What is neonatal herpes? | Infectious diseases | NCLEX-RN | Khan Academy

What is neonatal herpes? | Infectious diseases | NCLEX-RN | Khan Academy


– [Voiceover] A pregnant woman
that’s infected with herpes and who delivers a baby with
open sores can give their baby Neonatal Herpes, Neonatal Herpes. And I’ve got a picture of a
baby here, and we’re going to go through the three different
types of Neonatal Herpes a newborn baby can have. The first type of Neonatal
Herpes that a baby can have is referred to as SEM Herpes, SEM Herpes. And the name actually helps us
remember what gets affected. The S refers to the fact
that the baby’s skin can have these herpes lesions or
sores, and these mainly occur wherever the baby has
skin tears, so skin tears. So for example, if the baby
was delivered with forceps, there may be tears on the baby’s scalp where the forcep was applied. And these places can get in
contact with the herpes lesions that a mother may have,
and they can cause the baby to have sores there like I’ve drawn here. Other than the skin, the
baby can also have herpes in the eyes, and we’ve already talked a little bit about this. Herpes in the eyes affects
the most central part of the eye called the
cornea, and so you’ll see sort of a lattice-like
or a, what’s termed, dendritic lesion on the center
or the cornea of the eye. And if it’s left untreated, this can actually lead to blindness. So that’s the E in SEM Herpes. The M refers to the mouth, and these will be your classic
coldsores, so your coldsores that can occur on the lips,
on the inside of your cheeks or even on the tip of the tongue. Now what I’ve hope you’ve noticed through these three different
systems that get affected is that none of them
involve the internal organs, so there’s no internal organ involvement, which makes this the least
severe type of the three we’re going to discuss. The next severe level of
Neonatal Herpes a baby can have is what’s referred to
as Disseminated Herpes, which as the name suggests
is disseminated more throughout the body, which now means that internal organs are involved. And the organ that’s most
commonly infected or affected is the liver, so I’m
drawing the liver over here, and I am purposely drawing it to be huge because the baby will have
the herpes virus spread here and white blood cells, so
I’ll make sure to write that this symbol refers
to the herpes virus. So the herpes virus will spread
here, and white blood cells will fight the herpes
virus here in the liver, causing the liver to swell with the incoming white blood cells and the fluid that results from it. So when your liver is
affected, the term for this is hepato, hepato referring
to the liver, megaly, hepatomegaly, which
just means large liver. And of the three types of
herpes we’re going to talk about here, this type of Neonatal Herpes has the highest mortality or
has the highest rate of death associated with it. And finally, the last
type of Neonatal Herpes is what’s referred to as CNS Herpes or herpes of the central nervous system, and that means that the herpes can spread to either the spine or the brain, and you have a different set of symptoms, depending on what part
of the CNS is affected. For the spine up here, what you’ll most commonly see are tremors. There are these tremors
that the baby will have. If you take a look at
their hands or their feet, there’s going to be a
very steady shake to them, which makes sense because the spinal cord gives off nerves that
control the rest of your body beyond the brain. Now in the brain though,
once we have this type of dynamic, where white
blood cells are fighting the herpes virus up there, you can start to make the baby tired. And so, they could be
in a state of lethargy, so I’ll draw some Zs right there because the baby’s going to sleep. And this is actually kind of a bad finding because what it indicates
is that the nerves that are in the brain that
are supposed to send messages to the rest of the body
or to keep the baby awake are being destroyed because
of the white blood cells fighting the virus there. Another thing you might
see is that the baby could have seizures that
result from this type of inflammation, so the
white blood cells fighting the herpes virus and causing inflammation, so I’ll write that term here
’cause that’s an important term to keep in mind, so there’s
inflammation that’s happening within the brain. And as a result of inflammation,
you’re going to have increased pressure in the brain. And the term for that is
increased intracranial, the cranium being the skull,
so intracranial pressure, so increased intracranial pressure, which actually has its own
symptom associated with it. You could get a bulging fontanelle
or multiple fontanelles, bulging fontanelles, and
fontanelles are just the soft spots of a baby’s skull that are still healing. Classically, there’s
the anterior fontanelle that sits at the top or
the vertex of the skull, and it’s usually very soft, and it’s within the shape of the skull. But sometimes, if you’re having increased intracranial pressure, it will bulge, and you’ll see it
actually as a protuberance at the top of the skull right here. And that’s an indication
that you have inflammation causing increased intracranial
pressure in the baby. And because the brain is
responsible for so much, one of the things that
makes sense that occurs because of CNS Herpes is that
this type of Neonatal Herpes is associated with the highest morbidity or the highest rate of
long-term complications that can include mental
retardation, cerebral palsy, or other types of neuronal
slowing that exists throughout life, which
makes it very important to catch a pregnant woman that is infected with herpes early on.

Prezcobix a Prescription Medication Used to Treat HIV Infection in Adults – Overview

Prezcobix a Prescription Medication Used to Treat HIV Infection in Adults – Overview


Prezcobix is a prescription medication used
to treat human immunodeficiency virus (HIV) infection in adults. It is a single product containing 2 medications:
darunavir and cobicistat. Darunavir belongs to a group of drugs called
protease inhibitors. It works by decreasing the amount of HIV in the blood. Cobicistat belongs to a group of drugs called
pharmacokinetic enhancers. Cobicistat helps to keep darunavir in the body longer so that
the medication will have a greater effect. This medication comes in tablet form and is
taken typically once a day, with food. There are many medications that can interact
with Prezcobix and either cause more side effects or can increase the risk of Prezcobix
not working against HIV. Even over the counter medications like antacids can interact, so
make sure to talk to you doctor or pharmacist before taking any medications (even over the
counter ones) with Prezcobix. Common side effects of Prezcobix include nausea,
vomiting, diarrhea, headache, and abdominal pain. You should call your doctor or pharmacist
if you experience a skin reaction like a severe rash. Like all HIV medications, Prezcobix will not
keep you from giving HIV to others. Always practice safe sex even if your partner also
has HIV

Herpes (oral & genital) – causes, symptoms, diagnosis, treatment, pathology

Herpes (oral & genital) – causes, symptoms, diagnosis, treatment, pathology


Most of the time, when herpes simplex virus
or HSV infects a person, there are no symptoms. In fact, it also usually moves from one person
to another in the absence of symptoms, so it can therefore it can move through a population
silently. Once in a while, though, it can cause symptoms, and typically those are in
the form of skin and mucous membrane lesions which can be divided into infections “above
the waist”—mostly involving the mouth and tongue, and those “below the waist”—involving
the genitals. There are two types of herpes simplex viruses—HSV1 and HSV2—both of
which are part of a larger family of enveloped double-stranded DNA viruses: the herpesviridae
family. Generally speaking, HSV1 tends to cause infections above the waist and HSV2
tends to cause infections below the waist, but there’s a lot of crossover because both
viruses can cause both types of infections. Although herpes is most contagious when there
are virus-filled lesions present, it can also spread by asymptomatic shedding which means
that herpes viruses can be in saliva or genital secretions even when there are no signs of
a cold sore or genital lesion. Typically, when herpes virus lands on a new host, in
other words a person that’s never had herpes before, it dives into small cracks in the
skin or mucosa and binds to epithelial cell receptors, which triggers those cells to internalize
the virus. Once inside, the virus starts up the lytic
cycle, which is where its DNA gets transcribed and translated by cellular enzymes which help
to form viral proteins which are packaged into new herpes viruses which can leave to
go off and infect neighbouring epithelial cells. HSV1 and HSV2 also infect nearby sensory neurons,
and travel up their axon to the neuron’s cell body to start up the latent cycle. The
sensory neurons of the face have their cell bodies in the trigeminal nuclei and those
around the genitalia are located in the sacral nuclei. So that’s ultimately where the herpes virus
settles in—for life! You see, the sensory neurons aren’t destroyed, instead, they
become a permanent home for the herpes virus, and from time to time, the herpes virus makes
a few viral copies of itself and sends those virus particles back down the axon so they
can get released and infect epithelial cells. Since the trigeminal and sacral nuclei serve
just one side of the face or body, herpes vesicles and ulcers develop on the ipsilateral
or same side as the affected nuclei. This can happen over and over again throughout
a person’s lifetime, with classic triggers being things like stress, skin damage, and
viral illnesses. Recurrent episodes are usually less severe than the primary infection, and
sometimes there are no symptoms at all. When there are symptoms, there might be a characteristic
tingling or burning sensation, called a prodrome, one or two days before the blisters appear. In oral and genital herpes, the primary infection
is most often asymptomatic. Having said that, in oral herpes when it does cause symptoms
it usually affects children and it causes lesions on the palate, gums, tongue, lip,
and facial area, as well as a fever and enlarged lymph nodes. The lesions themselves are typically
clusters of small, painful, fluid-filled blisters, that ooze and ulcerate, and then eventually
heal after a few weeks. In older children and adults, a common symptom is pharyngitis.
Most of the time, like primary infection, reactivation doesn’t cause any symptoms,
but when it does, the most common pattern is having a handful of blisters at the vermillion
border—the border of the lip—on one side of the face. These blisters are typically
smaller and heal over a week. With genital herpes, primary infection can
cause symptoms like ulcers and pustules which form on the labia majora, labia minora, mons
pubis, vaginal mucosa, and cervix in women and on the shaft of the penis in men. Like
oral herpes, most of the time reactivation doesn’t cause any symptoms, but when it
does, the most common pattern is to have a few blisters that resolve rapidly in about
a week. In addition to oral and genital infections,
HSV can also affect other areas. When it affects the fingertip or nail bed, it’s called herpetic
whitlow, and this might happen if the finger rubs up against an active lesion around the
mouth or genital area. Once it affects the fingertip, it’s also easy for it to get
carried over to other areas on the body to spread the infection—a process called autoinoculation. HSV can sometimes involve the trunk, extremities,
or head—a pattern that’s common among wrestlers because they have a lot of skin-to-skin
contact; and is therefore called herpes gladiatorum. Finally, individuals with burn injuries or
with atopic dermatitis can have really serious herpes infections in those areas, the latter
even has a specific name—eczema herpeticum. HSV can also affect the eye causing keratoconjunctivitis,
which is inflammation of both the cornea and conjunctiva. In addition to symptoms of conjunctivitis
which are pain, redness, tearing, and sensitivity to light, there can some classic signs of
corneal involvement like blurry vision and a branching dendritic lesion which looks a
bit like the tree-like dendrites of a neuron, which happens on the cornea itself, and this
pattern is classic for herpes infection. In rare cases, herpes viruses can spread to
the central nervous system and cause meningitis or encephalitis, typically affecting the temporal
lobe, in individuals of all ages. These can happen from a primary infection, but more
commonly happen during reactivation when some of the virus can escape into the bloodstream
and reach the brain. When there is brain involvement, a lumbar puncture often has specific findings
like an increase in red blood cells, increase in white blood cells, and elevated protein
levels. There are also some CT, MRI, and EEG changes that can help to make the diagnosis. HSV can also pass from a mother to a baby.
Rather than causing a congenital infection while the fetus is in the uterus, most of
the transmission happens at birth when the baby passes through infected maternal vaginal
secretions during delivery. Neonatal HSV causes three different patterns of illness each occurring
about ⅓ of the time. The first is skin, eye, or mucous membrane infection, where lesions
pop up 1-2 weeks after delivery typically at sites of damaged skin like the site where
fetal scalp electrodes may have been attached. The second is central nervous system infection
which typically causes lethargy, irritability, and even seizures 2-3 weeks after delivery
and can cause some of the same lumbar puncture, CT, MRI, and EEG findings as that in older
children and adults with HSV encephalitis. If not treated, both the first and second
type can transition into the third type which is disseminated infection, where herpes virus
causes sepsis and failure of various organs including the heart and brain. HSV can cause unique symptoms in immunocompromised
individuals who tend to have more frequent reactivation, more severe symptoms, and a
wider range of symptoms, like lesions in the esophagus or lungs. Herpes can usually be diagnosed based on how
the skin or mucous membrane lesions look, and can be confirmed with tests looking for
viral DNA, like polymerase chain reaction, an antibody response to the virus, or by growing
the virus with a viral culture. Although infections typically resolve without treatment within
a couple of weeks, there are antiviral drugs like acyclovir, famciclovir, and valacyclovir
that can be used topically or systemically to reduce pain and speed up healing. For recurring
episodes, these treatments usually work best if taken when the prodrome starts; in other
words, before the blisters develop, and high-dose intravenous antivirals may be given in more
severe, or life threatening situations. Alright, as a quick recap, most of the time,
herpes simplex virus 1 and 2 cause asymptomatic latent infections that set up in the trigeminal
and sacral nuclei for life, but sometimes they can cause symptoms like recurrent oral
and genital lesions. They can also cause more severe infections like HSV keratoconjunctivitis,
meningitis, and encephalitis, as well as neonatal infections which usually get transmitted when
a baby passes through infected vaginal secretions. Thanks for watching, you can help support
us by donating on patreon, or subscribing to our channel, or telling your friends about
us on social media.

Pneumonia – causes, symptoms, diagnosis, treatment, pathology

Pneumonia – causes, symptoms, diagnosis, treatment, pathology


Pneumonia is an infection in the lung tissue
caused by microbes, and the result is inflammation. The inflammation brings water into the lung
tissue, and that extra water can make it harder to breathe. During inhalation, air reaches your lungs
by traveling down your trachea, then it continues through the bronchi and the bronchioles and
ends up in the alveoli. The alveoli are tiny air sacs that look like
tiny clumps of grapes, that are wrapped up in a net of capillaries. This is where the majority of gas exchange
happens in the lungs. Oxygen leaves the air in the alveoli and crosses
into the bloodstream while carbon dioxide leaves the bloodstream and is then exhaled
out of the body. Now, now in addition to air, you’re constantly
breathing in other stuff, like microbes. But we’re usually good at protecting ourselves. For example, we have mechanical techniques
like coughing, a mucociliary escalator that lines the entire airway and moves out larger
bacteria, and macrophages that are nestled deep inside the alveoli and ready to destroy
anything that lands there. But sometimes, a particularly nasty microbe
might succeed in colonizing the bronchioles or alveoli, and when that happens – Congratulations! You’ve got pneumonia. Those microbes typically multiply and cross
over from the airways into the lung tissue, creating an inflammatory response. The tissue quickly fills with white blood
cells as well as proteins, fluid, and even red blood cells if a nearby capillary gets
damaged in the process. Now, there are lots of different pneumonia-causing
microbes. Usually it’s caused by viruses and bacteria,
but it can also be caused by fungi and a special class of bacteria called mycobacteria. In adults, the most common viral cause of
pneumonia is influenza, sometimes just called the flu. In adults, bacterial causes include streptococcus
pneumoniae, haemophilus influenzae, and staphylococcus aureus. There are also more unusual bacteria like
mycoplasma pneumoniae, chlamydophila pneumoniae, and legionella pneumophila, which don’t
have a cell wall and are well known for causing an “atypical or walking pneumonia” because
they often cause vague symptoms like fatigue. In individuals with a normal immune system,
fungi are a rare cause of pneumonia and often it’s regional – for example, there’s Coccidioidomycosis
in California and the Southwest – which you can remember because there’s a “C” in
both cocci and california, Histoplasmosis in the Ohio and mississippi river valleys
– “H” in Histo and in O”H”io, and Blastomycosis which are broad based budding
yeast which are in the east – you can remember that with the “east” in yeast. And the broad based budding refers to the
fact that under a microscope, when the fungi bud off of each other there is a broad versus
a narrow based. To round out the fungal causes in the US,
there’s Cryptococcus which is “cryptic” because geographically it can pop up really
anywhere. Now, one special fungal culprit is pneumocystis
jiroveci which is a risk for immunocompromised individuals. Finally, there’s mycobacteria which are
slow-growing like fungi, hence the “myco” in their name even though they’re still
bacteria. The most well known one is mycobacterium tuberculosis,
also just called TB. Pneumonia can also be categorized by how it’s
acquired. The most common, is community acquired pneumonia,
and it’s called that when a person gets sick outside of a hospital or healthcare setting. Next is hospital-acquired pneumonia or nosocomial
pneumonia, which is when a person gets pneumonia when they are already hospitalized for something
else. This type tends to be more serious because
sick patients often have a weakened immune systems and the microbes in hospitals are
often resistant to the common antibiotics. That’s because hospitals bring together
the bacteria that are often the most virulent – think great offense – as well as the most
resistant – think great defence. These bacteria are able to swap some of the
antibiotic resistance genes with one another. A well known example is Methicillin-resistant
staphylococcus aureus, or MRSA. Non resistant staph aureus can cause pneumonia
and other infections, but it can also be killed by common antibiotics like ampicillin. MRSA on the other hand is resistant to many
antibiotics and is therefore harder to treat. Another category of pneumonia is ventilator
associated pneumonia, which is a subset of the hospital-acquired pneumonia, but it specifically
develops when ill individuals are connected to a ventilator. Oftentimes, there’s a biofilm – which is
a mix of bacteria and sugars and proteins that can coat a surface – that forms on the
endotracheal tube. Individuals on a ventilator can’t cough
and are often quite sick already, so over time microbes can move from the tube directly
into the lung and cause a pneumonia. Now in addition to inhaling microbes there
are other ways to develop pneumonia. Think about this: you’re eating some french
fries, and instead of swallowing one, you accidentally breath it in. Informally we call that going down the wrong
pipe, but we could also say that you aspirated that french fry. Normally, you’d automatically gag and start
coughing, and work that french fry out of your lungs. These gag reflexes can be compromised, however,
by drug and alcohol abuse, brain injuries, or swallowing issues. So in these cases the french fry might stick
around in your lower airways. Now, of course, that french fry isn’t sterile,
there might be some microbes stuck to it. If those microbes infect the lungs and you
get pneumonia, we would call that this french fry pneumonia—just kidding—we call it
aspiration pneumonia. Aspiration pneumonia can also happen with
drinks, or even gastric contents, like after a bout of vomiting. Aspirated gastric contents can be particularly
nasty because the stomach acid can cause a chemical irritation in addition to the possible
infection. Another way we can characterize pneumonia
is by where the infection is. In bronchopneumonia, the infection can be
throughout the lungs involving the bronchioles as well as the alveoli. In atypical or interstitial pneumonia, the
infection is mainly just outside the alveoli in the interstitium. And in a lobar pneumonia, the infection causes
complete consolidation of a whole lobe of the lung, meaning that the entire region is
filled with fluid. The vast majority of these are caused by the
streptococcus pneumoniae. Usually, lobar pneumonia happens in stages. The first stage is congestion, and it happens
between 1 and 2 days. This is where the blood vessels and alveoli
start filling with excess fluid. The next stage is red hepatization, and it
happens between days 3 and 4. This is where exudate, which contains red
blood cells, neutrophils, and fibrin starts filling the airspaces and makes them more
solid. The name hepatization refers to the lungs
taking on a liver-like appears from the reddish brown color of the exudate. The third stage is gray hepatization, which
happens around days 5 to 7. In this stage the lungs are still firm but
the color has changed because the red blood cells in the exudate are starting to break
down. The last stage is called resolution, and this
happens around day 8 and can continue for 3 weeks. In this stage the exudate gets digested by
enzymes, ingested by macrophages, or coughed up. Pneumonia most often causes dyspnea, or shortness
of breath, chest pain, and a productive cough, meaning that pus or bloody sputum might come
up. Often there are also systemic symptom like
fatigue and fever. Diagnosis of pneumonia is usually made in
a person who’s working hard to breath or breathing quickly. A chest xray of bronchopneumonia typically
shows patchy areas that are spread out throughout the lung, in atypical or interstitial pneumonia,
the pattern is also often spread throughout the lungs but is often concentrated in the
perihilar region and looks reticular, meaning there will be more line shaped opacities visible
in a chest x-ray. In a lobar pneumonia, fluid is localized to
a single lobe or set of lobes. Another way to detect a lobar pneumonia, though,
is to look for dullness to percussion which suggests that there’s a lung consolidation. There’s also tactile vocal fremitus, which
is when you can feel more vibrations from a person’s chest or back after they repeat
certain phrases. This is because sound travels better through
the fluid-filled consolidated tissue than air-filled healthy tissue. Late inspiratory crackles may also be heard,
along with bronchial breath sounds, bronchophony and egophony. The treatment of pneumonia depends on the
type and severity of pneumonia. Since bacteria are the most likely cause antibiotics
are often prescribed. In addition, cough suppressants and pain medications
are often used to help with symptoms. Alright … as a quick recap. Pneumonia is an infection of the lungs that
results in air sacs being filled with fluid. The disease can be classified by being either
community-acquired, hospital acquired with some of those being ventilator associated
pneumonias, or aspiration pneumonias. Pneumonia can also be characterized by where
the infection is in the lungs. Bronchopneumonia is spread throughout the
lungs, atypical or interstitial pneumonia happens interstitium around the alveoli, and
lobar pneumonia usually infects an entire lobe of the lung.

The Unstoppable Epidemic Could Start in China | China Uncensored

The Unstoppable Epidemic Could Start in China | China Uncensored


On this episode of China Uncensored, the exceptionally dangerous thing China is
doing that could accidentally kill millions of people… and not just inside China. Hi, welcome to China Uncensored, I’m your host Chris Chappell. Bacteria. Basically the bad guys from the Matrix. Only real. And everywhere. A hundred years ago, outbreaks of infectious disease were fairly
common. But then better sanitation and the discovery
of antibiotics changed that. Which is how we can have a world as connected
as it is today, without this happening. “The most optimistic projection that USAMRIID
is willing to make for the spread of the virus is this. 24 hours. 36 hours. 48 hours.” OK, I know the movie Outbreak was about a
virus, and I’m talking about bacteria. But they can both kill people following the
same terrible pattern. Anyway, antibiotics have saved a lot of lives. But there’s a problem. Over time, bacteria can evolve resistance
to antibiotics. Which means you have to use stronger antibiotics. And when the bacteria become immune to that, you have to use stronger antibiotics. And so on. It’s like that episode of the Simpsons where
Springfield solves its pigeon problem with lizards that eat the pigeons. “What happens when we’re overrun with lizards?” “No problem, we just release Chinese lizard
snakes. They’ll wipe out the lizards.” “But aren’t the snakes even worse?” “Yes, but we’re prepared for that. We’ve lined up a fabulous type of gorilla
that thrives on snake meat.” “But then we’re stuck with gorillas!”
“No, that’s the beautiful part. When wintertime rolls around the gorillas
simply freeze to death.” But what happens when you don’t have the snake-eating
gorilla version of an antibiotic? Well, the world enters what scientists call
“the post-antibiotic era.” It’s a time when bacteria have evolved resistance
to all forms of antibiotics. The BBC says this “could plunge medicine back
into the dark ages.” Which is why I’ve come up with “Dr.” Chappell’s
Live Leeches. Guaranteed to suck out all the bad humors. So unless you’re in the leech business, this is something you really, really don’t
want to happen. Well, haha, it’s happening. “The very last line of defense, the last drug doctors used when all other
antibiotics failed, no longer works because bacteria have become
resistant to it things like surgery will no longer be effective.” The drug he’s talking about the last line of defense is called colistin. It was first introduced in 1959, but hardly ever used, even though it’s really effective against
bacteria. That’s because it’s also really effective
at destroying your kidneys. But it’s still useful in those rare cases
where all other antibiotics failed. Fortunately, since Colistin wasn’t used much, it also meant bacteria hadn’t built up resistance
to Colistin. Did you notice how I said all that in the
past tense? It turns out, Chinese farmers have been feeding
Colistin to farm animals for more than a decade. You see, low levels of antibiotics can help
fatten animals up, plus keep them alive in the really, really
unsanitary conditions of a factory farm. This unnecessary use of antibiotics is a very
short-sighted way of doing things, but it’s done all over the world usually with other antibiotics. But because almost no one else uses Colistin, it also means it’s cheap. Perfect for the poorly regulated pig farms
of China. Except, according to a report in the Lancet
Infectious Disease journal, this has led to a gene that grants immunity
to “the last line of defense.” Researchers first discovered it in 2013 when
they found E. coli bacteria that couldn’t be killed with Colistin in a pig on a farm
near Shanghai. Then, they found bacteria with colistin resistance
in supermarkets and slaughterhouses, and even in hospital patients. That’s right, it’s already spread to humans. And this new resistant gene discovered in
China is not in the bacteria’s chromosomes. It’s in the bacteria’s plasmid which means it can be easily passed around
to other species of bacteria. The transfer rate has been called “ridiculously
high.” In fact, this resistant gene already been
discovered in Malaysia, Laos, and now, Europe. The fear is this new gene will get passed
around along with other antibiotic resistant genes. That could eventually create a pan-drug resistant
bacteria. In other words, a bacteria that can’t be killed
by anything we throw at it. According to the authors of this report, “pan-drug resistance is inevitable and will
ultimately become global.” Doctors will “face increasing numbers of patients
for whom we will need to say, ‘Sorry, there is nothing I can do to cure
your infection.'” Now you might be asking, well why don’t we just make new, more powerful
antibiotics? Surely there’s some kind of gorilla-eating
shark, or shark-crushing meteor we can use, right? Well it turns out, making a new antibiotic is extraordinarily
difficult. It’s been 30 years since the last antibiotic
was created. Early this year, researchers at the Northeastern University
in Boston said they may have at last discovered a new one that could help push back the post-antibiotic
era. But it hasn’t gone through human trials yet. And it can only push back the inevitable. Every year bacteria become more resistant
to the antibiotics we have. The Centers for Disease Control and Prevention
estimates that by 2050, antibiotic resistant bacteria will kill 10
million people. Worst case scenario? A global epidemic that can’t be stopped by
any form of antibiotics. On the bright side though, this isn’t the first time something like this
has happened. In the early 2000s, a strain of staph infection developed an immunity
to an antibiotic similar to Colistin, and the gene was also on its plasmid. Scientists then had the same fears. In 15 years, there’s only been 14 infections
in the US. The difference, though, is that this time, the resistant gene could spread more quickly
because of Colistin’s widespread use on Chinese pig farms. One piece of good news is that the US doesn’t
import pork from China. In fact, you’re most likely to eat tilapia
imported from China. Which is safe, right? What, what’s that, Shelley? Tilapia feed premixed with colistin?! So what do you think? Is this the start of the post-antibiotic era? Leave your comments below and share this episode! Make it go viral! Thanks for watching this episode of China
Uncensored. Till next time, stay safe and healthy. Once again I’m (cough cough)

Bullet Ant Venom

Bullet Ant Venom


– So the other group of ants
[Dr. Corrie Moreau, curator/ants] that we have today are bullet ants.
[Dr. Corrie Moreau, curator/ants] – Why are they called bullet ants?
[Bullet ant, Paraponera clavata] – Well, they’re called bullet ants
[Bullet ant, Paraponera clavata] because their sting is so painful
[* causing excruciating pain, numbness & trembling] it feels like you were shot by a gun.
[* causing excruciating pain, numbness & trembling] – And you’ve experienced
this firsthand? – I have, just once, I’d like
to keep it that way. And so you can see they’re
actually quite tremendous ants, I mean, they’re really foreboding,
[* worker bullet ants are 18–30 mm long] they’re crazy big and they’re cool.
[* worker bullet ants are 18–30 mm long] – Are they the largest ant? – They’re one of the largest ants. There’s another genus called Dinoponera.
[Dinoponera, Dinoponera australis] In some ways larger.
[* females may surpass 30–40 mm in length] Not as painful of a sting, though.
[* females may surpass 30–40 mm in length] This is Paraponera.
[Bullet ant, Paraponera clavata] We’re studying the gut bacteria
actually in this group of ants. But we’re also
interested in the venom. And so what I was telling
you is part of the reason I brought them back
alive is that at one point I had tried to milk them, because
my colleague was like, “It’s because we weren’t sure if
we’d have permits to bring back alive.” – Yeah.
– You can just milk them. So I can show you how
I attempted to do it and I will tell you that it
didn’t work in the end. When I got the venom back
it was actually not usable. But let me grab my equipment. – It’s not every day you get to
milk a venomous ant. At work. – So this is our fancy equipment. So if you think about, like, how they milk the venom
from spiders, right? Usually they just have
them bite something and squirt the venom inside
and it’s the same principle. So again, we just have
our empty tubes, and we have a little
bit of parafilm, right, which is essentially just like
a waxy kind of paper-y thing that we can stretch
across the top of this. And we’re going to get them
to try to sting through the tube and deposit their venom
on the side of the tube. – Wow.
– Yeah. One thing I have noticed is, what’s really interesting
actually, is with these bullet ants, when you collect them in the
wild they’re incredibly aggressive. You disturb them at all, and they
just go into immediate attack mode. In fact in the field, if you
even like blow on them, you can physically
hear them stridulate, which is a way of communicating
between individuals. And now that they’ve been
in the lab for just a few days, they’re actually almost docile. And so I’m curious to see whether
they’ll even sting through this. But we’ll try. Yeah, see, this one stridulates. So now let’s see if we
put her abdomen up, yeah, she is depositing
her sting through. – Oh!
– See that? – Sting it! Sting it! – So you see, she’s got her sting out, this is where I don’t want
to lose control of her. She’ll try to sting through, oh, there, you saw that sting go? That’s huge.
– Yeah. Wow. Focus your anger. – We will try to get another one to sting
– Come on, ladies. – You look like a new victim,
raaah, let’s get her all mad. – Yeaaaah! Oh, she’s stridulating. – She’s actually kinda not
mad as much anymore. – They’re—they’re just
like, they’re like, “Corrie, we wanna hang out,
I thought we were cool.” – I know, that’s probably
exactly what they think. – Like, “Come on, Corrie,” “I read your latest paper about
climactic regional distribution” “of my sister species.” I don’t even know if that’s
what you’ve written about, I don’t even know if that—
those words even make sense. – You don’t read all my
scientific publications? – Um, I probably couldn’t
get through the abstract. Not—not just yours, but most. – I won’t take it personally. Oh, yeah, she’s got a very big sting,
so let’s see if I can get her to— – Yeah. Sting it. – So that’s how you milk a
bullet ant for their venom. So essentially, just getting them
to sting through this material, they have now
deposited their venom all over the top of this
and inside of that tube, so I can just shove
that in there and then take it back
to an analytical lab to look at what are the—what’s
the chemistry within the venom. Now, I’ve already told you that
that didn’t work so successfully, so in a sense, what we need to do
is dissect out the venom glad, and that’s where it
gets a little more tricky, because in this case, you
can see they’re big and— – Cranky. – Cranky. And they
don’t like to hold still. Do this under the microscope. Okay, so now, again, we’re
gonna just pull off her abdomen, oh God, these are some tough ants.
[* abdomen] Even tougher than the bullet ants.
– Wow. – So now we’ve got—
– You did it. – —her body separated
from her abdomen. I wanna just tease apart some
of the parts of the abdomen and then we can usually pull the
venom gland out through the sting. So I’m just gonna start
pulling apart the body, and since I don’t want to
rupture the venom gland, I wanna try not to stab too much. – Yeah, this is meticulous work, dissecting ants.
– Yeah. – What is the smallest ant that
you’ll work on under a microscope? – Oh, I’ll work on anyone. – Even the ones
that are so small that you can’t even see
them on the labels? – Yep, even those. I’ve had to
dissect out their guts, too. – How do you even get
forceps that small? – Suspense, right?
– Yeah, the pressure. – Yeah, nothing like having
to dissect on camera, too. As if it’s not hard enough, right? – Yeah, all the viewers are
at home, quietly judging you. They’re like, “Well, when
I dissected ants last—” – I was thinking they were biting
their fingernails in suspense. – Yeah, that too. – So at the one end, let’s see if I can put it
in a good orientation— you can actually
see the left side, if you look through
the microscope, you can actually see the sting hanging all the way out.
[* sting] – Oh yeah!
– It’s like a giant hypodermic needle. – Yeah. – And then starting at the
other end on the right side, we can actually start to see
those parts of the digestive system. So first you have the crop, right?
[* crop] So it’s that social food sharing organ,
which then transitions into the mid gut and then into what’s called the ileum
[* mid gut, * ileum] and then finally into the rectum,
[* rectum] and then alongside that is where the venom gland sits.
[* venom gland] – That’s amazing.
– Yeah, it’s really awesome. One of the things that’s cool
when you first open them up is that the contents within the gut, you can see fat and
you can see the trachea and all those other things,
and even within the gut, it’s either clear like it
almost looks like water, or sometimes you can see
things that look like waste, but within the venom sac,
it’s actually almost like oil. And so when you burst it,
it’s literally like oil coming out, not like liquid, like, you
know, in the same sense. – Cool.
– Yeah. – Nice.
– So now the question is, are you gonna hold
a bullet ant for 10 seconds? The Brain Scoop is brought to you by the Field Museum in Chicago It still has brains on it.

Sulfamethoxazole and Trimethoprim Treat Bacterial Infections – Overview

Sulfamethoxazole and Trimethoprim Treat Bacterial Infections – Overview


Sulfamethoxazole and trimethoprim is a prescription
medication used to treat bacterial infections of the urinary tract, lungs, intestines, ears,
and infections that cause traveler’s diarrhea. It is a single product containing 2 drugs,
sulfamethoxazole and trimethoprim, which belong to a group of drugs called antibiotics. These
work by stopping bacterial growth. Sulfamethoxazole and trimethoprim come in tablet and oral suspension
forms and is taken up to 4 times a day, with or without food. Common side effects of this
medication include diarrhea, vomiting, anorexia, and skin reactions like hives or itching.
Take this medication only if it is prescribed for you by health care provider. For RxWiki,
I’m Teresa Brucker.

Poliomyelitis diagnosis and treatment | Infectious diseases | NCLEX-RN | Khan Academy

Poliomyelitis diagnosis and treatment | Infectious diseases | NCLEX-RN | Khan Academy


– Diagnosis of Poliomyelitis is really based off of two things. So first of all you’re
going to want to think about what symptoms the patient is having. And the symptoms should
paint a clear picture of polio, so it should be like
oh, ok these are the symptoms, this should get you thinking about polio. To confirm the diagnosis, the next step you’ll take a look at is the lab values, or specific lab tests I should say, that will determine that
there is actually polio, or an active polio infection in the body. So first of all before we talk about the active polio infection, what are the symptoms we can see? Well the buzzword that you’re
going to encounter for polio is acute asymmetric, asymmetric, flaccid paralysis. So a patient is having an acute infection, it’s a sudden onset. The patient, and usually
we’re thinking of a child. In fact, the term floppy baby is often associated with a polio diagnosis. Or really any other flaccid paralysis. So in polio, it’s children less
than six months old that are the most commonly affected. Really anybody can be
affected, adults, children, but they are the most commonly affected. And they’ll appear floppy
because as you remember in polio, it’s the motor
neurons that are being affected. So you’ve got a motor neuron that innervates a muscle, so it provides energy to a muscle. And these motor neurons are damaged. And they may be damaged
in an asymmetric pattern. So you might have this motor neuron getting shut down by the polio virus, but this other motor neuron,
being completely active. So you’ll see an asymmetric pattern. So we’ve got acute, sudden onset, asymmetric and flaccid so
there’s really no innervation to that muscle so the patient is weak. The baby is weak and appears flaccid, so you get this floppy baby syndrome. I’m not really great at drawing babies, so I just want you to
picture in your mind’s eye a baby that’s just flopping on one side of the body, like their arm isn’t able to move and
that should alert you to this asymmetric paralysis. Now once these symptoms
have been identified, lab tests should be underway. And there are actually several
lab tests that you can really think about for this asymmetric paralysis. And all of them relate to
the pathway that the virus, the polio virus, is going
to take in the body. So the polio virus gets into the mouth, gets to the throat and can replicate here. It can also travel into the intestines, into the stomach and the intestines, and replicate in the small intestines. So it has two sites of replication. Then, the virus can actually
spread to the spinal cord, to the central nervous system. So now there’s three locations in which you can find the polio virus. So there are actually three
lab tests that you can perform to diagnose polio. So one, let’s go ahead and
erase some of this here, and reveal this. You can isolate the virus
from a throat culture. You can also isolate the
virus from a stool culture. And the virus can also be
isolated from the spinal fluid. So let me write that down,
remember you can get a throat culture, you can get a stool culture, and you can get it from the
cerebrospinal fluid, CSF. And this is usually
done with a spinal tap, where the doctor inserts
a needle into the spine, and withdraws some of this
fluid that can be found. This fluid surrounds all of
the central nervous system, it surrounds the brain, and it encoats the spinal nerve as well. So these are the lab tests,
three different tests that can be performed. And any of them will work. The cerebrospinal fluid
is the most accurate. If you can find the polio
virus isolated in this fluid, that confirms diagnosis
of Poliomyelitis, in fact, as a reminder, myelitis means
inflammation in the spine. So right there, that shows,
if you can isolate the virus, in this CSF, cerebrospinal fluid, then that confirms your diagnosis. But also because the virus can
be shed through the mouth and in the feces, you can
collect stool cultures or throat cultures as well. And stool cultures are one
of the cheapest methods and fairly accurate, more
accurate than throat cultures in determining if a person is
infected by the polio virus. So stool cultures are
fairly commonly used. Now once diagnosis is made, we need to progress to treatment. And unfortunately treatment is, well there is really no
treatment for a person who has polio, it’s really
symptomatic support. If a patient, for example has
their respiratory muscles, like the muscles like the diaphragm, if that is dysfunctional
and they can’t breathe, then they might need support
through a breathing tube, put a breathing tube into the
mouth to support the lungs. In fact in the old days,
let’s go ahead and scroll down while I show you this. In the old days, there was
this thing called an iron lung. And here’s a view of it right here, you can also see a patient sitting inside the iron lung in this picture. They have their head poking out, and this essentially
allows pressure changes to expand the chest cavity
and allow breathing. And this was before the
time of having ventilators. And this has since been long retired, but it still provides you
an idea of how serious the condition can be, and sometimes warrants
respiratory support. Now though there is no
treatment currently, for polio virus, there
is a way to prevent it, and that’s through a polio vaccine. Through vaccination
and through the efforts of the World Health
Organization and many other organizations that have contributed, eradication of polio is very real. The entire western hemisphere,
including the United States, North America, Europe,
are completely polio free. Now there are still cases in
the world where polio exists, but the widespread eradication
because of these vaccines has been considered one of the world’s greatest medical achievements. And hopefully in the future
polio can be completely eliminated by the widespread
use of vaccination.

Diflucan A Prescription Medication For Fungal Infections

Diflucan A Prescription Medication For Fungal Infections


Diflucan, the brand-name form of fluconazole,
is a prescription medication used to treat fungal infections. It is also used to prevent
fungal infections in people with a weak immune system. Diflucan belongs to a group of drugs
called azole antifungals, which work by inhibiting a fungal enzyme needed for the fungus to grow.
This medication comes in tablet and oral suspension forms. The oral form is usually taken once
a day by mouth, with or without food. Some of the common side effects of Diflucan include
headache, diarrhea, nausea, and dizziness. Do not drive or operate machinery until you
know how Diflucan will affect you. This medication is only to be used if prescribed by your healthcare
provider. For RxWiki, I’m Bethany Muhlstein.

What is trichomoniasis? | Infectious diseases | NCLEX-RN | Khan Academy

What is trichomoniasis? | Infectious diseases | NCLEX-RN | Khan Academy


– [Voiceover] Trichomonas
vaginalis is responsible for a sexually transmitted infection known as trichomoniasis and as we’ll talk about in a minute, the symptoms mainly occur
in women in the vagina. Now this STI is not caused by a bacterium, but rather a protozoan which is a more advanced
form of microorganism than a bacterium and this protozoan
specifically is a parasite and it exists mainly by eating cells that they destroy, so
eating cell fragments and this protozoan uses
these cell fragments or these pieces of cells for nourishment. Now they typically have
a pear shape to them, so I’ll draw this pear shape here. So this is their body, the cell body. These trichomonas, or you
can also refer to them as trichomonads have one cell to them, so this is the one cell pear body and they move around because
of these protein strands, these whips that they have, that are called flagella, flagella. And finally, one of the
other things you might see if you take a look at this
guy under a microscope, as we will in a minute, is the nucleus. So here’s the nucleus. Now because trichomoniasis is a sexually transmitted infection, we have to consider the
mode of transmission, or how does it commonly spread from one person to the other, and as the name sort of sugggests, this occurs only through vaginal sex and what makes this
infection very interesting is that the trichomonad
protozoan can’t survive anywhere else. So they can only live
within the urogenital tract. Now this means they can live within women, like in the vaginal
tract or in the urethra, or they can also live in men, but the tricky thing about that with men is that they rarely have symptoms. So they’re asymptomatic, which means that they’re
carriers of this infection. So they’re asymptomatic carriers that can spread this STI to women without even realizing it. So if we take a look at
this woman right here, and I’ve drawn here urogential tract so we’re taking a look
at a sagittal section or if we chop them in
half from head to toe down the middle through the legs, you can see here is the bladder that leads out the urethra. So here’s the urethra. And here’s the vagina, so the vagina. At the top of the vaginal tract is the cervix over here and this part that I won’t label for our conversation, because we won’t be talking much about it, this is the anus that
leads up to the rectum and the rest of the GI tract. So if a woman is infected
with trichomonas, they’re going to spread into the vagina and spread up the vaginal walls and we can take a look at
this on a larger scale here. Here are the vaginal
walls and we’re leading up to the cervix. Let’s say that the trichomonas is climbing up the vaginal tract using
its flagella right here. I’ll draw these green. And it latches on there. It’ll use this type of mechanism to whip itself upward and in doing so, it causes stress to the cell membrane that over time, as I’ll show up here, causes the cell to die, producing fragments
that used to be the cell that are scattered into the vaginal tract and eaten up by this parasite. Now your immune system will recognize this and in response to the trichomonas, white blood cells will be sent here to combat them and release toxins and try and engulf them and eat them to stop them from
killing cells in our body and as a result of this, we will get inflammation. Inflammation meaning more
cell death in response to the ones that have been
affected by the trichomonas as well as a fever and
other systemic responses and that causes irritation. If we have white blood cells
fighting the trichomonads within the urethra, you can get urethritis which will cause pain when you urinate and that’s referred to
a dys, meaning painful, urea, meaning urinations. So painful urination. The same thing happens
up here with the vagina as well as with the cervix, because you can get vaginitis as well as cervicitis, cervicitis. Irritation of these two will
then make sex rather painful, causing what’s referred to
as dys, again, meaning pain, pareunia, dyspareunia or painful sex. And as this battle continues,
you’ll have more dead cells, dead white blood cells,
dead protozoa falling through the vaginal tract out producing frothy, green discharge. And this also has a
characteristically bad smell or it’s malodorous. Over time this inflammation
can actually cause some pretty bad effects as well. In women, especially
those that are pregnant, chronic irritation or long-term irritation can cause them to deliver a
baby earlier than they should. So that leads to preterm labor. Also, long-term inflammation
can cause irregularities in cell formation or cell
division at the cervix, over time producing cervical cancer. The idea though is because women tend to have symptoms, we will
catch the trichomonads earlier on and we’ll treat
them as we’ll talk about. In men, there’s a greater concern though, because they’re asymptomatic. So one of the things that you can get with chronic inflammation
is prostate cancer which why, as we’ll see in a few minutes, why it’s important to treat
the symptomatic patient as well as their
asymptomatic sexual partner. Now, let’s move on and talk about how do we diagnose trichomoniasis? Well there are two main
tests that we can employ. The first is what’s
referred to as a wet mount, which is exactly kind
of what it sounds like. You take a swab of the vaginal tract. You take a swab. Let me
draw that swab right here. And if we swab the vaginal tract, we’ll get a sample of cells, mucus and hopefully some of
the protozoa as well.>From there, you put the
sample on the slide, so you put it on the slide. So there’s our sample and you take a look at
it under a microscope and this is what you’ll see. They’ll be some squamous cells. So this simple squamous
vaginal epithelial cells as well as these two
guys which are actual, microscopic views of these trichomonads. Now that you can see
here, there’s the nucleus, the pear shaped body and the flagella that are present here. The second test you can do
is a culture, a culture, or just try and grow out the
trichomonads on a petri dish. So here’s our petri dish over here and I’ve smeared our sample
from this swab right there and we’ll let it grow
over about five days. Then, what you’ll see here
are these trichomonad colonies that are growing on this petri dish. Okay, so now that we’ve
diagnosed trichomoniasis, how do we treat it? Well, here to we’re
going to use antibiotics and we can use the culture up here to determine what
antibiotics the trichomonads will be sensitive to. So say let’s put antibiotic
number one down there and antibiotic two up here. Over time we will see that antibiotic two wasn’t very useful. We still had these trichomonads grow even though we had it
on our petri dish here, whereas down here, antibiotic one created this space where no
trichomonads could grow. So that way we can have our culture determine what antibiotics
the trichomonads are sensitive to. So we can have our culture
determine sensitivity. And another important thing
about treating infected patients with trichomoniasis, is
that their sexual partner should be treated as well, because remember if
their partner was a male, they may not have any symptoms, but are at risk for developing
diseases down the line. Now, if we wanted to prevent
trichomoniasis all together? How do we achieve prevention? Well, the trick here like most STI’s is to block transmission and we do that by limiting the amount of direct contact during
these modes of transmissions. So, in this case, during vaginal sex use of a condom, so condoms,
can greatly reduce the rate of spreading trichomonads potentially from an asymptomatic carrier to a susceptible patient and because trchimonas
vaginalis can only live within the human urogenital tract, if we treated everyone that
was carrying this parasite, we could eradicate the
disease from the planet.