Speaker 1: 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. Yo, there's lots of them, and
to focused on the high steel topics that are frequently
tested on bartonella, batchelism, chlamydia, cute roumatic fever, can pull
bactor jay Juni, as well as many others. Got plenty
of nomonics 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 and E O. You put
a two between the H and E O. That makes
H two 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 menifestations involves water. So
if you can remember H two oh, 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 cholera. Fibrio choler is a comma
shaped gram negative rod and again everything ties back to water,
just like we talked about before, and even with fibrio
rio rio, if you speak Spanish you may already see it,
but vibrio ends in real, which means river in Spanish.
So when you see vibrio rio, think river, think water,
think H two O. So where are people typically expose
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 namonic shellfish live in you
gott 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 flecks 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
a symptomatic cases depending on the strain that's involved. There
can be nause of vomiting and fever is actually uncommon
and the presence should prompt the search for concombinant 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 Straightford 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 and
severe cases from over ten percent to less than zero
point five 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 lactape,
which is water, electrolytes and sodium lactape. 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 H two. Oh. 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 cholera rioaka river and that's cholera.
Let's talk about lamydia next, specifically chlamydia trichomitis, 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 eurogenital tract,
leading to classic eurogenital syndromes such as eurethritis with mucoid
or watery urethral discharge and dysyria, serviceitis with vaginal discharge
or purulent endocervical discharge, and epididymitis with testicular pain and swelling.
There are extragenital manifestations depending on the zero type involved,
including conjunctivitis, pharyngitis, perihepatitis, 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 trachomatis goes untreated in FEMA, 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 Yueld association is reactive arthritis.
Chlamydia is actually the most common sexually transmitted pathogen linked
to reactive arthritis, so this connection is absolutely worth knowing.
Moving onto diagnosis nexts, which will be made with nucleic
acid amplification testing or naat net, a test which detects
the genetic material DNA or RNA of viruses or bacteria
by amplifying it to detectable levels through sample obtained. For chlamydia,
samples are typically obtained via a vaginal swab and female patients,
or a urine sample in male patients. One other important
thing to consider when conducting diagnostic testing is that Niceria
gannorea coinfection is common, so all patients with chlamydia trichomitis
infection should also be tested for Nicia ganorea as they
have similar clinical manifestations and coinfection is common. Finally, let's
talk about treatment. One med to commit to memory here
is going to be doxy cycling. Doxy is your treatment
of choice in non pregnant individuals. As compared with a zythromycin,
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 clamydia clamydia,
what word sticks out? Clam right? And where do you
find clams in a dock by the sea? Doc C cycling,
So anytime you hear clamydia, think about finding those clams
in a dock by the sea, and you'll remember your
first line med doc C cycling. 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 GNAT testing So for clamydia, remember your clams
on a dock by the sea being swarmed by gnats,
and you remember your first line med and diagnostic test,
and that's chlamydia. Let's talk about ganoia next, So gunnoia
infection with gram negative bacterium niceria gonorrhea, which you will
forever remember instead as ni Siria gadoreea, set of Nicicyria gounoriea.
Remember it as knie Syria gunoreea, as in the joint
the knee knee Syria gonoreea. More about that in a minute.
So in the US knee Syria gunnoreea. It's the second
most commonly reported commuticable disease. There's not a whole lot
to know here, and there is 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 as that's likely what will be
tested on. So in females will see service citis. This
can manifest as vaginal paritis and or mucopurulent discharge, and
just like in chlamydia, this can spread and develop into
pelvic inflammatory disease, which occurs in approximately ten to twenty
percent of females. With cervical GANNERRIEA, both males and females
will see eurethritis, so dysyria, urinary urgency, or frequency purulent discharge,
which is more common in males. This organism can also
affect areas outside of the genitalia ghanacoc conjunctivitis, which mainly
affects infants born to untreated mothers. Perihepatitis known as fits
you Curtis syndrome and disseminated infection can occur, and this
is the highest heeled thing to know about GONNERRIEA as
it's always tested on so Ganococcal infection can spread from
the initial site and up to three percent of patients.
Disseminated infection often leads to one of two clinical syndromes,
which is a triad of tenosinovitis, dermatitis, polyalthralgis or and
this is the one to know, purulent authritis, which can
involve the wrist or ankles, but most commonly the need
This vignette always seems to pop up on exams time
and time again. It'll be a young patient complaining of
dysyria and knee pain, recently engaging in unprotected sexual intercourse,
et cetera. 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 gonorehea again, remember it as knee
syria gonoreea, just to help you remember the purulent authritis
most commonly involving the knee. Don't forget it all right. Diagnosis,
just as in chlamydia, you're going to use GNAT 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 sef triaxone. As of the time
of this recording, sef triaxone is the standard of care
for treatment of gonerrhea and has the lowest rate of
ganococcal drug resistance. This may change in the future, but
as of now, no sef triaxon, which is usually administered
as a single intramuscular dose. With that being said, if
you're treating gonnerrhea, what other presumptive treatment should likely be considered.
That's right, Like we talked about before, chlamydia, chlamydia and
gonerrihea are unfortunate friends and often come together, So doxycycling
likely will be added to this regiment unless it's been
excluded through testing. So that's gonoriea serviceitis eurethritis possible to
progress to PID. Most importantly, know of the potential for
purilent arthritis, most commonly in the knee. Remember knee siri
gonerhea diagnose with NAT, treat with sef triaxone, and as
coinfection with chlamydia as common, doxy will likely be added
to your regimen. Next, let's talk about Bartonella. And while
there are a number of Bartnella species that can infect humans,
when we're talking about the exam, the species you need
to know is Bartonella hens lay which is the causative
organism for cat scratch disease. So Bartnella hens layan is
the most common form of Bartonellosis in the United States
and the one you'll be tested on. So Bartnella henslay
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 Bartnella
hens lay, and that's why this is called cat scratch
disease as cats serve as a natural reservoir for Bartnella
hens lay. By scratch or a bite from an infected
cat as well as exposure to cat fleas infected with
this species can lead to transmission. In humans. Most commonly
see this in young individuals, more than fifty percent of
cases in children younger than eighteen 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 limphatinopathy. Regional
limphatinopathy 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 in large
lymph nodes that will appear proximel to the site of inoculation,
so near the bite or scratch, there'll be tender arethema
of the overlying skin, usually appearing around two weeks after
the bite or scratch. So remember lymphat anopathy. That's the
highest yield thing to know for clinical manifestations. Nothing high
yield for diagnosis, generally a clinical diagnosis that can be
supported with zerol logic tests or biopsy treatment. Next, there's
one meth that you need to know, and that is ezythromycin.
Even though many patients will have resolution of symptoms without antibiotics,
the whole point is to prevent serious complications, which as
many as fourteen percent of patients will have diseminated disease.
So patients with mild to moderate disease with just lymphat
aopathy are going to get a five day course of exythromycin.
There are alternative cipro, etc. But focus on ezythromycin as
that's your first line. In patients with as seminated disease,
you'll usually add or a fampin too. Axythromycin main take
away for treatment though for your exam, I would just
focus on azythromycin. Okay, So cat scratch disease A few
high old things to know how to remember all of
those high old points. Well, this is cat scratch disease.
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 ack contains all of
the hild things you need to know. Starting with B
for Bartnella Henslay. Cat scratch disease is an infectious disease
caused by Bartnella Hensley. Next L, which stands for lymphat aopathy.
This disease is usually characterized by self limited regional lymphat aopathy.
Gotta remember that. Next, the A stands for xythromycin, which
is your first line med for most patients. See of
course stands for cats, as they serve as the natural
reservoir for Bartonella hensley. I. 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 hens Lay lymphat aopathy is xythromycin
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 Laustridium botulinum, a group
of gram positive rod shaped spore forming anaerobic bacteria. Let's
hit the high old 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 and these
sources of infection in each And because there's three sources
that do have high old 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 old associations, which we're
going to talk about now, starting with baby, which helps
you remember infant botulism, which happens when a baby swallows
sea bochulinum spores. Because infants have poorly developed gut flora,
these spores can actually settle, colonize, and release talks and
right inside the GI tract. In the US, 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
infect In just twenty twenty five, there was an outbreak
of botulism that was actually associated with 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 sea bochulinum infects wounds, puncture wounds,
et cetera. 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 have this exact question in school, So remember
black tar heroin. It's very specific, but it does come up.
Last is food born botulism, which you'll remember as bottle
because bottle helps remind you of canned or bottle foods,
which often contain preform boculinum toxin, an exam favorite. So
food born botulism is often seen with home canned foods, vegetables,
and fish, and the US higher rates occur Alaska native
populations due to the consumption of aged or fermented fish,
while in China it's commonly to home fermented tofu and
bean products. All right, So to tie everything together, remember
Baby's black bottle for the types of botulism and their sources.
Baby for infant botulism or sports colonized the gut, Black
for wound botulism with IV drug use, particularly with black
tar heroin, and bottle for food born botulism with improper
bottled or canned foods. Next, clinical manifestations, so Claustrinium botulinum
can cause muscle weakness or flacid paralysis by blocking the
release of acetyl coline at the neuromuscular junction. This happens
because the toxin cuts something called a snare protein, which
are what nerve cells need to release acetyl coline 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 visions, 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 d's of botulism, which are dilated fixed pupils,
diplopia which is double vision, dysphasia which is difficulty swallowing,
dysarthria which is difficulty speaking, and descending muscle weakness or paralysis.
So that's your clinical meniphesations. Remember the key here is
the muscle weakness and cranial nerve dysfunction. Focus on the
five d's 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 indubation for patients with respiratory failure,
but botulinum anatoxin 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 where spores
colonize the gut, Black for wound botulism with ib drug use,
particularly black tar heroin, and bottle for food born botulism
with improperly bottled or canned foods. Remember your five d's
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 anti toxin. That's botulism.
Moving on to Campelobacter specifically campelo Bacter J. Juny, which
is a gram negative, curved or comma shaped bacteria. Camplow
Bacter A juni, or CJ as we'll call them, is
a common food borne 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,
and 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 a 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 fifteen percent of adults. In children,
it's much more common, closer to fifty percent. 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 adominal pain
that radiates to the right aliac fossa 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 suspects CJ and
a patient with abdominal pain and diarrhea in the context
of risk factors for transmission somebody who is drinking milk
straight from the utter, 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 divies disease,
antibiotics can be used, typically as if the remycin is recommended,
fluoroquino loans 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
geon Berat syndrome. CJ is actually the most common precipitate
of geon Beret syndrome, so you need to know this.
Reactive arthritis, post infectious irriable bowel syndrome are other late
onset complications of CJ, but please focus on gion Beret
syndrome as this will very likely be tested on. All Right,
so there's a few high eel things to know for CJ.
Here's a quick way to remember the important details. When
you think of Camp low Bacter 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
trustee camp counselor at Camp Elobacter is grilling up some
food for the campers, and on the grill we see
a big old raw chicken. Since it's hot at camp elobacter,
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 Gyon beret syndrome. In his front
pocket there is a big oversized fake pen, like something
from a gag store, which helps us remember the pseudo
apenn dicitis commonly associated with his 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 CJ is warring helps you to
remember Gyon beret syndrome, the oversized fake pen in his
pocket represents pseudo apendicitis, and the diaper helps remind you
of the diarrhea often bloody, associated with camp Blowbackter Jay JUNI.
That's cj X. Let's talk about diphtheria. So dip theia
is an infectious disease caused by the gram positive Bacillis
griny Bacterium diph THEORYA or C dip theoria, and for
the sake of this lecture, it will now be called
CE dip theory gray instead of CE dip theory A.
Remember it as see 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 aaa Y. Remember that it will help you
get the exam question right and I'll explain why in
a minute. So ceed dip theory gray. 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 vaccina, but seed dip theory 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 dip thory gray, you can have a sore throat, malaise,
cervical impot andopathy. These patients can actually have some pretty
severe swelling of the neck. They can develop what's called
a bull neck where you have this massive swelling of
the tonsils, uvulas, cervical lymphanodes. And finally, the most important
finding and the 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
pseudo membranes. So at least a third of patients infected
with this organism will have these adherent gray what they
call pseudo membranes covering the pharynx, soft palate, nasal membrane.
These will often bleed if scraped, and the reason people
with dip theory 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 cellular debris lead to the appearance of
this gray, leathery adherent membrane. These pseudo membrane can also
dislodge and wind up in the baranchial 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 pseudo membrane. That's why
you will always call this seed dip theory gray. All right,
less important, but no, there is cutaneous disease which patients
may develop these unhealing sores or shallow gray ulcers. But
again focus on gray pseudo membranes in respiratory seed dip
theory gray all right. So for diagnosis and a patient
you suspect may have dip theory gray, you'll culture. In
PCR testing, diagnosis is a little bit involved. You first
start with a swab of the throat, naars or any
cutaneous lesion that demonstrates signs of infection. Then you send
them out for culture. Cultur will identify the Karni Bacterium species.
Then we have to determine if these species identified is
dune undone toxogenic, 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 is 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 seedp
theory gray on culture? Isn't that enough? Why do we
need to know if it's a toxic strain? Well? Determining
toxogenicity is important, one because toxogenic 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 a symptomatic carriers. The main takeaway is
here is toxogenic 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 DIP theory GRAY
treatment are airway antiitoxin and antibiotics. Although cultures and toxin
testing should be obtained for diagnosis, you do not want
to wait for confirmation before initiating a treatment. Therapy has
started immediately based on clinical suspicion. If toxogenic DIP theoryray
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 dip theory 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 antiitoxin is in a quine derived antibody
that's obtained from the plasma of horses imminized against diphtheria toxin,
so this antiitoxin binds to and inactivates the toxin. Not only.
The last A stands for antibiotics. Per up to date,
xythromycin is now the preferred agent. Luckily another A penicillin
and erythromycin used to be preferred and are of course
still used, but a xythromycin is preferred for dip theory
gray due to increased penicillin resistance and preferred over erythromycin
due to 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 dip theory Gray is prevention with immunization.
All right, So dip theory Gray. Infectious disease caused by
the gram positive Bacillis karini bacterium theory Gray. Remember sore throat,
cervical and fatinopathy, that big old bullneck and of course
the star of the show Gray, pseudo membranes that can
bleed have scraped. DIP theory Gray. Diagnose 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 as zythrope.
That's dip theory Gray. Moving on to acute rheumatic fever
or rf ARF, 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 brings us to
the highest sealed part of the 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 doctor T.
Duckett Jones, who first described the diagnostic rules for a
cue romatic fever in the nineteen forties. 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'll 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, et cetera carditis, so
we can see pericarditis. Myocarditis most commonly will see involvement
of the mitral and aortic valves, with mitrol regurgitation being
the most common Valvular legion. Next sitaham Korea, which is
a neurologic disorder consisting of a erratic, abrupt involuntary movements,
muscle weakness, et cetera. Erethema marginatum. This is a pink
or faintly red, non pruitic 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 demarketed outer
border and diffuse inner margin forming a continuous ring. And finally,
cutaneous 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
our You got to know those. The demonic for Jones
major criteria is Luckily Jones jo Nes. 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
you will help you remember your migratory polyarthritis. OH stands
for oh my heart, what you will help you remember
carditis mutual 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 arithmo 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 Sinnaham Korea. But I knew damn well.
On an exam, I would not remember what the heck
that stood for, So instead I just remembered it as shaky.
Because even if you remember Sidnaham Korea on an exam,
they're not going to say the patient presents with Sinnaham Korea.
They're going to say the patient presents with uncoordinated jerking movements.
So just remember the S as shaky, just to make
it easier. So remember the five manifestations of r F.
Remember Jones, J, O, N, E, S, J for joint
for the polyothritis, O for oh my heart for carditis,
N for nodules, E for arithemo marginatum, and S for
shaky aka Sinaham Korea. And then we have the minor manifestations,
which are going to be feverthralgia, which is joint pain
usually involving several joints. Elevated acus phase reactants, so most
patients with RF will have elevated inflammatory markers to increase
levels of E, s R and CRP and finally abnormalodies
on ECG specifically a prolonged PR interval, So again fever arthragia,
elevated acute phase reactants prolonged PR, which I used to
remember umber as fat as an faat so f for fever,
A for our thralgia, the second A for acute phase
reactants which are elevated and then T for two long
PR for your prolonged PR interval. So minor criteria again
is fat faat fever aarthralgia, acute phase reactants too long PR.
So how do we diagnose are f 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 a recurrent episode. Some criteria cannot be counted twice,
like arthralgia, and the minor criteria can't be used alongside
arthritis in the major criteria. But for example purposes, let's
keep the simple unfocused on the basics. So diagnosis is
made with evidence of a preceding gas infection. So this
can be a positive rapid strep test, a positive throw culture,
elevated or rising anti streptococcal antibody tighter, plus two major
manifestations or one major plus two minor. So again remember
for diagnosis, two major manifestations or one major plus two
minor are sufficient for diagnosis of an initial episode OFF
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 youat 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 aase strap. You do that with antibiotics, and the
preferred antibiotic is penicillin G benzethene, which is a long
acting intramuscular injection. Of course, if PENG isn't available or
they have penicillin allergies, there are alternatives, but definitely you
should know penicillin G for the exam. Now, there are
other treatments depending on what other manifestations are present. URF
associated arthritis, for instance, N SAIDs will be your first
line to proxy and ambiprofen. So for treatment, remember penge
and n sets to keep it nice and simple, penge
being the highest deal component. All right, ourf acute rhumatic fever,
it's tested on a lot. There's a decent amount of
information to know, but you remember the high yield stuff.
It's actually pretty easy. Instead of RF 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 old information you need to know for a
cute rheumatic fever. So picture this. You're at the Zoos,
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 bee, 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 ur, themo marginatum, and shaky fat.
For the minor criteria fever, arthralgia, acute phase reactants, too long,
pr penguin, I'll give you a second and think about it.
The first four letters are pe n G as in
peng or penicillin G, your first line medication, and then
finally gas, which helps you remember the infectious organism that
caused this whole mess in the first place. Group a strip,
so remember arf becomes barf as in barf Jones. The
fat penguin has gas. That's a cute rhumatic fever. Let's
talk about Rocky Mountain spotted fever next. So Rocky Mountain
spotted fever is a tick born disease that can be
fatal if not treated. In fact, prior to the introduction
of antibiotics, the fatality rate was as high as eighty
percent in some regions. More recently, with widespread antibiotic availability
and improved disease recognition, mortality rate has dropped to approximately
zero point one two point six percent. So who is
responsible for this terrible disease? Well, that's an organism by
the name of Rickettsia rickettsi, which is a gram negative
obligate intracellular bacterium named after the pathologist Howard Rickets. 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 rockets cii. And that's because you're going
to remember Rocky Mountain spoted 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 rickettsii. This is the only Ricketzial 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 nineteen oh six, 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 snowwater. So
Ricky Mountain spotted fever is usually transmitted via tick bite
and 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
rocketsia 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 US is the
derma center of Verabilis tick derma center and DERSNY 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 as a tick. Clinical menifestations next.
Early symptoms of ricky mountain spotted fever are non specific fever, headache,
as well as malaise, myalagias, abdominal pain, confusion. But the
main clinical menaphisation 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 and approximately eighty eight to ninety percent of patients.
It is uncommon at the initial clinical presentation, but it
usually pops up the third to fifth day of illness.
The hallmark is a blanching arithmatose 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 old part. You'll be tested on
the appearance of the rash usually begins on the ankles
and risks and spreads to the trunk. So remember when
we're talking about a ricky rash, the rash begins on
the risks 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 focus primarily on the
rash 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 serology
is obtained in the first few days are often falsely
negative and second infulmentate 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 immunofluorescent 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 thrombocytopenia, hyponatremia,
and elevation and serum aminotransferrace levels can all be seen
with a Ricky infection. Finally, we have treatment which is
very easy. You really just need to know one met
and that's going to be doxy cycling. Doxy is your
treatment of choice in both adults and children, even in
pregnant women. The only alternative, which is chlorinmphenicol, 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 wagh
for serologic testing. As we talked about before, Okay, so
you will never forget that Rocky Mountain spot of fever
is caused from the organism ricketsia ricketsia, because again you'll
remember it as Ricky Mountain spotted fever, super easy. But
there's other highield 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, ricketsi.
I got bit by a tick, which we know is
the vector for this disease. Stood on the docks, which
helps you remember doc cy cycling 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 spreads 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 tested on
clinical manifestation. If you can remember that little ryme, 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 tetanose, 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 Deatonnis is caused by the toxin producing bacteria Claustridium
tetani which is an anaerobic gram positive spore forming bacilline
which typically live in soil and surprisingly even present in
the gut of mammals. So these guys don't like oxygen.
They are 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 immunity, 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 deliveries with unsanitary cutting of the umbilical cord. Okay,
And then we have the final key predisposing factor, and
that's devitalized tissue. So a schemic or necrotic tissue as
we see in many infections, is an important predisposing factor
for developing tetanus. And why is that? Why can't tetani
grow in healthy tissue? While it's what we talked about before.
Tetani 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
a schemic tissue which has little to no blood flow.
So this low oxygen environment allows tetni 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 a schemic 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 localized tetanus
that involves only the cranial nerves, natal tetanus, and then
generalized tetanus, which is the most common, and that's what
we'll focus on. So generalized tetanus, you will have spastic
muscle contractions. Now, really quickly, I want to just talk
about why this disease causes these severe muscle contractions, so
Claustridium tetana can produce a horrible toxin called tetanospasmen. This
toxin blocks inhibitory neural transmitters like gaba and glysine, which
normally tell muscles to relax, and without the inhibition, alpha
modor neurons fire continuously causing severe, rigid, sustained muscle contractions.
So we'll see things like tristmas, which is present in
more than eighty percent of cases, involving these strong, painful
spasms of the meceder muscles and an inability to open
the mouth. That's why sometimes referred to as lock jaw
opis thoughtness, which is the spasm of the spinal extensors
leading to the severe arching of the back. Rhesis sardenticus,
which is also known as a sardonic smile, which is
caused by persistent face 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 tetanus exists, but they're not reliable at
low tighters and impatients who received antiitoxin. 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's been inadequately immunized. So a treatment
is multifaceted, including airway management, wound agreement. Adequate wound to
agreement is actually really important because tetani can persist in
wounds even after these patients are started on antibiotic therapy. Antibiotics,
which in most cases will be metronitasol penicyllerg is an alternative,
and then tetanus immune globulin, which is an antiitoxin that
binds to and can neutralize any remaining circulating unbound tetnos spasmin,
that horrible toxin we talked about before, And benzodiazepines like diazepam,
which are usually the first line madule used to help
control the muscle spasms. And ultimately the goal is prevention
with immunization with your tetanus vaccine. Once the 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
twenty eight year old unvaccinated male presents to the emergency
department with a three day history of sore throat, low
grade fever thirty eight degrees celsius one hundred point four
degrees fahrenheit, and difficulty swallowing. An examination, you note a
gray adherent membrane covering both tonsils and the posterior FHARINGX.
When you attempt to remove a small portion for culture,
it bleeds. The patient has prominent cervical and fatinopathy 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 throughat culture. Then start
antibiotics while awaiting results. C reassure and provide symptomatic treatment
only d initiates supportive care and observe for twenty four
to forty eight hours before starting antimicrobial therapy or E
arranged for ton select me to remove the pseudo membrane,
So that is going to be a administer DIP theory, antitoxin, intravenous,
antibiotic and airway management. So even if you have no
idea what disease is being referenced in the vignette, you
may recognize de gray adherent membrane being mentioned, which would
trigger you to remember DIP theory gray spelled with three a's,
and DIP theory gray should certainly be suspected in this
patient with the presence of a gray pseudo membrane that
bleeds with scraping, unvaccinated, low grade fever, prominent cervical infatinopathy,
and what empiric treatment should be started in patients with
suspected respiratory DIP theory Gray well the three a's, which
is why gray is spelled with three a's to help
you remember anti toxin, antibiotic, airway metam so for respiratory
DIP theory gray urgent empiric treatment with diphtheria antitoxin and
antibiotics 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 dip theory anti toxin, intravenous antibiotic and airway management
is the correct answer for this patient. Question two. A
thirty two year old woman presents the emergency department with
profuse watery diarrhea and abdominal cramping for the past forty
eight hours. She reports passing copious amounts of pale, watery
diarrhea that is non bloody and has a milky, cloudy
appearance with small white flecks. She reports severe thirst, lightheadedness
when standing, and is not urinated in over twelve 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 eight raw oysters at a
local market. She has no significant past medical history. Vital
science revealed tachycardian hypotensionation is a febrie. On examination. She
appears ill and lethargic, with sunken eyes, markedly dry mucous membranes,
and skin tentting. The that persists for over two seconds.
Her abdomen is soft with mild diffuse 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 answered b intravenous isotonic fluids due to the
combination of profuse, non bloody rice water stools, absence of fever,
rapid severe dehydration, consumption of likely contaminated water, and rast shellfish.
Even though we can't definitively say this, cholera should be
high on your list of differentials. And with choloro we
know to put a two between the H and the
O to make H two O because the hygy old
stuff involves H two oh. Including the treatment, we know,
the initial and most important form of treatment before antibiotics
or 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 immortality.
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 rests in observation
would be dangerous and potentially fatal. Spatial has severe dehydration,
requiring immediate aggressive fluid resuscitation with intravenous isotonic fluids, making
answer be the correct answer. Question three. A nineteen year
old male presents the emergency department with a three day
history of fever, headache. Myologist M malays two days ago
he developed a rash on his wrists and ankles. He
denies nause vomiting or abdominal pain. One week ago, he
spent four days deer hunting in the wooded areas of
North Carolina. Herport's checking himself for ticks each evening and
recalls finding what he thought might be a small tick
on his lower leg, although he is 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 talk phytoscience. Temperature thirty eight point
eight degrees celsius one oh one point eight degrees fahrenheit,
heart rate one o two beats per minute, blood pressure
one hundred and eighteen over seventy two. He's alert and oriented.
A faint arithmatose macular rash consisting of two to four
millimeters 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
one hundred and forty thousand, normal range being one hundred
and fifty to four hundred thousand, and sodium one hundred
and thirty one normal range being one hundred and thirty
five to one hundred and forty five. Which of the
vowing organisms is most likely the cause of this patient's
presentation A Burellia berg de Ferry b Grini, Bacterium, Diphtheria,
c Ricketsia ricketsii, or D. Campilowbackter jay juni. So the
correct answer is c Ricketzia ricketsii. All right, So the
question is asking for the most likely most likely causative organism,
and our answer is c ricrick. But first let's start
with while the other answer choices are incorrect, A Burellia
bergdo ferry, which we did not go over today, but
is an important differential as it is another tick borne
disease and the causative organism in lime disease. And while
the early presentation can be quite similar with the fatigue, myalgia, fever,
et cetera, the cutaneous findings are usually different lime disease,
and around eighty percent of patients will present with what's
known as erythema migrants. This expanding araythematose lesion that begins
at the tick bite site. Lesion is usually a single arithmatose,
non painful, round or oval patch that expands slowly, and
in some cases central clearing may occur, causing this bulls
eye appearance. Unlike our patient who has multiple small blanching
macules on distal extremities bilaterally not an expanding lesion at
a bite site. B Crinibacterium, diphtheria or dip theory gray,
as we know, will likely have a gray pseudo membrane
mentioned in the pharynx sore throat, low grade fever, cervical
and patanopathy with a bullneck appearance, cam Blowbacter jay junior
answer D remember cg at camp Elobacter with the diarrhea,
domino pain, cramping, mention of consuming undercooked poultry, drinking raw milk,
none of which are mentioned here. So in this patient
with fever, headache, characteristic macular blanching rash beginning on the
wrists and ankles following take exposure in an endemic area,
as well as the thrombocytopenia and hyponatremia on labs, we
know in this case the most likely pathogen would be
Rickettsia ricketsii or rick rick which we know by remembering
Rocky Mountain spoty fever instead as Ricky Mountain spoty fever.
Question four, Which of the following treatments should be started
immediately in the patient mentioned above in the absence of contraindications.
A trimethiprim, sulfomethoxizol, B doxy cycling, cmoxiscillin, d azithromycin, or
E chlorinmphenicol. So that's going to be answered. B doxy cycling,
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 chlorinmphenicol, although it's less effective and would really only
be recommended if it has a history of a very
severe adverse reaction to doxy. So remember the de monic
rick got bit by a tick because he stood on
the docks aka doxy cycling, and forgot to wear gloves
and socks, And then I'll help you remember your answer here.
Last question, Question five, a ten 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 has experienced pain that began in her left knee,
then moved to a right ankle, and now affects both risks.
She also reports a non itchy rash on her trunk
that appears and then disappears on examination. Our temperature is
thirty nine point one degree celsius one hundred and two
point four fahrenheit, heart rate one hundred and fifteen beats
per minute, and blood pressure one hundred and over sixty.
Both risks are swollen, warm, and tender to pal patient.
A faint pink rash with sharply demarketed outer borders is
noted on the trunk and limbs, sparing the face. Cardac
examination reveals a grade two out of six high pitched
apical holosysolic murmur rating to the axilla. Laboratory studies show
elevated inflammatory markers ESO, RNCRP and elevated anti streptolicin O tiers.
Echocardiography demonstrates mitro regurgitation. Which of the following findings in
this patient are classified as minor criteria under the twenty
fifteen revised Jones criteria? Select all that apply A carditis, B,
elevated acute phase reactants, c rithema, marginatum, D fever or
E subcutaneous nodules, so that is going to be answered,
B elevated acute phase reactance and D fever. So this
patient's presentation is most consistent with acute rheumatic fever or
r F supported by recent untreated group A strap 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 nomonic Jones being the major criteria and fat faat
standing for minor criteria. Faat we know stans for fever, arthralgis,
acute phase reactants, and too 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 era athemum marginatum and subcutaneous nodules being classified
as major criteria under the Joones 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