S1E57 Bacterial Disease Review

<v Speaker 1>Okay, So I've been getting a lot of requests for
<v Speaker 1>some more infectious disease topics, So today we're going to
<v Speaker 1>go over bacterial diseases. Yo, there's lots of them, and
<v Speaker 1>to focused on the high steel topics that are frequently
<v Speaker 1>tested on bartonella, batchelism, chlamydia, cute roumatic fever, can pull
<v Speaker 1>bactor jay Juni, as well as many others. Got plenty
<v Speaker 1>of nomonics in here, maybe too many. So we'll get started.
<v Speaker 1>But as always, a quick thank you for all of
<v Speaker 1>the nice comments, the support everybody who's bought a T
<v Speaker 1>shirt donated to the channel. I really do appreciate it,
<v Speaker 1>so thank you so much. Let's go ahead and get started,
<v Speaker 1>starting first with cholera. So when you see cholera C
<v Speaker 1>H O L E R A on an exam question,
<v Speaker 1>the first thing I want you to do is put
<v Speaker 1>a two between the H and E O. You put
<v Speaker 1>a two between the H and E O. That makes
<v Speaker 1>H two O. Why Because every time you see cholera,
<v Speaker 1>I want you to be thinking of water as everything
<v Speaker 1>you need to know about this disease from the infectious organism.
<v Speaker 1>The mode of transmission, treatment clinical menifestations involves water. So
<v Speaker 1>if you can remember H two oh, you can likely
<v Speaker 1>get the question right on the exam. So. Cholera is
<v Speaker 1>a life threatening infection caused by toxin producing strains of
<v Speaker 1>an organism called vibrio cholera. Fibrio choler is a comma
<v Speaker 1>shaped gram negative rod and again everything ties back to water,
<v Speaker 1>just like we talked about before, and even with fibrio
<v Speaker 1>rio rio, if you speak Spanish you may already see it,
<v Speaker 1>but vibrio ends in real, which means river in Spanish.
<v Speaker 1>So when you see vibrio rio, think river, think water,
<v Speaker 1>think H two O. So where are people typically expose
<v Speaker 1>to this organism? This will most commonly be through the
<v Speaker 1>fecal to oral route through consumption of contaminated water. Ingestion
<v Speaker 1>of water contaminated with feces is often cited as one
<v Speaker 1>of the most common sources of transmission of cholera, and
<v Speaker 1>it's why this is more common in settings with poor
<v Speaker 1>sanitation and limited access to clean drinking water. Water water water.
<v Speaker 1>With that being said, contaminated food is another one, so
<v Speaker 1>consumption of specific contaminated foods can also spread the disease.
<v Speaker 1>And while there are a number of foods that can
<v Speaker 1>become contaminated. Contaminated shellfish is an exam favorite and I
<v Speaker 1>personally got a question on this in school. And luckily
<v Speaker 1>for you, me and my namonic shellfish live in you
<v Speaker 1>gott it water. So for transmission, remember contaminated water and shellfish. Next,
<v Speaker 1>let's talk about clinical manifestations. The main thing you need
<v Speaker 1>to know is this infection can cause profuse watery diarrhea.
<v Speaker 1>So the hallmark of this disease is profuse watery diarrhea.
<v Speaker 1>It will sometimes be described as rice water stool, which
<v Speaker 1>is this pale and cloudy looking with little flecks of mucus,
<v Speaker 1>basically looking like the water that's left over after you
<v Speaker 1>rinse or cook rice. So once Fibrio gets into the
<v Speaker 1>small bowel, it releases a toxin, which is the main
<v Speaker 1>issue as this toxin hijacks the cells lining the intestine,
<v Speaker 1>which can lead to massive amounts of water and electrolytes
<v Speaker 1>being dumped. This disease can be fatal if it's not treated,
<v Speaker 1>as it can lead to rapid dehydration and electrolyte loss
<v Speaker 1>from all of the fluid being dumped. There can be
<v Speaker 1>a symptomatic cases depending on the strain that's involved. There
<v Speaker 1>can be nause of vomiting and fever is actually uncommon
<v Speaker 1>and the presence should prompt the search for concombinant infection.
<v Speaker 1>But most importantly know your profuse watery diarrhea and or
<v Speaker 1>rice water stool water water water diagnosis. I won't go
<v Speaker 1>too deep into it as it's pretty Straightford often made
<v Speaker 1>clinically and confirmed via stool culture. But treatment is very important,
<v Speaker 1>and I'll give you a second to think about what
<v Speaker 1>the treatment might be. That's right, water and to be
<v Speaker 1>more specific, IV fluids or oral rehydration solutions. So fluid
<v Speaker 1>management is the cornerstone of cholera treatment, reducing mortality and
<v Speaker 1>severe cases from over ten percent to less than zero
<v Speaker 1>point five percent. The type and amount of fluid depends
<v Speaker 1>on the degree of dehydration. Mild dehydration can be treated
<v Speaker 1>with oral rehydration solutions composed of water and electrolytes. Moderate
<v Speaker 1>and severe cases require IV fluids, often using ringers lactape,
<v Speaker 1>which is water, electrolytes and sodium lactape. Antibiotics can also
<v Speaker 1>be used as adjunctive treatment in more severe cases as well.
<v Speaker 1>But remember the main state treatment for cholera is water
<v Speaker 1>aka your fluid replacement. That's what you need to know. Okay, cholera,
<v Speaker 1>Remember add a two between the H and the O.
<v Speaker 1>You get H two. Oh. Remember, transmission is often through
<v Speaker 1>contaminated water. Clinical manifestations are profuse watery diarrhea or rice
<v Speaker 1>water stool treat with water aka fluid replacement. And the
<v Speaker 1>organism here is Vibrio cholera rioaka river and that's cholera.
<v Speaker 1>Let's talk about lamydia next, specifically chlamydia trichomitis, which is
<v Speaker 1>a gram negative bacteria and is the most commonly reported
<v Speaker 1>STI in the United States. What do we need to know.
<v Speaker 1>Let's start with clinical manifestations. Surprisingly, a great majority of
<v Speaker 1>chlamydia infections are asymptomatic, but that's not what you'll be
<v Speaker 1>tested on, so let's focus on the symptomatic patient. So
<v Speaker 1>when symptoms do occur, they most commonly involve the eurogenital tract,
<v Speaker 1>leading to classic eurogenital syndromes such as eurethritis with mucoid
<v Speaker 1>or watery urethral discharge and dysyria, serviceitis with vaginal discharge
<v Speaker 1>or purulent endocervical discharge, and epididymitis with testicular pain and swelling.
<v Speaker 1>There are extragenital manifestations depending on the zero type involved,
<v Speaker 1>including conjunctivitis, pharyngitis, perihepatitis, among others. And while these are
<v Speaker 1>important to know, the next two complications are tested on
<v Speaker 1>far more often, so make sure you know them well.
<v Speaker 1>If Chlamydia trachomatis goes untreated in FEMA, it can lead
<v Speaker 1>to pelvic inflammatory disease presenting with lower abdominal or pelvic
<v Speaker 1>pain and cervical motion tenderness, and ultimately can lead to
<v Speaker 1>infertility and chronic pain. Another high Yueld association is reactive arthritis.
<v Speaker 1>Chlamydia is actually the most common sexually transmitted pathogen linked
<v Speaker 1>to reactive arthritis, so this connection is absolutely worth knowing.
<v Speaker 1>Moving onto diagnosis nexts, which will be made with nucleic
<v Speaker 1>acid amplification testing or naat net, a test which detects
<v Speaker 1>the genetic material DNA or RNA of viruses or bacteria
<v Speaker 1>by amplifying it to detectable levels through sample obtained. For chlamydia,
<v Speaker 1>samples are typically obtained via a vaginal swab and female patients,
<v Speaker 1>or a urine sample in male patients. One other important
<v Speaker 1>thing to consider when conducting diagnostic testing is that Niceria
<v Speaker 1>gannorea coinfection is common, so all patients with chlamydia trichomitis
<v Speaker 1>infection should also be tested for Nicia ganorea as they
<v Speaker 1>have similar clinical manifestations and coinfection is common. Finally, let's
<v Speaker 1>talk about treatment. One med to commit to memory here
<v Speaker 1>is going to be doxy cycling. Doxy is your treatment
<v Speaker 1>of choice in non pregnant individuals. As compared with a zythromycin,
<v Speaker 1>which is an alternative, doxy has better microbial cure rates.
<v Speaker 1>So really you just need to remember doxy. And it's
<v Speaker 1>actually easy to remember why because when you hear clamydia clamydia,
<v Speaker 1>what word sticks out? Clam right? And where do you
<v Speaker 1>find clams in a dock by the sea? Doc C cycling,
<v Speaker 1>So anytime you hear clamydia, think about finding those clams
<v Speaker 1>in a dock by the sea, and you'll remember your
<v Speaker 1>first line med doc C cycling. And if you want
<v Speaker 1>to get really fancy, remember those clams have been sitting
<v Speaker 1>out in the sun for a little too long, getting
<v Speaker 1>all nasty and they're getting swarmed with gnats. And then
<v Speaker 1>I'll help you remember your first line test Nucleic acid
<v Speaker 1>amplification or GNAT testing So for clamydia, remember your clams
<v Speaker 1>on a dock by the sea being swarmed by gnats,
<v Speaker 1>and you remember your first line med and diagnostic test,
<v Speaker 1>and that's chlamydia. Let's talk about ganoia next, So gunnoia
<v Speaker 1>infection with gram negative bacterium niceria gonorrhea, which you will
<v Speaker 1>forever remember instead as ni Siria gadoreea, set of Nicicyria gounoriea.
<v Speaker 1>Remember it as knie Syria gunoreea, as in the joint
<v Speaker 1>the knee knee Syria gonoreea. More about that in a minute.
<v Speaker 1>So in the US knee Syria gunnoreea. It's the second
<v Speaker 1>most commonly reported commuticable disease. There's not a whole lot
<v Speaker 1>to know here, and there is definitely some overlap with chlamydia.
<v Speaker 1>Let's first start with clinical manifestations. So while there are
<v Speaker 1>areas outside of the genitalia that can be infected, genital
<v Speaker 1>infections are the most common associated with this organism, and
<v Speaker 1>just like in chlamydia, a large number of patients may
<v Speaker 1>be asymptomatic, so keep that in mind. But let's talk
<v Speaker 1>about your symptomatic patients as that's likely what will be
<v Speaker 1>tested on. So in females will see service citis. This
<v Speaker 1>can manifest as vaginal paritis and or mucopurulent discharge, and
<v Speaker 1>just like in chlamydia, this can spread and develop into
<v Speaker 1>pelvic inflammatory disease, which occurs in approximately ten to twenty
<v Speaker 1>percent of females. With cervical GANNERRIEA, both males and females
<v Speaker 1>will see eurethritis, so dysyria, urinary urgency, or frequency purulent discharge,
<v Speaker 1>which is more common in males. This organism can also
<v Speaker 1>affect areas outside of the genitalia ghanacoc conjunctivitis, which mainly
<v Speaker 1>affects infants born to untreated mothers. Perihepatitis known as fits
<v Speaker 1>you Curtis syndrome and disseminated infection can occur, and this
<v Speaker 1>is the highest heeled thing to know about GONNERRIEA as
<v Speaker 1>it's always tested on so Ganococcal infection can spread from
<v Speaker 1>the initial site and up to three percent of patients.
<v Speaker 1>Disseminated infection often leads to one of two clinical syndromes,
<v Speaker 1>which is a triad of tenosinovitis, dermatitis, polyalthralgis or and
<v Speaker 1>this is the one to know, purulent authritis, which can
<v Speaker 1>involve the wrist or ankles, but most commonly the need
<v Speaker 1>This vignette always seems to pop up on exams time
<v Speaker 1>and time again. It'll be a young patient complaining of
<v Speaker 1>dysyria and knee pain, recently engaging in unprotected sexual intercourse,
<v Speaker 1>et cetera. I've seen this question so many times, so
<v Speaker 1>it's in your best interest just remember this, and that's
<v Speaker 1>why instead of niceria gonorehea again, remember it as knee
<v Speaker 1>syria gonoreea, just to help you remember the purulent authritis
<v Speaker 1>most commonly involving the knee. Don't forget it all right. Diagnosis,
<v Speaker 1>just as in chlamydia, you're going to use GNAT again,
<v Speaker 1>nucleic acid amplification testing. This will be your test of
<v Speaker 1>choice for initial diagnosis. Treatment one med to know and
<v Speaker 1>that's going to be sef triaxone. As of the time
<v Speaker 1>of this recording, sef triaxone is the standard of care
<v Speaker 1>for treatment of gonerrhea and has the lowest rate of
<v Speaker 1>ganococcal drug resistance. This may change in the future, but
<v Speaker 1>as of now, no sef triaxon, which is usually administered
<v Speaker 1>as a single intramuscular dose. With that being said, if
<v Speaker 1>you're treating gonnerrhea, what other presumptive treatment should likely be considered.
<v Speaker 1>That's right, Like we talked about before, chlamydia, chlamydia and
<v Speaker 1>gonerrihea are unfortunate friends and often come together, So doxycycling
<v Speaker 1>likely will be added to this regiment unless it's been
<v Speaker 1>excluded through testing. So that's gonoriea serviceitis eurethritis possible to
<v Speaker 1>progress to PID. Most importantly, know of the potential for
<v Speaker 1>purilent arthritis, most commonly in the knee. Remember knee siri
<v Speaker 1>gonerhea diagnose with NAT, treat with sef triaxone, and as
<v Speaker 1>coinfection with chlamydia as common, doxy will likely be added
<v Speaker 1>to your regimen. Next, let's talk about Bartonella. And while
<v Speaker 1>there are a number of Bartnella species that can infect humans,
<v Speaker 1>when we're talking about the exam, the species you need
<v Speaker 1>to know is Bartonella hens lay which is the causative
<v Speaker 1>organism for cat scratch disease. So Bartnella hens layan is
<v Speaker 1>the most common form of Bartonellosis in the United States
<v Speaker 1>and the one you'll be tested on. So Bartnella henslay
<v Speaker 1>is a gram negative bacteria that can spread between animals
<v Speaker 1>and humans, which is by definition a zoonotic disease. As
<v Speaker 1>far as transmission, this will most often be from a
<v Speaker 1>scratch or a bite from a cat infected with Bartnella
<v Speaker 1>hens lay, and that's why this is called cat scratch
<v Speaker 1>disease as cats serve as a natural reservoir for Bartnella
<v Speaker 1>hens lay. By scratch or a bite from an infected
<v Speaker 1>cat as well as exposure to cat fleas infected with
<v Speaker 1>this species can lead to transmission. In humans. Most commonly
<v Speaker 1>see this in young individuals, more than fifty percent of
<v Speaker 1>cases in children younger than eighteen years of age, so
<v Speaker 1>likely will be a child in the vignette. As far
<v Speaker 1>as clinical manifestations, a number of things can be seen fever, malaise,
<v Speaker 1>even disseminated disease affecting the liver, spleen, bone, etc. What
<v Speaker 1>you need to know for the exam is limphatinopathy. Regional
<v Speaker 1>limphatinopathy is the hallmark of this disease due to a
<v Speaker 1>granulomatose inflammatory response, and it's what you have to know.
<v Speaker 1>This will definitely be in the question so in large
<v Speaker 1>lymph nodes that will appear proximel to the site of inoculation,
<v Speaker 1>so near the bite or scratch, there'll be tender arethema
<v Speaker 1>of the overlying skin, usually appearing around two weeks after
<v Speaker 1>the bite or scratch. So remember lymphat anopathy. That's the
<v Speaker 1>highest yield thing to know for clinical manifestations. Nothing high
<v Speaker 1>yield for diagnosis, generally a clinical diagnosis that can be
<v Speaker 1>supported with zerol logic tests or biopsy treatment. Next, there's
<v Speaker 1>one meth that you need to know, and that is ezythromycin.
<v Speaker 1>Even though many patients will have resolution of symptoms without antibiotics,
<v Speaker 1>the whole point is to prevent serious complications, which as
<v Speaker 1>many as fourteen percent of patients will have diseminated disease.
<v Speaker 1>So patients with mild to moderate disease with just lymphat
<v Speaker 1>aopathy are going to get a five day course of exythromycin.
<v Speaker 1>There are alternative cipro, etc. But focus on ezythromycin as
<v Speaker 1>that's your first line. In patients with as seminated disease,
<v Speaker 1>you'll usually add or a fampin too. Axythromycin main take
<v Speaker 1>away for treatment though for your exam, I would just
<v Speaker 1>focus on azythromycin. Okay, So cat scratch disease A few
<v Speaker 1>high old things to know how to remember all of
<v Speaker 1>those high old points. Well, this is cat scratch disease.
<v Speaker 1>When you think of cat scratch disease, I want you
<v Speaker 1>to think of black cat scratch disease. So think of
<v Speaker 1>a black cat. So B l ack contains all of
<v Speaker 1>the hild things you need to know. Starting with B
<v Speaker 1>for Bartnella Henslay. Cat scratch disease is an infectious disease
<v Speaker 1>caused by Bartnella Hensley. Next L, which stands for lymphat aopathy.
<v Speaker 1>This disease is usually characterized by self limited regional lymphat aopathy.
<v Speaker 1>Gotta remember that. Next, the A stands for xythromycin, which
<v Speaker 1>is your first line med for most patients. See of
<v Speaker 1>course stands for cats, as they serve as the natural
<v Speaker 1>reservoir for Bartonella hensley. I. Finally, K stands for kids,
<v Speaker 1>as this will most commonly be a disease of children
<v Speaker 1>and young adults. So again, cat scratch disease. Remember black
<v Speaker 1>cat scratch disease. Bartnella hens Lay lymphat aopathy is xythromycin
<v Speaker 1>cats and kids. Next, let's talk about botulism. What's botulism? Well,
<v Speaker 1>this is a rare but potentially life threatening paralysis caused
<v Speaker 1>by a neurotoxin that's produced by Laustridium botulinum, a group
<v Speaker 1>of gram positive rod shaped spore forming anaerobic bacteria. Let's
<v Speaker 1>hit the high old topics. So there's three common types
<v Speaker 1>of botulism. These are infant botulism, food borne botulism, and
<v Speaker 1>wound botulism. And each of these are associated with high
<v Speaker 1>old sources or little things that you need to know.
<v Speaker 1>So let's talk about the three common types and these
<v Speaker 1>sources of infection in each And because there's three sources
<v Speaker 1>that do have high old associations, I have a mnemonic
<v Speaker 1>for you to remember them. So what I want you
<v Speaker 1>to remember is Baby's black bottle, Baby's black bottle, to
<v Speaker 1>help you remember the three high old associations, which we're
<v Speaker 1>going to talk about now, starting with baby, which helps
<v Speaker 1>you remember infant botulism, which happens when a baby swallows
<v Speaker 1>sea bochulinum spores. Because infants have poorly developed gut flora,
<v Speaker 1>these spores can actually settle, colonize, and release talks and
<v Speaker 1>right inside the GI tract. In the US, even though
<v Speaker 1>we have typically associated this with consumption of honey, most
<v Speaker 1>cases actually come from everyday environmental dust and soil that
<v Speaker 1>contain these spores that infants are susceptible to. So even
<v Speaker 1>though honey can contain spores, it's likely not the main source,
<v Speaker 1>as even after years of warning parents to avoid honey,
<v Speaker 1>the rates of infant botulism haven't gone down, which tells
<v Speaker 1>us honey is likely only a minor source of this
<v Speaker 1>infect In just twenty twenty five, there was an outbreak
<v Speaker 1>of botulism that was actually associated with with a popular
<v Speaker 1>brand of powdered formula. So for babies it's not so
<v Speaker 1>much a specific source as it is their susceptibility. Next
<v Speaker 1>is wound botulism, which I want you to remember the
<v Speaker 1>word black, as in baby's black bottle. So there's something
<v Speaker 1>known as wound botulism when sea bochulinum infects wounds, puncture wounds,
<v Speaker 1>et cetera. But the most important and the one that
<v Speaker 1>will likely be in your vignette, and the reason this
<v Speaker 1>one is labeled black is because wound botulism has often
<v Speaker 1>been associated with injection drug use, particularly with black tar heroin,
<v Speaker 1>which I have this exact question in school, So remember
<v Speaker 1>black tar heroin. It's very specific, but it does come up.
<v Speaker 1>Last is food born botulism, which you'll remember as bottle
<v Speaker 1>because bottle helps remind you of canned or bottle foods,
<v Speaker 1>which often contain preform boculinum toxin, an exam favorite. So
<v Speaker 1>food born botulism is often seen with home canned foods, vegetables,
<v Speaker 1>and fish, and the US higher rates occur Alaska native
<v Speaker 1>populations due to the consumption of aged or fermented fish,
<v Speaker 1>while in China it's commonly to home fermented tofu and
<v Speaker 1>bean products. All right, So to tie everything together, remember
<v Speaker 1>Baby's black bottle for the types of botulism and their sources.
<v Speaker 1>Baby for infant botulism or sports colonized the gut, Black
<v Speaker 1>for wound botulism with IV drug use, particularly with black
<v Speaker 1>tar heroin, and bottle for food born botulism with improper
<v Speaker 1>bottled or canned foods. Next, clinical manifestations, so Claustrinium botulinum
<v Speaker 1>can cause muscle weakness or flacid paralysis by blocking the
<v Speaker 1>release of acetyl coline at the neuromuscular junction. This happens
<v Speaker 1>because the toxin cuts something called a snare protein, which
<v Speaker 1>are what nerve cells need to release acetyl coline into
<v Speaker 1>the synapse. So without that signal the muscle can't contract
<v Speaker 1>and we have the clinical presentation will go over next.
<v Speaker 1>So the classic presentation of botulism is acute onset of
<v Speaker 1>bilateral cranial neuropathies with symmetric descending weakness, so we can
<v Speaker 1>see things like double visions, slurred speech, and difficulty swallowing.
<v Speaker 1>If you want to focus on the five main clinical
<v Speaker 1>manifestations you'll most likely see on an exam question. Remember
<v Speaker 1>the five d's of botulism, which are dilated fixed pupils,
<v Speaker 1>diplopia which is double vision, dysphasia which is difficulty swallowing,
<v Speaker 1>dysarthria which is difficulty speaking, and descending muscle weakness or paralysis.
<v Speaker 1>So that's your clinical meniphesations. Remember the key here is
<v Speaker 1>the muscle weakness and cranial nerve dysfunction. Focus on the
<v Speaker 1>five d's diagnosis This is usually going to be made
<v Speaker 1>on clinical findings alone. This can later be confirmed by
<v Speaker 1>botulinum toxin detected in serum, stool, or wound specimens. Confirmatory
<v Speaker 1>testing can take a while to come back though, and
<v Speaker 1>generally you do not want to wait for these test
<v Speaker 1>results before moving on to treatment, which will be with
<v Speaker 1>botulinum antitoxin, which is the main therapeutic option for botulism.
<v Speaker 1>Of course, be aware of supportive treatment like nasogastric feedings
<v Speaker 1>to minimize aspiration risk indubation for patients with respiratory failure,
<v Speaker 1>but botulinum anatoxin is the main focus here. Okay, recap
<v Speaker 1>for botulism. Remember Baby's black bottle for the types of
<v Speaker 1>botulism and their sources. Baby for infant botulism where spores
<v Speaker 1>colonize the gut, Black for wound botulism with ib drug use,
<v Speaker 1>particularly black tar heroin, and bottle for food born botulism
<v Speaker 1>with improperly bottled or canned foods. Remember your five d's
<v Speaker 1>for clinical manifestations dilated, fixed pupils, diplopia, dysphasia, dysarthria, and
<v Speaker 1>descending muscle weakness. Diagnosis can be made clinically and confirmed
<v Speaker 1>with toxin detection. Later treat with anti toxin. That's botulism.
<v Speaker 1>Moving on to Campelobacter specifically campelo Bacter J. Juny, which
<v Speaker 1>is a gram negative, curved or comma shaped bacteria. Camplow
<v Speaker 1>Bacter A juni, or CJ as we'll call them, is
<v Speaker 1>a common food borne pathogen that can cause diarrhea in
<v Speaker 1>all age groups. Let's start with transmission. So CJ can
<v Speaker 1>be found in a variety of domestic and wild animals,
<v Speaker 1>and infection may be acquired through consuming these animals, usually
<v Speaker 1>raw or undercooked meat, So poultry is a common one.
<v Speaker 1>Know this one for sure. Contamination of beef, pork, or
<v Speaker 1>lamb is less common, so really focus on poultry. Milk
<v Speaker 1>is another big one, specifically, consumption of unpasteurized milk is
<v Speaker 1>a common source and definitely an exam favorite. And contaminated water.
<v Speaker 1>Nearly any natural water source can be infected. There's other
<v Speaker 1>routes person a person transmission via fecal oral route, vertical
<v Speaker 1>transmission from mom to baby. Even domestic pets like puppies
<v Speaker 1>can be a source. But poultry, unpasteurized milk. That's what
<v Speaker 1>you got to know for the exam, all right. So
<v Speaker 1>clinical manifestations as you'd expect, abdominal pain, cramping, fever, diarrhea,
<v Speaker 1>which can be watery or bloody. So bloody diarrhea can
<v Speaker 1>be seen in around fifteen percent of adults. In children,
<v Speaker 1>it's much more common, closer to fifty percent. And this
<v Speaker 1>is an important differentiating factor. Remember, because things like cholera
<v Speaker 1>was typically watery but not bloody, and that's because CJ
<v Speaker 1>invades the intestinal mucosa, causing inflammation, damaging capillaries, and allowing
<v Speaker 1>blood to leak into the stool. Another important thing to
<v Speaker 1>know is that CJ can closely mimic other conditions, most
<v Speaker 1>notably acute appendicitis, because sometimes abdominal pain may occur before
<v Speaker 1>the onset of diarrhea, which can delay recognition of an
<v Speaker 1>infectious cause. So someone that comes in with adominal pain
<v Speaker 1>that radiates to the right aliac fossa tenderness on exam
<v Speaker 1>very similar to appendicitis, which is why this is called
<v Speaker 1>pseudo appendicitis. And you can of course use ultrasound or
<v Speaker 1>CT to help differentiate the two. But remember this as
<v Speaker 1>it's sometimes tested on. It definitely was for me and
<v Speaker 1>of course good to know when you're out there practicing
<v Speaker 1>as well as far as diagnosis, so suspects CJ and
<v Speaker 1>a patient with abdominal pain and diarrhea in the context
<v Speaker 1>of risk factors for transmission somebody who is drinking milk
<v Speaker 1>straight from the utter, for instance, and then diagnosis can
<v Speaker 1>be established with stool testing, usually with stool culture. Finally,
<v Speaker 1>treatment it's pretty straightforward. For most patients, this is going
<v Speaker 1>to be supportive care, and in patients with severe divies disease,
<v Speaker 1>antibiotics can be used, typically as if the remycin is recommended,
<v Speaker 1>fluoroquino loans are an alternative. One last thing I want
<v Speaker 1>you to know for CJ is that CJ can cause
<v Speaker 1>some pretty high yield complications that are often tested on,
<v Speaker 1>and the main one to know is going to be
<v Speaker 1>geon Berat syndrome. CJ is actually the most common precipitate
<v Speaker 1>of geon Beret syndrome, so you need to know this.
<v Speaker 1>Reactive arthritis, post infectious irriable bowel syndrome are other late
<v Speaker 1>onset complications of CJ, but please focus on gion Beret
<v Speaker 1>syndrome as this will very likely be tested on. All Right,
<v Speaker 1>so there's a few high eel things to know for CJ.
<v Speaker 1>Here's a quick way to remember the important details. When
<v Speaker 1>you think of Camp low Bacter camp Elobacter, think of
<v Speaker 1>a camp, a summer camp named Camp Elobacter, with a
<v Speaker 1>camp counselor named you guess it's CJ. Now CJ, our
<v Speaker 1>trustee camp counselor at Camp Elobacter is grilling up some
<v Speaker 1>food for the campers, and on the grill we see
<v Speaker 1>a big old raw chicken. Since it's hot at camp elobacter,
<v Speaker 1>he's drinking a cold glass of milk to cool him down.
<v Speaker 1>The raw chicken and milk help us to remember the
<v Speaker 1>undercooked meat, most commonly poultry and unpasteurized milk, which are
<v Speaker 1>common methods of transmission for this pathogen. Now, a few
<v Speaker 1>other things you'll notice about CJ. He's wearing a beret,
<v Speaker 1>which helps you remember Gyon beret syndrome. In his front
<v Speaker 1>pocket there is a big oversized fake pen, like something
<v Speaker 1>from a gag store, which helps us remember the pseudo
<v Speaker 1>apenn dicitis commonly associated with his condition. And finally, poor
<v Speaker 1>CJ is wearing a diaper, which helps us remember the diarrhea,
<v Speaker 1>sometimes bloody, seen with CJ infections. So quick recap. The
<v Speaker 1>raw chicken and glass of milk points to the common
<v Speaker 1>transmission sources. The beret CJ is warring helps you to
<v Speaker 1>remember Gyon beret syndrome, the oversized fake pen in his
<v Speaker 1>pocket represents pseudo apendicitis, and the diaper helps remind you
<v Speaker 1>of the diarrhea often bloody, associated with camp Blowbackter Jay JUNI.
<v Speaker 1>That's cj X. Let's talk about diphtheria. So dip theia
<v Speaker 1>is an infectious disease caused by the gram positive Bacillis
<v Speaker 1>griny Bacterium diph THEORYA or C dip theoria, and for
<v Speaker 1>the sake of this lecture, it will now be called
<v Speaker 1>CE dip theory gray instead of CE dip theory A.
<v Speaker 1>Remember it as see dip theory gray gray gray gray gray.
<v Speaker 1>Remember that word also for the sake of the mnemonic
<v Speaker 1>gray is spelled with three a's, So dip theory gray
<v Speaker 1>g r aaa Y. Remember that it will help you
<v Speaker 1>get the exam question right and I'll explain why in
<v Speaker 1>a minute. So ceed dip theory gray. Infection can lead
<v Speaker 1>to respiratory or cutaneous disease. Some patients may also be
<v Speaker 1>asymptomatic carriers. We don't see this as often since the
<v Speaker 1>availability of vaccina, but seed dip theory gray is reappearing
<v Speaker 1>in some regions. So what do you need to know.
<v Speaker 1>Let's keep it simple, starting with the clinical manifestations. So
<v Speaker 1>with respiratory dip thory gray, you can have a sore throat, malaise,
<v Speaker 1>cervical impot andopathy. These patients can actually have some pretty
<v Speaker 1>severe swelling of the neck. They can develop what's called
<v Speaker 1>a bull neck where you have this massive swelling of
<v Speaker 1>the tonsils, uvulas, cervical lymphanodes. And finally, the most important
<v Speaker 1>finding and the one that you will not forget and
<v Speaker 1>the reason you'll always call the seed with theory gray,
<v Speaker 1>is because the hallmark finding is going to be gray
<v Speaker 1>pseudo membranes. So at least a third of patients infected
<v Speaker 1>with this organism will have these adherent gray what they
<v Speaker 1>call pseudo membranes covering the pharynx, soft palate, nasal membrane.
<v Speaker 1>These will often bleed if scraped, and the reason people
<v Speaker 1>with dip theory gray develop these is because these organisms
<v Speaker 1>attached to the pharynx or surrounding areas and it can
<v Speaker 1>release a toxin, a DT toxin, which causes inflammation and
<v Speaker 1>ultimately necrosis of the tissue. This resulting necrotic epithelium mixed
<v Speaker 1>with inflammatory cells cellular debris lead to the appearance of
<v Speaker 1>this gray, leathery adherent membrane. These pseudo membrane can also
<v Speaker 1>dislodge and wind up in the baranchial tree, leading to
<v Speaker 1>respiratory compromise. There are systemic manifestations which can involve the heart,
<v Speaker 1>nervous system, kidneys. But the main takeaway you do not
<v Speaker 1>want to forget your hallmark gray pseudo membrane. That's why
<v Speaker 1>you will always call this seed dip theory gray. All right,
<v Speaker 1>less important, but no, there is cutaneous disease which patients
<v Speaker 1>may develop these unhealing sores or shallow gray ulcers. But
<v Speaker 1>again focus on gray pseudo membranes in respiratory seed dip
<v Speaker 1>theory gray all right. So for diagnosis and a patient
<v Speaker 1>you suspect may have dip theory gray, you'll culture. In
<v Speaker 1>PCR testing, diagnosis is a little bit involved. You first
<v Speaker 1>start with a swab of the throat, naars or any
<v Speaker 1>cutaneous lesion that demonstrates signs of infection. Then you send
<v Speaker 1>them out for culture. Cultur will identify the Karni Bacterium species.
<v Speaker 1>Then we have to determine if these species identified is
<v Speaker 1>dune undone toxogenic, and the PCR testing helps with that.
<v Speaker 1>It will help detect the presence of the toxin gene,
<v Speaker 1>which is a good start, but it won't tell us
<v Speaker 1>if there is active toxin production, so we need additional
<v Speaker 1>testing like with an elix test to help establish active
<v Speaker 1>toxin production. So why do we need to do all
<v Speaker 1>of this? Why can't we just stop at identifying seedp
<v Speaker 1>theory gray on culture? Isn't that enough? Why do we
<v Speaker 1>need to know if it's a toxic strain? Well? Determining
<v Speaker 1>toxogenicity is important, one because toxogenic strains generally cause the
<v Speaker 1>more severe systemic disease we worry about. And two it
<v Speaker 1>helps direct appropriate treatment and isolation protocols, as some patients
<v Speaker 1>may only be a symptomatic carriers. The main takeaway is
<v Speaker 1>here is toxogenic strains are the issue, and for the exam,
<v Speaker 1>I would focus on just remembering your culture and PCR
<v Speaker 1>testing for diagnosis. Next, let's talk about treatment. Treatment involves
<v Speaker 1>the three a's, which is why you remembered gray spelled
<v Speaker 1>with three a's. The three a's of DIP theory GRAY
<v Speaker 1>treatment are airway antiitoxin and antibiotics. Although cultures and toxin
<v Speaker 1>testing should be obtained for diagnosis, you do not want
<v Speaker 1>to wait for confirmation before initiating a treatment. Therapy has
<v Speaker 1>started immediately based on clinical suspicion. If toxogenic DIP theoryray
<v Speaker 1>treatment is later rolled out, certain treatments can be discontinued,
<v Speaker 1>but early intervention is critical to prevent complications. So starting
<v Speaker 1>with the first A, which stands for airway, so aggressive
<v Speaker 1>airway management and patients with respiratory dip theory gray is
<v Speaker 1>very important as respiratory failure due to airway compromises a
<v Speaker 1>major complication and a cause of mortality, so intubation may
<v Speaker 1>be needed. Also keep in mind these patients will usually
<v Speaker 1>be placed on isolation precautions. Next A stands for antitoxin.
<v Speaker 1>Specifically diphtheria antitoxin or DAT is used, which is interesting
<v Speaker 1>as the diphtheria antiitoxin is in a quine derived antibody
<v Speaker 1>that's obtained from the plasma of horses imminized against diphtheria toxin,
<v Speaker 1>so this antiitoxin binds to and inactivates the toxin. Not only.
<v Speaker 1>The last A stands for antibiotics. Per up to date,
<v Speaker 1>xythromycin is now the preferred agent. Luckily another A penicillin
<v Speaker 1>and erythromycin used to be preferred and are of course
<v Speaker 1>still used, but a xythromycin is preferred for dip theory
<v Speaker 1>gray due to increased penicillin resistance and preferred over erythromycin
<v Speaker 1>due to better side effect profile. Just a few other
<v Speaker 1>side notes. You want to also identify and test close
<v Speaker 1>contacts and potentially administer prophylactic antibiotics if needed. And remember
<v Speaker 1>the ultimate goal with dip theory Gray is prevention with immunization.
<v Speaker 1>All right, So dip theory Gray. Infectious disease caused by
<v Speaker 1>the gram positive Bacillis karini bacterium theory Gray. Remember sore throat,
<v Speaker 1>cervical and fatinopathy, that big old bullneck and of course
<v Speaker 1>the star of the show Gray, pseudo membranes that can
<v Speaker 1>bleed have scraped. DIP theory Gray. Diagnose with culture and PCR.
<v Speaker 1>Treat with your three a's. That's why Gray is spelled
<v Speaker 1>with three a's. Airway antitoxin and antibiotics, especially as zythrope.
<v Speaker 1>That's dip theory Gray. Moving on to acute rheumatic fever
<v Speaker 1>or rf ARF, which is a delayed immune mediated complication
<v Speaker 1>that occurs two to four weeks after exposure to a
<v Speaker 1>specific organism. It's highly tested on you got to know it.
<v Speaker 1>So the organism in question is Group A Streptococcus or
<v Speaker 1>gas so ARF is a systemic immune mediated inflammatory condition
<v Speaker 1>that occurs two to four weeks after group A strep
<v Speaker 1>or gas infection. There's this broad immune response to the
<v Speaker 1>infectious organism that can lead to multiple organ systems being damaged,
<v Speaker 1>including the joints, skin, and heart, which brings us to
<v Speaker 1>the highest sealed part of the disease. The clinical manifestations
<v Speaker 1>which also form the framework for diagnosis. So ARF is
<v Speaker 1>diagnosed using the Jones criteria, which are divided into major
<v Speaker 1>and minor criteria. These criteria are named after doctor T.
<v Speaker 1>Duckett Jones, who first described the diagnostic rules for a
<v Speaker 1>cue romatic fever in the nineteen forties. The five major
<v Speaker 1>Jones criteria, which typically present one to five weeks after
<v Speaker 1>a gas infection, include arthritis, which is usually the earliest
<v Speaker 1>manifestation of ARF. This is sometimes described as migratory as
<v Speaker 1>it'll start in one joint then quickly jump to another,
<v Speaker 1>so the knee for a few days, then a few
<v Speaker 1>days later the elbow, wrist, ankle, et cetera carditis, so
<v Speaker 1>we can see pericarditis. Myocarditis most commonly will see involvement
<v Speaker 1>of the mitral and aortic valves, with mitrol regurgitation being
<v Speaker 1>the most common Valvular legion. Next sitaham Korea, which is
<v Speaker 1>a neurologic disorder consisting of a erratic, abrupt involuntary movements,
<v Speaker 1>muscle weakness, et cetera. Erethema marginatum. This is a pink
<v Speaker 1>or faintly red, non pruitic rash that involves the trunk
<v Speaker 1>and sometimes the limbs, usually sparing the face, often evanescent
<v Speaker 1>where it'll pop up and then disappear in a matter
<v Speaker 1>of hours. The lesion usually has a sharply demarketed outer
<v Speaker 1>border and diffuse inner margin forming a continuous ring. And finally,
<v Speaker 1>cutaneous nodules, which are these firm, painless lesions ranging from
<v Speaker 1>a few millimeters to two centimeters in size, often located
<v Speaker 1>over bony surfaces. So that's your Jones major criteria for
<v Speaker 1>our You got to know those. The demonic for Jones
<v Speaker 1>major criteria is Luckily Jones jo Nes. This is an
<v Speaker 1>old demonic that I learned in school, but I modified
<v Speaker 1>it a little bit to make it a little easier
<v Speaker 1>to remember. Starting with J that stands for joint which
<v Speaker 1>you will help you remember your migratory polyarthritis. OH stands
<v Speaker 1>for oh my heart, what you will help you remember
<v Speaker 1>carditis mutual regurgitation being a common manifestation. N stands for nodules,
<v Speaker 1>your subcutaneous nodules, the firm, painless lesions usually located over
<v Speaker 1>a bony surface. E stands for arithmo marginatum, the pink
<v Speaker 1>non pruritic rash most often on the trunk and sometimes
<v Speaker 1>the limbs. And then finally the S, which the original
<v Speaker 1>mnemonic stood for Sinnaham Korea. But I knew damn well.
<v Speaker 1>On an exam, I would not remember what the heck
<v Speaker 1>that stood for, So instead I just remembered it as shaky.
<v Speaker 1>Because even if you remember Sidnaham Korea on an exam,
<v Speaker 1>they're not going to say the patient presents with Sinnaham Korea.
<v Speaker 1>They're going to say the patient presents with uncoordinated jerking movements.
<v Speaker 1>So just remember the S as shaky, just to make
<v Speaker 1>it easier. So remember the five manifestations of r F.
<v Speaker 1>Remember Jones, J, O, N, E, S, J for joint
<v Speaker 1>for the polyothritis, O for oh my heart for carditis,
<v Speaker 1>N for nodules, E for arithemo marginatum, and S for
<v Speaker 1>shaky aka Sinaham Korea. And then we have the minor manifestations,
<v Speaker 1>which are going to be feverthralgia, which is joint pain
<v Speaker 1>usually involving several joints. Elevated acus phase reactants, so most
<v Speaker 1>patients with RF will have elevated inflammatory markers to increase
<v Speaker 1>levels of E, s R and CRP and finally abnormalodies
<v Speaker 1>on ECG specifically a prolonged PR interval, So again fever arthragia,
<v Speaker 1>elevated acute phase reactants prolonged PR, which I used to
<v Speaker 1>remember umber as fat as an faat so f for fever,
<v Speaker 1>A for our thralgia, the second A for acute phase
<v Speaker 1>reactants which are elevated and then T for two long
<v Speaker 1>PR for your prolonged PR interval. So minor criteria again
<v Speaker 1>is fat faat fever aarthralgia, acute phase reactants too long PR.
<v Speaker 1>So how do we diagnose are f well? The diagnosis
<v Speaker 1>is made by combining the clinical findings we just reviewed
<v Speaker 1>with evidence of a preceding group a strep infection. There
<v Speaker 1>are stipulations depending on whether this is a first episode
<v Speaker 1>or a recurrent episode. Some criteria cannot be counted twice,
<v Speaker 1>like arthralgia, and the minor criteria can't be used alongside
<v Speaker 1>arthritis in the major criteria. But for example purposes, let's
<v Speaker 1>keep the simple unfocused on the basics. So diagnosis is
<v Speaker 1>made with evidence of a preceding gas infection. So this
<v Speaker 1>can be a positive rapid strep test, a positive throw culture,
<v Speaker 1>elevated or rising anti streptococcal antibody tighter, plus two major
<v Speaker 1>manifestations or one major plus two minor. So again remember
<v Speaker 1>for diagnosis, two major manifestations or one major plus two
<v Speaker 1>minor are sufficient for diagnosis of an initial episode OFF
<v Speaker 1>in a patient with evidence of preceding gas infection. What
<v Speaker 1>about treatment, It's actually pretty simple, luckily, because there's a
<v Speaker 1>whole bunch of other crap youat to remember this. The
<v Speaker 1>most important thing to know is going to be penicillin G.
<v Speaker 1>Treatment of ARF consists of eradication of the gas infection
<v Speaker 1>group aase strap. You do that with antibiotics, and the
<v Speaker 1>preferred antibiotic is penicillin G benzethene, which is a long
<v Speaker 1>acting intramuscular injection. Of course, if PENG isn't available or
<v Speaker 1>they have penicillin allergies, there are alternatives, but definitely you
<v Speaker 1>should know penicillin G for the exam. Now, there are
<v Speaker 1>other treatments depending on what other manifestations are present. URF
<v Speaker 1>associated arthritis, for instance, N SAIDs will be your first
<v Speaker 1>line to proxy and ambiprofen. So for treatment, remember penge
<v Speaker 1>and n sets to keep it nice and simple, penge
<v Speaker 1>being the highest deal component. All right, ourf acute rhumatic fever,
<v Speaker 1>it's tested on a lot. There's a decent amount of
<v Speaker 1>information to know, but you remember the high yield stuff.
<v Speaker 1>It's actually pretty easy. Instead of RF acute rheumatic fever,
<v Speaker 1>you're going to add a B and remember it as barf.
<v Speaker 1>Arf becomes barf, and you're going to remember this sentence
<v Speaker 1>Barf Jones, The fat penguin has gas. Barf Jones, the
<v Speaker 1>fat penguin has gas. That one sentence contains most of
<v Speaker 1>the high old information you need to know for a
<v Speaker 1>cute rheumatic fever. So picture this. You're at the Zoos,
<v Speaker 1>standing at the penguin exhibit, and this fat penguin names
<v Speaker 1>Jones right in front of you just keeps farting NonStop,
<v Speaker 1>so the point where it's making you want to barf.
<v Speaker 1>So when you see arf, add the bee, remember barf
<v Speaker 1>and lock in this visual. Barf Jones, the fat penguin
<v Speaker 1>has gas. Joan helps you remember the major criteria joints,
<v Speaker 1>oh my heart, nodules ur, themo marginatum, and shaky fat.
<v Speaker 1>For the minor criteria fever, arthralgia, acute phase reactants, too long,
<v Speaker 1>pr penguin, I'll give you a second and think about it.
<v Speaker 1>The first four letters are pe n G as in
<v Speaker 1>peng or penicillin G, your first line medication, and then
<v Speaker 1>finally gas, which helps you remember the infectious organism that
<v Speaker 1>caused this whole mess in the first place. Group a strip,
<v Speaker 1>so remember arf becomes barf as in barf Jones. The
<v Speaker 1>fat penguin has gas. That's a cute rhumatic fever. Let's
<v Speaker 1>talk about Rocky Mountain spotted fever next. So Rocky Mountain
<v Speaker 1>spotted fever is a tick born disease that can be
<v Speaker 1>fatal if not treated. In fact, prior to the introduction
<v Speaker 1>of antibiotics, the fatality rate was as high as eighty
<v Speaker 1>percent in some regions. More recently, with widespread antibiotic availability
<v Speaker 1>and improved disease recognition, mortality rate has dropped to approximately
<v Speaker 1>zero point one two point six percent. So who is
<v Speaker 1>responsible for this terrible disease? Well, that's an organism by
<v Speaker 1>the name of Rickettsia rickettsi, which is a gram negative
<v Speaker 1>obligate intracellular bacterium named after the pathologist Howard Rickets. And
<v Speaker 1>as difficult as the name may be to say, it's
<v Speaker 1>super easy to remember that Rocky Mountain spotted fever is
<v Speaker 1>caused by Rickettsia rockets cii. And that's because you're going
<v Speaker 1>to remember Rocky Mountain spoted fever instead as Ricky Mountain
<v Speaker 1>spotted fever. Swap Rocky for Ricky. Ricky Mountain spotted fever
<v Speaker 1>helps you remember this disease is caused by rick aka
<v Speaker 1>Rickettsia rickettsii. This is the only Ricketzial infection that has
<v Speaker 1>the name rick twice. So remember rick for Ricky Mountain
<v Speaker 1>spotted fever, all right. That brings us to our next
<v Speaker 1>important tidbit, the vector. So in nineteen oh six, Howard
<v Speaker 1>Ricketts demonstrated that Ricky Mountain spotted fever was an infectious
<v Speaker 1>disease transmitted by ticks, which prior to that people actually
<v Speaker 1>thought you got this from drinking the melted snowwater. So
<v Speaker 1>Ricky Mountain spotted fever is usually transmitted via tick bite
<v Speaker 1>and is most commonly seen in the spring and early summer,
<v Speaker 1>when outdoor activity is the highest. Transmission occurs after a
<v Speaker 1>tick has been attached for several hours, during which time
<v Speaker 1>rocketsia organisms are released from the tick's salivary glands into
<v Speaker 1>the human host. The type of tick that carries this
<v Speaker 1>varies by location. Eastern and south central US is the
<v Speaker 1>derma center of Verabilis tick derma center and DERSNY is
<v Speaker 1>the primary vector in the mountain states west of the
<v Speaker 1>Mississippi River. Probably wouldn't go too hard here with memorization,
<v Speaker 1>just remember the vector as a tick. Clinical menifestations next.
<v Speaker 1>Early symptoms of ricky mountain spotted fever are non specific fever, headache,
<v Speaker 1>as well as malaise, myalagias, abdominal pain, confusion. But the
<v Speaker 1>main clinical menaphisation I want you to remember, which is
<v Speaker 1>the hallmark of this disease and is always tested on,
<v Speaker 1>is the rash. So Ricky is going to cause a
<v Speaker 1>rash and approximately eighty eight to ninety percent of patients.
<v Speaker 1>It is uncommon at the initial clinical presentation, but it
<v Speaker 1>usually pops up the third to fifth day of illness.
<v Speaker 1>The hallmark is a blanching arithmatose rash with macules, so
<v Speaker 1>small flat spots that become particular over time, so more
<v Speaker 1>red or purple pinpoint spots. So that's great to know.
<v Speaker 1>But here's the high old part. You'll be tested on
<v Speaker 1>the appearance of the rash usually begins on the ankles
<v Speaker 1>and risks and spreads to the trunk. So remember when
<v Speaker 1>we're talking about a ricky rash, the rash begins on
<v Speaker 1>the risks and ankles and spreads what they call centripetally
<v Speaker 1>to the trunk, which just means towards the center. There
<v Speaker 1>are also complications secondary to ricky, like seizures, other neurologic
<v Speaker 1>abnormalities non cardiogenic pulmonary edema, but focus primarily on the
<v Speaker 1>rash centripetal distribution for the exam. Okay diagnosis not super
<v Speaker 1>high yield, but a presumptive clinical diagnosis of ricky is
<v Speaker 1>made based upon clinical signs and symptoms in a patient
<v Speaker 1>who are from an endemic area or visited one recently.
<v Speaker 1>So fever, rash, tick bite in the right location, treat it.
<v Speaker 1>Don't wait for serologic testing to come back. Why don't
<v Speaker 1>you want to wait for serologic testing to come back
<v Speaker 1>before you give them antibiotics? Well, first, because early serology
<v Speaker 1>is obtained in the first few days are often falsely
<v Speaker 1>negative and second infulmentate cases of Ricky death can occur
<v Speaker 1>in as early as five days. So treat based on
<v Speaker 1>clinical suspicion and confirm retrospectively through serologic testing, which will
<v Speaker 1>be obtained through indirect immunofluorescent testing or in some cases
<v Speaker 1>PCR testing, which can be used to make a definitive diagnosis.
<v Speaker 1>And then finally, there are some lab findings that can
<v Speaker 1>be obtained to help support the diagnosis. Things like thrombocytopenia, hyponatremia,
<v Speaker 1>and elevation and serum aminotransferrace levels can all be seen
<v Speaker 1>with a Ricky infection. Finally, we have treatment which is
<v Speaker 1>very easy. You really just need to know one met
<v Speaker 1>and that's going to be doxy cycling. Doxy is your
<v Speaker 1>treatment of choice in both adults and children, even in
<v Speaker 1>pregnant women. The only alternative, which is chlorinmphenicol, has been
<v Speaker 1>associated with a higher risk of death, so it's really
<v Speaker 1>doxy all the way. Nothing more to know here except
<v Speaker 1>for the fact that you treat asap, do not wagh
<v Speaker 1>for serologic testing. As we talked about before, Okay, so
<v Speaker 1>you will never forget that Rocky Mountain spot of fever
<v Speaker 1>is caused from the organism ricketsia ricketsia, because again you'll
<v Speaker 1>remember it as Ricky Mountain spotted fever, super easy. But
<v Speaker 1>there's other highield stuff to know, and for that I
<v Speaker 1>have to tell you a little rhyme about Ricky or Rick.
<v Speaker 1>So here's the rhyme that contains all of the juicy
<v Speaker 1>details for the exam. Rick got bit by a tick
<v Speaker 1>because he stood on the docks and forgot to wear
<v Speaker 1>gloves and socks. Rick got bit by a tick because
<v Speaker 1>he stood on the docks and forgot to wear gloves
<v Speaker 1>and socks. So Rick, that's your cue for rickettsia, ricketsi.
<v Speaker 1>I got bit by a tick, which we know is
<v Speaker 1>the vector for this disease. Stood on the docks, which
<v Speaker 1>helps you remember doc cy cycling is the first line
<v Speaker 1>med and forgot to wear gloves and socks. Gloves and
<v Speaker 1>socks help you remember where the rash originates, super important,
<v Speaker 1>the ankles and wrist then spreads centripetally. So Rick got
<v Speaker 1>bit by a tick because he stood on the docks
<v Speaker 1>and forgot to wear gloves and socks. It's got your
<v Speaker 1>infectious organism vector, first line med and most tested on
<v Speaker 1>clinical manifestation. If you can remember that little ryme, you'll
<v Speaker 1>likely get the exam question right. All right, So that's
<v Speaker 1>Rocky aka Ricky Mountain spotted fever. We're almost there. Last
<v Speaker 1>one is going to be tetanus, so tetanus, which is
<v Speaker 1>derived from the Greek word tetanose, which literally means tension
<v Speaker 1>tight or to stretch, which makes sense when you're familiar
<v Speaker 1>with the manifestations of the disease, which will go over shortly.
<v Speaker 1>So Deatonnis is caused by the toxin producing bacteria Claustridium
<v Speaker 1>tetani which is an anaerobic gram positive spore forming bacilline
<v Speaker 1>which typically live in soil and surprisingly even present in
<v Speaker 1>the gut of mammals. So these guys don't like oxygen.
<v Speaker 1>They are anaerobes, so when they get exposed to beautiful
<v Speaker 1>fresh oxygen or an unfavorable environment, they get stressed and
<v Speaker 1>shed these little spores almost like safe little transport vehicles
<v Speaker 1>for them to hang out in until a new anaerobic
<v Speaker 1>environment presents itself for them to sprout back into Clostridia.
<v Speaker 1>So let's go over the predisposing factors. So the first
<v Speaker 1>is going to be lack of immunity, which, of course
<v Speaker 1>we know that we do have tetanus vaccines available to
<v Speaker 1>prevent this disease, and most patients who develop tetanus are
<v Speaker 1>either incompletely immunized and or receive inadequate prophylaxis following a wound.
<v Speaker 1>Next is going to be inoculation of spores. So those
<v Speaker 1>little spores we talked about before, they got to get
<v Speaker 1>into the body somehow, and this typically happens through some
<v Speaker 1>sort of penetrating trauma, splinters, gunshots, lacerations, burns, compound fractures.
<v Speaker 1>There needs to be an entry point for those spores.
<v Speaker 1>There are even some cases of neonatal tetanus which result
<v Speaker 1>from home deliveries with unsanitary cutting of the umbilical cord. Okay,
<v Speaker 1>And then we have the final key predisposing factor, and
<v Speaker 1>that's devitalized tissue. So a schemic or necrotic tissue as
<v Speaker 1>we see in many infections, is an important predisposing factor
<v Speaker 1>for developing tetanus. And why is that? Why can't tetani
<v Speaker 1>grow in healthy tissue? While it's what we talked about before.
<v Speaker 1>Tetani is an anaerobic bacteria. It thrives in the absence
<v Speaker 1>of oxygen. So when it enters the body through those
<v Speaker 1>dormant spores, what key element can wake them up and
<v Speaker 1>allow them to sprout? An environment void of oxygen, where
<v Speaker 1>can we find that in the body. A necrotic or
<v Speaker 1>a schemic tissue which has little to no blood flow.
<v Speaker 1>So this low oxygen environment allows tetni to thrive and
<v Speaker 1>germinate and do the terrible things we'll talk about next.
<v Speaker 1>So you need a combination of these three factors. Lack
<v Speaker 1>of immunity, a tetanus prone injury like a puncture wound,
<v Speaker 1>and then a schemic or necrotic tissue. All right, clinical
<v Speaker 1>manifestations next. So there are different types of tetanus. Localized
<v Speaker 1>tetanus which is only localized to a specific part of
<v Speaker 1>the body. Cephalic tetanus is a form of localized tetanus
<v Speaker 1>that involves only the cranial nerves, natal tetanus, and then
<v Speaker 1>generalized tetanus, which is the most common, and that's what
<v Speaker 1>we'll focus on. So generalized tetanus, you will have spastic
<v Speaker 1>muscle contractions. Now, really quickly, I want to just talk
<v Speaker 1>about why this disease causes these severe muscle contractions, so
<v Speaker 1>Claustridium tetana can produce a horrible toxin called tetanospasmen. This
<v Speaker 1>toxin blocks inhibitory neural transmitters like gaba and glysine, which
<v Speaker 1>normally tell muscles to relax, and without the inhibition, alpha
<v Speaker 1>modor neurons fire continuously causing severe, rigid, sustained muscle contractions.
<v Speaker 1>So we'll see things like tristmas, which is present in
<v Speaker 1>more than eighty percent of cases, involving these strong, painful
<v Speaker 1>spasms of the meceder muscles and an inability to open
<v Speaker 1>the mouth. That's why sometimes referred to as lock jaw
<v Speaker 1>opis thoughtness, which is the spasm of the spinal extensors
<v Speaker 1>leading to the severe arching of the back. Rhesis sardenticus,
<v Speaker 1>which is also known as a sardonic smile, which is
<v Speaker 1>caused by persistent face muscle spasms causing this exaggerated or
<v Speaker 1>abnormal grin. We can also see autonomic overactivity, so these
<v Speaker 1>patients can present with excessive sweating, fever, tachycardia, cardiac arrhythmias.
<v Speaker 1>For the exam certainly focus on the intense spastic muscle contractions. Okay,
<v Speaker 1>So for diagnosis, tetanus is going to be diagnosed clinically.
<v Speaker 1>Antibody tests for tetanus exists, but they're not reliable at
<v Speaker 1>low tighters and impatients who received antiitoxin. So again, this
<v Speaker 1>is a clinical diagnosis and you should suspect this in
<v Speaker 1>a patient with intense muscle spasms, especially after a tetanus
<v Speaker 1>prone injury, someone who's been inadequately immunized. So a treatment
<v Speaker 1>is multifaceted, including airway management, wound agreement. Adequate wound to
<v Speaker 1>agreement is actually really important because tetani can persist in
<v Speaker 1>wounds even after these patients are started on antibiotic therapy. Antibiotics,
<v Speaker 1>which in most cases will be metronitasol penicyllerg is an alternative,
<v Speaker 1>and then tetanus immune globulin, which is an antiitoxin that
<v Speaker 1>binds to and can neutralize any remaining circulating unbound tetnos spasmin,
<v Speaker 1>that horrible toxin we talked about before, And benzodiazepines like diazepam,
<v Speaker 1>which are usually the first line madule used to help
<v Speaker 1>control the muscle spasms. And ultimately the goal is prevention
<v Speaker 1>with immunization with your tetanus vaccine. Once the patient is stabilized,
<v Speaker 1>they should receive active immunization with a full series of
<v Speaker 1>tetanus and diphtheria toxoid containing vaccines, as having tetanus unfortunately
<v Speaker 1>does not provide immunity. All right, we did it. That
<v Speaker 1>was your bacterial disease review. Let's do five quick questions
<v Speaker 1>to see what you've retained. Starting with question one, A
<v Speaker 1>twenty eight year old unvaccinated male presents to the emergency
<v Speaker 1>department with a three day history of sore throat, low
<v Speaker 1>grade fever thirty eight degrees celsius one hundred point four
<v Speaker 1>degrees fahrenheit, and difficulty swallowing. An examination, you note a
<v Speaker 1>gray adherent membrane covering both tonsils and the posterior FHARINGX.
<v Speaker 1>When you attempt to remove a small portion for culture,
<v Speaker 1>it bleeds. The patient has prominent cervical and fatinopathy with
<v Speaker 1>visible neck swelling. What is the most appropriate immediate management
<v Speaker 1>for the suspected diagnosis? A Administer diphtheria antitoxin, intravenous antibiotic
<v Speaker 1>and provide airway management b obtained throughat culture. Then start
<v Speaker 1>antibiotics while awaiting results. C reassure and provide symptomatic treatment
<v Speaker 1>only d initiates supportive care and observe for twenty four
<v Speaker 1>to forty eight hours before starting antimicrobial therapy or E
<v Speaker 1>arranged for ton select me to remove the pseudo membrane,
<v Speaker 1>So that is going to be a administer DIP theory, antitoxin, intravenous,
<v Speaker 1>antibiotic and airway management. So even if you have no
<v Speaker 1>idea what disease is being referenced in the vignette, you
<v Speaker 1>may recognize de gray adherent membrane being mentioned, which would
<v Speaker 1>trigger you to remember DIP theory gray spelled with three a's,
<v Speaker 1>and DIP theory gray should certainly be suspected in this
<v Speaker 1>patient with the presence of a gray pseudo membrane that
<v Speaker 1>bleeds with scraping, unvaccinated, low grade fever, prominent cervical infatinopathy,
<v Speaker 1>and what empiric treatment should be started in patients with
<v Speaker 1>suspected respiratory DIP theory Gray well the three a's, which
<v Speaker 1>is why gray is spelled with three a's to help
<v Speaker 1>you remember anti toxin, antibiotic, airway metam so for respiratory
<v Speaker 1>DIP theory gray urgent empiric treatment with diphtheria antitoxin and
<v Speaker 1>antibiotics should be administered right away, even before confirmatory diagnostic
<v Speaker 1>tests come back. And of course aggressive airway management is
<v Speaker 1>important due to the risk of obstruction. So answer a
<v Speaker 1>administer dip theory anti toxin, intravenous antibiotic and airway management
<v Speaker 1>is the correct answer for this patient. Question two. A
<v Speaker 1>thirty two year old woman presents the emergency department with
<v Speaker 1>profuse watery diarrhea and abdominal cramping for the past forty
<v Speaker 1>eight hours. She reports passing copious amounts of pale, watery
<v Speaker 1>diarrhea that is non bloody and has a milky, cloudy
<v Speaker 1>appearance with small white flecks. She reports severe thirst, lightheadedness
<v Speaker 1>when standing, and is not urinated in over twelve hours.
<v Speaker 1>She returned yesterday from a medical mission trip to a
<v Speaker 1>remote region of South America, where she had limited access
<v Speaker 1>to clean drinking water and eight raw oysters at a
<v Speaker 1>local market. She has no significant past medical history. Vital
<v Speaker 1>science revealed tachycardian hypotensionation is a febrie. On examination. She
<v Speaker 1>appears ill and lethargic, with sunken eyes, markedly dry mucous membranes,
<v Speaker 1>and skin tentting. The that persists for over two seconds.
<v Speaker 1>Her abdomen is soft with mild diffuse tenderness and hyperactive
<v Speaker 1>bowel sounds. What is the most appropriate initial treatment for
<v Speaker 1>this patient A oral rehydration solution with glucose and electrolytes,
<v Speaker 1>b intravenous isotonic fluids, c intravenous broad spectrum antibiotics only
<v Speaker 1>or D bowel rest and observation. So that is going
<v Speaker 1>to be answered b intravenous isotonic fluids due to the
<v Speaker 1>combination of profuse, non bloody rice water stools, absence of fever,
<v Speaker 1>rapid severe dehydration, consumption of likely contaminated water, and rast shellfish.
<v Speaker 1>Even though we can't definitively say this, cholera should be
<v Speaker 1>high on your list of differentials. And with choloro we
<v Speaker 1>know to put a two between the H and the
<v Speaker 1>O to make H two O because the hygy old
<v Speaker 1>stuff involves H two oh. Including the treatment, we know,
<v Speaker 1>the initial and most important form of treatment before antibiotics
<v Speaker 1>or anything else is fluids. In mild cases, this can
<v Speaker 1>be with oral rehydration solution, but in moderate or severe cases,
<v Speaker 1>which is clearly evident in this patient, urgent administration of
<v Speaker 1>IV fluids is the cornerstone of treatment for reduction immortality.
<v Speaker 1>Answer A oral rehydration solution would only be recommended in
<v Speaker 1>mild cases, which this is not c Antibiotics are appropriate
<v Speaker 1>as an adjunct, but rehydration is the absolute priority and
<v Speaker 1>must precede antibiotic administration and d bowel rests in observation
<v Speaker 1>would be dangerous and potentially fatal. Spatial has severe dehydration,
<v Speaker 1>requiring immediate aggressive fluid resuscitation with intravenous isotonic fluids, making
<v Speaker 1>answer be the correct answer. Question three. A nineteen year
<v Speaker 1>old male presents the emergency department with a three day
<v Speaker 1>history of fever, headache. Myologist M malays two days ago
<v Speaker 1>he developed a rash on his wrists and ankles. He
<v Speaker 1>denies nause vomiting or abdominal pain. One week ago, he
<v Speaker 1>spent four days deer hunting in the wooded areas of
<v Speaker 1>North Carolina. Herport's checking himself for ticks each evening and
<v Speaker 1>recalls finding what he thought might be a small tick
<v Speaker 1>on his lower leg, although he is uncertain whether it
<v Speaker 1>was a tick or just debris. He has no significant
<v Speaker 1>past medical history and takes no medications on examination. He
<v Speaker 1>appears ill but not talk phytoscience. Temperature thirty eight point
<v Speaker 1>eight degrees celsius one oh one point eight degrees fahrenheit,
<v Speaker 1>heart rate one o two beats per minute, blood pressure
<v Speaker 1>one hundred and eighteen over seventy two. He's alert and oriented.
<v Speaker 1>A faint arithmatose macular rash consisting of two to four
<v Speaker 1>millimeters blanching pink macules is present on both wrists and
<v Speaker 1>ankles Bilaterally, the remainder of the skin is clear. Cardiovascular, pulmonary,
<v Speaker 1>and abdominal examinations are normal. Laboratory studies reveal platelets at
<v Speaker 1>one hundred and forty thousand, normal range being one hundred
<v Speaker 1>and fifty to four hundred thousand, and sodium one hundred
<v Speaker 1>and thirty one normal range being one hundred and thirty
<v Speaker 1>five to one hundred and forty five. Which of the
<v Speaker 1>vowing organisms is most likely the cause of this patient's
<v Speaker 1>presentation A Burellia berg de Ferry b Grini, Bacterium, Diphtheria,
<v Speaker 1>c Ricketsia ricketsii, or D. Campilowbackter jay juni. So the
<v Speaker 1>correct answer is c Ricketzia ricketsii. All right, So the
<v Speaker 1>question is asking for the most likely most likely causative organism,
<v Speaker 1>and our answer is c ricrick. But first let's start
<v Speaker 1>with while the other answer choices are incorrect, A Burellia
<v Speaker 1>bergdo ferry, which we did not go over today, but
<v Speaker 1>is an important differential as it is another tick borne
<v Speaker 1>disease and the causative organism in lime disease. And while
<v Speaker 1>the early presentation can be quite similar with the fatigue, myalgia, fever,
<v Speaker 1>et cetera, the cutaneous findings are usually different lime disease,
<v Speaker 1>and around eighty percent of patients will present with what's
<v Speaker 1>known as erythema migrants. This expanding araythematose lesion that begins
<v Speaker 1>at the tick bite site. Lesion is usually a single arithmatose,
<v Speaker 1>non painful, round or oval patch that expands slowly, and
<v Speaker 1>in some cases central clearing may occur, causing this bulls
<v Speaker 1>eye appearance. Unlike our patient who has multiple small blanching
<v Speaker 1>macules on distal extremities bilaterally not an expanding lesion at
<v Speaker 1>a bite site. B Crinibacterium, diphtheria or dip theory gray,
<v Speaker 1>as we know, will likely have a gray pseudo membrane
<v Speaker 1>mentioned in the pharynx sore throat, low grade fever, cervical
<v Speaker 1>and patanopathy with a bullneck appearance, cam Blowbacter jay junior
<v Speaker 1>answer D remember cg at camp Elobacter with the diarrhea,
<v Speaker 1>domino pain, cramping, mention of consuming undercooked poultry, drinking raw milk,
<v Speaker 1>none of which are mentioned here. So in this patient
<v Speaker 1>with fever, headache, characteristic macular blanching rash beginning on the
<v Speaker 1>wrists and ankles following take exposure in an endemic area,
<v Speaker 1>as well as the thrombocytopenia and hyponatremia on labs, we
<v Speaker 1>know in this case the most likely pathogen would be
<v Speaker 1>Rickettsia ricketsii or rick rick which we know by remembering
<v Speaker 1>Rocky Mountain spoty fever instead as Ricky Mountain spoty fever.
<v Speaker 1>Question four, Which of the following treatments should be started
<v Speaker 1>immediately in the patient mentioned above in the absence of contraindications.
<v Speaker 1>A trimethiprim, sulfomethoxizol, B doxy cycling, cmoxiscillin, d azithromycin, or
<v Speaker 1>E chlorinmphenicol. So that's going to be answered. B doxy cycling,
<v Speaker 1>So you have to know this for Rocky Mountain spotted
<v Speaker 1>fever for adults and children, doxy is going to be
<v Speaker 1>your first line med. The only alternative listed here would
<v Speaker 1>be chlorinmphenicol, although it's less effective and would really only
<v Speaker 1>be recommended if it has a history of a very
<v Speaker 1>severe adverse reaction to doxy. So remember the de monic
<v Speaker 1>rick got bit by a tick because he stood on
<v Speaker 1>the docks aka doxy cycling, and forgot to wear gloves
<v Speaker 1>and socks, And then I'll help you remember your answer here.
<v Speaker 1>Last question, Question five, a ten year old girl presents
<v Speaker 1>the emergency department with a four day history of fever,
<v Speaker 1>joint pain, and rash. She had a sore throat three
<v Speaker 1>weeks ago that resolved without treatment. Over the past four days,
<v Speaker 1>she has experienced pain that began in her left knee,
<v Speaker 1>then moved to a right ankle, and now affects both risks.
<v Speaker 1>She also reports a non itchy rash on her trunk
<v Speaker 1>that appears and then disappears on examination. Our temperature is
<v Speaker 1>thirty nine point one degree celsius one hundred and two
<v Speaker 1>point four fahrenheit, heart rate one hundred and fifteen beats
<v Speaker 1>per minute, and blood pressure one hundred and over sixty.
<v Speaker 1>Both risks are swollen, warm, and tender to pal patient.
<v Speaker 1>A faint pink rash with sharply demarketed outer borders is
<v Speaker 1>noted on the trunk and limbs, sparing the face. Cardac
<v Speaker 1>examination reveals a grade two out of six high pitched
<v Speaker 1>apical holosysolic murmur rating to the axilla. Laboratory studies show
<v Speaker 1>elevated inflammatory markers ESO, RNCRP and elevated anti streptolicin O tiers.
<v Speaker 1>Echocardiography demonstrates mitro regurgitation. Which of the following findings in
<v Speaker 1>this patient are classified as minor criteria under the twenty
<v Speaker 1>fifteen revised Jones criteria? Select all that apply A carditis, B,
<v Speaker 1>elevated acute phase reactants, c rithema, marginatum, D fever or
<v Speaker 1>E subcutaneous nodules, so that is going to be answered,
<v Speaker 1>B elevated acute phase reactance and D fever. So this
<v Speaker 1>patient's presentation is most consistent with acute rheumatic fever or
<v Speaker 1>r F supported by recent untreated group A strap infection
<v Speaker 1>and the presence of multiple Jones criteria, And the question
<v Speaker 1>is specifically asking which of the following findings in this
<v Speaker 1>patient are classified as minor criteria and if you remember
<v Speaker 1>the mnemonic answering this is easy. Remember Jones the fat
<v Speaker 1>penguin nomonic Jones being the major criteria and fat faat
<v Speaker 1>standing for minor criteria. Faat we know stans for fever, arthralgis,
<v Speaker 1>acute phase reactants, and too long pr which we can
<v Speaker 1>see answer B Elevated acute phase reactants and D fever
<v Speaker 1>fall under minor criteria, with the remainder of the answer
<v Speaker 1>choices carditis era athemum marginatum and subcutaneous nodules being classified
<v Speaker 1>as major criteria under the Joones demonic. All right, So
<v Speaker 1>that was your bacterial diseases. I hope that was helpful.
<v Speaker 1>Thank you so much for watching, and thank you so
<v Speaker 1>much for the support