Pneumonia

PneumoniaH&P, CXR, procalcitonin, invasive proceduresDefense mechanisms: nose, mucociliary escalator of tracheobronchial ciliated epithelium, alveolar macrophagesSteroids decrease effective macrophage clearanceL respiratory tract usu sterileMicrobial 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 situationsOrganisms are 1-10microns, eg TB, influenza, histoplasmosis

Hematogenous spread, direct penetration, or direct extension from a close infectionLobar 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 pneumonia4 stages if untreated: Congestion: lung starts to become heavy b/c leaky dilated interstitial vessels in response to infx/inflamRed Hepatization: Alveolar spaces fill w/ pus red, SOLID like liverGrey Hepatization: red cells break down, still looks like grey liverResolution: 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 autopsyMicro shows PMNs in alveolar space around larger bronchi

Grossly scattered foci 3-4cmCXR: patchy whiteout

INTERSTITIAL PNEUMONIAInflammation in interstitium NOT in alveolar space, NO gross evidence of consolidation, micro-lymphocytes in the interstitiumDRY, non-productive coughCXR: hazy, dirty looking lung: widened alveolar walls but still filled w/ airMost common causes: mycoplasma pneumonia, virusesComplications: 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 & CXRInfection 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 CXRInfection by bacteria that produce patchy inflammatory changes that are confined to alveolar septum and the

interstitium of the lung; no alveolar infiltration or purulent sputumHospital acquiredImmunocompromised

Pneumococcus (95%): fever, productive cough, consolidation on PE & CXRLancet shaped G+ diplococcic w/ polysaccharide capsule (virulence factor: antigenic, antiphagocytic) + pili + IgA protease

+ autolysin pneumolysin mammalian cell lysisAlpha-hemolytic

Path: colonization, aspiration, attachmentantiphagocytic capsule pneumolysinMicro: 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 laryngotracheobronchitisMicro: 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 stainCulture on buffered charcoal yeast extract (BCYE) agar + cysteinePathogenesis: colonizes air conditioner condensers

Blocks formation of phagolysosome Ruptures macrophages via pore forming toxins

Gross: Bacterial, shows consolidation (broncho type pattern)Micro: PMN’s and macrophagesClinical: depends on the health of the host

If healthy: flu-like = Pontiac feverCOPD + steroids: do not clear organism well: assoc w/ males, respiratory failure, shock

Dx via urinary antigen testing

Anaerobic community-acquired pneumonia, bacterial typeEtiology: bacteriodes, fusobacteria, actinomyces, microaerophilic cocciPath: bad teeth + aspiration (sometimes w/ aerobes that use up O2 and allow anaerobes to thrive)Gross: bronchopneumo or rarely lobar, but can form abscessMicro: heavy PMN infiltrate (b/c bacterial)Clinical: bad teeth, high fever, productive cough

CO-MRSA: community acquired methicillin resistant Staph aureusPath: more likely to be in skin or soft tissue infx than HA-MRSAGross/Micr: similar to othersClinical: often seen in younger, healthier pt w/ a BILATERAL NECROTIZING

pneum + abscess

Community acquired pneumonia, NON bacterial type

Mycoplasma pneumoniaStrictly aerobic, encapsulated, lacks cell wall = pleomorphic; cytoplasmic wall

composed of STEROLSPath: can interfere w/ cilia +/- desquamation of surface epithelium, passed

by respiratory dropletsP1 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 grosslyMicro: classic INTERSTITIAL pneumonitisClinical: classic DRY cough & dirty CXR (no pus)

Gradual onset of HA, fever, chills, malaise followed by dry cough, earacheChlamydia pneumonia: Chlamydial pneum

Path: unclear transmission, obligate intracellular parasite

LPS stimulate inflammationGross: varies upon severityMicro: interstitial lymphs/histiocytesClinical: usu in young adults 1-3wks post pharyngitisPCR gold standard for dx

Viral pneumoniaEtiology: influenza, adenovirus, RSV, etc….Path: spread via droplets, varies w/ severity, often results in bacterial superinfx secondary bacterial pneum Gross: congestion but no consolidationMicro: interstitial lymphs/histiocytesClinical: sx often not respiratoryDx via nasal swab (but insensitive), PCR often done

HOSPITAL ACQUIRED PNEUMONIAPseudomonas aeruginosa pneum: aerobic G- rod w/ LPS, pili, alginate, flagellum, & toxin production tissue invasion

Exotoxin A INH euk elongation factor = protein syn INH cell deathExotoxin S acts on G protein in cell cytoskeleton disruption = cell apoptosisElastase + phospholipase tissue damage & dissemination

>50% of hospital acq pneums (ventilator asso, immunocompromised, eg CF, neutropenic)Gross: BronchoMicro: PMNs w/in alveolar spaceClinical: fever, dyspnea +CXRDx sputum, blood cultures

Enteric G- bacilli: Klebsiella, Serratia, EnterobacterPathogenesis: colonization and aspiration

Klebsiella has an antiphagocytic capsuleGross: Bronchopneumonia or rarely lobar

Klebsiella can produce abcessesMicro: PMN rich in alveolar spaceClinical: fever, sputum and + CXR.

Blood cultures are very important both aerobic and anaerobicRales may be influenced by hydration of patient

Staphylococcal pneum: Staphylococcus aureus, incl hospital-acquired MRSA (HA-MRSA) sepsis + secondary pneumPath: colonization-aspiration or hematogenous infx from infected IV siteGross: broncho, lobar, or abscessMicro: multifocal if hematogenousClinical: varies w/ pt health and route of transmission

IMMUNOCOMPROMISED PNEUMONIANote: typical bacterial pneumonias still occur and can be quite severeSome pulm infiltrates on CXR are NOT infx, rather are lung Karposi’s sarcomaCD4+ T cell counts: >200 bacterial pneum; 50-200 CMV; <50 pneumocystis

Pneumocystis pneumonia = pneumocystis jiroveciPathogenesis: ubiquitous organism fills alveolar spaces with little reactionGross: lung is solid and airlessMicro: alveoli look “foamy” Clinical: may present as resistant infiltrateDx: confirmed by BAL and silver stain

PCR can be done but is usually reserved for non-immunocompromised patients

CMV pneumonia: CytomegalovirusPathogenesis-Similar to “mono” in normal, but immunocompromised pt are overwhelmed

Gross: patchy or diffuse infiltrate seenMicro: classic intranuclear inclusionsClinical: in HIV, common with PCPDx: 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 ptsGross: Can be focal airless consolidationMicro: granulomas not seen, only yeastClinical: can look like miliary TB with fever, night sweats, & weight

lossDx by urine antigen testing or culture. PCR is insensitive