gene, which is a good start. But it won't tell us if there's active toxin production. So we need additional testing, like with an ELIX test, to help establish active toxin production. So why do we need to do all of this? Why can't we just stop at identifying Cid theory gray on culture? Isn't that enough? Why do we need to know if it's a toxic strain? Well, determining toxicinicity is important, one, because toxicogenic strains generally cause the

more severe systemic disease we worry about. And two, it helps direct appropriate treatment and isolation protocols as some patients may only be asymptomatic carriers. The main takeaway here is toxicogenic strains are the issue. And for the exam, I would focus on just remembering your culture and PCR testing for diagnosis. Next, let's talk about treatment. Treatment involves the three A's, which is why you remembered gray, spelled with three A's. The three A's of diphtheri treatment are airway antitoxin and antibiotics. Although cultures and toxin testing should be obtained for diagnosis. You do not want to wait for confirmation before initiating treatment. Therapy is started immediately based on clinical suspicion. If toxicogenic diphtheri gray treatment is later

rolled out, certain treatments can be discontinued, but early intervention is critical to prevent complications. So starting with the first A, which stands for airway. So aggressive airway management and patients with respiratory diphthery gray is very important as respiratory failure due to airway compromises a major complication and a cause of mortality. So intubation may be needed. Also keep in mind, these patients will usually be placed on isolation precautions. Next A stands for antitoxin. Specifically, diphtheria antitoxin or DAT is used, which is interesting as the diphtheria antitoxin is an equine-derived antibody that's obtained from the plasma of horses immunized against diphtheria toxin. So this antitoxin binds to and it activates the toxin. Finally, the last A stands for

antibiotics. Per up to date, Zithromycin is now the preferred agent. Luckily, another A. Penicillin and erythromycin used to be preferred and are of course still used, but azithromycin is preferred for diphthery gray due to increased penicillin resistance and preferred over erythromycin due to a better side effect profile. Just a few other side notes, you want to also identify and test close contacts and potentially administer prophylactic antibiotics if needed. And remember, the ultimate goal with diphtheri gray is prevention with immunization. All right. So diphthery gray, infectious disease caused by the grand positive bacillus carini bacterium diphthery gray. Remember, sore throat, lymphatinopathy, that big old bullneck, and of course the star of the show gray pseudomebranes

that can bleed if scraped. Diphtheri-gray, diagnosed with culture and PCR, treat with your three A's, that's why gray is spelled with three A's, airway, antitoxin and antibiotics, especially azithro. That's diphthery gray, moving on to acute rheumatic fever or ARF, AARF, which is a delayed immune mediated complication that occurs two to four weeks after exposure to a specific organism. It's highly tested on, you got to know it. So the organism in question is group A streptococcus. or gas. So ARF is a systemic immune-mediated inflammatory condition that occurs two to four weeks after group a strep or gas infection. There's this broad immune response to the infectious organism that can lead to multiple organ systems being damaged, including the joints, skin, and heart,

which bring us to the highest ill part of this disease, the clinical manifestations, which also form the framework for diagnosis. So ARF is diagnosed using the Jones criteria, which are divided into major and minor criteria. These criteria are named after Dr. T. Duckett Jones, who first described the diagnostic rules for acute rheumatic fever in the 1940s. The five major Jones criteria, which typically present one to five weeks after a gas infection, include arthritis, which is usually the earliest manifestation of ARF. This is sometimes described as migratory, as it will start in one joint, then quickly jump to another. So the knee for a few days, then a few days later, the elbow, wrist, ankle, etc. Carditis, so we can see pericarditis, myocarditis,

most commonly will see involvement of the mitral and aortic valves, with mitral regurgitation being the most common volvular lesion. Next, Sitaam Korea, which is a neurologic disorder consisting of erratic, abrupt, involuntary movements, muscle weakness, etc. Erythema marginatum, this is a pink or faintly red non-proeretic rash that involves the trunk and sometimes the limbs, usually sparing the face, often evanescent where it'll pop up and then disappear in a matter of hours. The lesion usually has a sharply demarcated outer border and diffuse inner.

margin forming a continuous ring. And finally, obcutaneous nodules, which are these firm painless lesions ranging from a few millimeters to two centimeters in size, often located over bony surfaces. So that's your Jones major criteria for ARF. You've got to know those. The demonic for Jones major criteria is luckily Jones, J-O-N-E-S. This is an old demonic that I learned in school, but I modified it a little bit to make it a little easier to remember. Starting with J, that stands for joint, which will help you remember your migratory polyarthritis. O stands for oh my heart, which will help you remember carditis,

much of regurgitation being a common manifestation. N stands for nodules, your subcutaneous nodules, the firm, painless lesions usually located over a bony surface. E stands for erythema marginatum, the pink non-pruritic rash, most often on the trunk and sometimes the limbs. And then finally, the S, which the original mnemonic stood for Scytham-Korea, but I knew damn well on an exam. I would not remember what the heck that stood for.

So instead I just remembered that as shaky, because even if you remember Siddham Korea on an exam, they're not going to say the patient presents with Sineham Korea. They're going to say the patient presents with uncoordinated jerking movements. So just remember the SS shaky, just to make it easier. So remember the five manifestations of ARF, remember Jones, J.O.N.S. J for joint for the polyarthritis. O for O my heart for carditis, N for nodules, E for erythema marginatum, and S for shaky,

aka Sinaham, Korea. And then we have the minor manifestations, which are going to be fever, arthralgia, which is joint pain, usually involving several joints, elevated, accused phase reactants, so most patients with ARF will have elevated inflammatory markers, so increased levels of ESR and CRP. And finally, abnormalities on ECG, specifically a prolonged PR interval. So again, fever, arthritis, elevated acute phase reactants, prolonged PR, which I used to remember as fat, as an F-A-A-T, so F for fever, A for arthritis, the second A for acute phase reactants, which are elevated, and then T for too long PR for your prolonged PR interval. So

minor criteria, again, is fat FAA-T, fever, orthrologia, acute phase reactants, too long PR. So how do we diagnose ARF? Well, the diagnosis is made by combining the clinical findings we just reviewed with evidence of a preceding group A strep infection. There are stipulations depending on whether this is a first episode or recurrent episode. Some criteria cannot be counted twice, like orthology and the minor criteria can't be used alongside arthritis in the major criteria. But for exam purposes, let's keep the simple unfocus on the basics. So diagnosis is made with evidence of a preceding gas infection. So this can be a positive rapid stress test, a positive throat culture, elevated or rising antistreptychoccal antibody tighter, plus two major

manifestations or one major plus two minor. So again, remember for diagnosis, two major plus two minor are sufficient for diagnosis of an initial episode of ARF in a patient with evidence of preceding gas infection. What about treatment? It's actually pretty simple, luckily because there's a whole bunch of other crap you had to remember this. The most important thing to know is going to be penicillin G treatment of ARF consists of eradication of the gas infection group A strep you do that with antibiotics and the preferred antibiotic is penicillin G benzateen which is a long acting intramuscular injection of course if pen G isn't available or they have penicillin allergies there are alternatives but definitely you should know penicillin for the exam now there are other treatments depending

on what other manifestations are present arf associated arthritis for instance nseds will be your first line to proxin ibuprofen so for treatment remember pen G and inseds to keep it nice and simple pen G being the highest yield component. All right, ARF acute rheumatic fever. It's tested on a lot. There's a decent amount of information to know. But to remember the high yield stuff, it's actually pretty easy. Instead of ARF, acute rheumatic fever, you're going to add a B and remember it as barf.

Arf becomes barf, and you're going to remember this sentence. Barf Jones, the fat penguin has gas. Barf Jones, the fat penguin has gas. That one sentence contains most of the high-yield information you need to know for acute rheumatic fever. So picture of this, you're at the zoo. standing at the penguin exhibit, and this fat penguin names Jones right in front of you just keeps farting nonstop. So the point where it's making you want to barf.

So when you see arf, add the B, remember barf, and lock in this visual, barf, Jones, the fat penguin has gas. Joan helps you remember the major criteria, joints, oh my heart, nodules, eryema, marginatum, and shaky, fat for the minor criteria, fever, arthrologia, acute phase reactants, too long PR. Penguin, I'll give you a second and think about it. The first four letters are PENG, as in PENG or Penicillin G, your, you're first-line medication. And then finally, gas, which helps remember the infectious organism that caused this whole mess in the first place, group A strep. So remember, ARF becomes barf, as in Barf,

Jones, the Fat Penguin has gas. That's a acute rheumatic fever. Let's talk about Rocky Mountain Spotted Fever next. So Rocky Mountain Spotted Fever is a tick-borne disease that can be fatal, if not treated. In fact, prior to the introduction of antibiotics, the fatality rate was as high as 80% in some regions. More recently, with widespread antibiotic availability and improved disease recognition, mortality rate has dropped to approximately 0.1 to 0.6%. So who is responsible for this terrible disease? Well, that's an organism by the name of Rickettsia rickettsia, which is a gram-negative obligate intracellular bacterium named after the pathologist Howard Ricketts.

And as difficult as the name may be to say, it's super easy to remember that Rocky Mountain Spotted Fever is caused by Rickettsia-Rickettsia. And that's because you're going to remember Rocky Mountain Spotted Fever instead as Ricky Mountain Spotted Fever. swap Rocky for Ricky. Ricky Mountain Spotted Fever helps you remember this disease is caused by Rick, aka Rickettsia Rickettsia. This is the only Rickettsial infection that has the name Rick twice. So remember Rick for Ricky Mountain Spotted Fever. All right, that brings us to our next important tidbit, the vector. So in 1906 Howard Ricketts demonstrated that Ricky Mountain Spotted Fever was an infectious disease transmitted by ticks, which prior to that, people actually thought you got this from drinking the melted snow water. So Ricky Mountain Spotted Fever is usually transmitted via tick bite. And it's a infectious disease transmitted by ticks bite. And it's a infectious disease transmitted by ticks bite. And it's, is most commonly seen in the spring and early summer when outdoor activity is the highest. Transmission occurs after a tick has been attached for several hours,

during which time rickettsia organisms are released from the tick's salivary glands into the human host. The type of tick that carries this varies by location. Eastern and South Central U.S. is the Dermacenter Verabalus tick. Dermacenter and Dersone is the primary vector in the mountain states west of the Mississippi River. Probably wouldn't go too hard here with memorization. Just remember the vector is a tick. Clinical manifestations next. So early symptoms of Ricky Mountain Spotted Fever are non-specific, fever, headache, as well as malaise, myologous, abdominal pain, confusion.

But the main clinical manifestation I want you to remember, which is the hallmark of this disease and is always tested on, is the rash. So Ricky is going to cause a rash in approximately 88 to 90 percent of patients. It is uncommon at the initial clinical presentation, but it usually pops up by the third to fifth day of illness. The hallmark is a blanching erythematous rash with macules, so small flat spots that become particular over time. so more red or purple pinpoint spots. So that's great to know, but here's the high-yield part you'll be tested on. The appearance of the rash usually begins on the ankles and wrists and spreads to the trunk. So remember when we're talking about a Ricky rash, the rash begins on the wrists and ankles

and spreads what they call centripetally to the trunk, which just means towards the center. There are also complications secondary to Ricky-like seizures, other neurologic abnormalities, non-cardiogenic pulmonary edema, but focused primarily on the rash with centripetal distribution for the exam. Okay, diagnosis, not super high yield, but a presumptive clinical diagnosis of Ricky is made based upon clinical signs and symptoms in a patient who are from an endemic area or visited one recently. So fever rash, tick bite in the right location, treat it. Don't wait for serologic testing to come back. Why don't you want to wait for serologic testing to come back before you give them antibiotics? Well, first, because early serologies obtained in the first few days are

often falsely negative. And second, in fulminate cases of Ricky, death can occur in as early as five days. So treat based on clinical suspicion and confirm retrospectively through serologic testing, which will be obtained through indirect immunoflorescent testing or in some cases PCR testing, which can be used to make a definitive diagnosis. And then finally, there are some lab findings that can be obtained to help support the diagnosis. Things like thrombocytopinia, hyponatremia, and elevation and serum immunotransferase levels can all be seen with a ricky infection. Finally, we have treatment, which is very easy. You really just need to know one med, and that's going to be doxycycline. Doxy is your treatment of choice in both adults and children, even in pregnant women.

The only alternative, which is chloramphenicol, has been associated with a higher risk of death, so it's really doxy all the way. Nothing more to know here except for the fact that you treat ASAP. Do not wait for serologic testing as we talked about before. Okay, so you will never forget that Rocky Mountain spotted fever is caused from the organism, Rickettsia rickettsia. Because again, you'll remember it as Ricky Mountain Spotted Fever. Super easy.

But there's other high-yield stuff to know. And for that, I have to tell you a little rhyme about Ricky or Rick. So here's the rhyme that contains all of the juicy details for the exam. Rick got bit by a tick because he stood on the docks and forgot to wear gloves and socks. Rick got bit by a tick because he stood on the docks and forgot to wear gloves and socks. So Rick, that's your cue for Rickettsia Rickettsia. Got bit by a tick, which we know is the vector for this disease. Stood on the docks, which helps you remember doxycycline is the first line med,

and forgot to wear gloves and socks. Gloves and socks help you remember where the rash originates. Super important. The ankles and wrist then spread centripetally. So Rick got bit by a tick because he stood on the docks and forgot to wear gloves and socks. It's got your infectious organism, vector, first line med, and most tests that on clinical manifestation. If you can remember that little rhyme, you'll likely get the exam question right. All right, so that's Rocky, aka Ricky Mountain Spotted Fever.

We're almost there. Last one is going to be tetanus. So tetanus, which is derived from the Greek word tetanos, which literally means tension, tight, or to stretch, which makes sense when you're familiar with the manifestations of the disease, which will go over shortly. So detainous is caused by the toxin-producing bacteria, clostridium, tetanai, which is an anaerobic, gram-positive spore-forming bacilli, which typically live in soil and surprisingly even present in the gut of mammals. So these guys don't like oxygen, they're anaerobes.

So when they get exposed to beautiful, fresh oxygen or an unfavorable environment, they get stressed and shed these little spores, almost like safe little transport vehicles for them to hang out in until a new anaerobic environment presents itself for them to sprout back into Clostridia. So let's go over the predisposing factors. So the first is going to be lack of immune. which of course we know that we do have tetanus vaccines available to prevent this disease. And most patients who develop tetanus are either incompletely immunized and or receive inadequate prophylaxis following a wound.

Next is going to be inoculation of spores. So those little spores we talked about before, they got to get into the body somehow. And this typically happens through some sort of penetrating trauma, splinters, gunshots, lacerations, burns, compound fractures. There needs to be an entry point for those spores. There are even some cases of neonatal tetanus, which result from home to live. with unsanitary cutting of the umbilical cord. Okay.

And then we have the final key predisposing factor, and that's devitalized tissue. So ischemic or necrotic tissue, as we see in many infections, is an important predisposing factor for developing tetanus. And why is that? Why can't tetanai grow in healthy tissue? Well, it's what we talked about before. Tetanai is an anaerobic bacteria. It thrives in the absence of oxygen.

So when it enters the body through those dormant spores, what key element can wake them up and allow them to sprout, an environment void, of oxygen. Where can we find that in the body, a necrotic or ischemic tissue, which has little to no blood flow. So this low oxygen environment allows tetanine to thrive and germinate and do the terrible things we'll talk about next. So you need a combination of these three factors, lack of immunity, a tetanus prone injury like a puncture wound, and then ischemic or necrotic tissue. All right, clinical manifestations next. So there are different types of tetanus, localized tetanus, which is only localized to a specific part of the body. Cephalic tetanus is a form

of a localized tetanus that involves only the cranial nerves, neonatal tetanist, and then generalized tetanus, which is the most common, and that's what we'll focus on. So with generalized tetanus, you'll have spastic muscle contractions. Now, really quickly, I wanted to talk about why this disease causes these severe muscle contractions. So Clostridium tetanic can produce a horrible toxin called tetanospasmin. This toxin blocks inhibitory neurotransmitters like gabin glycine, which normally tell muscles to relax. And without the inhibition, alpha motor neurons fire continuously, causing severe, rigid, sustained muscle contractions. So we'll see things like Trismus, which is present in more than 80% of cases involving

the strong, painful spasms of the macedar muscles and an inability to open the mouth. That's why it sometimes referred to as lockjaw. Opistothotonous, which is the spasm of the spinal extensors, leading to the severe arching of the back. Reesis Sardinicus, which is also known as a sardonic smile, which is caused by persistent facial muscle spasms, causing this exaggerated or abnormal grin. We can also see autonomic overactivity, so these patients can present with excessive sweating, fever, tachycardia, cardiac arrhythmias. For the exam, certainly focus on the intense spastic muscle contractions.

Okay, so for diagnosis, tetanus is going to be diagnosed clinically. Antibody tests for tetanists exist, but they're not reliable at low titers and in patients who received antitoxin. So again, this is a clinical diagnosis, and you should suspect this in a patient with intense muscle spasms, especially after a tetanus prone injury, someone who has been inadequately immunized. So a treatment is multifacetely. including airway management, wound debremen. Adequate wound debreedment is actually really important because tetanite can persist in wounds even after these patients are started on antibiotic therapy. Antibiotics, which in most cases will be metronidazol. Penicillin is an alternative.

And then tetanus immune globulin, which is an antitoxin that binds to and can neutralize any remaining circulating unbound tetanospasmin, that horrible toxin we talked about before. And benzodiazepines like diazepam, which are usually the first line manual used to help control the muscle spasms. And ultimately, the goal is prevention with immunization with your tetanus vaccine. Once a patient is stabilized, they should receive active immunization with a full series of tetanus and diphtheria toxoid-containing vaccines, as having tetanus, unfortunately, does not provide immunity. All right, we did it. That was your bacterial disease review. Let's do five quick questions to see what you've retained. Starting with question one. A 28-year-old unvaccinated

male presents to the emergency department with a three-day history of sore throat, low-grade fever, 38 degrees Celsius 100.4 degrees Fahrenheit and difficulty swallowing. On examination, you note a gray adherent membrane covering both tonsils and the posterior pharynx. When you attempt to remove a small portion for culture, it bleeds. The patient has prominent cervical lymphadenopathy with visible neck swelling. What is the most appropriate immediate management for the suspected diagnosis? A, administer diphtheria antitoxin intravenous antibiotic and provide airway management. B, obtained throat culture, then start antibiotics while awaiting results. C, reassure and provide symptomatic treatment only.

D, initiate supportive care and observe for 24 to 48 hours before starting antimicrobial therapy. Or E, arrange for tonsillectomy to remove the pseudomebrate. So that is going to be A, administer diphtheria antitoxin, intravetis antibiotic, and airway management. So even if you have no idea what disease is being referenced in the vignette, you may recognize the gray adherent membrane being mentioned, which would trigger you to remember diphthery gray, spelled with three A's.

And diphthery gray should certainly be suspected in this patient with the presence of a gray pseudomebrane that bleeds with scraping, unvaccinated, low-grade fever, prominent cervical and fatanopathy, and what empiric treatment should be started in patients with suspected respiratory diphthery gray? Well, the three A's, which is why gray is spelled with three A's to help you remember, antitoxin, antibiotic airway management. So for respiratory diphthery gray, urgent empiric treatment with diphtheria, antitoxin, and antibiotic should be administered right away, even before confirmatory diagnostic tests come back. And of course, aggressive airway management is important due to the risk of obstruction.

So answer A, administer diphtheria antitoxin, intravenous antibiotic, and airway management is the correct answer for this patient. Question two. A 32-year-old woman presents the emergency department with profuse watery diarrhea and abdominal cramping for the past 48 hours. She reports passing copious amounts of pale watery diarrhea that is non-bloody and has a milky, cloudy appearance with small white flex. She imports severe thirst, lightheadedness when standing, and is not urinated in over 12 hours. She returned yesterday from a medical mission trip to a remote

region of South America, where she had limited access to clean drinking water and ate raw oysters at a local market. She has no significant past medical history, vital signs reveal tachycardia and hypotension. The patient is afebrile. On examination, she appears ill and lethargic with sunken eyes, markedly dry mucus membranes, and skin tenting that persists for over two seconds. Her average diminis soft with mild diffused tenderness and hyperactive bowel sounds, what is the most appropriate initial treatment for this patient? A, oral rehydration solution with glucose and electrolytes, B, intravenous isotonic fluids, C, intravenous broad spectrum antibiotics only, or D, bowel rest and observation. So that is going to be answer B, intravenous isotonic fluids.

All right, due to the combination of profuse, non-bloody rice water stools, absence of fever, rapid severe dehydration, consumption of likely contaminated water and raw shellfish. Even though we can't definitively say this, cholera should be high on your list of differentials. And with cholera, we know to put a tube between the H and the O to make H2O, because the high-yield stuff involves H2O, including the treatment. We know the initial and most important form of treatment before antibiotics where anything else is fluids.

In mild cases, this can be with oral rehydration solution, but in moderate or severe cases, which is clearly evident in this patient, urgent administration of IV fluids is the cornerstone of treatment for reduction in more. mortality. Answer A, oral rehydration solution would only be recommended in mild cases, which this is not. C, antibiotics are appropriate as an adjunct, but rehydration is the absolute priority and must precede antibiotic administration, and D, bowel rest and observation would be dangerous and potentially fatal. This patient has severe dehydration requiring immediate aggressive fluid resuscitation with intravenous isotonic fluids, making answer be the correct answer.

Question three. A 19-year-old male presents the emergency department with a three-day history of fever, headache, myelogist, and malaise. Two days ago, he developed a rash on his wrists and ankles. He denies nausea vomiting or abdominal pain. One week ago, he spent four days deer hunting in the wooded areas of North Carolina. He reports checking himself for ticks each evening and recalls finding what he thought might be a small tick on his lower leg, although he was uncertain whether it was a tick or just debris.

He has no significant past medical history and takes no medications. On examination, he appears ill but not toxic. Vital signs, temperature 38.8.8 degrees Celsius, 101. point eight degrees Fahrenheit, heart rate 102 beats per minute, blood pressure 118 over 72. He is alert and oriented. A faint erythematous macular rash consisting of 2 to 4 millimeter blanching pink macules is present on both wrists and ankles bilaterally. The remainder of the skin is clear. Cardiovascular, pulmonary, and abdominal examinations are normal. Laboratory studies reveal platelets at 140,000, normal range being 150 to 400,000, and sodium 131, normal range being 135 to 145.

which of the following organisms is most likely the cause of this patient's presentation? A. Borrelia burgdoferi. B. Corrinebacterium diphtheria. C. Riketia rick. Or D. Campelobacter J. Juni. So the correct answer is C. Riketia. All right. So the question is asking for the most likely, most likely causative organism.

And our answer is C. Rick, Rick. But first let's start with why the other answer choices are incorrect. A. Borrelia burgdoferi, which we did not. go over today, but is an important differential as it is another tick-borne disease and the causative organism in Lyme disease. And while the early presentation can be quite similar with the fatigue, myalgia, fever, etc., the cutaneous findings are usually different. Lyme disease and around 80% of patients will present with what's known as erythema migrans. This expanding erythematous lesion that begins at the tick bite site lesion is usually a single erythematous, non-painful, round or oval patch that

expand slowly, and in some cases central clearing may occur, causing this bull's eye appearance. Unlike our patient who has multiple small blanching macules on distal extremities bilaterally, not an expanding lesion out of bite site. B. Corrini bacterium diphtheriae, or diphtheri gray, as we know, will likely have a gray pseudomembrain mentioned in the pharynx, sore throat, low-grade fever, cervical and fetonopathy with a bullneck appearance. Camplobacter J. Juni answered D. Remember C.J. at Camp Elobacter with the diarrhea, abdominal pain cramping, mention of consuming undercooked poultry, drinking, drinking,

raw milk, none of which are mentioned here. So in this patient with fever, headache, characteristic, macular, blanching rash beginning on their wrists and ankles following tick exposure in an endemic area, as well as the thrombocytopinia and hyponitremia on labs. We know in this case the most likely pathogen would be Rickettsia, Rickzii, or Rick Rick, which we know by remembering Rocky Mountain spotted fever instead as Ricky Mountain spotted fever. Question four, which of the following treatments should be started immediately in the patient mentioned above in the absence of contraindications?

A, trimethyprym-Mothozyzol, B, doxycycline, C, amoxicillin, D, azithromycin, or E, chloramphenicol. So that's going to be answer B, doxycycline. So you have to know this for Rocky Mountain Spotted Fever. For adults and children, doxy is going to be your first line med. The only alternative listed here would be chloramphenicol, although it's less effective and would really only be recommended if a patient has an history of a very severe adverse reaction to doxy. So remember the motic, Rick got bit by a tick because he stood. on the docks, aka doxycycline, and forgot to wear gloves and socks, and that'll help you remember your

answer here. Last question, question five. A 10-year-old girl presents the emergency department with a four-day history of fever, joint pain, and rash. She had a sore throat three weeks ago that resolved without treatment. Over the past four days, she's experienced pain that began in her left knee, then moved to her right ankle, and now affects both wrists. She also reports a non-itche rash on her trunk that appears and then disappears.

On examination, her temperature is 39.1 degrees Celsius, 102.4.5. Fahrenheit, heart rate 115 beats per minute, and blood pressure 100 over 60. Both wrists are swollen, warm, and tender to palpation. A faint pink rash with sharply demarcated outer borders is noted on the trunk and limbs, sparing the face. Cardiac examination reveals a grade two out of six high-pitched apical, holococytic murmur rating to the axilla. Laboratory studies show elevated inflammatory markers, ESR and CRP, and elevated antistreptolycin

O titers. Ecocardiography demonstrates mitral regurgitation. which are the following findings in this patient are classified as minor criteria under the 2015 revised Jones criteria, select all that apply. A, carditis, B, elevated acute phase reactants, C, erythema marginatum, D, fever, or E subcutaneous nodules. So that is going to be answer B, elevated acute phase reactants and D, D, fever. So this patient's presentation is most consistent with acute rheumatic fever or ARF, supported by recent untreated group A strep infection and the presence of multiple Jones criteria.

And the question is specifically asking which of the following findings in this patient are classified as minor criteria. And if you remember the mnemonic, answering this is easy. Remember Jones the fat penguin mnemonic, Jones being the major criteria and fat FAAAT, standing for minor criteria. FAAAT, we know stands for fever, arthrologes, acute phase reactants, and two long PR, which we can see answer B, elevated acute phase reactants, and D, fever fall under minor criteria with the remainder of the answer choices carditis erythema marginatum and subcutaneous nodules

being classified as major criteria under the jones demonic all right so that was your bacterial diseases i hope that was helpful thank you so much for watching and thank you so much for the support