Ants colour vision may help march towards robot technology


Well what we thought before was that ants
have only two photoreceptors to see colours, which gives them colour vision but very poor
colour vision. A bit more similar to your dog or your wallaby
which can see colours but see more on a relative scale, they see colours out of green, or bluer
or redder. They don’t have such a rich colour experience. What we found is we looked at the colour vision
system of ants and we found that an ant have actually three photoreceptors that see different
types of colours. Which gives them a colour vision system that
is not dissimilar to ours, so they have very good colouration. But interestingly what we don’t have is they
can see UV light, so they’re system is short wavelengths shifting from ours. They see UV,
blue and green light where as we see blue green, yellow and red light. One of the species we studied is night active,
so they actually operate on light intensities where you and I would be totally colourblind,
we only have one receptor, our rods, that function at night and so we can’t see any
colours at night. These animals, even in the middle of the night
will probably be able to see full range of colours. For us the interesting thing is that these
animals are really small, so they have a very small visual system and have an even smaller
brain, that has a very low capacity to process information. Yet when you look at the animal they are very
sophisticated, they can navigate on their own they are good decision makers. So how do they do it with such limited recourses. And that’s something that biologists and the
robotics world is really interested in. How you can make a miniturised system that
can make autonomous decisions. There are many examples of how biology have
inspired engineers to build better robots because it tells us how can you make short
cuts in your design. So you dont have the time to crunch all the numbers to find something
out but you just use those bits of information that are really critical to achieve a certain
goal. But that’s what animals have evolved to do
and that’s what they’re good at.

CMV infection after transplant

CMV infection after transplant


Cytomegalovirus, or CMV, is an enveloped double-stranded
DNA virus that belongs to the herpesviridae family. It’s one of the most common viruses to cause
severe infection in individuals undergoing transplantation of bone marrow or solid organs
like the liver or kidney. It can affect almost every organ in the body
resulting in encephalitis, retinitis, pneumonia, hepatitis, gastroenteritis, and of course,
transplant rejection. In the post-transplantation period, the recipient
is usually given immunosuppressive medication in order to prevent their immune system from
recognizing the transplanted tissue as foreign and causing rejection. However, one major disadvantage of this approach
is that the weakened immune system is unable to protect the body against pathogens like
CMV. CMV can be transmitted through blood and other
body fluids like saliva, genital secretions, and urine of an infected person; or from the
transplanted organ itself! During the primary infection, the virus usually
invades the epithelial cells, like those that make up the oral, GI, or urinary mucosa; and
starts to multiply. CMV damages the infected cells by breaking
down the cytoskeletons which maintain the cell structure. That results in enlarged cells with intranuclear
viral inclusion bodies, giving it the typical owl’s eye appearance. CMV also infects monocytes in the blood and
sets up a latent infection, which means that the virus remains dormant for long periods
of time. The dormant virus can reactivate at times
when the immune system weakens, causing disease. Most of the time primary infection occurs
years before the transplant with resultant reactivation of the virus during immunosuppressive
therapy. In about 25% of transplants primary infection
occurs which is usually much more severe compared to reactivation. In either case, the virus can spread throughout
the body, damaging various organs. The transplanted organ is almost always affected. This is because viral infected cells attract
an army of immune cells to the site, which in the process of killing the virus also recognise
the foreign transplanted cells and may attack them, causing collateral damage. If it spreads to the liver, it can cause viral
hepatitis, which is the inflammation of the liver. If the virus moves into the lower respiratory
system, it can cause pneumonia. It can also affect epithelial cells of the
GI tract, particularly those of the esophagus and large intestine, causing gastroenteritis. In rare cases, CMV can also affect the retina
causing retinitis, and the brain causing encephalitis. Symptoms usually begin 1 to 4 months after
the organ transplantation in the absence of antiviral prophylaxis. In the setting of prophylaxis the onset, when
it occurs, is usually within 6 months of discontinuation of prophylaxis. Depending on the organ transplanted, symptoms,
when they occur are generally accompanied by fever and malaise. Pneumonia can cause symptoms of cough and
shortness of breath. Gastrointestinal symptoms include pain and
difficulty while swallowing, abdominal pain, nausea, vomiting, and diarrhea. In addition, hepatitis can cause jaundice. Retinitis presents with blurring of vision,
dark spots in the visual field called scotomas, or even total blindness. Encephalitis presents with symptoms like altered
mental status, seizures, and weakness. Diagnosis of CMV infections involves isolation
of the virus from tissues and body fluids; polymerase chain reaction, or PCR, to detect
viral DNA, and serological tests like immunofluorescence assays to detect CMV specific antibodies in
the blood. Increased CMV-IgM titer may indicate acute
infection, and increased CMV-IgG titer indicates past infection. Specific DNA studies are more sensitive and
specific than antibody studies. As of now, there is no cure for CMV infections,
but they can be treated with the help of antiviral medications like ganciclovir, valganciclovir,
and foscarnet. Also, CMV IVIG, or intravenous immunoglobulin,
which contains anti-cytomegalovirus antibodies, can be given to help boost the immune response. Now, in high-risk individuals, like those
with a previous history of CMV infection, prophylactic antiviral therapy can be given
after the transplant to prevent reactivation. All right, as a quick recap… Cytomegalovirus, or CMV, is one of the most
common viruses to cause severe infection in transplant recipients receiving immunosuppressive
medication. It can affect almost every organ in the body
resulting in encephalitis, retinitis, pneumonia, hepatitis, gastroenteritis, and transplant
rejection. Symptoms vary based on the organ affected. CMV is diagnosed with the help of PCR and
serological testing of tissues and body fluid, and treated using antiviral medications like
ganciclovir, valganciclovir, and foscarnet; and CMV IVIG.

How Do I Know If I Have A Yeast Infection


Today I would like to answer a question that
I frequently get asked. How do I know if I have a yeast infection? Well, there are many ways I can answer this
question. One of the most intelligent ways to answer it is to say, let’s just see if
there are any particular causes which could have contributed to your yeast infection in
the first place. I think that’s quite a smart move. So let’s have a look. Have you taken an antibiotic in the past several
years or recurrent rounds of antibiotics? Have you been on the oral contraceptive pill
for any prolonged period of time? Do you have cravings for sugar? Have you had any other
medications? Have you been on any steroid based drugs like prednisone or cortisone for
a while or perhaps inhaled steroids for asthma? They’re called preventatives. These are all
quite pertinent questions. Do you feel worse in a damp surrounding? Perhaps you live in
a moldy sort of environment. Does it make you cough or wheeze? These are all important
questions to ask, you know, if you have a yeast infection. Look at the signs and symptoms of yeast infection.
Can you relate to any of these? Do you have any aches or pains in the body? Any digestive
problems? Fogginess in the head? Do you have any toenail fungus or jock itch or vaginal
thrush? That’s how you’re going to know if you’ve got a yeast infection. If you go to yeastinfection.org, you can see
a lot of the common signs and symptoms on one of my pages there. There’s a very comprehensive
page I’ve written about the signs and symptoms of yeast infection. But probably one of the
most intelligent things you can do is to go to my quiz on CandidaCrusher.com. Very, very
good quiz you will find online. In fact, it’s the world’s best online Candida quiz. So by
going there and you can just follow the 20 odd screens for man, woman or child and just
go through the screens and you’re going to find out whether there’s a low probability,
moderate or high probability that you’ve got a yeast infection. It took a long time for me to put this quiz
together and many, many thousands of people now have done this quiz. I’ve had some incredibly
good feedback, so that’s a very smart way to find out if you’ve got a yeast infection. One of the best anti-fungal products you’ll
find anywhere in the world is called Canxida. It took me six months to develop Canxida and
I’m very proud of it, and it’s now being taken up by quite a few people. We’ve had incredibly
good feedback from Canxida. It’s unlike any other product you’ll find of its kind on the
market. It’s sustained release and contains 11 of the best ingredients in it. So thank
you everybody for your exceptional feedback for Canxida. So don’t forget, if you really want to know
if you’ve got a yeast infection, go to CandidaCrusher.com and please complete my online quiz. That’s
how you’re going to find out if you’ve got Candida or not. Thank you for your attention.

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.