This is Robert Bauch. I am going to now review community-acquired pneumonia cases you should know. As part of the multi-professional critical care review course, I'm at Rush University Medical Center in Chicago, Illinois. And my charge this review is to go over the definitions and risk factors for the development of severe pneumonia. We'll discuss the common ideologies of severe pneumonia. We'll review the guidelines for initial antibiotic treatment of severe pneumonia and describe the prognosis and some strategies for preventing severe pneumonia in the future. Let's start with a brief review. Pneumonia and lower respiratory tract infections are the second most common cause of death worldwide and the most common cause of death from infection in developed countries. It's important to remember that hospitalized community-acquired pneumonia is associated with increased mortality, development of acute respiratory failure and ARDS, and leads to ventilatory support and costs about $10 billion a year in the U.S. and 10 billion euros in Europe. The clinical manifestations typically consist of cough, purulent sputum, pleuritic chest pain in about half of the people, and usually fever and dyspnea. It's important to ensure that there is an abnormality on the chest x-ray compatible pulmonary infiltrate. And just to get you into board review mode, here's the chest x-ray, typical quality that you might see on a board exam. So look for an infiltrate, and I hope you're able to see my cursor on this. And as you can see from the gram stain of the sputum, here's some gram-positive diplococci consistent with pneumonia. I know a lot of you are probably using point-of-care ultrasound, and it's been touted as a way to diagnose pneumonia, but remember that it is very operator-dependent and may be subject to the interpreter views of what they are seeing. So right now it is not the gold standard for diagnosing pneumonia. To get you in board review mode, let's also deal with a question. Which of the following is not a risk factor for the development of community-acquired pneumonia? Use of ACE inhibitors, proton pump inhibitors, inhaled corticosteroids, and alcohol use? The answer is ACE inhibitors. But there are a lot of risk factors for pneumonia, and we just reviewed some of them. Alcoholism, asthma, maybe the inhaled steroids are the big component of that. Gastric acid suppression, proton pump inhibitors, and H2 blocker use. Opioids and other substances like benzodiazepines that may obscure one's ability to protect their airway or level of consciousness. Immune suppression, having heart disease, being institutionalized, and unfortunately being elderly and over age 70 increases your risk, as does the increased risk for having comorbid conditions. This is a nice review paper by Mandel and Niederman on the impact of micro aspiration on pneumonia and realized that there are a number of situations that can impair swallowing, impair your level of consciousness, and increase the chance that gastric contents may end up in the airways and the lung. And these are again listed in some of the risk factors we just talked about. Also remember that not all aspiration ends up leading to a pneumonia. When you're dealing with community-acquired pneumonia, we typically are going to be in a situation where we do not have a positive pathogen identified, and we'll go over this in the next couple of slides. When we have been successful at identifying a positive pathogen by culture or other means, strep pneumonia continues to be the most common of the bacterial pathogens, and depending on the patient and the circumstance, you may have atypicals and other organisms as you see on this slide. The bacteriology of severe community-acquired pneumonia has also changed over the years, and here you see two periods of time, 84 to 87 and 1996 to 1998, and you see that the strep pneumonia frequency has changed. Legionella certainly changed a lot. Pseudomonas aeruginosa was about the same, and atypicals are being more commonly encountered as time goes on. As far as what is currently thought to be responsible for the etiology of hospitalized community-acquired pneumonia, the CDC sponsored an epidemiology of pneumonia in the U.S., and using a pretty intense diagnostic approach using nasal cultures, sputum cultures, urinary antigens for Legionella, streptococcus, blood cultures, getting pleural fluid, lavage fluid when available, and even using blood for PCR, and of course serologies for various viral agents. Looking at patients who were included in this hospitalized cohort, the most common identifiable pathogen was human rhinovirus. You see, of the bacterial pathogens, strep pneumonia was still the most common, but 62% of the time, even with this intense diagnostic approach, no pathogen was identified in a patient who is treated and managed as having community-acquired pneumonia that results in hospitalization. Also, from this same cohort study, you can see that as people age and you go from 18 to greater than 80, the organism's prevalence will change. You'll see a lot more of the strep pneumonia as people age, and kind of a smattering of different etiologies, mostly viral and in the younger age group. As you're taking boards, a big part of the challenge is correctly reading the question and deciding what are they asking me. And as far as pneumonia is concerned, a lot of important information, and I'm going to call these pearls, are hidden in the question. So if you look at the stem and you read carefully, you'll pick up clues that may help you answer the question correctly. And in pneumonia, there's a lot of historical features that will go into correctly answering the question to help you identify what organism or organisms are we talking about. So if you have a patient who was driving a truck through the Southwest and gets pneumonia, think about coccidioidomycosis. Nursing home residents, you have strep pneumonia, H flu, staph aureus, anaerobes, MTB, don't forget MTB when you're talking about pneumonia, and chlamydia. If they're exposed to bats or they're in a cave, think about histoplasmosis. Exposure to birds, think about chlamydia, cryptococcus, and again, histoplasma. If they're around rabbits, think about tularemia. If they're around farm animals, especially sheep, think about coxellia, burnetti, Q fever. If they're an IV drug abuser, think about staph aureus, anaerobes, MTB, and pneumocystis. When you have an endobronchial obstruction and foul-smelling sputum, think of anaerobes. Recent antibiotic treatment, think about drug-resistant organisms, including strep pseudomonas and multi-drug-resistant enterobacteriaceae. Pneumonia in the summer and winter is typically thought of as legionella. And then we have the more rare things that might come up like hantavirus and some of the coronaviruses. And I think the boards have not recognized the SARS-CoV-2, but future years, I'm sure there will be questions on SARS. If the sputum is mucopurulent, typically we think about bacterial, but occasionally it can be viral or mycoplasma. Scant, watery, it's usually the sputum of mycoplasma and atypical pneumonia. Rusty is characteristically strep pneumonia. Current jelly sputum is typically klebsiella. The foul-smelling is mixed anaerobic. And a lot of white cells, few bacteria, think of legionella. If the physical exam has a patient who has a fever, but doesn't have the typical tachycardia that goes along with a fever, we call that a pulse temperature deficit. And think about viral infections, mycoplasma, cysticosis, tularemia, and legionella. They have furunculosis, think of staph. They have herpes labialis, think of strep pneumonia. Bad periodontal disease, well, you're probably looking at somebody who may have anaerobic infection. And if the patient looks reasonably well, but their x-ray looks terrible, think of viral, like we see with some of this COVID, and mycoplasma disease. So we think about pneumonia and it's usually a pretty straightforward definition of, and clinical descriptor that we go with, but realize that the presence of underlying cardiopulmonary disease may delay our diagnosis of CAP or may obscure that diagnosis. And unfortunately, can delay your treatment, which may be associated with increased morbidity and mortality. So it's important that you recognize that when you have an abnormal chest x-ray, that it's not always pneumonia when it looks like you have this defined infiltrate. It could be pneumonitis, could be heart failure, and heart failure may typically be unilateral. Could be a pulmonary infarct, could be patient having acute exacerbation of pulmonary fibrosis or bronchiectasis, may have hypersensitivity pneumonitis, could have vasculitis. And some people who have various other habits can have cracked lung or can have heroin-induced pulmonary edema. And of course, people can have respiratory symptoms with a normal chest x-ray and you should be cognizant of those conditions that can lead to that. It's important for getting the right treatment in the right scenario that you put the patient in the right risk strategy. And we're going to go over that on the next couple of slides. But it's also important that you recognize that communicable pneumonia may be associated with acute coronary syndromes. And 5 to 7 percent of acute CAT patients have a concomitant cardiac event. It's thought that the inflammatory cascade that the pneumonia induces may induce cardiac lesions. And that can result in typical ischemia. And there is a pretty high association, up to 30 percent of CAT patients have adverse cardiac events occurring at the time of their presentation. As we approach a patient with a presentation of community-acquired pneumonia, we'd like to be able to define what is their severity index. The most common is the Port Pneumonia Severity Index, where basically if you're under age 50 and you have no comorbid conditions, well, you have a pretty low risk of having to be hospitalized and you can go on a pretty low risk antibiotic regimen. Unfortunately, if you have amassed a lot of points, and you see here listed a number of different physical findings and demographic factors, as well as laboratory and radiographic findings that can amass points. If you have over 130 points, you're in the risk class 5, which is associated with a 27 percent mortality rate from the community-acquired pneumonia. And this is just a table to better define the classes 1 through 5. 1 through 3 are usually low levels of severity. Most often, all of these are handled as an outpatient unless there is a need for inpatient care, usually not related to the pneumonia. Class 4 and class 5 require inpatient care and class 5 is in the ICU. Another way to help determine the severity of community-acquired pneumonia that's a little less complex than adding all those points is the IDSA ATS severe cap guideline. And that can be easy to identify the major criteria. If they need to be on an invasive ventilator or they have septic shock and need vasopressors, that would qualify as severe cap that needs to be in the ICU. Otherwise, if you have three or more of these minor criteria, and the minor criteria may not sound very intense to you, but a respiratory rate that's a true respiratory rate over 30 breaths per minute is a marker. Same thing with oxygenation abnormalities, and here we see a PaO2-FiO2 ratio less than 250, having multilobular infiltrates, having the presence of uremia, and here we call uremia BUN over 20, leukopenia, thrombocytopenia, hypothermia, and of course hypotension that requires aggressive fluid resuscitation. All of those should be associated with getting you to recognize that this patient, if they have three or more of these, qualifies for severe cap treatment and should be in your intensive care unit. The British Thoracic Society simplified it even more saying a respiratory rate over 30, diastolic blood pressure less than or equal to 60, and a serum BUN level greater than 7, which again correlates to that's millimoles to are greater than or equal to 20. Two or more of these would qualify as severe cap. The CURB-65 is one that you'll hear a lot of people use. A lot of past studies have validated this, and it's again looking at confusion, elevated BUN, respiratory rate greater than or equal to 30, systolic blood pressure less than 90, or diastolic blood pressure less than or equal to 60, and age over or equal to or over 65. Here if you have three or more, you have a high risk for severe cap, and those are people who should be in the ICU. And then the Spanish came up with the CUROX. That's six factors, again looking at confusion, the BUN, respiratory rate above 30, multilobular infiltrates or bilateral infiltrates, and having a PaO2 less than 54 or PaO2-FiO2 ratio less than 250, as well as an age greater than or equal to 80. And here having two or more of these, or if you go by their point scale, as you see at table three, these are the people who you would put in the ICU and have a high risk of severe community-acquired pneumonia. And then for completeness, there's a number of other scoring systems that have been utilized, but I don't think this test is going to dwell on all of the various scoring systems. But realize the common variables are confusion, BUN, tachypnea, multifocal infiltrates, hypoxemia, hypotension, and these are the things that should get your eye as well as the patient. It's important to realize that patients who get admitted to the floor when they should go to the ICU actually have worse outcome than if they went to the ICU to begin with. And this is a secondary analysis of 28-day mortality of 453 community-acquired pneumonia patients who ended up actually having to go to the ICU. But if they were initially admitted to the floor, they had a higher 28-day mortality rate and decreased hospital discharge compared to those patients who were initially admitted to the ICU for management of their community-acquired pneumonia. So it's important to manage the patient in the correct location. Now we're all used to all sorts of biomarkers to help us. We use it in dealing with myocardial infarction, pulmonary embolism, and other clinical conditions. There's a whole host of different biomarkers that have been utilized in community-acquired pneumonia. We have procalcitonins, C-reactive protein, proadrenomodulin, beta-natriuretic peptide, and even troponins. At this point in time, I don't think any of these have passed the mustard to make them a part of our diagnostic routine. And particularly, none of them are going to help us decide who does not need antibiotic therapy if we think there is a bacterial infection. And we'll talk more about this. Choice one, piptazo plus amikacin. Choice two, levofloxacin plus tobramycin. Choice three, lenazolid plus meropenem. Choice four, ceftriaxone plus azithromycin. The answer is choice four. So let's talk about some community-acquired pneumonia management issues. As we've said, the causative pathogen is frequently not found. Up to 50, 60% of the time, we don't know the causative pathogen. So we have to look at guidelines, and we have to know our antibiogram, and our ecology of organisms that we have in our environment to help us determine what is which bacteria, which pathogens we need to be covering. Most of the time, our important ones are pneumococcal pneumonia, atypical pathogens, and in select circumstances, community-acquired MRSA. Most of our treatment is given empirically, guideline-directed. We want to start it early. We want to know about the antibiotic resistance patterns in our institution, in our city, in our locale. It may even be in your unit that it becomes very important. And you should know the antibiogram to let you know which antibiotics are going to be more or less successful. And there is data that suggests that combined antimicrobial management, particularly with a macrolide, may have a beneficial effect in community-acquired pneumonia. From the 2007 IDSA ATS-CAP guideline, they bring out some important considerations for us in our management of our patient with severe community-acquired pneumonia. And that is in the ICU, we do want to ensure we get blood cultures, sputum if possible, look at the urinary antigen for Legionella and pneumococci. And if they have a endotracheal tube in place, you can do a deep tracheal aspirate, you can do a bronchoscopy with BAL. And if they have a pleural effusion, sample the pleural fluid, not only to see the organism, but to ensure that it's not a complicated perineumonic effusion or empyema that may need additional forms of management. We know from the guidelines that there are certain modifying factors that we need to take into consideration when we're thinking of a patient potentially having penicillin and other drug-resistant pneumococci. And some of these that will again be important historical features to come into reading your stem. If they've had a beta-lactam within the past three months, if they're an alcoholic, if they're on any immune suppressing medications, or they have an immune suppressing illness, they have a lot of medical comorbidities. And frequently they like to have the grandfather who picks up the kid at the daycare center. And that puts that grandfather at risk of potentially having a drug-resistant pneumococcus. Gram-negative organisms, think about patients who are residing in nursing homes who have underlying cardiopulmonary disease, multiple medical comorbidities, or recent antibiotic therapy. And the patients who are more susceptible to pseudomonas are those with structural lung disease like bronchiectasis who have been on chronic corticosteroid therapy, and that's defined as prednisone at more than 10 milligrams per day, or who have been on broad spectrum antibiotic therapy for more than seven days in the past month. And again, the impact of malnutrition on the individual with pneumonia, you would think about pseudomonas aeruginosa. Now for, I'll say antibiotic guideline recommendations, we have a quandary here because the 2007 guideline has been updated in 2019. And I'm gonna share those updated guidelines with you, but I'm right now focusing on 2007 because I don't believe the board has updated their questions based on 2019 data. I don't know for sure, so that's why I'm gonna give you both. So focusing on the 2007 IDSA ATS-CAP treatment guidelines, outpatient treatment, we shouldn't need to know for a critical care test, but inpatients in the ICU, they would recommend a beta-lactam antibiotic plus either azithromycin or a respiratory fluoroquinolone. And that was the answer to our test question. And if there are special concerns like pseudomonas, then you need not only the antinumococcal antibiotic, but you have to add an anti-pseudomonal beta-lactam plus either ciprofloxacin or levofloxacin, or you can add a beta-lactam plus an immunoglycoside and azithromycin, or a beta-lactam plus an immunoglycoside and an antinumococcal fluoroquinolone. If you worry about the presence of communiquired MRSA, then add vancomycin or lenazol. Now here's the 2019 IDSA ATS-CAP treatment guidelines, which basically says the same thing. They help break this down as to prior respiratory isolation of MRSA. That's gonna move you even more toward adding anti-MRSA therapy. If they have prior respiratory isolation of pseudomonas, again, you're gonna be adding anti-pseudomonal coverage. And if they're recently hospitalized and had parenteral antibiotics, you're even more move towards covering for those organisms. Communiquired MRSA is a significant pathogen that we need to not only recognize, but treat appropriately. It is a distinct illness. Usually it's associated with severe necrotizing disease, associated with the elaboration of a panton-valentin-leukocidin toxin, which leads to the necrotizing infection, and mandates that our treatment include not only an antibiotic, but something that can handle the protein synthesis and take care of the toxin. So if you're using vancomycin, you would add clindamycin. If you're gonna use lenazolid, it can counteract toxin production on its own. Remember to not use daptomycin for pneumonia treatment because it is inactivated by surfactant. And this is just a nice cartoon to show you the PVL necrotizing communiquired MRSA pneumonia and its inflammatory reaction. And you'll think about communiquired MRSA when you have cavitary infiltrates or necrosis, a rapidly increasing pleural fusion, patient presents with gross hemoptysis, has a concurrent influenza infection, they're neutropenic, they have an erythematous rash, may have skin pustules. And oftentimes it's a young previously healthy patient who developed severe pneumonia in the summer. Lots of data comparing lenazolid versus vancomycin. Here's a study that suggests that lenazolid may be better. There's other data that says at least in ventilator-associated pneumonia, lenazolid may be better. You can also say they're equivalent except for we need to take care of the impact on the toxin production by MRSA. And here is another study in meta-analysis and systematic review of 1,641 patients in eight trials saying lenazolid is not superior to glycopeptides. Another controversial area is the use of corticosteroids in community-acquired pneumonia. So we'll turn to a meta-analysis to determine if adjunctive steroids are beneficial with severe CAP treatment. Unfortunately, with a meta-analysis, we have a meta-elaboration of different steroid preparations. So we're looking at the use of corticosteroids steroid preparations. So we're looking at different steroids, dexamethasone, prednisone, prednisolone, hydrocortisone, different durations, anywhere from one dose to 10 days, different doses. So it truly is a very difficult thing to make exact sense out of. But if you look at the data in severe pneumonia, using steroids does improve all-cause mortality. Less seen in less severe pneumonia, but in severe pneumonia, there seems to be a benefit. So not only was there a severe pneumonia decrease in mortality of 3%, but steroid treatment seemed to decrease the need for mechanical ventilation. Steroid treatment shortened hospital stay, but steroid treatment was associated with more hyperglycemia. So optimal treatment of community-acquired pneumonia means that you've got to get the right antibiotic and you got to get it in fast. So getting it in within three hours will improve survival. We all know surviving sepsis says, get that in within one hour, if possible. Seems that there is improved survival with multiple antibiotics. And there's some data that suggests that there's improved survival with community-acquired pneumonia when azithromycin is part of the regimen. And this is despite the fact that there's an increased resistance of strep pneumonia to azithromycin. So this may be the anti-inflammatory effect of the macrolide. It may be an unknown mechanism up to this point in time. It's also important that you treat for the appropriate duration. Most would say five to seven days in conjunction with the clinical response. And I think most people are treating for five days. There are some that are suggesting three days may be adequate, but we need more data for that. There was a recent report in the Lancet that will not be on the boards. Lots of data though that says delayed appropriate antibiotic treatment has detrimental effects on outcome. All the outcomes you want to look at, whether overall 20 to 30 days, ICU outcome, whether looking at septic shock with gram negatives, gram positive, and severity of illness. So treat with the right antibiotic as soon as possible. And following guidelines will improve your ability to get the patient stable, to deescalate to a less intense and more tailored antibiotic regimen, decrease the length of hospital stay, and improve hospital mortality. And again, getting the patient with severe community-acquired pneumonia on the right antibiotic therapy and being compliant with the guidelines leads to better outcomes, shorter stays on the ventilator, and better survival. So back to the 2019 ATS IDSA treatment guidelines. I put in some of the summaries that you can see here and read on your own since this is now a virtual discussion. I will highlight a few things with the strength of the evidence and the quality of the evidence. So the new guidelines suggest getting gram stain and sputum culture insensitivities for severe caps, especially if you're thinking about MRSA or pseudomonas. If there's previous infection with MRSA or pseudomonas, or they were hospitalized or received parenteral antibiotics in the past 90 days. And you can see most of that is at least strong recommendation, conditional recommendation with relatively low quality data. Blood cultures and severe cap, again, a strong recommendation, very low quality data. And again, particularly in the patients with MRSA or pseudomonas or those who had previous infection with MRSA or pseudomonas, or who were hospitalized or received parenteral antibiotics in the past 90 days. There's a conditional recommendation for obtaining the urinary antigen for strep and Legionella detection. Influenza testing when the virus is circulating is actually a strong recommendation with moderate quality data. Empiric antibiotics in radiologic community acquired pneumonia, regardless of procalcitonin level is a strong recommendation with moderate quality data. Using a clinical prediction rule, and they particularly picked out the pneumonia severity index is a strong recommendation with moderate quality. And they liked their IDSA rule for diagnosing severe community acquired pneumonia with also got a strong recommendation, low quality data. Antibiotic treatment based on risk factors, severity, local antibiogram is strong recommendation for the beta-lactam plus the macrolide with moderate quality. Beta-lactam plus respiratory fluoroquinolone was also strong, but lower quality data. No need for anaerobic coverage unless there's a lung abscess or emphysema. They recommend against steroid for non-severe CAP. Severe CAP is a conditional recommendation and influenza is a conditional recommendation. So recommending against the use of steroids, they endorse surviving sepsis recommendation for physiologic steroids in severe CAP with refractory shock. Again, the new guidelines, if you aren't familiar with it is like the hospital acquired pneumonia ventilator associated pneumonia guideline where they took out the healthcare associated pneumonia definition. And they think that promotes unnecessary antibiotic escalation. So that's a strong recommendation with moderate quality data and the duration of treatment, they would support five to seven days along with evidence of clinical improvement. So how do you know the patient is clinically improving? Well, you see the reversal of all the clinical abnormalities so they're no longer having a fever, their heart rate's lower, the respiratory rate's lower, blood pressure's higher, oxygen saturation's better, they're taking in oral intake and their mental status is normal. And as you would expect, if you are able to deescalate your antibiotic therapy as the patient improves, the patients do a lot better than if you have to escalate therapy. So looking at mortality, people, and these are ventilator associated pneumonia patients, people who deescalate therapy have the lowest mortality, people who escalate therapy, the highest mortality. When you're looking for failure to improve or suboptimal response to your treatment, you need to look at the patient and see what about that patient may be responsible for that. So some of the factors when the patients are not improving, you can see if they have underlying liver disease, if they have a pleural effusion, multilobar disease, cavitary disease, if they're leukopenic, these are patients who you might have to intervene, you might actually have to tap that effusion if you haven't kept it before. If it's cavitary disease, there may be a need to sample that cavity, whether bronchoscopically or in a percutaneous fashion. In addition, if you look at patients early on who have a greater risk of not improving, those are the people with multilobar infiltrates who are more severely ill. Importantly, it's those with have either gram-negative pneumonia or Legionella are not likely to rapidly improve. So you might have to wait that out a little bit or investigate a little bit more. And of course, if you're giving the wrong antibiotic agents or discordant therapy, that may be a reason the patient has not improved. So we've already reviewed a lot of these, but most of the time, you're gonna see risk factors for treatment failure are liver disease, increased severity of illness, leukopenia, multilobar disease, pleurofusion, and cavitary disease. And with poor response to therapy, you're gonna see a higher mortality in those treatment failures, 25% versus 2%. So our third question is, which of the following suggests a poor prognosis for a patient with severe communiquered pneumonia in the ICU? Subsegmental infiltrates, falling procalcitonin level at 24 hours, high bacterial load for pneumococci, prior immunization with pneumovex. And the answer is high bacterial load for pneumococci. We do have a pretty big meta-analysis of 134 studies, 35,000 CAP patients, that brings out that people who have a lot of comorbid conditions, a high respiratory rate, hypothermia, hypotension, have elevated BUN, leukopenia, leukocytosis, hypoxemia, and multilobar infiltrates are more likely to have higher mortality from their communiquered pneumonia. But it's also borne out that the higher the bacterial load, the more likely the patient is to develop septic shock and to have higher mortality. So it's important that they be diagnosed quickly and started on effective therapy. Now, a very disconcerting finding in elderly communiquered pneumonia patients is that even if they survive the hospital stay, that they have a higher mortality over the subsequent one to two years compared to other elderly patients who have been hospitalized for non-communiquered pneumonia conditions. And some of that may reflect an increase in MIs and cardiac events. As it points out here, the acute inflammation can destabilize atheromatous plaques and maybe induce a procoagulant state. Supporting that study is another study that came from Kentucky where in Louisville, they looked at, again, the adult Medicare population who was admitted with communiquered pneumonia and they looked not only at in-hospital deaths as whether they were an early ICU admission or a late ICU admission, but subsequent deaths in the next 30 days, next six months, and even the next year. And you'll see that of the population, about half of them had died within that subsequent year of follow-up. So communiquered pneumonia in elderly people is a bad prognostic sign. So we need to give it a lot of respect. And part of that respect is by preventing communiquered pneumonia. And that's where influenza vaccine, the two pneumococcal vaccines come in handy. Smoking cessation is also a big part of trying to prevent pneumonia. And you can decrease ICU admission and decrease mortality in pneumococcal pneumonia by giving them influenza vaccine and pneumococcal vaccine. And here you can see just influenza vaccine in about 17,390 adults hospitalized with CAPS during the flu season, the vaccine recipients had decreased in-hospital all-cause mortality. And this was a significant factor even after adjusting for various comorbidities. So we've talked about severe communiquered pneumonia as the most common infectious disease cause of death. It's important for us to rapidly diagnose, effectively triage, and begin timely initiation of appropriate antibiotic therapy. We should use guideline-directed therapy because it's been shown to improve outcome. Data suggests that there's improved outcome with early multiple antibiotics, meaning include a macrolide if possible. And as far as biomarkers are concerned right now, their role is uncertain, may be helpful in the future for prognosis or assisting in antibiotic stewardship by shortening antibiotic duration of treatment. But at least right now, our antibiotic treatment is usually five to seven days and maybe even moving shorter than that. We'll see what the future holds. I wanna thank you all for your attention and wish you good luck on the exam.

community-acquired pneumonia

definitions

risk factors

common pathogens

treatment guidelines

bacterial pathogen

atypical pathogens

scoring systems