Gram Negative Bacteria: Neisseria meningitidis
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Assalamu alaikom everyone, and welcome to a new ATP video. Today we’ll be talking about the gram-negative bacteria that
have a Diploccocus arrangement, probably the only pathogenic bacteria that have
this arrangement is: Neisseria! Neisseria has two main important species:
the first one is Neisseria meningitidis, and the second one is Neisseria
gonorrhea. In this video we’ll talk about the first one, Neisseria meningitidis. But
first let’s start with the shared features between these two species. First
of all they’re both gram-negative diplococci, and second of all, they are
both oxidase positive. For the lab stuff, Neisseria species grow on chocolate agar, but what is that? Do we actually use chocolate? No not really 😀 Neisseria
species can’t grow on blood agar because it’s inhibited by some of the elements
in the blood agar. However when we heat the blood agar these inhibitory elements
become inactive, and thus, Neisseria can grow. This heated blood is in fact the
famous chocolate agar! The other medium that we use for Neisseria growth is
Thayer-Martin agar, which is selective agar that only allows Neisseria species
to grow while inhibiting other organisms from growing. This is also known as VCN
agar, referring to the antibiotics used to inhibit the other organisms which are:
vancomycin, colistin, and nystatin. Now let’s move to the shared virulence
factors. First we have pili which allows attachment to mucosal surfaces. These
pili also display antigenic variation, which makes it difficult for our immune
system to target, because as you know they always change, they “camouflage”. Then we have IgA protease which will cleave IgA antibodies at its hinge point.
This facilitates Neisseria survival along the mucosal surfaces. Because if
you remember, IgA antibodies are found predominantly at the mucosal surfaces.
Since Neisseria meningitidis is a gram-negative bacterium, he has the
ability of producing endotoxin, but be aware the Neisseria endotoxin is a
little different than the original one that we already know about. It has a lipo-oligosaccharide instead of the
lipopolysaccharide in the previous examples. You can think of it as an
alternative version of the lipopolysaccharide found in other
gram-negative bacteria. Lastly you need to know that patients with C5 – C9
deficiency, also known as terminal complement deficiency, are more
susceptible to Neisseria infection, because these particular complement
proteins are essential to form the MAC, or also known as membrane attack complex, that is usually used to cause bacterial lysis. So when these proteins are
deficient the MAC won’t be produced enough, and that will cause them to be
more prone to infections. Now let’s talk about our main topic today: Neisseria
meningitidis. The first unique feature that distinguished Neisseria
meningitidis from other Neisseria species is that it’s the only one that
ferments maltose in addition to glucose, while other Neisseria species ferment
glucose only. You can remember that from the M letter in its name. Another
differentiating feature is that it has a polysaccharide capsule. This capsule
inhibits phagocytosis, and thus, it’s a very important virulence factor for this
particular species, in addition to the other valence factors that it has. A
quick note here is that patients with sickle cell disease or asplenic
patients, asplenic means they don’t have a spleen, are more susceptible to gain
Neisseria meningitidis infection or any other infection with
encapsulated organisms. Now let’s discuss the pathogenesis of Neisseria meningitidis infection. First it spreads by respiratory secretions like respiratory
droplets that come from sneezing, coughing, or kissing; thus, it spreads more easily in crowds and between people in close quarters like college dorm
residence or military recruits. Neisseria meningitidis colonizes the nasopharynx first, and he uses the pili to attach to the nasopharynx mucosal surface, and then it will use the IgA protease to escape IgA antibody, then he uses the
blood to spread through the entire body, and we call this the hematogenous
spreading. At the same time it will utilize the
polysaccharide capsule it has to protect it from phagocytosis, like we mentioned
before. Then Neisseria meningitidis will cause two main diseases: meningitis also known as meningococcal meningitis and/or disseminated meningococcemia. Let’s begin with meningitis. Once inside the bloodstream, Neisseria meningitidis
preferentially travels to the brain, then it crosses the blood CSF barrier and
enters the cerebrospinal fluid or CSF where it replicates and causes
inflammation of the surrounding meninges. Meningitis patient presents with
symptoms like headache, fever, neck stiffness, photophobia, photo means: light in greek and phobia: comes from Phobos or fear, and it means feeling of discomfort
in the presence of light, and lastly phonophobia, phono: comes from sound in
Greek and it means feeling of discomfort in the presence of loud sounds. Now let’s
talk about disseminated meningococcemia. when Neisseria meningitidis spreads
through the blood all over the body, it will release the endotoxin lipooligosaccharide and this will result in massive inflammation response that were
result in increased capillary permeability, and activation of
coagulation. When there’s extensive coagulation inside the blood vessel
throughout the body we call this condition: disseminated intravascular
coagulation, intra means inside and vascular means blood vessel, so inside
the vessels. This disseminated coagulation will consume the platelets
and results in thrombocytopenia. The thrombocytopenia will result in
increased tendency of bleeding, because you don’t have platelets and that will
happen throughout the body, and will present as petechial rash,
especially over the trunk and lower extremities. Lastly when there is damage
to endothelial cells and increased capillary permeability subsequently, this
will lead to leakage of blood to the interstitial space and this will
ultimately result in generalised hypovolemia, and clinicians call this:
hypovolemic shock, hypo means less and volemic from volume. Now we’ll talk
about Waterhouse Frederickson syndrome. When the inflammatory response
happens in the small blood vessels of the adrenal gland, it will result in
endothelial damage and rupture of the blood vessels. The DIC condition will
make it harder to form clot properly, because we’re using the platelets
somewhere else, and this will lead to leakage of blood into the interstitial
space of the adrenal gland. This along with the generalized hypoperfusion will
result in ischemia and necrosis of the adrenal glands, which eventually leads to
acute adrenal insufficiency, also known Adissonian crisis. Okay
I know it’s a lot, so let’s do a quick recap. Neisseria meningitidis infects a
patient through the respiratory secretions. Then Neisseria meningitidis
will colonize the nasopharynx, then it will disseminate hematogeneously and
release the endotoxin lipooligosaccharide, which will result in
massive inflammatory response throughout the entire body. This will lead to
increased capillary permeability and activation of coagulation inside the
blood vessels, and this will lead to DIC, which will consume the platelets and
lead to thrombocytopenia, and petechial rash, in addition to that, the increased
capillary permeability will lead to the blood leakage throughout the body, and
lead to generalized hypoperfusion or shock. When all that happens and results
in ischemia necrosis of the adrenal gland, we will have adrenal insufficiency,
or acute adrenal insufficiency, and we call this condition what? Waterhouse
Frederickson syndrome. For treatment we use a third-generation
cephalosporin: ceftriaxone and for the close contact of the affected patient we
use rifampin as prophylaxis. For prevention we have a vaccine for certain
strains, and these are: Group A and C. The vaccine we use is a purified capsular
polysaccharide which is immunogenic from these strains. Immunogenic means it induces an immune response from the body. However we don’t have a vaccine yet for
Group B, because type B strain capsule is not immunogenic.
So most of the infections all around the world are caused by type B strain
usually. That is all you need to know about Neisseria meningitidis. We hope
you enjoyed the video! Please give us your feedback so we can improve in the
next videos. And don’t forget to Like, share, and subscribe to get our new
videos and explanations. Thank you!

46 thoughts on “Gram Negative Bacteria: Neisseria meningitidis

  1. rifampin is it the rifampicine or the rovamycine?? because in algeria we usually use the rovamycine or spiramycine ..thanks for the videos they are really interessting .

  2. Wa alaikum assalam . Very helpful if you have not a problem we need more videos about microbiology you are the best

  3. I really don't know what to say 😢😢😢 thanks A lot
    Keep moving on …….
    To help me in my study

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