PNEUMONIA

Microbiology of Pneumonia

Clinical Setting Etiologies

Community-

acquired (CAP)

(NEJM

2014;371:1619 &

373:415; Lancet

2015;386:1097)

No pathogen identified in 50–60%, virus alone in ~25%, bacteria alone in ~10%, virus-bacteria

coinfection in <5%

Viruses: influenza, RSV, hMPV, rhinovirus (unknown significance), parainfluenza virus,

coronavirus
S. pneumoniae (most common bacterial cause)

S. aureus (esp. postinfluenza)

Mycoplasma, Chlamydia (esp. in young & healthy)

H. influenzae, M. catarrhalis (esp. in COPD)

Legionella (esp. in elderly, smokers, ↓ immunity, TNF inhibitors)

Klebsiella & other GNR (esp. in alcoholics & aspiration)

Hospital-acquired or

ventilator-assoc.

(HAP/VAP)

S. aureus, Pseudo., Klebsiella, E. coli, Enterobacter, Acinetobacter, Stenotrophomonas. IV abx

w/in 90 d RF for MDR.

Viral~ 20% cases (Chest 2017; 154:1)

Immunosuppressed Above + PCP, fungi, Nocardia, non-TB mycobacteria (NTM), CMV

Aspiration (NEJM

2019;380:651)

Chemical pneumonitis due to aspiration of gastric contents

Bacterial pneumonia ≥24–72 h after aspiration event outPt: oral flora (strep, S. aureus, anaerobes)

inPt or chronically ill: GNR (Pseudomonas) and S. aureus

Clinical manifestations

Presenting features are variable and depend upon several host factors (esp. age)

Classically: fever, cough w/ purulent sputum, consolidation on CXR

Atypical pathogens (Legionella, Mycoplasma, Chlamydia, virus): historically classified as

“atypical” b/c they failed to grow on routine cx. Presentation varies from insidious to

acute; imaging features vary from interstitial infiltrates to tree-in-bud opacities, to

dense consolid.
Clinical and imaging features do NOT distinguish “typical” from “atypical”

Aspiration pneumonitis/PNA: can be infectious or non-infectious; may p/w acute

inflammatory syndrome (fever, ↑ WBC, etc.) or insidious course

HAP/VAP: develops w/in 48 h after admission or mechanical ventilation, respectively

Diagnostic studies

Sputum Gram stain/Cx: reliable if high quality (ie, sputum not spit; <10 squamous

cells/lpf) & if PNA should be purulent (>25 PMNs/lpf). Yield ↓ >10 h after abx (CID

2014;58:1782).

Blood cultures (before antibiotics!): ⊕ in ~10% of inPts, depending on pathogen

Procalcitonin: ↑ in acute bacterial (not viral) PNA. Consider stopping abx if levels <0.25

ng/ml (<0.5 ng/ml in ICU Pts) or ↓ ≥80% from peak. ↓ abx exposure by 2–3 d (Lancet ID

2016;16:819 & 2018;18:95). Not validated in immunocompromised hosts. Levels harder to

interpret in CKD. False ⊕ in cardiac arrest, shock, surgery.

CXR (PA & lateral; see Radiology inserts) → tap effusions if >5 cm or severe PNA