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Neisseria meningitidis, also called N. meningitidis or just meningococcus, is a gram-negative
round bacterium that causes meningitis in humans, as well as life-threatening conditions
like sepsis and disseminated intravascular coagulation.
Now, N. meningitidis has a thin peptidoglycan layer, so it doesn’t retain the crystal
violet dye during Gram staining.
Instead, like any other Gram-negative bacteria, it stains pink with safranin dye.
N. meningitidis typically live in pairs called diplococci, stacked side to side, so the pair
looks like a coffee bean.
They are also non-motile, non-spore forming, and obligate aerobes, which means that they
absolutely need oxygen to grow.
Finally, they’re catalase and oxidase positive - which means they produce both these enzymes.
N. meningitidis grows on a special chocolate medium called Thayer-Martin agar, which mainly
consists of sheep’s blood... err, yum?
Some antimicrobials, like vancomycin and nystatin are usually added to the Thayer-Martin agar,
to inhibit the possible growth of undesired bacteria or fungi, and maximize the growth
of Neisseria species.
However, other Neisseria species, like N gonorrhoeae, also share these properties.
So the maltose fermentation test is done to differentiate the two.
The gist of it is that N. meningitidis can ferment maltose, whereas N. gonorrhoeae cannot.
To check for this, a pure sample from the culture is transferred to a sterile tube containing
a mix of phenol red and maltose, which is then incubated at 36 degrees Celsius for 24
N. meningitidis causes acidic fermentation of maltose, and the resulting byproducts make
the solution turn yellow.
With N. gonorrhoeae, the solution stays red.
Now, N. meningitidis has a number of virulence factors, that are like assault weaponry that
help it attack and destroy the host cells, and evade the immune system.
First, N. meningitidis is encapsulated - meaning it’s covered by a polysaccharide layer called
The capsule has pili, which are hair-like extensions that help the bacteria attach to
Underneath the capsule, there’s the outer cell membrane, which has two opacity proteins,
called Opa and Opc, that also help N. meningitidis attach to host cells.
Additionally, N. meningitidis produces toxins - and the most important one is is IgA protease,
a toxic protein that this bacterium uses to destroy Immunoglobulin A – IgA.
IgA is an immune system protein found in the nasopharyngeal mucosa secretions that normally
osponizes invading bacteria - meaning it tags them so neutrophils can recognize and destroy
So IgA protease neutralizes the first line of mucosal defense!
However, not all IgA molecules get neutralized, so some N meningitidis bacteria are still
opsonized, and they get attacked by the neutrophils.
Within a neutrophil, N meningitidis gets wrapped in a phagosome, which is like a bubble inside
which reactive oxygen species, such as H2O2, are released to kill it.
However, N. meningitidis releases catalase, which breaks down H2O2.
Unfortunately, this translates as a win for N. meningitidis, which now takes over the
neutrophil and uses its energetic resources to multiply.
The neutrophil eventually becomes too full, bursting open, and releasing N. meningitidis
in the bloodstream, what’s known as meningococcemia.
Inside the bloodstream, N. meningitidis uses another toxin called factor H binding protein,
which disables factor H, a protein involved in the alternate complement pathway, which
plays a role in anti-bacterial immunity.
This allows N. meningitidis to spread, multiply and produce toxins in the bloodstream, causing
destruction of the capillary endothelial cells, which result into leaky capillaries.
N. meningitidis also has a cell wall antigen called Lipooligosaccharide, or LOS, which
can trigger a widespread immune reaction that results in sepsis - meaning blood vessels
dilate, so blood pressure drops, and vital organs don’t get enough blood.
Finally, meningococcal sepsis can lead to disseminated intravascular coagulation, or
That’s because the damaged endothelial cells release procoagulant-like tissue factor, which
makes clots form inside the blood vessels, and that depletes platelets and clotting factors.
Unfortunately, this leads to severe bleeding throughout the body.
If a lot of blood pools within the adrenal gland, local pressure increases, which makes
the adrenal blood vessels pinch shut.
This results in ischemia and eventually, necrosis of the various hormone-producing cells in
the adrenal gland, a condition known as Waterhouse-Friderichsen syndrome.
Insufficient production of adrenal hormones, especially aldosterone and cortisol, can further
worsen the shock.
Now, the good news is that meningococcus can actually colonize the nasal and pharyngeal
mucosa of many people, where it doesn’t do any harm so long as the immune system keeps
them in check, restricting their growth and preventing them from getting into the bloodstream.
Problems arise in individuals with weaker immune systems, like infants and the elderly.
Other immune-weakening conditions include an HIV infection, diabetes, malignancy, or
Additionally, since the spleen plays an important role in immunity against encapsulated bacteria,
N. meningitidis infections are more common in people who’ve had a splenectomy, meaning
their spleen was surgically removed, or in those with sickle cell disease who have functional
Most commonly, meningococcemia results in meningitis.
N. meningitidis is actually the only bacteria known to cause meningitis epidemically, most
likely in people living in close quarters like soldiers in a camp, or among larger communities
that share the same source of freshwater.
Meningitis happens when the bacteria move within the bloodstream up in the brain, and
use its toxins to break through the endothelial cells that make up the blood-brain barrier.
This way, it gets into the cerebrospinal fluid or CSF, resulting in meningitis.
People with meningitis typically present with headache, fever, and neck stiffness.
Symptoms of meningococcemia include a petechial rash, which are small, red or purple, spots
that often appear on the trunk and lower extremities, and with sepsis, there may be signs of shock,
like hypotension and tachycardia.
Diagnosis requires blood cultures to look for N meningitidis in the blood, as well as
a lumbar puncture for CSF analysis and culture.
Treatment relies on prompt administration of ceftriaxone.
Following the results of the antibiogram, treatment can be switched to penicillin G.
Additionally, prophylactic ceftriaxone, rifampin, or ciprofloxacin should be given to close
contacts of the affected individual.
Finally, it is recommended that people who are at risk of a meningococcal infection get
vaccinated, and these include babies, children and teens, adults with spleen issues, or those
who travel in places where N. meningitidis is endemic.
Currently, there’s two kinds of vaccines against N. meningitidis.
One is the meningococcal conjugate vaccine typically given to children and teens.
The other is is the meningococcal recombinant vaccine, and it’s the one typically given
Alright, as a quick recap, Neisseria meningitidis is a Gram-negative diplococcus, that grows
on Thayer-Martin agar.
It is non-motile, non-spore forming, oxidase positive, catalase positive, and it can ferment
Its virulence factors include the capsule, the pili, and proteins like Opa, Opc, IgA
protease and LOS.
Meningococcemia mainly causes meningitis, but it can also result in other severe conditions
such as sepsis, disseminated intravascular coagulation, and Waterhouse-Friderichsen syndrome.
Treatment with intravenous ceftriaxone, and it’s rapidly started upon clinical suspicion,
the treatment can then be adjusted afterwards, as soon as the CSF culture
and antibiogram are available.