Transcript for:
Comprehensive Overview of Pneumonia

What's up, Ninja Nerds? In this video today, we are going to be talking about pneumonia. There's a lot to discuss. We'll go over the pathophys. We'll go over the different types of ways that we can classify pneumonia based upon the microbes, based upon how you acquire it, based upon the location. We'll talk a lot about that stuff. Then we'll go over some of the features and complications, really tying things together. We'll talk about diagnostics and finish up with some treatment. All right, so when we talk about first things first, first the kind of the pathophys behind pneumonia whenever patients develop pneumonia you have to think about the different mechanisms by which they can develop pneumonia obviously pneumonia is an inflammation infection of the lung tissue itself due to a particular pathogen this could be bacterial this could be be viral, this could be fungal, could be a lot of different entities, right? Most common, it's going to be bacterial though. But the ways that the bacteria get into the respiratory tract is important. Now, one of the ways that this can happen is usually aspiration, right? And so when I mean aspiration, this usually means that some type of secretion, whether this be like secretions within our oral pharynx, so some of the salivary secretions and things from our oral cavity, nasal cavity, all of those things kind of draining down, unfortunately, into the airway. So, oral pharyngeal aspiration is actually... tends to be one of the most common ones. I'm gonna represent that with this orange arrow here, where some of the secretions within this oropharyngeal portion here, instead of it going down into the esophagus, which is this green tube, it unfortunately goes right down into the blue tube, right into the airway, right? And whenever these pathogens that are within these secretions get socked up down here into like a little bronchial or alveoli, they have the ability to cause damage to the lung tissue, inflammation of the lung tissue, infect it, and then lead to pneumonia. Now, another mechanism besides oropharyngeal, secretion so let's actually put like a little one here so one is to represent the oral pharyngeal type of aspiration the second aspiration which is really nasty really scary is gastric right so someone has some type of situation here where some of their gastric secretions go right into their air tube this would be the second one so some type of gastric type of aspiration so if someone has gastric aspiration there could be a lot of different reasons for this particular problem but either way that's a way for the bacteria to to be able to move from parts of our esophagus, from our stomach, some of the natural flora within this area naturally to get into the lung tissue, cause injury, inflammation, infection, and then you got pneumonia. So my question for you is how would these particular pathogens that are coming from oral pharyngeal secretions or from a gastric secretions even get into the actual lung tissue? How does it get into the airway? That's the question, right? Because we should naturally have protective reflexes there to prevent us, right? You try to go and stab like the back of the tonsils of the throat, you're going to have gag reflex or something kind of gets in the proximal airway, agitates the tissue there, cough reflex. Or instead of oral pharyngeal secretions or things coming from our GI tract going upwards into the airway, they should naturally go down into the GI tract. So the normal swallowing process. Those should also all be intact. But what if a patient doesn't have those intact? So what if for some particular reason you have, right, for example here, we have our central nervous system. Here's going to be like the parts that control a lot of these particular reflexes. Let's say here's a lot of the different cranial nerves that are involved in some of the particular gag reflex, particularly within the cough reflex or particularly within the swallowing reflex. So now you have a disease process for whatever particular reason it may be. And what it's going to do is there's going to be some type of disease process or depression, whatever it may be, that's shutting down this cough, gag and swallowing reflex. So in these patients, the primary reason by which they aspirate is the loss of the cranial nerve. of the gag reflex or a decrease in the gag reflex, a decrease in the cough reflex, or a decrease within the swallowing reflex. And that basically prevents us from being able to prevent things from going into the airway and also prevent us from naturally letting things to go into the GI tract and then undesirably go right into the airway and create an opportunity for pneumonia. Now my question to you is what kind of things would actually cause this disease process where you inhibit this? Central nervous system diseases baby. baby? Nothing crazy to think about it, right? So one would be if you have any kind of CNS disease, think about this. It's not too complicated. You have a stroke, you damage part of the brain, seizures, Parkinson's disease, multiple sclerosis, lots of different diseases, which are going to lead to this inhibition of this pathway, ALS, right? The other one is any kind of CNS depression. And I think this is important also to be able to remember. So it may not be a disease process, but if you have patients who are on some some type of opioids, or they're also taking particularly maybe some type of benzodiazepine, or they're being sedated, or they're being paralyzed because of the ventilator, or they're having to be intubated, whatever, you're taking away that natural type of reflex from the central nervous system. So any type of CNS depression, would also be a big one. The really big ones that I really want you to remember here especially is alcohol use as well. So alcohol use is a big one here as well as any kind of sedation. So I would remember sedation or neuromuscular blockade, things of that nature. But either way, you're shutting down the cough, gag, swallowing reflex, allowing for aspirated material. Now here's the thing. This kind of things happen and then the microbe gets in. What are some of the microbes that we should really be concerned with whenever patients aspirate? There's a lot of different bugs, but the ones that I really, really want you to be thinking about, especially in patients with some type of underlying aspiration, the particular bugs that I would actually be somewhat concerned with, the microbes, if you will, that I would think about in this particular scenario. is Klebsiella. So one would be Klebsiella. This is a really, really nasty bug. This is very common in patients who are an alcohol user, have some type of aspiration from a CNS disease. Other ones would be anaerobes. So anaerobes are really, really nasty. When you want to know why anaerobes, because this will come from the GI tract. GI tract naturally is going to have a lot of anaerobic bacteria. And the other one that I would also consider here is going to be Staphylococcus. aureus. So the ones that I would actually be really, really potentially considering and patients who have some type of aspiration would think about Klebsiella, anaerobic bacteria, and potentially Staphylococcus aureus due to aspiration loss of or decrease in gag, cough, swallowing reflex due to CNS disease or CNS depression of some particular etiology. All right, boom, roasted. Next particular thing, what would be another reason why someone actually has a pathogen get into the actual airways, cause inflammation, infection, and lead to pneumonia? One is you inhale a really nasty kind of hardy pathogen. And what would that potential pathogens have to be? What would be some of the risk factors that would be associated with it? So let's say that you're in a population in a particular environment where there's a high kind of volume population, lots of close contact. In situations where there's lots of this close contact, lots of highly populated individuals, you're at risk for some particular types of pathogens that I think are worthy of remembering. And the ones that I would... really want you guys to potentially think about here in situations where there's lots of close contact a lot of people horded together within a very tight population is really be thinking about mycoplasma pneumonia this is a really big one mycoplasma i would also think about chlamydia and i would also think about influenza Think about an influenza as well. Okay? So these are really, really big things to be able to consider in these particular patient populations. Again, whenever you have a lot of close contact, there's an opportunity for a lot of these particular pathogens to be passed on via respiratory droplets and ha- and have the ability to cause a particular infection. So think about influenza, mycoplasma, chlamydia, sometimes Legionella as well. But I would put a plus minus with Legionella because the real particular thing that you really wanna remember here with Legionella. I'm just going to put here, think about water sources. I really want you to think about contaminated water sources, but this could still be in highly populated types of areas. Hot tubs, pools, showers, AC units within a lot of different hotels and things. like that. All right, but we got aspiration, we got inhalation, particularly within close contact airborne pathogens. But here's another one. Maybe it's not like a person to person transmission via mycoplasma, chlamydia, influenza, or lesionella maybe it's some type of like soil or dust exposure or like nasty droppings from particular animals that put these patients at high risk and it's dependent upon the geographic location which is very high yield so sometimes you can have a lot of fungal infections really really nasty fungal infections and the ones I want you to remember that they may test you on the exams they may say there was a patient who had potentially has pneumonia and he was just hiking in southwestern United States near California whenever you hear southwestern portion of the actual United United States, you want to think about something called coccidio mycosis. So what I'm going to put coccidio here. So think about coccidio mycosis. Whenever some people say they were, you know, doing a lot of spelunking, they were looking at different birds and bats and stuff like that near the Mississippi or Ohio river Valley areas. You want to think about histoplasmosis. So look for that on the clinical vignette. So histoplasmosis, particularly, think about that kind of buzzword terms, bird backdroppings, Ohio, Mississippi, River Valley area, or spelunking. And the next one is if you think about broad-based yeast in the east, right? This is going to be particularly more on the western side, I'm sorry, the eastern side of the United States. So if you see kind of like the southeastern, northeastern part of the United States, think about the broad-based yeast in the east. This is going to be blastomycosis. So think about blasto, okay? So these are the particular types of fungal infections that I would want you guys to be aware of and potentially... Airborne inhalation. So this would again be the particular microbes, but again when we talk about these particular microbes we're really talking about a fungal type of infection. So this would be a fungal. type of population that i would want you guys to think about all right so these are the big big big things that i really want you guys to be aware of for the potential etiologies first one aspiration second one inhalation now what if a patient let's say for whatever reason they don't have any particular problem with maybe an aspiration or an inhalation but they have something other kind of problem down here that has to do with their normal respiratory function because they have underlying types of diseases that are altering their natural immune system defenses such as mucociliary clearance. Let's talk about how that potentially could be another problem for patients that are developing pneumonia. If a patient does have no problem where they didn't aspirate something, right? They didn't have any situation where they inhaled like a hearty pathogen, like a fungal infection or a mycoplasma, chlamydia, lesionella, or viruses, then you want to be thinking about, is there something wrong with the actual anatomy of the respiratory tract? Is their defense system a little bit altered in a particular way? And so one of the big kind of defense mechanisms that our actual respiratory tract has is what's called mucociliary clearance. It's really interesting. Interesting concept. So you have cilia right there beating, beating, beating. They're usually beating things upwards. So if you have something kind of stuck within the bronchi or the trachea, generally these little guys will beep, beep, beep, beep, beep, beep the bacteria and mucus upwards so we can spit it out or swallow it so it doesn't stay within our respiratory tract. And sometimes we'll have little mucus globules that will trap the pathogen and again make it easy to be able to beat that bacteria up via the cilia. But let's say that there's disease processes that either really chalk up the mucus where the cilia now they can't handle all this mucus. They're trying to beat against this thick, thick mucus wall. Or there's damage to the cilia. Now you don't have the ability to move that mucociliary clearance or escalator. What are disease processes that would alter this and then lead to an opportunity for pathogens to kind of like get locked up in the lower airways, cause inflammation and infection, leading to pneumonia? One disease process that would really kind of increase this mucus production, think about it, guys. It's not really hard. What about cystic fibrosis? So think about potentially someone who has what's called cystic fibrosis or a They have the other disease, maybe it's not due to cystic fibrosis, but it's due to other particular things such as malignancies or such as primary ciliary dyskinesia, a lot of other inflammation of the airways, and this could be something like what's called bronchiectasis, bronchiectasis. And so in these particular situations, you know that this is gonna increase a lot of the mucus. If you increase the mucus, are the cilia gonna be able to beat the bacteria and all that mucus upwards? No, because now the mucus is gonna get so thick. Imagine that these like cilia, they're trying to be able to push like 2,000 pounds versus like 10 pounds. Now they got this big thing that they gotta try to move. That's not gonna allow for the bacteria to be easily cleared. Plus it's gonna create an opportunity for bacteria to not get moved. And so then what happens is some of these like nasty little pathogens, they're supposed to get cleared. Guess what? They kind of just stay in these areas and then they move down to like the smaller bronchioles and alveoli and create an infection. Other situations is maybe it's not an increase in the mucus. Maybe the problem is that their cilia is all jacked up. Maybe we inhibit the potential cilia. What if I damage the cilia? You know what kind of disease is what actually damaged the cilia what about copd right or maybe they don't have underlying copd but they are a smoker so sometimes patients who are like big big smokers we know that the tobacco also will cause destructive damage to the cilia and elderly individuals so as you get older you kind of lose some of that natural function of the cilia so elderly individuals will also have this high risk potentially here now we have an understanding of like these are the patient populations now what i want I want you to think about is what kind of microbes would potentially be present here because if our cilia isn't beating or the mucus is getting too thick, it creates an opportunity for the bacteria to not get mobilized. They stick down here and they cause pustiform and then they lead to infection, pneumonia. The potential pathogens that I would want you guys to really be aware of potentially within the situation here is there's a lot of them. One is I want you to be thinking about this very, very specifically with your COPD patients. So in these COPD patients, patients and patients who have COPD they're at very high risk for something called Haemophilus influenza and something called Marexella catarrhalis. These are really really nasty types of bugs that actually can accumulate here and cause nasty nasty infection. The other thing is that patients who are actually going to have cystic fibrosis and bronchiectasis, you know what's really bad with this one? With cystic fibrosis and bronchiectasis. These are at really high risk for a really nasty bug called Pseudomonas. So it's called Pseudomonas originosa. So I really, really want you guys to be able to remember that one as well. The next particular thing that I also want you guys to be thinking about is that patients who are elderly and who smoke, so smokers and elderly individuals, are at very high risk for Pseudomonas. High risk for another type of pathogen, particularly this one that I would want you guys to be thinking about is Legionella. Remember we talked about that one with the contaminated water sources? So contaminated water sources, but also be thinking about this as an atypical pathogen in patients who are smokers and elderly. So these are the big things that I really want you guys to be thinking about in this situation here. Alright, so let's say that there's a problem where, again, patient aspirated. They aspirated some of these particular pathogens into the airway because of the alteration in their natural central nervous system function. Or they inhaled a really hardy, nasty pathogen because of close contact. Or they were in a particular geographic location that put them at high risk for a fungus. Or they have some type of alteration within the normal defense system of the respiratory tract, like impaired mucociliary. clearance what if by some terrible situation we get a pathogen that gets into the bloodstream when it gets into the bloodstream it then spreads to the lungs oh that'd be a terrible situation but guess what patients who are iv drug abusers are very high risk from whenever they're using dirty needles you know on the skin you have a potential pathogen called staphylococcus aureus so in patients who are iv drug abusers they have this risk of taking this pathogen from dirty needles getting into the bloodstream and spreading to the lung tissue where it can then cause inflammation and infection. Obviously, they can get endocarditis and things like that as well, but this is a big one. So because of that, I really want you guys to be thinking about Staphylococcus aureus in patients who are IV drug abusers. The only other thing that I would potentially want you guys to think about with Staphylococcus aureus is not just from IV drug abuse, but sometimes, add this into your memory, don't forget this one, is that sometimes in a patient population where they just had the influenza, so they just got influenza, after they have influenza, their immune system system is a little bit kind of like not as protective, they're at high risk for Staphylococcus aureus. So post-influenza infections, these patients are at high risk for Staphylococcus aureus. Remember two things, IV drug abuse and post-influenza for Staphylococcus aureus. All right, but that's another route. That's another way that patients can develop pneumonia. They can aspirate, they can hail, they lose their mucociliary clearance, or they get it in the blood and it spreads to the lungs. Here's the other thing. What if the patient gets it spread from the blood, right? So it comes from the blood, hematogenously, gets into the lungs, or it's inhaled, it's aspirated, or there's an impaired mucociliary clearance, and it gets into the lungs. Either way, the same result is the same kind of thing here. We develop inflammation, infection, and then we develop pneumonia. What if, naturally, our immune system is, there's another altered, there's another defense. We have macrophages, we have our immune system that will come and try to be able to clear and get rid of the pathogen and get rid of all that kind of infected material. That's our natural kind of immune system. immune response. But what if a patient doesn't have a good immune system? What if for whatever reason whenever they come in exposure to that actual pathogen, their macrophages aren't doing very well, they try to recruit a lot of lymphocytes and neutrophils, but all of this is particularly depressed. And so their ability, all of these immune system cells to be able to work and clear this infection is inhibited because their immune system is depressed. They have a decreased function of their macrophages, particularly decreased number of lymphocytes would be the big reason. big one that I want you guys to think about. And again, just decrease activity of the immune system in general. What kind of patients would be really, really high risk? HIV. So I want you guys to be thinking about patients particularly who are immunocompromised such as HIV. Or what else? Maybe they have diabetes. Maybe they have CKD. Maybe they're alcoholics. Maybe they're status post transplant. Right? Or maybe they're on some type of immunosuppressant medication. What are some types of immunosuppressants that you guys would really want to be aware of that they may present on the actual exam? exam. Think about TNF alpha inhibitors. Think about your DMARs, any kind of things like that. Steroids would be a really big one. So any of those DMARs, any of the actual types of steroids would be really, really big things to think about. So these are the things I really want you guys to be able to be aware of. But now here's the thing. Microbes that patients are really high risk of when they're immunocompromised is also really, really important. So if a patient is immunocompromised, they are really, really at high risk for a lot. of different microbes and I think it's worthy of mentioning some of these. One of them, especially in these immunocompromised patients you want to be thinking about is pseudomonas. Pseudomonas is very high risk in these patients with underlying disease processes and immunosuppression. depression. The other one that I would really want you guys to think about here, especially in this patient population, is lesionella. Lesionella is another really big one. It's an atypical type of pathogen that we talked about with the contaminated water sources, elderly and smokers. The other big thing here is something called PJP, pneumocystic jereviscite pneumonia. This is a fungus. And the big, big population that you need to be aware of when they present this on the exam is patients with HIV, and I can't stress how important this is. a CD4 count less than 200. If they present that on the exam, they're trying to point you to this. It's a PJP that's causing the pneumonia. So a patient who's immunosuppressed with HIV, CD4 count less than 200, think about that particular pathogen. The next thing that I want you guys to be thinking about besides this one is also think about, you know, sometimes some of the viruses like CMV would also be another particular one to be thinking about and any type of really other underlying kind of nasty fungal infection. would be a big one. But the big ones I really think about is Pseudomonas, Legionella, PJP, CMV, and there could be a lot of other nasty ones as well. Potentially other fungal infections. But for right now, I'd say that these are the primary ones that I really want you guys to be able to remember. So let's stick with these. these ones as the primary ones here, okay? All right, so we have, I think, a pretty good understanding now of how patients can develop pneumonia. It could be from an aspiration problem, it could be from an inhalation problem, it could be from an impaired mucociliary clearance problem, it could be because it spread via the blood to get to the lung tissue, IV drug abusers, or it could be because they got it in from the blood or they got it inhaled, aspirated, impaired mucociliary clearance, any one of these mechanisms, but their immune system wasn't competent enough to clear the infection, okay? The last thing I want to talk about here is whatever patients we talk about, about pneumonia we talked about it with respect to pathophysiology mechanisms we talked about it with respect to microbes but we didn't talk about the acquisition of pneumonia so what I mean by this I want to briefly talk about it cuz we'll talk about later in the diagnostics or something called community acquired pneumonia and hospital acquired pneumonia it's really straightforward it's not hard community acquired pneumonia you acquired the infection the pathogen from the community which means it's a special type of bug streptococcus pneumonia is a really really important one that I can't let you guys forget so Whenever you have a patient who has what's called community acquired pneumonia, think about streptococcus pneumonia. That's going to be one of the most common types. Usually you'll see that with the elderly patients as well. So if you really wanted to add it into the list here for the elderly, I would also add in here streptococcus pneumonia. And this is going to be the most common cause of community acquired pneumonia in most patients. But they acquired it within the community or they got admitted into the hospital and with less than two days in the hospital. It has to be key. Less than two days in the hospital. hospital or out in the community they acquired the infection from strep pneumo. If it's hospital acquired there's a usually a very specific definition. So hospital acquired pneumonia is they've been in the hospital for more than 48 hours, more than two days, and now the bug changes from strep pneumo to a very very nasty resistant bugs that you can encounter in the hospital. And usually the most common type of HAP or hospital acquired pneumonia is a subtype called VAP, ventilator associated pneumonia. These are patients who have an endotracheal tube within their airway or some type of trach, like they have a trach or they have an endotracheal tube. happens is once they're in the hospital for greater than two days, they now have nasty bugs that they can actually form. And the two bugs that I really want you guys to remember here is going to be MRSA. So methicillin resistant staphylococcus aureus. And the other one is going to to be pseudo monas now in patients who develop ventilator associated pneumonia do they have an endotracheal tube you obviously need that and more than two days they have the actual diagnosis so they haven't have an endotracheal tube in for greater than two days or 48 hours what are potential things that put these patients at risk I think that this is one that I would actually consider remembering for the exam okay they may ask you this because it's relatively high-yield oftentimes when patients are in the ICU we give them particular drug to suppress their gastric acid production to prevent them from getting like stress ulcers. And so we may give them things like proton pump inhibitors. We may give them things like H2RAs, like famotidine. And what that does is that suppresses their gastric acid production so they don't get ulcers. But you know what else it does? It increases the gastric pH. Do you think bacteria survive better in a high pH or a low pH? They survive better in a high pH. And if that's the case, and for whatever reason, they reflux some of this around the edges of the endotracheal tube and it gets into the lungs, this can really cause a little nasty. pneumonia. So I really want you guys to remember that gastric acid suppression tends to be a very, very big potential cause for ventilator-associated pneumonia. The other one here is when patients are being sedated. Normally, if you have pathogens there, you cough and cough and cough, and you'll clear those secretions, or you'll get suctioned. If patients aren't getting actively suctioned, so there's decreased suctioning, decreased suctioning of potential secretions that can build up, form a film, and then lead to an infection. Or if you're having a lot of increased sedation. So when patients are on lots of sedation, they don't have a lot of that cough reflex to clear a lot of their secretions, or you know what else is really bad? If they're paralyzed. If you're paralyzed, can you cough? No. And so whenever you're either not suctioning out the secretions and getting them to cough, or you're taking away their cough and their natural kind of like mechanisms to clear secretions, such as an increased sedation or increased paralysis, for whatever potential reason, these potential things really increase the risk of ventilator-associated pneumonia. But you need an endotracheal tube for two days. days. And think about these particular bugs. For CAP, what I say, less than two days in the community or in the hospital, and strep pneumo. All right, let's move on to features and complications. All right, my friends, so a patient develops pneumonia, right? They have an infection of their lung tissue. Whenever they start having this infection of their lung tissue, what are some of the features, the complications? When they present this on the vignette, they're going to say, oh, this patient has pneumonia. No, they're going to say, okay, the patient's coming in and they're presenting with blah, blah, blah, blah, blah, blah. And then they may present some of their underlying lung disease that maybe puts them at risk for aspiration. They were in very tight control crowds. They were like hiking in southwestern parts of the United States. They have an immunosuppressive condition. They are an IV drug abuser. You get the point. So it's important to be able to understand what are those features and complications that really point you towards pneumonia. Now, remember I told you that I used the terms a little bit loosely. I didn't really mention them and discuss them in detail, but there's a typical pneumonia. And what I really mean by typical pneumonia is this is the pneumonia. that most people think about that are like a very specific bacteria subset. So this is like your streptococcus pneumonia, your Klebsiella, your Haemophilus influenzae, your Staph aureus, etc. All of those nasty bugs, Pseudomonas, and so on and so forth. When we talk about atypical pneumonia, we're talking about a very specific subset. Okay, so what I want to do is I want to write down here because I didn't mention them a ton But you talked about something called atypical Pneumonia and when I talk about atypical pneumonia really what I'm saying is this is a very specific subset I like to just break it down a little easy Mycoplasma Chlamydophilia and lesionella are the three atypical pathogens that I really want you to remember and so I'm not gonna write all this down I'm gonna abbreviate it to help you guys remember it as well I always remember atypical MCL mycoplasma chlamydia lesionella And then the other one to remember is your viruses. Remember I told you influenza, parainfluenza, CMV, SARS-CoV-2, and COVID-19. So there's a lot of different viruses out there that could also fit within that atypical umbrella. The key thing that you have to remember is that with atypical pneumonia due to mycoplasma, due to chlamydia, due to lesionella, or due to viruses, they won't present with a lot of the classic features that we're going to see with typical pneumonia. Oftentimes, the key ways to differentiate this subset is they present with upper respiratory tract infection-like symptoms. So that's really what I want you guys to remember for the atypical types of pneumonias due to these pathogens. Think about upper respiratory tract. infection type symptoms. What does that include? Well, it can cause headache. So think about headaches. Think about some type of like nasal congestion or rhinorrhea. You know what else is a really big one? How about a sore throat? So some type of sore throat. Sometimes here's the other big one that I would want you guys to remember, earaches. So I want to show you guys a potential picture here, especially with mycoplasma pneumonia. You know, Even with mycoplasma, it can cause a really nasty infection of the tympanic membrane and cause bullous meningitis. They may present this on the actual exam. So think about this when they say ear pain, atypical features like upper respiratory tract infection symptoms, go looking in that ear. This is what it would look like. All right, so that's some of the big things. Now sometimes upper respiratory tract infections, they may have very low grade fevers and myalgias and arthralgias. So you can also add those features in there as well. So think about a low grade fever. Okay. But these would be the big things to think about. Upper respiratory tract infections are really going to be the key things. So headaches, sore throat, nasal congestion, earaches with the bolus meningitis, and then again some low-grade fevers, myalgias, arthralgias, things like that. Here's the big, big stuff. With the typical Now everything else that we're going to talk about now is typical pneumonia. For the typical pneumonia, you see a lot of classic features. Whenever you have, let's say, here's this area of infection. So you have all of this part of the lung is all locked up with bacteria. it's all locked up with bacteria, it's going to cause a massive inflammatory type of process, which release a lot of cytokines, interleukin one, interleukin six, all these things that you probably don't really care about. But what they do is they really kind of work on your central nervous system and particularly at the level of the hypothalamus. And your hypothalamus says, Ooh, got to increase the body temperature so that the bacteria can't survive, baby. Ooh, I may have to make these patients shake a little bit due to this type of problem. So they may develop fever and rigors, very common features in patients with a typical pneumonia. And I'd be really important to remember here that it would be more of a high grade fever rather than a low grade fever. The other thing is as you lock up this kind of like alveoli, now look at this. Look at this. I'm going to lock up these poor little alveoli with pus, and I'm going to even maybe hit some of the bronchioles. Normally, whenever we have a Good measurement of oxygenation is dependent upon the ventilation of the alveoli and the perfusion to the alveoli. Let's say in this situation, the perfusion is normal. So the ability to move blood through the pulmonary vessels and pick up oxygen is good. But the ventilation in this situation is decreased. Because now I got to try to send oxygen into this locked up alveoli. It's going to stop right there. And I got to try to send oxygen down here. And now the oxygen has to try to move across these all socked up and pus-filled alveoli. Imagine how little oxygen is going to move into these alveoli. So what's the end result here? Because I have something called a low ventilation and a normal perfusion, I get something, a combined effect of these called a V. Do you guys remember this from our hypoxemic respiratory failure lecture? That whenever you have a VQ mismatch, this can lead to hypoxemia due to this alveoli being filled with pus. Here's the next thing. When a patient gets hypoxemic, what are the potential reflexive reactions that they may present on the vital signs? Let's come down and talk briefly about that. Here's another really interesting thing that they may present. So they may say, okay, the patient's coming in, they have high grade fever. they got rigors, they have low O2 saturation on their pulse ox, and then when they look at the vitals also maybe in the vignette, they may also say something else. And I want to just kind of explain why this usually happens because it's a pretty concept dependent type of thing. So whenever you have this locked up area that causes that VQ mismatch, right? So decreased ventilation to this portion of the lung. So whenever you mismatch that portion, decreased ventilation, good perfusion, it leads to hypoxemia. So low levels of oxygen within the blood. blood. So there's going to be poor oxygenation at this point here. Now we know that when that gets into the pulmonary circulation that'll go back to the left side of the heart right? We know pulmonary veins return to the left heart and whenever they return to the left heart you'll empty all that blood into the left ventricle. From the left ventricle, you'll take this blood and then send it outwards into your aorta and into the carotid system. Now, what you guys probably remember is that there's all these different chemoreceptors within the aorta and the carotid bifurcation there that pick up the sensation of oxygen or pick up the concentration of oxygen. And whenever the concentration of oxygen is low, it really activates these chemoreceptors and they send these impulses into the central nervous system. And the pneumodula goes like haywire and it says, oh, geez, the oxygen is low. I got to increase the blood flow out of my heart to the lungs to increase perfusion and I need to increase the respiratory rate to increase my ventilation. And so subsequently what happens is you'll notice that the patient may have an increase in their heart rate and they also may have an increase in their respiratory rate and depth. So they may present tachypneic or dyspneic and tachycardic hypoxemic. fevers and rigors. Okay. What else? If you think about this locked up area here, and let's say that some of this pneumonia is involving some of the actual bronchi and bronchioles, and you got some of this pus that's kind of filling into the lungs here. Here it's filling into the alveoli. It's involving some of the bronchi. Whenever you inflame the bronchi and bronchioles, they're really, really heavily innervated by a lot of different types of nociceptors and kind of like cough receptors. And so when you stimulate this because of a lot of inflammation, they're going to go haywire, send that information into your center. central nervous system. And your central nervous system will say, oh, okay, there's a lot of secretions and mucus within the airways. If I cough, I may be able to clear some of those secretions up. And so it then produces this intense cough reflex. But the cough should be what? Productive. All right. So that is going to be a big thing to think about here with these patients. So look for a productive cough filled with a lot of mucopurulent sputum, high fevers, rigors, hypoxemia, reflexive, tachycardia, tachypnea. which may look like they're breathing hard and working hard to breathe. The other thing here, key types of basic foundation stuff, is whenever you have, let's say, inflammation of the lung parenchyma here, and it gets close to involving the nearby pleura. If you agitate or inflame the pleura, guess what else there is near that pleura? Pain receptors, agitation receptors that are going to be able to pick up that sensation of inflammation and send that to the center. central nervous system. And these are somatic motor fibers that present with referred type of pain. And so they'll have pain in their chest whenever they take a breath. What is that called? Pleuritic chest pain. Very common in any type of pulmonary pathology to present with a pleuritic chest pain. So look for pleuritic chest pain, productive cough, hypoxemia, reflexive tachypnea, tachycardia, high-grade fevers, and rigors. Typical you don't really get a lot of that stuff. You know what I'm saying MCL viruses the other thing that I really want you guys think about here is These are really high yield concepts, these are your physical exam findings. So, you know when a patient gets a locked up portion of the lung, let's say here's a big old consolidation in their lung. When they have this consolidation, you go and you try to do your physical exam, there's big, big things that they may ask you. They may even ask you these questions, they may present it in the clinical vignette. Where you have this area of consolidation, so that's filled with fluid, that's filled with pus, that's filled with cells, all of those things is a really kind of fluid consolidation. Here's the best big term, I actually want you guys to get away. So, consolidative findings. So, consolidation. Consolidation is a big, big thing that they sometimes will ask you on the exams. So if you have a consolidation, there is this concept that air, right, whenever sound is moving through particular substances, if it moves through air and it moves through fluid, so between the two, which one would it actually move faster through and better through? It moves better and faster through the fluid than it does the air. And so it increases the intensity of a lot of physical exam findings. So one of the things that would actually be very, very important to consider here is you go to the chest and you percuss. If. if you really do that, you'll hear something called dullness to percussion. So you'll have a lot of dullness to their percussion. If you listen and you take the stethoscope and you put it over their chest and you have them perform some specialized types of activities where first thing you do is you have them say 99. And you're listening to their lungs. where the area of consolidation is. When that sound is moving through the consolidation, when they say 99, it's going to sound so dang clear. And it shouldn't sound clear. So because of the air, usually that's filling that space. So if they have what's called a able to hear. the 99 clearly during auscultation that's called a positive bronchophony that's a really big one the other one is that sometimes you'll have the patient say e and when you say e whenever the sound moves through that consolidation it really kind of amplifies it and changes to where it can sound like a so if it goes from e to a that's a consistent with a consolidated finding so we call that positive e golfing remember e and it go off in the e going to a egophony. Okay, the next thing here is that sometimes we can have them whisper. And so when you're normally having them whisper, you're like, one, two, three, one, two, three. What that will do is you shouldn't be able to hear that really at all in a patient who has all air-filled lungs. But if you have a consolidation, that sound's going to move really, really easily and you're going to be able to hear it relatively well. So if you can hear one, two, three when they whisper very, very easily, it's consistent with a consolidation. So it's called whispered pectilarquy. I'm not going to spell that out. out because I'll probably butcher it. The next thing that I also want you guys to consider here is if you do something called tactile fremitus. You take the hypothenar immanences and you put it on the area of where the consolidation is. Normally, vibration that's moving from the sound waves, moving through their airway, through the pleura, through the chest wall, onto your hypothenar immanence is kind of dependent upon air, right? But also, the fluid that it actually is moving through or the substance that it's moving through. When that sound waves move through a flow of fluid consolidation, the actual vibrations are intensified. And so you'll feel that way more intensely in a patient who has a consolidation in the nose with normal lungs. And we call that increased tactile fremitus. So they will have increased tactile fremitus. Alright my friends, these are big, big findings that I would really don't forget for your exam because they will probably ask you this as consolidated findings. Okay, so we have these as the features of typical pneumonia. And here's what's the scary thing with pneumonia. When patients develop pneumonia, they can develop a couple associated complications. So let's say here we have a pneumonia in this left lower lobe. Left lower lobe is all locked up with bacteria and pus. Well, that's going to cause a localized inflammation. So the capillaries are going to become leaky. They're going to become vasodilated. and fluid's going to start leaking out into the pleural space. If the fluid leaks into the pleural space around that area of a pneumonia, what is this called? It's called a paranemonic effusion. Sometimes, though, it can really get locked up, and actually some of the bacteria, so sometimes you know what can happen is you can have some of the fluid here, but some of the bacteria... actually kind of spreads contiguously into the space and makes it really loculated type of appearance. And so you can get two potential complications. One is you have a sterile inflammation around the pneumonia and one is you have a lot of inflammation with a lot of loculated bacteria and pus. pus within the pleural cavity. What are these called my friends? This is called first one, a paranemonic effusion. A paranemonic effusion. We talked about this in the pleural disease lecture. You guys remember that right? And then the other one, this one here where there's a loculated type of a pus and infection within the pleural cavity spreading from a localized area of pneumonia this is called a empyema. Empyema these are scary complications from this disease okay so empyema here, perinemonic effusion here. Alright what else can happen here? The other really big thing here is that sometimes if you get like a lot of anaerobes and staphylococcus aureus or klebsiella. Remember I told you that anaerobes, klebsiella, staphylococcus aureus, aspiration. In those situations, what can happen is you can have like an infection here, right? But then the bacteria get really smart, especially anaerobes. And those anaerobes... start kind of walling off the bacteria. And then you can have this infection here where you have this big, big cavity filled with, let's just kind of make it all nasty here, all this pus and bacteria here. What is this called? When you have this cavitation in the lungs where there's actually the ability for the anaerobes or Klebsiella or Staphylococcus aureus to wall themselves off. This is a lung abscess. This is another potential complication here that you would want to remember with patients who have pneumonia. The other thing, obviously, obviously, is that as you start causing inflammation and infection of multiple alveoli and bronchials, let's say that you just continue to keep spreading. This is very, very common with like bronchopneumonia. But you start causing multiple alveoli, diffuse alveolar damage to occur. And you can lead to ARDS. So acute respiratory distress syndrome is another one. Remember, we talked about that before as well. This is a pretty common etiology, right? Here's the big one, though. And I think this is really important to remember this one, because it leads into how we kind of like restratify. diagnose these patients to determine which one needs hospitalization which will probably test you on and which ones don't so sometimes let's say that you have a really really nasty pneumonia in this patient right here's their pneumonia and then what happens is some of the bacteria from this pneumonia seed into the circulation that's not good and if they seed into the circulation now you have bacteremia bacteremia doesn't necessarily mean sepsis but if it seeds into the circulation and it starts causing potential organ failure ooh then we might be getting into that kind of sepsis criteria, especially if the patient is having like hypoxemia, low blood pressure, tachycardia, tachypnea, fevers. You're getting into that range of sepsis now if you have a patient who has pneumonia and it starts seeding into the actual circulatory system. What happens is it causes vasodilation, increased capillary permeability when these pathogens get out here. And uh-oh, what do we get? We get a low blood pressure, low mean arterial pressure. We stop perfusing organs, my friends. And as we stop perfusing organs such as the kidneys the liver the brain multiple other organs you can lead to multi system organ failure and on top of that you start altering the normal coagulation system and decreasing the number of platelets that are important to form clots and then you start consuming them to make a bunch of different clots but then you have the chance of bleeding what is this called DIC so it's really really important to remember that patients who develop pneumonia have a very very high risk of sepsis. Especially going down the road of septic shock. All right, my friends, let's now go into the diagnostics of pneumonia. All right, my friends, so we've already talked a little bit about this already with the diagnostics. We talked about CAP versus HAP, but I just want to take a little quick second here because There was a couple things that I said and I didn't write down, but I just want to kind of like, I can't keep testing your knowledge, right? So a patient comes into the emergency department, they come into your clinic, whatever it may be, they're presenting with cough, shortness of breath, fever. They have a low two stats. They're a little tachypneic. They're working a little bit hard to breathe. They're short of breath. They're... complaining of that, right? Their heart rate's a little bit up. You hear evidence of consolidation on their physical exam. They got a productive cough. They have pleuritic chest pain, or maybe they just have the atypical. So they have low-grade fevers, upper respiratory tract infections like headaches, sore throat, nasal congestion, runny nose. Maybe they have a little bit of myalgias, arthralgias, et cetera. Whenever a patient comes like that and you think about the risk of them having pneumonia, such as the etiologies and pathophys, the next thing is to determine, is this a community-acquired or a hospital-acquired, right? community acquired pneumonia there's a couple different things I want you to know so obviously it was acquired within the community so we can say it was acquired within the community up to less than two days in hospital and the reason why this is important because this determines the risk of what types of bugs bacteria pathogens that the patient is most likely going to have and you can use that degree of suspicion to say it's likely that it's capped and so I therefore can use this particular antibiotic regimen. But if it's greater than two days in the hospital you can't say with confidence that this is the same bug. It might be a different one so you have to change your antibiotic regimen. That's why it's important. So community to less than two days in the hospital they develop this pneumonia if you will. Now when patients develop pneumonia within the community oftentimes it tends to be kind of this This low bar pneumonia and there's a very specific pathogen I already told you that you see in patients greater than 65 years of age elderly most common in nursing home facilities It's the most common one streptococcus pneumonia. So it's going to be most commonly streptococcus pneumonia. Second line would be haemophilus influenzae and Marexella catarrhalis in your COPD patients. Okay? The next thing that I want you guys to understand is hospital acquired, so this would be HAP, all right? Community acquired pneumonia. HAP on the other hand, is you have them greater than two days in the hospital. And this could be in the hospital, they got a tube down their airway, intubated, okay? VAP, which is the most common subset of HAP. this situation oftentimes this type of pneumonia is usually bronchial so it involves the bronchi the bronchioles and a little bit of the alveoli and it's a little bit more scattered in that sense we'll talk about this a little bit later when we get into the imaging but oftentimes for these patients for HAP the very specific types of pathogens that I want you guys to remember about for this one is oftentimes going to be generally when we we think about HAP what did I tell you before MRSA and we said pseudomonas these are the two bugs that's why it's really important to understand because when you're in the hospital you have multi drug resistant pathogens nasty pathogens that you'll have in the hospital that you won't have in the community that's why it's important to know this definition now when you establish whether it's a HAP or a CAP based upon this type of discussion that can help you to determine your antibiotic regimen then you kind of say okay I think this patient I have a certain degree of confidence that they have pneumonia let me get some labs let me get some imaging maybe they ask you on the clinical vignette what's some of the the labs that you would order for this patient or maybe they present you with the labs and you have to kind of use the clinical context the clinical features and based upon it being cap or hap which types of labs are more suggestive or better for you oftentimes it's not really that many there's a lot of extra labs and i don't think they're super critical so one of the things that i would do consider right away is what if they are presenting with features of upper respiratory tract infections so if they have any features of upper respiratory tract infections, I would just go right away and get a respiratory viral panel because this is going to be helpful to look for maybe influenza. Maybe it'll help me to rule out some type of SARS-CoV-2, like in COVID-19, RSV, et cetera. So there's so many that I can pick here. But that's the first thing that I would do. Do they have any of these features? Do they have the atypical presentation? Send that off first. I would do that first. The other thing here is oftentimes just get some basic blood work for the patient. Oftentimes, if they have this pneumonia, what did I tell you? That it's going to act. activate their immune system, right? And if they activate their immune system, it's gonna cause an immune response. It's gonna release all those cytokines. It'll activate their bone marrow, have them amp up their white blood cell production. So if I expect to see an increase in their white blood cells, whether this be lymphocytes more in viral or neutrophils more in bacterial, I would order a CBC. Not too bad, right? The other thing here is, so if I think that that could be one potential thing, the other thing here is that sometimes with these infections, they can cause that multisystem organ failure, right? And if I'm concerned about multisystem organ failure, I'm concerned about... So sometimes what can happen is I'll actually check maybe a BMP. Okay, and so if I check their BMP, what I'm looking for is, is there any evidence of an acute kidney injury increase in their BUN? Is there any increase in their BMP? the creatinine because this is telling me a little bit more about concern for organ failure. So is the pneumonia causing sepsis? It's not helpful in the diagnosis. You see what I'm saying? I'd say that in anything, CBC would be better than the BMP in this situation. What could be potentially helpful is that whenever you are really doing this for the exam, the BMP may also show you low sodium. If a patient presents with low sodium who is is elderly, smoker, immunocompromised, and has some type of exposure to contaminated water sources, which one should you think about, guys? Legionella. So think about Legionella. All right. The other thing here. Sometimes some of these pathogens, okay, they can get into the bloodstream and then they can get filtered across the kidney and can get filtered into the urine. Specifically some of their antigens can be tested and so we can test the urinary antigens. And so what I do is I'll test the urinary antigens specifically for strep pneumo and lesionella. All right, baby. So these are some of the things that I would start off with. A CBC to look for a leukocytosis. That's probably the easiest one. A BMP to look for any acute kidney injury or hyponatremia. Acute kidney injury would be more concerning for early sepsis. Hyponatremia is suggestive of lesionella. And then consider the urinary antigens to look for strep pneumonia or lesionella. The other thing here is that sometimes this inflammation can actually work on the liver. And when it works on the liver, you may have the liver increase the production of something called CRP. I don't think that this is super helpful. So I wouldn't really worry about this one the other thing is that sometimes some of these and some of these actual pathogens may get into the bloodstream and cause kind of injury to the liver and cause a bump in the LFTs and One of the things I would consider here is in a patient who has hyponatremia nausea vomiting diarrhea elderly smoker Immunocompromised and some type of contaminated water source you bet it lesion Look for this hyponatremia increased LFTs. Think about legionella. All right. The last thing that I would also consider here is if you're concerned that the patient is developing sepsis, I would get blood cultures. So consider also testing the blood to make sure that the pathogen hasn't seeded into the circulatory system. So checking blood cultures may also be a good thing. And then if you really want to figure out what's the specific type of pathogen, because oftentimes you'll start antibiotics and periodicals, and really sick patients, when you get the sputum cultures back, it'll tell you, oh, this is the pathogen. Oh, okay. It's strep pneumo. I don't need to have all these intense antibiotics. I can get rid of these and then use the specific antibiotic for that pathogen. So sputum cultures may also be helpful to take and really kind of run like a suction down there. And what you can do is if you can get the suction down there and pull some of the sputum out, or usually it's in the proximal airways, you suck some of that sputum out, you can suck some of that sputum out and then put it into a tube and then send that off to be tested for culture. So you can do what's called a sputum culture. And that's really just to help you kind of like narrow down the antibiotics once you get the bacteria back. Okay. All right, I hope that made sense with the labs. The big ones that I would really be worthy of considering here is your CBC, your blood cultures, your sputum cultures, and your respiratory viral panel, and then potentially a BMP to be looking for, and again, hyponatremia with increased LFTs thinking about lesion. They like to ask that on the exam. Okay, let's go through imaging, which is actually way more superior and way more important. I think the really, really important thing to be able to elucidate here is the imaging. So not only knowing a couple, two different things, what the actual image would suggest off the chest x-ray if they present it to you. Is it a lobar? Is it an interstitial? Is it a bronco? So we'll talk about that briefly here in a second and we'll take a look at some images. But also there's also other ways that we can define pneumonia, right? So microbe acquisition and also location. So when we think about the actual type of pneumonia based upon location, we can define them again here. We have lobar. and it's not too hard. Bronco pneumonia, because you know the nice thing about this is that they were very, very generous when they came up with these names and had them actually make sense. And then last one is interstitial. And I think there's two two particular things that I want you guys to take away from this kind of like location description of pneumonia. So low bar pneumonia, it's straightforward. It's a pneumonia that's occupying one of the lobes of the lung. So if I had a pneumonia here, I could have a bunch of different types. I could have a right upper lobe, a right middle lobe, right lower lobe, left lower lobe, left upper lobe pneumonia. In this situation, I'm just going to pick a right. Lower lobe pneumonia, right? That's all it is. But the big pathogen that I want you guys to be thinking about, because they may ask you this, is, I already talked about it up there, strep pneumo. Strep pneumonia. I'm going to put strep pneumonia right there, okay? The next one is if you have a bronchopneumonia. It's not hard. It's involving the bronchi and the bronchioles, maybe some of the alveoli as well. So it's going to have like patchy, it's going to be very patchy, and it's going to be extinct. kind of scattered throughout the lungs. So it'll be kind of like very, very patchy opacities that you'll see bilaterally. This is bronchopneumonia. And usually the microbes for this one, if it's hospital acquired, yes, it's MRSA. it's Pseudomonas. But if it's community acquired, that's a different situation. So what I want you to remember is if it's community acquired pneumonia, I just do it like this because it helps me to remember it. Staphylococcus aureus, Streptococcus pneumonia, Haemophilus influenza, and Klebsiella for the community acquired bronchodemonia. For the hospital acquired pneumonia, we already know MRSA. and Pseudomonas Originosum. I'll put PSA there. So that's really what I want you guys to be thinking about. Okay? So if we have a lobar pneumonia, it's situating to one of the lobes. If it's broncho, it's involving the bronchi, bronchials. It's scattered bilaterally, like these kind of like patches. Interstitial, it's involving the interstitial spaces. So the pathogen is kind of infecting, not the lung parenchyma itself. It's causing infection here in the interstitial spaces. And this, my friends, is very common with... your atypical pneumonia. What did I tell you was atypical pneumonia? The way that I wanted you guys to remember it? MCL and viruses. So MCL, mycoplasma, chlamydia, lesionella. Which one would be the most common out of those three? Mycoplasma. Young children in college dorm, like college or dorm rooms, very close contact, occupied spaces. They're young, healthy. And usually that's going to be one of the most common types of atypical. Don't forget that one. If it's like young kids. and very close contacts, generally like dorms are the best examples that they'll present this in, or like boot camps and things like that. But the other one would be viruses. All right, I think that gives us a pretty good idea of the types of pneumonia that we have on imaging. Now, let's take a look at a bunch of imaging. All right, my friends. So I think one of the big things to think about is, okay, we get imaging. Well, what kind of imaging do we get? Do we get a chest x-ray? Do we get a CT? Oftentimes, a chest x-ray should be the initial test. Whenever a patient's coming in with shortness of breath, dyspnea, pleuritic chest pain, and they got purulent... cough, any kind of thing like that, it's not a bad idea to just start off with a quick initial chest x-ray. It's ease of access and it's going to be a quick one that you can get done. So I would do that one first. The only time I really do a CT is if you don't really know what's going on off their chest x-ray. Their chest x-ray is inconclusive. You are treating them for pneumonia and they're not getting better. And then the only third reason I would say is if they're immunocompromised. So I'd say three reasons why you get a CT. Chest x-ray is inconclusive, but you still have a high degree of suspicion that it's pneumonia. You're treating them for pneumonia. They're not getting better. and then third is their immunocompromised and you think that they may have some type of weird pneumonia that was worthy of taking a better look at. Okay, so first one here is bronchopneumonia. How can I tell? It's not situated to like a particular lobe. I can see that there's like patchy. You see how there's like patchy consolidation here, patchy here. It's kind of patchy over here. So it's this patchy kind of bilateral consolidations in both lungs. That's bronchopneumonia. Think about this and out. patients with that staphylococcus, streptococcus, haemophilus, and klebsiella. If it's hospital acquired, think about MRSA and then pseudomonas. Okay, let's take a look at another chest x-ray. All right, my friends, here's another chest x-ray for a patient who came in, they had headaches, they had kind of like some nasal congestion, rhinorrhea, sore throat, earaches. or bullous meningitis. They had some low-grade fevers, myalgias, arthralgias. They're young. They're living in a dormitory, and boom, you think about mycoplasma, right, or chlamydia. That would be another one. And if I said contaminated water sources in an elderly young individual who smokes or immunosuppressed, et cetera, you think about lesionella or viruses. But this right here, when you see this kind of fine threading, it almost looks like a ground glass type of appearance. It just looks really, really awful. kind of like someone who's like out in the winter and you're blowing on like the the glass when it's really cold and it kind of looks like that it has that kind of ground glass opacities but it's very very fine reticular markings that are moving from the hilum outwards towards the Plura. This is very, very classic of your interstitial pneumonia. Okay. So this would be on your differential for mycoplasma, chlamydia, lesionella, and viruses. All right, my friends. So we're taking a look here at what's called a PA and lateral chest x-ray. That deserves another question. Which type of x-ray do I put into the thing? Like if they ask me like, what kind of x-rays best if they asked me. The best would be a PA and lateral chest x-ray. APs can kind of sometimes distort the anatomy and kind of not provide the best clinical picture. PAs are going to be really, really good pictures that will really kind of enhance the chest wall and show pathology. And lateral x-rays are really good because sometimes you can't see those lower lobes on a PA view. And so if we put them in a lateral x-ray, you can get that lower lobe view, which is really nice. So I'd say PA and lateral chest x-ray are going to be the best test that you can do if you had to pick between the chest x-rays. PA lateral because PA will give you the upper lobes and like maybe a little bit of like the right middle lobe, but the lower lobe sometimes can be hidden and then you can get that better on that lower, that lateral chest x-ray. So here we can see right upper lobes look good. Left upper lobe looks good. Right middle lobe looks good. Can't really see the right lower lobe. Left lower lobe, I'm seeing some opacity here because it's kind of like obscuring the edge of the heart, like that left heart border. I might be missing some of the lower parts going down into the behind this diaphragm portion. So I put a ladder. in there and look at that. I can see here in this like left lower lobe really consolidated area here they got a left lower lobe pneumonia. So that's what you'd be looking for and thinking about strep pneumo is a big one here. Okay let's take a look at another x-ray. All right my friends here's another x-ray look at that. right upper lobe looks clean, right lower lobe looks clean. I'm able to kind of pick out my right heart border, left heart border here. I can kind of make it out. So I definitely don't see any opacity of the left lower lobe, but I'm kind of obscuring over here near the left kind of portion of the mediastinum near the aorta and the pulmonary knob. I'm kind of obscuring my left upper lobe. It looks hazy. It looks so bad. pacified. That's a left upper lobe pneumonia. Okay. That's a lobar pneumonia. Let's take a look at another one. All right, my friends. So here I can see here, my right upper lobe looks clean. My left upper lobe looks clean. I can see pretty well my left heart border. So left lower lobe looks relatively good, but look at that. My right heart border, I can't actually make out completely. And there's a little opacity or hazy consolidation here on that right middle lobe portion. That's a right middle lobe pneumonia, my friends. All right, let's do a good look at another x-ray. All right, so here's another one. I look at my left upper lobe. It's clean. Look at my left lower lobe. It's clean. I can see the nice left heart border. Right heart border is nice and clear, so I don't have a right middle lobe pneumonia. If I had a lateral view, I'd be able to get a better view. of my right lower lobe and my left lower lobe a little bit better but I don't have that here but what I do see that pops out like a sore thumb is this kind of right upper lobe opacity and I can even kind of see it because here's the fissure. So if you're horizontal and your oblique fissure that would come down here, I can already see my horizontal fissure here. So there's kind of like that little fissure that's bulging there and then again I know that I have like this opacity that's evolving. my right upper lobe. So think about that one as well. Okay. All right. Let's take a look at another type of image. All right, my friends. So this is a CT. So again, in this patient, we ended up getting a chest x-ray. They had an interesting type of kind of consolidation involving like their right upper lobe, but even getting into a little bit of their middle lobe, but primarily kind of like their right upper lobe was really getting hit. And what we are concerned about is kind of like the way it looks. So what I wanted to do is I wanted to show you. you something really interesting on the CT, why it's so good. It really is like the best for pneumonia. But we try to just reserve it if we're kind of unclear, we don't have enough from our chest x-ray, they're not getting better with antibiotics or they're immunocompromised. When I look at the CT here, look at the right lung. You can already kind of see here in this right hemithorax here, you can see kind of this hazy opacities in comparison to the left one. It looks nice and aerated. And as they go down, it's getting worse, more opacities, more opacities, more opacities, more opacities. And boom, you see something really interesting. You see how here's like a bronchus. that's kind of coming off here and it's moving into this consolidation and it's open there's a lot of air moving into it and it stops it's like a cut off here these are called air bronchograms this is very characteristic of pneumonia so if you see a consolidation and you see these opened up air kind of filled cavities moving into the consolidation, that is called an air bronchogram, pretty consistent with a patient having pneumonia. Okay. So that would be a right kind of lobe pneumonia. Generally, it's kind of, if you kind of look here, you can see it's actually hitting more of, in this patient's case, it's definitely involving more of their upper lobe. All right, my friends, let's now talk about the treatment of pneumonia. So we're going to talk about this in particularly focusing on the antibiotics that we're going to use to treat the infection. It's It's an infection of the actual lung tissue, right? So the primary focus should be treating the actual infection. There's a lot of supportive measures that come into it as well. Obviously treating potentially the hypoxemia that they may have, the work of breathing. We're not gonna go into that. We talked about that with the acute respiratory failure of the lecture, but what I really want us to focus on is here the antibiotics. but the antibiotics are really, really kind of dependent upon what kind of pneumonia we have. And that's really dependent upon how we stratify these patients and determine their need for outpatient care in hospital care, but not in the ICU and then ICU level care, or they've been in the hospital for a couple of days, more than two days, more than 48 hours, and they've developed pneumonia. So they have a HAP, right? So let's talk about this really quickly. So you have a patient come in, and this is really only applying to what's called the community... acquired pneumonias. So this is really trying to determine, is this a community-acquired pneumonia that can go home, to the floor, or to the ICU? The way that we do this that they will likely ask you on the exam is something called the CURB-65 score. And so really what this consists of is confusion. So you're probably like, wait, Zach, where did confusion come into play? Remember I told you that if a patient gets pneumonia, one of the complications is the bacteria can seed into the bloodstream, cause a decrease in their mean arterial perfusion. They don't perfuse the brain as well. They don't perfuse the kidney. Don't perfuse the liver. They develop multi-system organ failure. One of the first things for elderly individuals is that they develop confusion or altered mental status. And this is due to the kind of the septic feature. So if they're already presenting with sepsis, isn't that a concerning sign? APSA, stink, and lowly it is. So confusion is a very concerning sign. The next thing here is Uremia. Now uremia, wait, Zach, uremia, wasn't that what the decrease, the increase in the urea off of the patients, particularly their B and P? And whenever we say the uremia is present, we say greater than like 20. So we're saying like greater than like 20. in this situation, that would be concerning. What that would tell me is that they have an acute kidney injury, telling me that they're decreasing the perfusion to their kidneys potentially. So they have an acute kidney injury. Yeah, that's a concerning sign. That means that they need to be hospitalized. Zach, what if their respiratory rate is like really high? It's like greater than 30 breaths per minute. They're like breathing super, super fast. They're super tic-tactic. Their work of breathing is very scary. Would I feel comfortable sending that patient home? No, that's a very concerning sign. And that is another big one. The next thing is blood pressure. Blood pressure. What is blood pressure? Well, that was the thing with the MAP, right? The main arterial pressure. That's dropping. If they're hypotensive, is that the problem? Absolutely. So if their blood pressure is low, and what I mean by low is we're talking about two particular parameters, that their systolic blood pressure is less than 90 millimeters of mercury. or if their diastolic blood pressure is less than 60 millimeters of mercury. This is a concerning sign. And the last thing is patients who are greater than 65 years of age, they're obviously at higher risk of worse outcomes. And so because of that, we're assuming that as you get older, your immune system is becoming compromised, you have an impaired mucociliary clearance, and also you likely have other comorbidities that put you at higher risk, and we don't feel comfortable sending those patients home sometimes. And so if you are 65 years of age or greater, you are a high risk. high risk. And what we do is we sum up all the points. So if you have one of these, you obviously get a point. And what we do is we kind of restratify based upon their score. If their score is between zero or one, that's a patient that I feel relatively confident that does not have sepsis, multisystem organ failure, and can decompensate. I can send these patients home. So this would be a CAP outpatient. Okay. If their score is two, okay. then I'm a little bit more concerned for this patient. This is a patient that could potentially decompensate, and they need just a little bit more observation. Maybe not an ICU-level care, but they need some observation. So this is a CAP, but this is going to be a non-ICU admission. Okay? And the last one is they have 3+. This is a patient that you're very concerned with. They have a very high mortality rate, and we should not send them to a home. We should not send them to a non-ICU. They need a very close observation and very aggressive care. These are patients that have a community-acquired pneumonia and require ICU-level care. So that's how we should re-stratify these patients, okay? But I want you to understand why we use the CURB-65 and what's the purpose of looking at these parameters, not just memorizing it. Okay, now we've re-stratified, we've determined those with high mortality, low mortality, intermediate mortality, and then we say, okay, now that I have kind of a sequence, I can treat these patients accordingly to CAP outpatient, CAP 9 ICU, CAP ICU, and then what else? HAP, hospital-acquired pneumonia. Let's talk about that. talk about that. All right, so when we talk about these patients, we now can kind of group them into the CAP outpatient, CAP inpatient, CAP ICU, and then we'll talk about the HAPs, right, greater than two days in the hospital. And then we'll briefly, briefly talk about aspiration pneumonia. We won't spend a lot of time on it. Now, with CAP outpatient, what I want you to remember is in these particular populations, you're really kind of thinking about the atypicals. That's the big, big one, possibly even strep pneumonia as well. So for that, what really covers the strep pneumonia, covers the atypicals pretty well. The The first option that I would consider in these patients would be your macrolides. So azithromycin would be kind of the one or doxycycline, which is one of those particular I'm going to put doxy, which is one of the actual tetracyclines that we can consider as well. So doxycycline would be a pretty good one as well as a macrolide is the other alternative option there. Okay, either one. The second option here would really be a respiratory fluoroquinolone. And the reason we would consider this, don't do this one first. just because of high resistance, I would really only do this if a patient has an underlying comorbidity that puts them at high risk or they've gotten antibiotics in less than the past 90 days. If they have, then you can consider that they may have a little bit higher resistance. And so because of that, I would then say, okay, a respiratory fluoroquinolone may work well if they've had antibiotics in the last 90 days or a comorbidity there present. Okay. All right. So that would be that situation there. Next one, if a patient has community acquired pneumonia and they're actually in the hospital but they're on observation, not in an ICU setting, you can do somewhat of the same thing here. We could still do a respiratory fluoroquinolone, that's definitely an option here as a monotherapy. The other option here is I would consider doing same thing up here, a macrolide. Or doxy plus a beta-lactam. And the preferred beta-lactam is obviously dependent upon where you are in the world. Hospital, but oftentimes the most preferred agent is ceftriaxone. Okay, ceftriaxone is one that I would definitely consider. All right, for a patient who is in the ICU, they have community acquired pneumonia, they're in the ICU in that situation, you could do somewhat of the same thing. But unfortunately, we kind of get rid of the doxycycline. And so all that changes here is we can do two options here. One is we can do a macrolide, so azithromycin, or we could do a respiratory fluoroquinolone. The only thing that's different is I add a beta-lactam to one of these particular regimens. It doesn't matter which one you pick. Okay? So you can pick either one of these as an option. So this would be how we would start. CAP outpatient, macrolide or doxy, just by itself. Or a fluoroquinolone only if you meet this criteria. CAP in the hospital, it's a little bit different. You can do respiratory fluoroquinolone by itself or you could do macrolide or doxy plus beta-lactam. When you get into the ICU, you don't use doxy, it's usually macrolide plus a beta-lactam or Or respiratory fluoroquinolone plus a beta-lactam. That's it. Preferred ceftriaxone is a beta-lactam of choice. Sometimes you can do Augmentin, which is amoxicillin clavulanae, is another option as well. Or ampicillin sulbactin, which is also known as Unicin. But this is usually the easy one to remember. HAP. This is generally greater than two days in the hospital. Right? So whether this is with a tube down your airway or not, you're in the hospital for two days or more, and you have pneumonia, it is now a HAP. You're covered. covering a different type of bug. What is the bugs that I told you to not forget? The first one is don't forget about MRSA. So generally you treat with vancomycin. Another option is called linazolid. Okay, Pseudomonas aeruginosa. In this situation, what are we covering with? There's so many of these. So I'm going to abbreviate it, but we call this piperacillin, tezobactam, sometimes piptezo or zosyn. The other one is called cefepime. And the other one that I would also potentially consider here is your aminoglycosides. So, tobramycin, gentamicin, amikacin. I would really avoid these, though. They're really harsh on the kidneys. So, I'm going to put aminoglycosides. But I would... really try to avoid these as an option in the test question as well as in real life okay the other thing that i would also consider here is if a patient is HIV positive, let's see if you guys remember this, HIV positive and their CD4 count is less than 200. I suspect PJP. What should I treat them with? Because PJP is a really, really nasty one. And this one I treat them with. with what's called Bactrim, trimethoprim sulfamethoxazole. The only other thing that I would add on is is that sometimes you can add on a fluoroquinolone, a respiratory fluoroquinolone like levofloxacin or amoxifloxacin if you think that the patient has... Legionella. If they do have Legionella, you can add on respiratory fluoroquinolone, but let's not get too far down that rabbit hole. These are the big things that I really want you to remember that you may get on the exam. The last one is aspiration. I don't want you to get too locked up on this just because I don't think that it's actually super correct, to be honest with you, according to what you'll need to know for the boards in comparison to true life. Aspiration, pneumonia, think about it. What kind of pathogens? Anaerobes is the big one. What is the lung? Is it aerated? Very, very aerobic? Or is it anaerobic? The lung is filled with oxygen, so it's going to be hard for an anaerobe to be able to survive in the lungs, right? So therefore, unless the patient has a lung abscess or unless they have an empyema, we don't really treat for anaerobic infections with these particular bugs. But on the exam, you do. But in real life, you don't. So what are these? Think about clindamycin. Clindamycin would be one potential option here. Another one may be what's called... Augmentin, so Augmentin. So we call that amoxicillin, clavulonate, it's called Augmentin. And the third option that you may consider, again, I really don't think that this is worth mentioning, but metronidazole plus a beta-lactam. These are things that that you may see on the exam. If you had to pick between one, I'd pick clindamycin if they really ask you. But oftentimes because the lung is so aerated, we don't treat aspiration pneumonia. With these types of pathogens, we just treat it as though it's a hap or a cap. Same treatment, unless they have a lung abscess or an empyema, then we treat with the clindamycin or the Augmentin or the beta-lactam and the metronidazole. All right, my friends, the only thing I would actually tell you guys to remember potentially for the treatment of pneumonia is just remember prevention. How do we prevent this? We'll talk about it more in the vaccinations lecture, but we're going to be talking about your pneumococcal vaccinations. So PCV13, generally at 2, 4, 6, and 12 to 15 months of age, and then the PPSV23 vaccination. Vaccinations you get at 65 years of age or older or if you have a lot of underlying conditions that make you at risk in patients 2 to 64 years of age. But that'd be a good prevention that they could ask you. All right, that covers pneumonia. All right, my friends, let's do another case study here. So here we have a 73-year-old male presented to the Ningenera Clinic with purulent cough, dyspnea, Rieger's, and progressive confusion. Past medical history is pregnant for COPD, diabetes, and HIV. So we know this patient is going to have pneumonia. But some of the features here that are suggestive of pneumonia and are concerning is because she has a purulent cough. So she's got a purulent speed in production. She has dyspnea. So dyspnea could be indicative of a lot of the consolidation causing hypoxemia to some degree. She's got Riger's, which could be due to the fevers from a bacterial type of source here. And she's got progressive confusion, maybe kind of suggesting to some degree that she has some type of organ dysfunction. She may not be kind of allowing for proper perfusion of the brain. And so especially in elderly individuals, we can see that. So concerning finding there. But her past medical history is also kind of supportive of worsening kind of lung problems. COPD. COPD can cause a lot of nasty bugs there. Diabetes makes her a little bit more of immunocompromised. Plus she's HIV positive. That also makes her super immunocompromised. So she's got a lot of risk factors here for increasing the risk of her having some type of pneumonia. COPD, again, a lot of thickening secretions, a lot of bronchospasm. And again, because of not being able to beat the mucociliar apparatus, that's a problem. Diabetics, she's also kind of immunocompromised. HIV immunocompromised may not be able to have the immune system response that she needs to fight off any kind of normal pathogens in her airway. So very concerning findings here. And she's 72, which makes her a little bit more elderly. And again, reduces the amount of cilia, reduces that kind of process there. So concerning findings here. Oh, vitals are not very good at all. She's in big trouble. So vitals, BP is 80 over 50. So she is hypotensive. She's slightly tachycardic. So heart rate's 110. Respiratory rate is 32. So she's slightly tachypneic as well. And then her temp is elevated. So she's got a temperature of... of 101 degree Fahrenheit. So she's febrile, tachypneic, tachycardic, and mildly hypotensive. And on top of that, her SpO2 is dookie. So she's on 84% and she's already on FiO2 of 60%. So she must be on some type of supplemental oxygen source that's giving her 60% FiO2. So maybe some type of like high flow nasal cannula or, you know, et cetera. So in general, this is a concerning finding for this patient. So she's hypoxemic on oxygen supplementation, febrile, tachycardic, and hypotensive. So very concerning findings. Now, when we go to the chest and we go to examine this patient, we want to think about signs of consolidation. So things that are going to actually alter the kind of like process of auscultating, altering the process of tactile fremitus, auscultating the process of like the sounds or whispers and percussion. So how do we find concerning findings of consolidation? So if we hear bronchial breath sounds, that means that there's a consolidation as the bronchus is actually trying to run into the smaller bronchials. It's It's running into a consolidated area. So we're going to hear the breast sounds proximal to that consolidation, such as bronchial breast sounds. When we're percussing, generally anything that's more fluid filled or pus filled in this kind of case is going to give a more dull type of percussion. And it's going to be louder on tactile fremitus too. So they'll have an increased tactile fremitus. They'll also have a positive bronchophony, egophony, and whisper pectiloquy on their specialized tests. So that's important as well. So these are all... findings that are supportive of consolidation here for this patient. So how do we go about diagnosing pneumonia? Well, there's a lot of different things that we can do. We can get a bunch of different labs. We can get a bunch of different imaging. I mean, obviously starting off with like a CBC wouldn't be a bad idea and the CMP. So what we would see with the CBC in this patient is that she has a leukocytosis. So she has an elevated white count, maybe supportive of an infectious etiology. Her CMP shows a BUN of 30. So she's got an elevated BUN. Her creatinine was also elevated slightly. Her LFTs are are normal. Her sodium is normal. Again, this is important when it comes to lesionella. Her blood cultures, when we actually tested her and then she ended up going to the floor, well, actually, we'll see where she'll be able to go, but she goes somewhere in the hospital. Her blood cultures actually came back positive for haemophilus influenza and streptococcus pneumonia. And then her sputum cultures were positive for PJP, H flu, and streptococcus pneumonia. Her CD4 count, because she is HIV positive, we wanted to check, is less than 200. And her imaging on chest x-ray shows bilateral patchy consolidations. So this woman has got a lot of different problems here. So what we're seeing is she has a bacterial infection, right? Both bacteremic and mnemonic. She has HIV with a very, very low CD4 count, and she's definitely got bilateral patchy consolidation supporting more of like a bronchopneumonia type of finding. So she's got a leukocytosis. She has potential signs. kinds of acute kidney dysfunction, bacteremia, positive sputum cultures, and the source of her bacteremia is probably from her lungs. And she's got a low CD4 count, putting her at high risk of PJP, which she's positive for. And her lungs are supportive of consolidated findings here. So she's definitely got a really, really bad pneumonia, secondary to strep pneumo and H fluid. And then she's also got a little bit of PJP due to her CD4 HIV, less than 200. Okay. So what are the three types of radiographic pneumonia? I talked about bronchopneumonia, but what are the different types? So there's lobar, broncho, and interstitial pneumonia. So lobar pneumonia is when it's usually like a socked-in pneumonia. It's consolidated to potentially usually one lobe or two lobes. So generally it would be like a right middle lobar pneumonia, right lower lobe, kind of like lobar pneumonia. So it's usually kind of socked up. Usually we very commonly see this in pneumococcal pneumonia. Bronchopneumonia is more scattered, bilateral, patchy, and usually we see that kind of involving like the smaller bronch. and alveolar tissue as well. Usually you can see a lot of different bugs that cause this one. And then the last one here is interstitial pneumonia. So you see a lot of kind of like interstitial infiltrates and usually like this reticular reticular nodular kind of opacification. And we usually see this with like the mycoplasma, the chlamydia, lesionella. So that's important to remember here. Whereas the bronco, you see things with like staph and strep and haemophilus and klebsiella, a lot of different bacteria. All right, so we have a patient who we're definitely concerned has pneumonia. I think the question that we have to ask ourselves is, is this a community-acquired pneumonia or a hospital-acquired pneumonia? Well, she just got into the hospital. She just arrived. She's not even been in the hospital for more than 48 hours. So because of that, I would say that this is a community- acquired pneumonia. She acquired this in the community. She hasn't even been in the hospital for very long at all. So what level of care is another great question to ask that this patient may require? And how does actually one go about determining what level of care? So remember I told you about the CURB-65 score. So what out of these does she have? And then based upon that, what puts her at high risk? So you see here her CURB-65 score, she has confusion. We actually see that in her HPI. She does have uremia. Her urea was greater than 20. It was actually 30. 30. Her respiratory rate was 34, I believe. So she's got tachypnea that kind of supports that. Her BPs are soft. So she had an 80 over like 50. So she kind of fulfills that. And she's 72. She's creating 65 years of age. She has all of those findings. And so generally when someone has like findings that potentially high, like three or more. that's very concerning and they require ICU level care. So this patient needs to go to the ICU. Now when we send her to the ICU, we're going to start her on antibiotics because obviously the source of this is a bacterial pneumonia. There's so many different types of bacteria that can cause pneumonia, but likely hers is, again, because she's 72 and the most common cause of community acquired pneumonia in elderly individuals is streptococcus pneumonia. And on top of that, she has COPD. and diabetes puts her at high risk for haemophilus influenza and she's got HIV, which puts her at risk for PJP. She's got a multi-bacterial type of polymicrobial pneumonia here and with evidence of sepsis too, my friends. So she's also septic. So with that being said, if we were to kind of treat, let's say that we excluded sepsis at this point in time, and we were only treating the pneumonia, we were not treating the sepsis, what kind of antibiotics would we put her on based upon her CURB-65 score, putting her in the ICU level care? Well, we would do a beta-lactam and a macrolide generally is going to be the first thing that we'll do here. Or we can do a fluoroquinolone and a beta-lactam of some type, right? But these would generally be what you would start a patient on. So you would do this and get them started on this. And then when their cultures come back, as we already have them now, we would narrow down according to what we think is best. But again, I think a beta-lactam and a macrolide or a beta-lactam and a fluoroquinolone would put her in this kind of ICU level. category. Now, if we had her becoming septic, we could potentially change the antibiotics up a little bit. Oftentimes, patients just get put on something like vancomycin and piperacillin tezobactam, but I think the best thing here is that she would be appropriate with a beta-lactam antibiotic such as ceftriaxone and a macrolide such as something, as we've talked about before, like azithromycin in this particular situation. If that wasn't appropriate, you could do a beta-lactam like ceftriaxone and a fluoroquinolone. If there was concerns that she had MRSA, which she does not have MRSA, because our cultures came back with no MRSA, we would treat her with vancomycin. If her cultures came back positive for pseudomonas aeruginosa, or we had concerns for that, then we put her on something like piperacel and tezobactam or cefepime. But she doesn't have that. So we're going to treat her for what we would suspect based upon what the guidelines are that we talked about on the whiteboard and what her sputum cultures and blood cultures came back positive for. Beta-lactam and a macrolide or beta-lactam and a fluoroquinolone would be appropriate here. There's one other thing that she did test positive for, which is PJP. And PJP, generally, we should treat these patients with Bactrim. So it would also add on Bactrim in this particular situation, which is the trimethoprim sulfamethoxazole. The next question that I actually did kind of lead into this is that when you have pneumonia, one of the complications of pneumonia, obviously you can get things like ARDS, you can get perinemonic effusions that can lead to empyemas. There's a lot of different things that can happen with this potential disease. But one of the worst case scenarios that we can see here is that the patient can actually kind of seed some of the bacteria into their circulation, their systemic circulation, which can cause worsening features of hypotension, tachycardia. severe fevers, and then sometimes becoming refractory to fluids and vasopressors, we can see the patient becoming septic and going into septic shock. So right now the patient does have features of sepsis and some degree of septic shock because they are lower on the blood pressures and we're seeing organ dysfunction now. So I would say that this patient is in the point of septic shock, which is concerning. And again, we would treat the patient accordingly for septic shock, such as putting them on vasopressors, fluids, you know, with a minimal kind of fluid approach. And then on top of that, considering things such as antibiotics, obviously, that we would already have this patient on for their pneumonia. So treating their pneumonia, vasopressors to support their blood pressure, plus or minus a little bit of fluids, just being careful not to fluid overload them. But anyway, that's how we would go about this patient. Now, getting back to the actual concepts here that I need you guys to remember for the exam is remembering these buzzword terms. And so thinking about the microbe can really come across on the clinical vignette. So if they kind of use the term strep pneumonia or you think that it's strep pneumonia, which one of these would be more of a support of strep pneumonia? And I want you to think that it's the most common cause of community acquired pneumonia in elderly individuals. That's strep. Streptococcus pneumonia. All right. Sapharius, I want you to think about post-influenza and IV drug abuse. And again, think about MRSA as a hospital-acquired pneumonia type of pathogen that's very, very dangerous. Pardon me. The next one is H. flu and Marexella. So for H. flu and Marexella, I want you to think about COPD years and even some degree bronchiectasis. The next one here is Klebsiella. Think about alcoholics and CNS disease and depression. Anything that increases the risk of aspiration would be Klebsiella. And then Pseudomonas. Definitely think about immunocompromised or immunosuppressed and cystic fibrosis is a harbinger for Pseudomonas as well. Mycoplasma. Think about young, healthy, and close quarter living, especially dormitories. Legionella, you want to think about contaminated water sources, their smoker, their elderly, their immunocompromised. That's the big one there. PJP, think about HIV, AIDS, CD4 count less than 200. Coccidomycosis is the fungus in the southwestern United States, so California. And then you have the next one here, which is histoplasmosis. This is the bird or bat droppings that you see during the spelunking kind of events in the Ohio and Mississippi River Valley. And then blastomycosis, think about the yeast from the east. So eastern United States, think about blastomycosis. And then lastly, anaerobic bacteria, think about in situations of aspiration events. All right, my friends, that covers pneumonia. I hope that it made sense. made sense. I hope that you guys enjoyed it. As always, love you, thank you, and until next time.