This video is on Neisseria meningitidis. Some defining characteristics. So Neisseria meningitidis is a gram-negative diplococcus, and that's an extremely unique image.
I'll show you that on the next slide, but you absolutely need to know what this looks like. It is a facultative intracellular, and it ferments both maltose and glucose, so another kind of unique feature that you probably should know. It colonizes the nasopharynx, and because of this, it is transmitted via respiratory droplets.
As the name implies, it is a major cause of community-acquired bacterial meningitis. But what's really high yield to know on exams is that it can cause a rare syndrome called Waterhouse-Friedrichsen syndrome, and we'll explain that later in this video. Here is the image of what this looks like, and because, again, this is so unique, you need to know that it is a diplococcus.
A lot of times on exams, they'll give you some buzzwords that are associated with the bacteria, but they're going to show you an image and it will really be the image that sells you on the fact that it's Neisseria meningitidis. So know that this is one of the diplococci. Now virulence factors are very important. Let's touch on these briefly.
The first is IgA1 protease. Now, what this does is it cleaves mucosal IgA. So the high yield thing to know for immunology and on exams is that if you see IgA, you want to think about mucosal surfaces.
So a protease that cleaves mucosal IgA thereby allows the bacteria to adhere to mucous membranes because IgA is involved in immunity specifically with mucous membranes. The other important thing is this the presence of a polysaccharide capsule. This prevents phagocytosis, and we'll talk about this in just a second because it's extremely high yield to know for exams. There's a lipo-oligosaccharide endotoxin.
So because this is an endotoxin that's very potent, it induces IL-1 and TNF-alpha, so you can get overwhelming sepsis. And then there are these adhesins. These adhesins promote bacterial attachment and prevent the activation of lymphocytes.
Now from this list, if I were to say which one is the highest yield. the one that you should spend the most amount of time understanding, it's the polysaccharide capsule. And specifically, you want to know that the polysaccharide capsule prevents phagocytosis, and in certain bacteria, like Neisseria meningitidis, you need to know something called overwhelming post-splenectomy infection, sometimes referred to as OPSI. So under normal circumstances, let's say you have a bacteria. When the body recognizes the bacteria, it undergoes a process called opsonization.
This is part of the complement cascade. Basically, a tag gets attached to the bacteria, and that tag is either IgG or C3b. Now, under normal circumstances, splenic macrophages will recognize the opsinin.
It'll recognize that tag, and then those splenic macrophages will be released, and they will go phagocytize the bacteria. So to be clear here, it's a two-part mechanism. Part one is opsinization, where the tag of IgG or C3b is applied to the bacteria.
And then part two is splenic macrophages identify that tag and go and eat up the bacteria and clear it from the body. Now, the problem with overwhelming post-splenectomy infection is that in certain patients who have a splenectomy, if they don't have a spleen, they cannot release those splenic macrophages. So you get all of these bacteria that get opsonized with IgG or C3b, but there are no macrophages to go and eat and clear those bacteria.
And so then what happens is those bacteria grow out of proportion and cause overwhelming systemic infection. Now it's the encapsulated organisms that allow the bacteria to survive post-obscenization. Because it has that thick capsule, the body essentially relies on this two-part process of obscenization and splenic phagocytosis. So specifically in bacteria with these thick capsules, and those bacteria are shown here, strep pneumoniae.
H. influenza, and N. meningitidis, which of course we're talking about in this video.
In these bacteria, if somebody is either asplenic because their spleen was removed, let's say they were in a car accident and their spleen was injured and the spleen had to be taken out, or if they're functionally asplenic, meaning they have a spleen but the spleen just doesn't work because of some other medical comorbidity, then those patients are at extremely high risk of sepsis and potentially death due to these bacteria that are encapsulated. Again, because these encapsulated organisms have to be removed through the two-part process of upsanization and splenic phagocytosis. So you need to memorize that N.
meningitidis, which we're talking about in this video, but also strep pneumoniae and also H. influenzae, these are encapsulated organisms that are very problematic for patients without a spleen. And they can develop this overwhelming post-splenectomy infection. Now the way to memorize this is the shin bacteria, S for S pneumoniae.
H-I for H influenza and N for Neisseria. And it's kind of easy to remember this because this is all about opsinization or opsonins, right? The tag that gets applied to the bacteria is called an opsinin. And so the way that I've always memorized this is opsinin sounds like opsi-shin. Opsy tells me the type of disease we'll see, right?
The overwhelming post-splenectomy infection. And shin tells me the different bacteria that I have to worry about, those encapsulated organisms. Opsy-shin sounds like opsinin, and this whole pathophysiology is all based around opsinins being tagged and then splenic macrophages clearing the bacteria.
So this is a very high yield aside, and of course we're talking in this video just about Neisseria meningitidis, but this also applies to strep pneumoniae and H influenza. So that is the major virulence factor that you need to know. Now let's get into the clinical features.
Now as again as the name implies, meningitis is in the name essentially. So this is a major cause of community acquired bacterial meningitis. And because of that, the symptoms that you want to look out for are what you see here. So fever, headache, photophobia, nuchal rigidity, and altered mental status. Now on exams, test writers really like to go after the physical exam maneuvers that you can use to elicit different types of nuchal rigidity.
And the two that show up most often are the Koenig's sign and the Brudzinski's sign. So in the Koenig's sign, as you see in this image, you do flexion at the thigh and extension at the knee. And either pain or inability to extend at the knee is a positive Koenig's sign. In Brudzinski's sign, you do neck flexion. And if neck flexion causes reflexive hip flexion, presumably due to that tension in the meninges, that's a positive Brudzinski's sign.
So on exams, they might give you... a little printout with vital signs and the only thing you'll see is an elevated temperature. And then they'll describe, they'll say on exam, when the patient's neck is flexed, there is reflexive hip flexion. That could literally be the only thing that they give you in the vignette. And you'd have to use that to start to think about different types of meningitis.
So understand the Koenig's sign and the Brzezinski's sign because test writers absolutely love these things. In addition to community acquired bacterial meningitis, the other disease process you want to look out for is something called Waterhouse-Friedrichsen syndrome. Essentially what happens here is somebody becomes infected with Neisseria meningitis and then they get adrenal gland hemorrhagic necrosis. That can lead to things like DIC and then physically you're going to see petechiae that evolve into purpura.
Functionally, this is like Addison's disease. Because it is adrenal gland hemorrhage, you're going to see if you look at labs or physical findings, what you would expect to see if somebody had Addison's. Again, the adrenal gland is hemorrhagic.
It's not working. So on exam, if they give you a patient who has symptoms suggestive of meningitis, and they have a petechial rash, you want to be thinking about as a follow up question or as a third order question, is this Waterhouse-Friedrichson syndrome. And the way that this will present on exams a lot of times is they'll give you somebody who has meningitis, and then they'll ask you what a potential complication is. The answer will have something to do with Waterhouse-Friedrichsen syndrome and it will have therefore something to do with adrenal gland insufficiency. So be on the lookout for Waterhouse-Friedrichsen syndrome.
Again, the radar needs to be going off if you see any type of meningitis plus a rash. Let's wrap up by talking about treatment. So treatment really not high yield as far as this bug goes.
You want to use a third generation cephalosporin or you can use rifampin. Nice here in meningitis, just to kind of summarize and close here, big things you want to understand are OPSI and how that works. Also, Waterhouse-Friedrichsen syndrome.
If you know those two things, I think you're in really good shape.