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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 doesnt 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, theyre 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 sheeps 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 its covered by a polysaccharide layer called

a capsule.

The capsule has pili, which are hair-like extensions that help the bacteria attach to

host cells.

Underneath the capsule, theres 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 AIgA.

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, whats 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 dont get enough blood.


Finally, meningococcal sepsis can lead to disseminated intravascular coagulation, or


Thats 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 doesnt 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

alcohol abuse.

Additionally, since the spleen plays an important role in immunity against encapsulated bacteria,

N. meningitidis infections are more common in people whove 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, theres 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 its the one typically given

to adults.

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 its rapidly started upon clinical suspicion,

the treatment can then be adjusted afterwards, as soon as the CSF culture

and antibiogram are available.

The Description of Neisseria meningitidis - causes, symptoms, diagnosis, treatment, pathology