Pneumonia

H&P, CXR, procalcitonin, invasive procedures

Defense mechanisms: nose, mucociliary escalator of tracheobronchial ciliated epithelium, alveolar
macrophages
Steroids decrease effective macrophage clearance
L respiratory tract usu sterile
Microbial transmission:
Most commonly: aspiration of organisms that colonize oropharynx (eg
during the night)
Transient colonization during the year, some organisms colonize the oropharynx only in
certain situations
Organisms are 1-10microns, eg TB, influenza, histoplasmosis
Hematogenous spread, direct penetration, or direct
extension from a close infection
Lobar pneumonia vs bronchopneumonia both are
bacterial
LOBAR PNEUMONIA: alveolar spaces filled w/ pus =
complete consolidation of entire lobe of lung
95% of time is Pneumococcus = Streptococcus
pneumonia
4 stages if untreated:
Congestion: lung starts to become heavy b/c leaky dilated
interstitial vessels in response to infx/inflam
Red Hepatization: Alveolar spaces fill w/ pus red,
SOLID like liver
Grey Hepatization: red cells break down, still looks like
grey liver
Resolution: healing stage, start to cough up pus/debris
CXR: looks white
BRONCHOPNEUMONIA: patchy consolidation through more
than one lobe (dz process centered around airway)
Usu bacterial in origin, common finding at autopsy
Micro shows PMNs in alveolar space around
larger bronchi
Grossly scattered foci 3-4cm
CXR: patchy whiteout
INTERSTITIAL PNEUMONIA
Inflammation in interstitium NOT in alveolar space, NO
gross evidence of consolidation, micro-lymphocytes in the
interstitium
DRY, non-productive cough
CXR: hazy, dirty looking lung: widened alveolar walls but
still filled w/ air
Most common causes: mycoplasma pneumonia, viruses
Complications:
Lung abscess, Empyema, Organization, Bacteremia/septicemia goes to heart valves, CNS, or
joints
Goal in pneum dx: what is the bug? Classification based upon clinical presentation
Community acquired: bacterial vs non-bacterial
Typical: Pneumococcus (95%), sx: fever, productive cough, consolidation on PE & CXR
Infection by bacteria that multiply extracellularly in alveoli and cause
inflammation and exudation of fluid into the air-filled spaces of alveoli (consolidation)
Other causes: Staph aureus (coagulase +, B-hemolytic); H. influenzae, Klebsiella
pneumoniae (encapsulated G- rods, common cause of aspiration pneum)

Atypical: Mycoplasma, walking pneumonia, at best low grade fever, dry hacking cough, no
evidence of consolidation on either PE or CXR
Infection by bacteria that produce patchy inflammatory changes that are
confined to alveolar septum and the interstitium of the lung; no alveolar infiltration or
purulent sputum
Hospital acquired
Immunocompromised
Pneumococcus (95%): fever, productive cough, consolidation on PE & CXR
Lancet shaped G+ diplococcic w/ polysaccharide capsule (virulence factor: antigenic,
antiphagocytic) + pili + IgA protease + autolysin pneumolysin mammalian cell lysis
Alpha-hemolytic
Path: colonization, aspiration, attachmentantiphagocytic capsule pneumolysin
Micro: PMNs (since bacterial)
Clinical features: typical pneum
Hemophilius Influenzae (type B or non-type B): usu broncho pneumonia (or progress to lobar)
Pathogenesis: colonization, aspiration, can result in laryngotracheobronchitis
Micro: PMNs (since bacterial)
Clinical: Pediatric emergency
Legionella pneumophilia: Legionnaires Disease
Lobar pneum w/ HA, high fever, chills, dry cough, chest
pain
Often multilobe w/ rapid progression (necrotizing)
Fastidious G- rod, poorly staining, use SILVER stain
Culture on buffered charcoal yeast extract (BCYE)
agar + cysteine
Pathogenesis: colonizes air conditioner condensers
Blocks formation of phagolysosome
Ruptures macrophages via pore forming toxins
Gross: Bacterial, shows consolidation (broncho type pattern)
Micro: PMNs and macrophages
Clinical: depends on the health of the host
If healthy: flu-like = Pontiac fever
COPD + steroids: do not clear organism well: assoc w/ males, respiratory failure, shock
Dx via urinary antigen testing
Anaerobic community-acquired pneumonia, bacterial type
Etiology: bacteriodes, fusobacteria, actinomyces, microaerophilic cocci
Path: bad teeth + aspiration (sometimes w/ aerobes that use up O2 and allow anaerobes to
thrive)
Gross: bronchopneumo or rarely lobar, but can form abscess
Micro: heavy PMN infiltrate (b/c bacterial)
Clinical: bad teeth, high fever, productive cough
CO-MRSA: community acquired methicillin resistant Staph aureus
Path: more likely to be in skin or soft tissue infx than HA-MRSA
Gross/Micr: similar to others
Clinical: often seen in younger, healthier pt w/ a BILATERAL NECROTIZING pneum + abscess

Community acquired pneumonia, NON bacterial type

Mycoplasma pneumonia
Strictly aerobic, encapsulated, lacks cell wall = pleomorphic;
cytoplasmic wall composed of STEROLS
Path: can interfere w/ cilia +/- desquamation of surface
epithelium, passed by respiratory droplets
P1 protein binds sialic acid R on ciliated bronchial epithelial
cells attach to luminal surface + INH ciliary action patches
of affected mucosa desquamate inflammatory rxn lack of
cilia = decreased mucus clearance = dry cough
Gross: very little seen grossly
Micro: classic INTERSTITIAL pneumonitis
Clinical: classic DRY cough & dirty CXR (no pus)
Gradual onset of HA, fever, chills, malaise followed by dry cough, earache
Chlamydia pneumonia: Chlamydial pneum
Path: unclear transmission, obligate intracellular parasite
LPS stimulate inflammation
Gross: varies upon severity
Micro: interstitial lymphs/histiocytes
Clinical: usu in young adults 1-3wks post pharyngitis
PCR gold standard for dx
Viral pneumonia
Etiology: influenza, adenovirus, RSV, etc.
Path: spread via droplets, varies w/ severity, often results in bacterial superinfx secondary
bacterial pneum
Gross: congestion but no consolidation
Micro: interstitial lymphs/histiocytes
Clinical: sx often not respiratory
Dx via nasal swab (but insensitive), PCR often done
HOSPITAL ACQUIRED PNEUMONIA
Pseudomonas aeruginosa pneum: aerobic G- rod w/ LPS, pili, alginate, flagellum, & toxin production
tissue invasion
Exotoxin A INH euk elongation factor = protein syn INH cell death
Exotoxin S acts on G protein in cell cytoskeleton disruption = cell apoptosis
Elastase + phospholipase tissue damage & dissemination
>50% of hospital acq pneums (ventilator asso, immunocompromised, eg CF, neutropenic)
Gross: Broncho
Micro: PMNs w/in alveolar space
Clinical: fever, dyspnea +CXR
Dx sputum, blood cultures
Enteric G- bacilli: Klebsiella, Serratia, Enterobacter
Pathogenesis: colonization and aspiration
Klebsiella has an antiphagocytic capsule
Gross: Bronchopneumonia or rarely lobar
Klebsiella can produce abcesses
Micro: PMN rich in alveolar space
Clinical: fever, sputum and + CXR.
Blood cultures are very important both aerobic and anaerobic
Rales may be influenced by hydration of patient
Staphylococcal pneum: Staphylococcus aureus, incl hospital-acquired MRSA (HA-MRSA) sepsis +
secondary pneum
Path: colonization-aspiration or hematogenous infx from infected IV site
Gross: broncho, lobar, or abscess

Micro: multifocal if hematogenous

Clinical: varies w/ pt health and route of transmission
IMMUNOCOMPROMISED PNEUMONIA
Note: typical bacterial pneumonias still occur and can be quite severe
Some pulm infiltrates on CXR are NOT infx, rather are lung Karposis sarcoma
CD4+ T cell counts: >200 bacterial pneum; 50-200 CMV; <50 pneumocystis
Pneumocystis pneumonia = pneumocystis jiroveci
Pathogenesis: ubiquitous organism fills alveolar spaces with little reaction
Gross: lung is solid and airless
Micro: alveoli look foamy
Clinical: may present as resistant infiltrate
Dx: confirmed by BAL and silver stain
PCR can be done but is usually reserved for non-immunocompromised patients
CMV pneumonia: Cytomegalovirus
Pathogenesis-Similar to mono in normal, but immunocompromised pt are overwhelmed
Gross: patchy or diffuse infiltrate seen
Micro: classic intranuclear inclusions
Clinical: in HIV, common with PCP
Dx: often with PCR on BAL or evidence of CMV cytopathic effect on cytology specimens
Histoplasmosis pneumonia: Histoplasma capsulatum
Pathogenesis: Histo lives in soil and is inhaled
Granulomas in normal pt but not in these pts
Gross: Can be focal airless consolidation
Micro: granulomas not seen, only yeast
Clinical: can look like miliary TB with fever, night
sweats, & weight loss
Dx by urine antigen testing or culture. PCR is
insensitive