The Causes of CABP and Patient Outcomes

In this podcast, Christian Sandrock, MD, MPH, talks about how the causative agents of community-acquired bacterial pneumonia (CABP) are identified and how patient characteristics and type of bacteria affect treatment options, duration, and the patient journey. This is part 2 of 3 podcasts on CABP from Dr Sandrock.

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Christian Sandrock, MD, MPH, is a pulmonary, critical care, and infectious disease physician and professor of medicine at the University of California Davis in Sacramento, California.



Amanda Balbi: Hello everyone, and welcome to another installment of Podcasts360, your go-to resource for medical news and clinical updates. I’m your moderator, Amanda Balbi with Consultant360. 

Our guest today is Dr Christian Sandrock, who is a pulmonary, critical care, and infectious disease physician and professor of medicine at the University of California Davis in Sacramento, California. Today he joins us to share his thoughts on the causative agents of community-acquired bacterial pneumonia (or CABP), as well as how patient characteristics contribute to treatment options and patient outcomes. Let’s listen in. 

So, what are the typical causative bacterial organisms of CABP?

Christian Sandrock: With community-acquired bacterial pneumonia by definition, in there is “bacterial,” so we're going to focus on the bacterial agents for now and not look at the viral and fungal.

When we look at the bacterial component of things, there is a little bit of variability when we're on the outpatient side and the inpatient side, both severe and nonsevere inpatient. Far and away the No. 1 organism is Streptococcus pneumoniae or Pneumococcus. That's really the biggest bacterial agent that we tend to see across all areas. Haemophilus influenzae, which is a small, comma-like gram-negative when seen on gram stain, also plays a big role both in the ICU, non-ICU, and the outpatient world as well.

But this is where things change a little bit. When we look at the outpatient side, the atypicals—Mycoplasma and Chlamydia tend to play a bigger role in the outpatient worlds. They can also play a little bit of a role in the inpatient side, but generally not in a severe component. From the atypical side, we often see Legionella playing the largest role in our inpatient and are hospitalized side when we focus on them the atypicals.

And then, lastly, particularly because a post-viral bacterial pneumonia plays a big role in the number of admissions we see, particularly in the winter months, is Staphylococcus aureus or Staph aureus. So, whether it's MSSA or MRSA, that tends to rear its ugly head sometimes when people are admitted on the inpatient side but definitely on the ICU side. So, those are the slight differences, so certainly atypicals are more common as outpatients.

Legionella is more common in the inpatient side. We see Staph aureus in the severe, which we don't often see in the outpatient side. But regardless of that, S pneumoniae and H influenzae and, to a lesser degree, Moraxella catarrhalis. They tend to play the real big role of across the board for the bacterial side.

Amanda Balbi: So how are the causative organisms identified, and what diagnostic tools are available for that?

Christian Sandrock: For the diagnosis of community-acquired pneumonia, you're going to look at symptomology. You're going to get chest radiography when indicated, showing either lobar or nonlobar patchy, alveolar infiltrates. That comes with it, but identifying the organisms is always an interesting discussion. 

Because if you read the ATS/IDSA guidelines from 2019, there is not a big push for the identification of these organisms, particularly on the outpatient setting. Once you get to the inpatient setting, most notably in the ICU, those are generally recommended. The easiest way to do it is just old school. You get yourself a great sputum culture, or if they're intubated, you can do it via bronchoscopy. Those are some ways to identify by culture and developing sensitivity. That's the easiest way to generally do it.

There are other diagnostic tools available. There are urine antigens, whether we're looking at Legionella or Strep pneumoniae, that's one option that's available. There are other rapid tests, where we can just look at PCR and other antigen-based testings, but most notably PCR testing on the sputum. That will can look at some of these causative agents.

Each of them have their pluses and minuses. The big impact and the big discussion we have is when we look for these causative organisms, how does it change our therapy? Very often, it may not change our therapy on the severe side. It might because our coverage for Staph aureus, for example, would change. But, on the outpatient side, is it really going to change our therapy or mild inpatient hibition? Maybe not.

I think where it does change therapy is not so much what bacterial agent does it have, but is it bacterial or viral? That will change our therapy, because if this appears to be viral, we're not going to give antimicrobials in these cases. I think those are really the best way to look at the bacterial side. I left out all the viral testing, because we're just focusing on the bacterial side, but those are another side of things as well.

Amanda Balbi: Next, can you talk about some instances when additional work up is warranted?

Christian Sandrock: This idea of looking for causative organisms in an extensive workup in a CAP patient, looking for bacterial causes, is often not started initially, but there are some red flags when additional workup is warranted. For example, in the more critically ill, that's where you may want to actually take a look and see if this is Staph aureus, and we mentioned that before.

Some patients will come in with community-acquired pneumonia that tends to be a bit more persistent or recurrent. So, examples there maybe we start looking for other additional structural lung disease or pulmonary issues that may lead to that recurrence. For example, things like bronchiectasis—do they have a large mass where this is presenting a post-obstructive pneumonia?

Then from there, the other areas that are really relatively clear where workup is warranted is if this is a new pleural fusion associated with pneumonia. If they come in, they have a bacterial pneumonia, and there's a new pleural fusion. That's something that's going to need to be tapped or have arthrocentesis performed, evaluated if it is infected or is an empyema—this is parapneumonic effusion or is an empyema repeat drainage—and certainly chest tube placement, if indicated, is going to be warranted. Also, if this is a pleural fusion, a complicated parapneumonic effusion, or an empyema, that's going to change your antimicrobial therapy as well. Most notably, the length of that therapy. So, I think those are certainly warranted. 

Lastly, there's a number of patient characteristics that we'll talk about in a second. But if they’re immunocompromised, if they're a patient who has an ANC of zero, if they're HIV positive and their CD4 cell count is low—these are areas where you're going to look for other etiologic agents outside of Pneumococcus and H influenzae.

Amanda Balbi: Like you alluded to, how do patient characteristics, such as age or comorbidities, affect the treatment options for CABP, the duration of treatment, and the patient journey?

Christian Sandrock: That's a great question. Patient characteristics always play a role. Age is one of them, but there's really this larger question. If you look at the community-acquired pneumonia guidelines, they highlight this. 

The first question really is whether this is inpatient or outpatient. Most notably, outpatient is, “Does this patient have comorbidities?” If the answer is “no,” you can start looking at monotherapy with a macrolide or doxycycline if your resistance rates are not high.

However, if this person does have comorbidities, that's where you're going to shift away from, for example, amoxicillin over to amox clavulanate plus a macrolide. Those characteristics, such as age and other comorbidities—and when we talk about comorbidities, things like hypertension, heart disease, diabetes, alcoholism, COPD; those sort of play the role of comorbidities—and that will shift you away from monotherapy, with a macrolide or amoxicillin over to amox clavulanate plus a macrolide or a fluroquinolone. Those are the big areas that we will see.

Now there are some newer agents as well that would fit under that age and comorbidities umbrella, such as lefamulin or omadacycline. Two of those newer agents also work on the comorbidities side, and they were briefly mentioned in the recent guidelines but not highlighted as strong.

Now the immune system status—this idea of being immunocompromised or if you've actually had a recent admission to the hospital or the ICU—this is where multidrug-resistant gram negatives or resistant patterns for that show up. That may be where we then are going to do an extensive workup and, as we talked about before, look for things such as Pseudomonas, Staph aureus. 

Maybe their immune status to so profound, it is actually not bacterial; it’s fungal. Or it's Pneumocystis, Yoruichi, or any of the other agents that may be present. I think the immune system status really pushes you in a direction to hunt more for the organism, and depending on that organism, the treatment may be a lot more broad. Ideally, comorbidities, with age being one of those comorbidities, is the big branch point of the types of treatment.

Now, duration is 5 days in general, so unless you're looking at an immune-mediated or more complicated nontraditional community-acquired bacterial pneumonia, good duration is going to be 5 days, whether there is or is not the presence of comorbidities.

Amanda Balbi: How would complications and/or multiorgan involvement affect the treatment options for CABP?

Christian Sandrock: Some complications will affect your treatment options. Multiorgan involvement may as well. The most common thing we see is whether, for example, your pneumococcal disease is invasive or noninvasive.

If this is somebody who's going to have Pneumococcus now in their bloodstream—so they're actually bacteremic and/or septic—or it's going to be in another sterile site, pleural space, CSF, and so forth, your treatment is no longer going to be your standard 5 days. That's now going to evolve into a longer treatment course. In general, if this is bacteremia, for example, it's going to be 2 weeks. If this is a complicated parapneumonic effusion or empyema, you're looking at probably a few weeks of therapy plus chest tube drainage. So, that idea of having multiorgan involvement may extend your therapy.

So, when we look at 5 days of treatment for community-acquired bacterial pneumonia, that's when it's isolated to just a pulmonary side of things, so this is an aveolar infection. When it starts moving into the pleural strays, bloodstream, central nervous system, that's where your length of treatment is going to push outwards of 2 weeks. 

Maybe IV only in some of those cases, where oral agents are not going to play the biggest role. Because, you can imagine, that's going to be the CSF, like when fluroquinolone is not your first line of therapy due to its ability to cross the blood-brain barrier.

Amanda Balbi: And so, how would you approach a patient with a polymicrobial infection?

Christian Sandrock: The one thing we do see community-acquired pneumonia, in general, it's going to be a single agent like pneumococcus or H influenzae driving it, but there are cases where you're going to see polymicrobial infections. Those are usually patients who have underlying structural lung disease like bronchiectasis or other forms of pulmonary scarring that may be from a recent hospitalization.

Or they now fall into this category where they're not quite community-acquired bacterial pneumonia, but they have had contact with skilled-nursing facilities, they may have other hardware in place, like a tracheostomy; those are then going to highlight a red flag in your head to say “Okay, this may be more than one organism.”

Generally, in that approach, it's going to be getting some diagnostics, just like we had talked about before, to really see what else is living down there. Most notably where we tend to see that is, again, bronchiectasis or structural lung disease. Or this may not be just H influenzae, maybe H influenzae plus Pseudomonas or H influenzae plus Staph aureus or Staph aureus plus some other gram-negatives, or even anaerobes. 

I think that is going to play a bigger role. That approach is going to be, “We have to get some sort of microbiology to help drive that.” Now, that's not always realistic, and sometimes those are the cases where we don't always have those diagnostic and microbiologic data available.

That's where we might say “Okay, in this case, I'm going to cover with an anaerobe.” I might use something like clindamycin. Or “The risk factors for Pseudomonas are present, even though I didn't actually isolate it. And I'm going to treat for Pseudomonas.” So again, those are often game-time decisions, but I think the cornerstone of the approach to any patient with polymicrobial infection is to find out all the bugs that are living there, and use microbiology to drive your treatment choices.

Amanda Balbi: Great, thank you so much for joining us today, Dr Sandrock. And for our listeners, we do have other parts of this podcast to come. Stay tuned for more!