Previously, my knowledge of MRSA-PNA was limited to something people get in the ICU: nosocomial, associated with repeated hospitalizations/ICU stays, VAP’s etc. Well, while pneumonia caused by methicillin resistant S. aureus only represents 1-5% of all MRSA infections1, turns out it causes a very severe pneumonia in young, healthy adults and children. As a PGY-4 about to graduate, I’m about to inflict my own brand of medicine on the Upper West Side of Manhattan. The thought of very young and healthy people presenting to my ED circling the drain makes all of my sphincters tighten.
So how do I catch these people. Question number one:
1. Do you practice in a location where community acquired MRSA (CA-MRSA) is common?
Check. Seems to me everyone I treat has MRSA, to the point that I have stopped culturing abscesses because they’re all MRSA. If I’m considering antibiotics for my skin and soft tissue infection (SSTI) I’m going to obviously cover for MRSA. Moving on:
2. Has your sick PNA patient recently or do they concomitantly have a viral infection, possibly with influenza A?
I wasn’t aware of this one. Some people even suggest that this might be a prerequisite for an CA-MRSA infection.2 Turns out that outbreaks of CA-MRSA PNA’s tend to follow outbreaks of influenza A outbreaks.3-5 The destruction of respiratory epithelium by the viral infection makes a perfect basement membrane landing area for MRSA to attach!
3. Any history from the patient of hemoptysis? Do labs show leukopenia?
One of the reasons that MRSA is so virulent is that certain strains produce an exotoxin known as Panton-Valentine leukocidin. PVL release causes neutrophil chemotaxis and the release of cytokines that cause tissue damage/death and neutrophil lysis.6 Neutrophil lysis = leukopenia, hemoptysis = lung tissue necrosis, speaking of necrosis….
4. Does the CXR show signs of cavitation, ARDS picture?
MRSA PNA initially will show uni- or multi-lobar infiltrates, but as the disease course progresses, effusions and cavitary lesions may appear on CXR from necrosis of lung tissue.7 The ARDS picture is sequelae from alveolar hemorrhage.
So to summarize, consider CA-MRSA PNA in:
- Severe PNA
- PNA with hemoptysis or leukopenia
- PNA during influenza season
It’s all well and good to recognize CA-MRSA PNA but what to do with it? Obviously we’re going to do all the standard PNA things (blood cultures, fluid resuscitation), but which antibiotics to choose? Vancomycin is the choice of most ER/DR’s given it’s effectiveness against MRSA. However, some recent evidence calls into questions whether Vancomycin becomes concentrated enough if the lung alveoli and may not remain above the mean inhibitory concentration (MIC) to be effective.8 Some advocate for use of Linezolid instead, with the addition of Clindamycin (thought to decrease production of VPL in MRSA PNA).2 But, on the other hand, it’s really expensive (up to $91 PER PILL) and runs the risk of myelosuppression. Here’s my take, if you think your patient is at high risk for CA-MRSA PNA:
CA-MRSA PNA: Vancomycin 15 mg/kg q12h + Clindamycin 900 mg q8h
By PCorey @pcoreyEM
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2. Wallin TR, Hern HG, Frazee BW. Community-Associated Methicillin-Resistant Staphylococcus aureus. Emerg Med Clin N Am 2008;26:431-455
3. Goslings WR, Mulder J, Djajadiningrat J, et al. Staphylococcal pneumonia in inﬂuenza in
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carrying gene for Panton-Valentine leukocidin and highly lethal necrotising pneumonia in
young immunocompetent patients. Lancet 2002;359:753–9.
7. Boussaud V, Parrot A, Mayaud C, et al. Life-threatening hemoptysis in adults with community-acquired pneumonia due to Panton-Valentine leukocidin-secreting Staphylococcus
aureus. Intensive Care Med 2003;29:1840–3.
8. Scheetz MH, Wunderink RG, Postelnick MJ, et al. Potential impact of vancomycin pulmonary distribution on treatment outcomes in patients with methicillin-resistant Staphylococcus aureus pneumonia. Pharmacotherapy 2006;26:539–50