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New notes

  • Gary Velan: "Clancy lecture theatre should be reserved only for when other lecture theatres overflow" HAHAHAHA
  • Definition: Microbial invasion of the lung parenchyma and the associated host response
    • Parenchyma = everything distal to the terminal bronchioles (the respiratory parts of the lung)
  • In influenza epidemics, the most common cause of death is a superimposed pneumonia

Classification schemes

  • Acute or chronic
    • (chronic is scarce)
  • Typical or atypical
    • Typical = inflammation primarily in the alveolar spaces, with interstitial infiltrate in the lungs
    • Atypical = inflammation primarily in the alveolar septa, with intra-alveolar protein exudate in many cases
  • Community acquired (CAP) or nosocomial (health care-associated pneumonia – HCAP)
  • Normal host or immunocompromised
  • Microbial agent
  • Radiological (pathological)
    • Lobar (in one lobe), or patchy (bronchopneumonia)

Common causes

  • Bacteria
    • Strep. pneumoniae <-- most common by far, particularly in community acquire pneumonia (a.k.a. pnemococcus)
    • Staph. aureus <-- common in the immunocompromised, results in abscess formation
    • H. influenzae
    • Legionella sp.
    • Pseudomonas aeruginosa
    • Enterobacteriaceae <-- common in the ventilated; often multi-drug resistant in hospital
      • E. coli
      • Klebsiella pneumoniae
      • Serratia sp.
      • Enterobacter sp.
    • Moraxella catarrhalis
  • Bacteria-like agents
    • Mycoplasma pneumoniae <-- causes atypical pneumonia, common in school epidemics
    • Chlamydia pneumoniae
    • Chalmydia psittaci
    • Coxiella burnettic
  • Viral
    • Influenza A and B <-- but often it's the bacterial superinfection that causes pneumonia
    • Adenovirus
  • Fungal
    • Aspergillus sp.
    • Crytococcus neoformans
    • Pneumocystis Jiroveci Pneumonia <-- immunocompromised, HIV patients CD4+ 200<
  • Mycobacteria
    • M. tuberculosis

Lung defences

Lung defenses
  • Our defences usually keep the parenchyma of the lung sterile
  • Cough reflex - rapidly expels things that we accidentally inhale
  • Mucus blanket coats the epithelium of the trachea and bronchi. It is continuously moved by synchronous beating of the cilia of the epithelium towards the larynx. It is subsequently coughed out or swalled
  • BALT produces secretory IgA to protect against invading bacteria
  • If any bacteria get into the alveoli, we have resident macrophages in the alveoli of the lung, ready to remove pathogens and particles
  • When our immunity is impaired, we're more likely to develop pneumonia

Pathogenesis

  • Failure of host defenses:
    • filtration & humidification of inspired air (in the nasopharynx - allows particles to reach the larynx)
    • epiglottic and cough reflexes (e.g. stroke, excessive alcohol intake, anaesthesia)
    • mucociliary transport (e.g. smoking, viral bronchitis)
    • innate immunity:
      • alveolar macrophages, neutrophils, complement (e.g. pulmonary oedema - more liquid and oxygen tension - reduces macrophage activity)
    • humoral immunity:
      • B lymphocytes, immunoglobulin, complement
    • cellular immunity:
      • T lymphocytes (e.g. HIV/AIDS - for both opportunistic and typical organisms)
  • Formula: Virulent organism and sufficient inoculum

Impaired defenses

  • Extremes of age
  • Impaired drainage of secretions: cystic fibrosis, bronchiectasis, obstructive neoplasm, foreign body
  • Impaired mucociliary apparatus – congenital, post- viral, cigarette smoke
  • Impaired consciousness (suppression of cough reflex): anaesthesia, coma, narcotic drugs, alcohol
  • Static fluid in alveoli - pulmonary oedema
  • Immunodeficiency (innate, humoral, cell-mediated)

Syndromes

  • Acute, community acquired pneumonia
  • Atypical pneumonia
  • Nosocomial (health care-associated) pneumonia
  • Pneumonia in the immunocompromised

Community acquired pneumonia

  • Epidemiology:
    • increased risk at extremes of age (although all ages affected), mid-winter, underlying disease (e.g. alcoholism)
  • Symptoms:
    • chills, rigors (shaking), productive cough (might look rusty due to exit of RBCs in alveoli), pleuritic chest pain (spread of inflammation to pleura surface)
  • Signs:
    • fever, tachypnoea, dullness to percussion, crepitations and/or bronchial breathing (harsh upper airway sounds are not interrupted by air entering alveolar spaces), pleural friction rub
      • fever, tachypnoea and tachycardia is pneumonia until proven otherwise
  • Laboratory findings:
    • neutrophil leucocytosis, hypoxaemia, sputum with PMN and causative organism found on Gram stain

Bacterial pneumonia - pathology

  • Lobar or bronchopneumonic (patchy) patterns (MOST IMPORTANT investigation is chest x-ray, to see pattern)
  • Suppurative inflammation
  • Classical stages
    1. congestion (vasodilation produces exudation in the alveoli due to inflammation; lung appears heavy, red and foggi)
    2. red hepatisation (alveoli filled with neutrophils and fibrinous exudate - a fibrinous suppurative exudate - causes the lung to become solid, like the liver. Congested with blood. Red due to red blood cells)
    3. grey hepatisation (alveoli appear grey after red blood cells lyse)
    4. resolution (exudate is liquified and phagocytosed, mainly by alveolar macrophages, and thencoughed out, leading to a complete return to normal structure and function)

Histology - normal lung

Normal lung
  • Peripheral lung tissue - no major airways
  • High power view of a terminal bronchiole and associated alveolar ducts and alveoli
  • This is the part of the lung affected by pneumonia

Histology - bacterial pneumonia - early

Bacterial pneumonia
  • Filling the alveoli, instead of air, are lots of PMNs, as well as proteinaceous exudate and fibrin
  • Alveolar capillaries would be dilated and congested with blood

Lobar vs broncho-pneumonia

Lobar vs broncho-pneumonia
  • Lobar = occupies and entire lobe/lobes in
  • Broncho = patch, often bilateral and near the base of the lung, often centred around terminal bronchioles (lobular distribution).

Lobar pneumonia - macroscopic

Lobar pneumonia - macroscopic
  • Bottom lobe is solid and in the stage of grey hepatisation
  • Expect fibrinous exudate on the surface of the lung, which would have led to pleuritic chest pain
  • Top lobe is normal but congested with blood


Bronchopneumonia -micro

Bronchopneumonia -micro
  • Patches of consolidation often centred around terminal bronchioles. Tend to be greyish and elevated over the surrounding cut surface of the lung.
  • Patchy in its distribution, some alveoli affected and some aren't. Inflammation can be in different stages at different parts of the lung

Bronchopneumonia - macro

Bronchopneumonia -macro
  • Patch consolidation in the lower lobe of the lung
  • In the upper lung, the patches have become confluent -- called confluent bronchopneumonia. This is a poor prognostic indicator because the pneumonia has spread, and occupied other parts of the lung (affecting gas exchange)

Community acquired pneumonia –Clinicopathological correlation

  • Symptoms:
    • cough: stimulation of the cough reflex by inflammatory process
    • shortness of breath: hypoxaemia (ventilation/perfusion mismatch, shunting)
    • pleuritic chest pain: stimulation of sensory nerve endings in parietal pleura by inflammatory products on visceral pleura
  • Signs
    • tachypnoea: chemoreceptor-mediated response to hypoxaemia
    • fever: re-setting of hypothalamic thermostat by IL-1, TNF-a
    • crepitations: opening of fluid (pus)-filled alveoli
    • dullness to percussion: loss of resonance in consolidated alveoli

Notes

  • Include hypoxaemia
  • Hypothalamic thermostate = PGE2
  • Shunting - if alveoli are full of inflammatory exudate, the the bloodflow through these alveoli go straight through to the pulmonary vein without oxygenation (as if there is shunting of some of the
  • Pleuritic chest pain is due to inflammation on surface of the pleura, due to inflammatory markers and fibrin stimulating pain fibres -- sharp, stabby chest pain exacerbated on breathing

Investigations

  • Imaging
    • Chest X-ray (most important diagnostic investigation; it shows you consolidation of the lung parenchyma, not just that there's microbe in sputum)
  • Cultures:
    • Sputum (Gram stain, culture, antibiotic sensitivities)
    • Blood (20-30% +ve)
  • Ancillary tests:
    • FBC: neutrophil leucocytosis
    • Inflammatory markers – CRP (acute inflammation and systemic inflammatory response)
    • Arterial blood gases – hypoxaemia (or just use pulse oximetry)

Community acquired pneumonia

  • Microbiology:
    • Streptococcus pneumoniae (most common; most common cause of lobar pneumonia due to polysaccharide capsule; induces a rapid wave of exudation when it reaches the alveoli. It's able to surf that wave of exudation through the alveolar spaces, to spread rapidly throughout the lung. Can also cause patchy pneumonia)
    • Haemophilus influenzae
    • Staphylococcus aureus
    • Legionella pneumophila (stagnant fresh water -- occurs in air conditioning cooling towers)
  • Radiology:
    • lobar or bronchopneumonia


Mostly pneumonia is a local organism (common in nasopharynx) and reaches alveolar spaces through accidental aspiration of microbes (e.g. during sleep, particularly with alcoholism). Gastrointestinal reflux also increases the risk of aspirating colonising organisms.

Chest X rays in pneumonia

  1. Right middle lobe pneumonia, can see consolidation
  2. Right upper lobe
  3. Patchy consolidation affecting mostly the right lung but also spreading to the left lung field in someone with bronchopneumonia

Atypical pneumonia

  • Epidemiology:
    • children, adolescents, young adults; institutions year round occurrence, specific risk factors
  • Symptoms: (nonspecific)
    • 3-4 day prodrome of malaise, then headache,fever, dry cough
  • Signs:
    • typically sparse (sparse signs; usually due to intercellular organisms causing interstitial inflammation rather than exudation in the alveolar spaces)
  • Laboratory findings:
    • typically limited

Atypical pneumonia - pathology

  • Interstitial pneumonia:
    • inflammation predominantly within alveolar septa
    • mononuclear leucocyte infiltrate
    • intra-alveolar protein exudate in many cases
    • hyaline membrane formation (reflects alveolar damage) (can lead to wikipedia:acute respiratory distress syndrome, particularly in influenza epidemics)

Atypical pneumonia - Microscopic

Atypical pneumonia - micro
  • Oedema and exudation into the alveolar septa
  • Shedding of cells into the alveolar spaces
  • Microbiology:
    • Mycoplasma pneumoniae (70%)
    • Chlamydia (Chlamydophila) pneumoniae,
    • Viral: influenza A & B, adenoviruses
    • Coxiella burnetii (Q fever)
    • Chlamydia (Chlamydophila) psittaci (birds)
  • Radiology:
    • typically diffuse, interstitial pattern (different to both those above)

X-ray

  • Diffuse haze in the lower lobes
  • Often radiologically silent

Diffuse alveolar damage

  • Fibrin released can combine with alveolar cell debris, producing hyaline membranes
  • This hyaline appearance is common in acute respiratory distress syndrome
    • Loss of surfactant (harder to breath)
    • Loss of gas exchange
    • Need 100% oxygen; need to treat the underlying disease

Chest X-ray in ARDS

  • Often complete white out of the lung field


Nosocomial (health-care associated) pneumonia

  • Epidemiology:
    • elderly and unwell, hospitals and nursing homes, recent surgery, intubation, broad spectrum antibiotic use
  • Symptoms:
    • fever, deterioration in clinical course
  • Signs:
    • tachypnoea, basal crepitations
  • Laboratory findings:
    • leucocytosis (particularly neutrophils), hypoxaemia
  • Microbiology:
    • Aerobic Gram negative bacilli (60%)
      • Klebsiella pneumoniae, E. coli, Serratia sp., Enterobacter sp., Pseudomonas aeruginosa
      • Like moist environments e.g. tubing of ventilators
      • Often have acquired resistance to antibiotics
    • Staph. aureus
    • Strep. pneumoniae
  • Radiology:
    • variable, often patchy, widespread bronchopneumonia

Pneumonia in the immunocompromised

  • Features closely related to immunodeficiency:
    • HIV: diffuse, interstitial pneumonia; insidious onset, commonly Pneumocystis carinii (jirovecii) (get typical bacteria pneumonia, but once the CD4 count gets low enough, can get opportunistic pneumonia; also can get CMV pneumonia)
    • Acute leukaemia: focal pneumonia, insidious onset with fever and productive cough, often due to Aspergillus fumigatus (can be evasive in the immunosuppressed and can cause systemic infection)
    • Bone marrow transplantation: severe, diffuse interstitial pneumonia, commonly Cytomegalovirus
  • CAUSE POINTS YOU TO LIKELY ORGANISM

Pneumonia - complications

(Mostly associated with typical bacteria pneumonia)

  • Abscess - localised collection of pus in an organ or tissue
  • Empyema - pus in an organ or cavity (e.g. pleural cavity)
  • Disseminated infection
    • Meningitis, septic arthritis, infective endocarditis
    • Septic shock and muliple organ failure (most likely cause of death)
  • Respiratory failure (particularly in widespread pneumonia)
  • Organisation of exudate (if you can't remove it, then scarring can produce permanent reduction in surface area available for gas exchange)

Lung abscess - pathogenesis

  • Aspiration of infective material (most common)
  • Certain bacteria associated with bronchopneumonia (especially S. aureus, Klebsiella pneumoniae, and type 3 pneumococcus; chemotaxis and produces coagulase to localise the infection by converting fibrinogen to fibrin, thus walling it off)
  • Septic embolism (especially from right-sided endocarditis, most common in IVDU)
  • Airway obstruction (obstructed part of the lung becomes infected, and inflammatory products can't be drained)
  • Penetrating injury to the lungs
  • Spread from adjacent organs
  • Hematogenous spread to the lung (e.g. from osteomyelitis in the bone)
  • Rim of consolidation with a hollow centre
  • Develops a sinus to the area of low pressure, giving a productive cough
  • This cough can produce mucus that is foul-smelling, particularly if the causative organism was brought in through the mouth (e.g. oral anaerobes)

Structure and complications

  • Neutrophils in the abscess produce lysosomal enzymes, tending to burrow through the wall, producing a sinus to the airway
  • If a second sinus forms to the pleural cavity, we get a fistula between the pleural cavity and the bronchus
    • Bronchopleural fistula
    • Air and pus can get into the pleural cavity -- pyopneumothorax

Empyema

  • Due to tricuspid endocarditis, leading to a septic embolus to the lung. The woman was an intravenous drug user, causing the tricuspid endocarditis. IVDU is one of the most common casuses of septic emboli to the lung.
  • Air-fluid level on the Lt side due to a pyopneumothorax

Bacterial pneumonia - organisation of exudate

  • Scar tissue filling the alveolar spaces, stopping gas exchange
  • This normally doesn't happen because of the proteases used by neutrophils to break down the fibrin wall, and the fibrrin is then phagocytosed and removed via cough or by lymph drainage

Summary table

Definition

Microbial invasion of the lung parenchyma and the associated host response (note: Parenchyma = everything distal to the terminal bronchioles (the respiratory parts of the lung))

Epidemiology
  • Community acquired pneumonia: increased risk at extremes of age (although all ages affected), mid-winter, underlying disease (e.g. alcoholism)
  • Atypical pneumonia: children, adolescents, young adults; institutions year round occurrence, specific risk factors
Risk factors
  • Extremes of age
  • Impaired drainage of secretions: cystic fibrosis, bronchiectasis, obstructive neoplasm, foreign body
  • Impaired mucociliary apparatus – congenital, post- viral, cigarette smoke
  • Impaired consciousness (suppression of cough reflex): anaesthesia, coma, narcotic drugs, alcohol
  • Static fluid in alveoli - pulmonary oedema
  • Immunodeficiency (innate, humoral, cell-mediated)
    • HIV - diffuse, interstitial pneumonia; insidious onset; commonly Pneumocystis carinii (jirovecii)
    • Acute leukaemia - focal pneumonia, insidious onset with fever and productive cough, often due to Aspergillus fumigatus
    • Bone marrow transplantation - severe, diffuse interstitial pneumonia, commonly CMV
Aetiology

Some examples are:

  • Typical:
    • Lobar: Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis
    • Bronchopneumonia: less likely to be pneumococcus. More likely to be nosocomial, with Staph aureus, Klebsiella, E. Coli and Pseudomonas aeruginosa
  • Atypical: Mycoplasma pneumoniae (70%), chlamydia pneumoniae, influenza A and B, adenoviruses, Coxiella burnetii, Chlamydia psittaci
  • Community acquired
    • Strep pneumoniae (most common)
    • Haemophilus influenzae
    • Staphylococcus aureus
    • Legionella pneumophilia
  • Nosocomial:
    • 60% caused by aerobic gram -ve bacilli
      • Klebsiella pneumoniae, E coli, Serratia sp, Enterobacter sp, Pseudomonas aeruginosa
    • Staph aureus
    • Strep pneumoniae
Pathogenesis
  • A fight between virulence and dose vs host defences
  • Failure of host defences
    • Filtration/humidification of inspired air – filter larger particles
    • Epiglottic, gag/cough reflexes – prevent aspiration that can lead to pneumonia
    • Mucociliary transport – normally transport foreign material from the trachea and bronchioles
      • Have ciliated pseudostratified columnar epithelium with goblet cells
  • Cilia move particles out of the trachea where it can be coughed/swallowed
  • Mucus traps the debris
    • Innate immunity – alveolar macrophages, neutrophils, complement
    • Humoral immunity – B-cells, immunoglobulins (IgG, IgA), complement
    • Cellular immunity – antigens presented to T-cells in hilar lymph nodes
  • Vs virulent organism and sufficient inoculum
  • NB: Failure of host defenses due to:
    • Extremes of age
    • Impaired drainage of secretions: cystic fibrosis, bronchiectasis, obstructive neoplasm, foreign body
    • Impaired mucociliary apparatus – congenital, post- viral, cigarette smoke
    • Impaired consciousness (suppression of cough reflex): anaesthesia, coma, narcotic drugs, alcohol
    • Static fluid in alveoli - pulmonary oedema
    • Immunodeficiency (innate, humoral, cell-mediated)
  • Formula: Virulent organism and sufficient inoculum
  • Suppurative inflammation

Classical stages (lobar pneumonia)

  1. congestion (vasodilation produces exudation in the alveoli due to inflammation; lung appears heavy, red and foggi)
  2. red hepatisation (alveoli filled with neutrophils and fibrinous exudate - a fibrinous suppurative exudate - causes the lung to become solid, like the liver. Congested with blood. Red due to red blood cells)
  3. grey hepatisation (alveoli appear grey after red blood cells lyse)
  4. resolution (exudate is liquified and phagocytosed, mainly by alveolar macrophages, and thencoughed out, leading to a complete return to normal structure and function)
  • Atypical pneumonia: interstitial pneumonia
    • inflammation predominantly within alveolar septa
    • mononuclear leucocyte infiltrate
    • intra-alveolar protein exudate in many cases
    • hyaline membrane formation (reflects alveolar damage) (can lead to wikipedia:acute respiratory distress syndrome, particularly in influenza epidemics)
Morphology
  • Microscopic lobar:
    • Filling the alveoli, instead of air, are lots of PMNs, as well as proteinaceous exudate and fibrin
    • Alveolar capillaries would be dilated and congested with blood
  • Macroscopic lobar (one example):
    • Bottom lobe is solid and in the stage of grey hepatisation
    • Expect fibrinous exudate on the surface of the lung, which would have led to pleuritic chest pain
    • Top lobe is normal but congested with blood
  • Microscopic broncho:
    • Patches of consolidation often centred around terminal bronchioles. Tend to be greyish and elevated over the surrounding cut surface of the lung.
    • Patchy in its distribution, some alveoli affected and some aren't. Inflammation can be in different stages at different parts of the lung
  • Macroscopic broncho (one example):
    • Patch consolidation in the lower lobe of the lung
    • In the upper lung, the patches have become confluent -- called confluent bronchopneumonia. This is a poor prognostic indicator because the pneumonia has spread, and occupied other parts of the lung (affecting gas exchange)
Clinical manifestation
  • Symptoms:
    • cough: stimulation of the cough reflex by inflammatory process
    • shortness of breath: hypoxaemia (ventilation/perfusion mismatch, shunting)
    • pleuritic chest pain: stimulation of sensory nerve endings in parietal pleura by inflammatory products on visceral pleura
    • chills, rigors: systemic inflammation
  • Signs
    • tachypnoea: chemoreceptor-mediated response to hypoxaemia
    • fever: re-setting of hypothalamic thermostat by IL-1, TNF-a
    • crepitations and/or bronchial breathing: opening of fluid (pus)-filled alveoli
    • dullness to percussion: loss of resonance in consolidated alveoli
    • pleural friction rub: inflamed lungs rubbing on pleura
    • hypoxaemia/cyanosis (test ABG)
  • Atypical pneumonia:
    • Symptoms: 3-4 day prodrome of malaise, then headache, fever, dry cough
    • Signs: typically sparse
    • Lab findings: typically limited
Investigations/diagnosis
  • Clinical symptoms and exam (note cyanosis)
  • Imaging
    • CXR (gold standard - to show consolidation)
      • lobar pneumonia shows consolidation of one lobe
      • bronchopneumonia shows patchy consolidation
      • atypical pneumonia shows diffuse haze, interstitial pattern
  • Cultures
    • Sputum sample (gram stain, culture, antibiotic sensitivities), PMNs and causative organism found on gram stain
    • Blood culture if you think there is sepsis -- 20-30% +ve
  • Ancillary tests
    • FBC, white cells (neutrophil leukocytosis), arterial blood gases
    • Inflammatory markers - CRP, ESR (acute inflammation and systemic inflammatory response)
    • Arterial blood gases (ABG) - hypoxaemia (alternatively use a pulse oximeter)
Disease outcome
  • Complications
    • Sepsis
    • Abscess (localised collection of pus in an organi or tissue) --> fistula
    • Empyema (pus in an organ or cavity e.g. pleural cavity)
    • Pulmonary oedema (CCF)
    • Disseminated infection
      • Infective endocarditis, meningitis, septic arthritis
      • Septic shock and multiple organ failure (most likely cause of death)
    • Respiratory failure (particularly in widespread pneumonia)
    • Organisation of exudate (scarring, permanent loss of function)
  • Prognosis

Old notes

Definition

  • Pneumonia (pneumonitis) - microbial invasion of the lung parenchyma and the associated host response
    • An expression of the acute inflammatory process
    • Parenchyma – the gas exchange part of the lung, distal to the terminal bronchioles
  • Pneumonia can be particularly fatal for people with cancer or heart failure
    • “captain of the men of death

Classification factors

See SH/SGs/Respiratory physiology and anatomy: interpretation of investigations

  • Acute or chronic – not very useful except in defining pyogenic infection vs TB
  • Typical or atypical – various microorganisms can express differently, and thus need different treatments
  • Community acquired pneumonia (CAP) or nosocomial/hospital healthcare associated pneumonia (HCAP)
    • CAP – has a certain spectrum of microorganisms, therefore there are certain treatments
    • HCAP – often involves multi-drug resistant strains
  • Normal/immunocompromised host – determines treatment/outcome
  • Microbial agent - makes diagnosis easy and allows specific treatment
  • Radiological (pathological) – eg: lobar, segmental, broncho-pnuemonia (Brisbane disease haha)

Causes

Immune response to airborne antigen
  • Background and setting guides the likelihood of different species
  • Bacteria
    • Streptococcus pneumoniae – pneumococcus (CAP)
  • Gram –ve bacteria like Enterobacteriaceae (E. coli, Klebsiella pneumoniae, Enterobacter sp.) – causes problems with ventilation
    • Pseudomonas aeruginosa – especially a problem in cystic fibrosis
    • Legionella species – can be spread by air conditioned cooling towers
  • Bacteria-like
    • Mycoplasma pneumoniae
    • Chlamydia pneumoniae
    • Chlamydia psittaci – associated with birds
    • Coxiella burnetti – causes Q-fever
  • Viruses
    • Influenza A and B
    • Adenovirus
    • Can predispose to bacterial infections because they lower lung defences
  • Fungal
    • Especially affect immunosuppressed
    • Aspergillus
    • Cryptococcus neoformans – causes HIV meningitis
  • Mycobacteria
    • Mycobacteria tuberculosis

Pathogenesis

  • A fight between virulence and dose vs host defences
  • Failure of host defences
    • Filtration/humidification of inspired air – filter larger particles
    • Epiglottic, gag/cough reflexes – prevent aspiration that can lead to pneumonia
    • Mucociliary transport – normally transport foreign material from the trachea and bronchioles
      • Have ciliated pseudostratified columnar epithelium with goblet cells
  • Cilia move particles out of the trachea where it can be coughed/swallowed
  • Mucus traps the debris
    • Innate immunity – alveolar macrophages, neutrophils, complement
    • Humoral immunity – B-cells, immunoglobulins (IgG, IgA), complement
    • Cellular immunity – antigens presented to T-cells in hilar lymph nodes
  • Vs virulent organism and sufficient inoculum

Causes of defence impairment

  • Extremities of age – old age and very young
  • Impaired mucus drainage – eg: CF, bronchiectasis (permanent dilation of the airways resulting in easy collapse and thus obstruction), obstructive neoplasm, foreign body
  • Impaired mucociliary apparatus – eg: congenital, post-viral (damage to cells), cigarette smoke
  • Impaired consciousness – cough/gag reflex suppressed (eg. anaesthesia, coma, narcotic drugs, EtOH)
  • Static fluid in alveoli – cardiac failure: pulmonary oedema forms a liquid medium of nutrients
    • Macrophages are less effective in fluid (anoxia and hypoxia also affect macrophages)
  • Immunodeficiency (innate, humoral, cell-mediated)

Pneumonia syndromes

  • Acute, CAP – typical syndrome
  • Atypical pneumonia
  • Nosocomial (HCAP) pneumonia
  • Pneumonia in the immunocompromised

Community acquired pneumonia

Terminal bronchioles and sparse blood vessels are surrounded by alveoli, capillaries are dilated
PMNs, red cells, (red hepatisation), proteinaceous material causes consolidation of the alveoli via fibrin meshwork
  • Epidemiology
    • Increased risk at extremes of age – all ages affected however
    • Increased incidence in mid-winter
    • Increased with underlying disease such as COPD (chronic obstructive pulmonary disease), diabetes mellitus

and alcoholism

  • Symptoms
    • Chills, rigors, productive cough, pleuritic chest pain
  • Signs
    • Fever, tachypnoea, dullness to percussion,
    • Crepitations, bronchial breathing – due to alveoli not opening up because of consolidation
    • Pleural friction rub – inflamed lungs therefore rubbing on pleura
  • Laboratory findings
    • Neutrophil leucocytosis, hypoxaemia (measured by oximetry),
    • Sputum with polymorphonuclear cells, gram stain or culture showing organism (gram +ve cocci)
  • Pathology
    • Lobar – diffuse throughout a certain lobe
    • Bronchopneumonic – multifocal following terminal airways
    • Suppurative (due to pyogenic bacteria)
      • Bacteria releases myopeptides that are chemotactic to neutrophils
    • Classical stages – often not seen anymore due to antibiotics
      • Congestion – exudate into alveoli
      • Red hepatisation – looks like a solid piece of liver made up of neutrophils, fibrin and exudate
        • Red because capillaries are damaged and red cells leak into lung
      • Grey hepatisation – red cells degenerate
      • Resolution
  • Histology:
    • Slide 1:Terminal bronchioles and sparse blood vessels are surrounded by alveoli, capillaries are dilated
    • Slide 2: PMNs, red cells, (red hepatisation), proteinaceous material causes consolidation of the alveoli via fibrin meshwork

Bronchopneumonia vs lobar pneumonia

Bronchopneumonia vs lobar pneumonia
  • Bronchopneumonia
    • Bacteria spread to multiple foci via the airways
    • Some parts are badly affected others are not
    • Can lead to confluent bronchopneumonia and this can appear like lobar pneumonia
  • Lobar
    • Particularly pathogenic strain of TB that can resist phagocytosis
    • Thus can spread in the exudate and infected entire lobe of lung

Symptoms

  • Cough – stimulated by the inflammatory process
    • Purulent sputum if there is exudate
  • Shortness of breath – hypoxaemia (due to low saturation of the blood)
    • A perfusion/ventilation mismatch results in blood perfusing but not being oxygenated and thus causing cyanosis (effectively, lung is not oxygenating blood, blood shunt form R to L heart)
  • Pleuritic chest pain (maybe pain on inspiration)
    • Stimulation of sensory nerve endings in the parietal pleura by inflammation of the visceral pleura

Signs

  • Tachypnoea – chemoreceptor mediated response to hypoxaemia
  • Fever – resetting of hypothalamic thermostat by IL-1, TNF-α
  • Crepitations – opening of fluid (pus)-filled alveoli
  • Dullness to percussion – consolidation of lung tissue (loss of resonance)

Investigations

  • Imaging: chest x-ray (most important diagnostic investigation)
  • Cultures
    • Sputum – can’t identify location of bacteria, can identify bacteria and determine antibiotic sensitivies
    • Blood – 20-30% of cases will turn up +ve
  • Ancillary tests:
    • FBC – neutrophil leucocytosis
    • Inflammatory markers – CRP (C-reactive protein), a systemic marker produced by the liver
    • Arterial blood gases – hypoxaemia

Microbiology

  • Streptococcus pneumoniae (most common)
  • Haemophilus influenzae – especially in COPD, viral infection
  • Staphylococcus aureus – especially with previous viral infection
  • Legionella pneumophila – often found in epidemic settings

Radiology

  • Can determine pattern: lobar or bronchopneumonia
    • Broncho – bilateral diffuse patterns, commonly in base of the lungs
  • More common in debilitated people, CHF, disseminated malignancy
  • Static secretions at base of the lungs provide medium for bacteria to grow
    • Lobar – isolated to one lobe
  • Consolidations appear as opacities

Atypical pneumonia – eg. mycobacterium pneumoniae (intracellular or viruses)

Atypical pneumonia

Epidemiology

  • Children, adolescents, young adults, institutions
  • Year round occurrence

Symptoms

  • 3-4 day prodrome of malaise
  • Then syndrome of headache, fever, and dry cough (non-specific symptoms)
    • Often mistaken for non-specific virus or bronchitis

Signs

  • Sparse, in the interstitium, not alveoli

Laboratory tests

  • Typically limited and unspectacular

Pathology (interstitial pneumonia)

Atypical pneumonia - chest X-ray
  • Inflammation in the alveolar septa (interstitium)
  • Infiltration of mononuclear leucocytes
    • Macrophage, plasma cells, T-lymphocytes
  • Proteinaceous exudate may occur
  • Hyaline membrane formation
    • Caused by alveolar epithelial damage
    • Made up of fibrin, surfactant proteins, and epithelial debris
    • Line alveolar walls and create a barrier between gas and blood causing hypoxaemia
  • This may lead to ARDS (acute respiratory distress syndrome)
  • Slide: alveolar septa are full, there is shedding of epithelial cells into the spaces

Microbiology

  • Mycoplasma pneumoniae (70%)
  • Chlamydia (Chlamydophila) pneumoniae
  • Viral: influenza A and B, adenovirus
  • Coxiella burnetti (Q fever)
  • Chlamydia psittaci

Radiology

  • Hazy reticulonodular appearance
  • Slide: ARDS – diffuse alveolar damage
    • Eosinophilic membranes line damaged alveoli
    • Cause very opaque x-ray

Nosocomial (healthcare associated) pneumonia

Epidemiology

  • Elderly, unwell
  • Hospitals and nursing home
  • Recent surgery, intubation – gram –ve rods colonise ventilator tubing
  • Broad-spectrum antibiotic use – multi-drug resistant strains

Symptoms

  • Fever, deterioration

Signs

  • Tachypnoea, basal crepitations

Laboratory findings

  • Leucocytosis, hypoxaemia

Microbiology

  • Aerobic gram –ve bacilli (60%)
    • Klebsiella pneumoniae, E. coli, Serratia species, Enterobacter species, Pseudomonas aeruginosa
  • Staphylococcus aureus
  • Streptococcus pneumoniae

Radiology

  • Variable, often patchy, widespread bronchopneumonia

Pneumonia in the immunocompromised

Lung abscess - chest X-ray
  • Features of pneumonia are often associated with immunodeficiency
    • HIV:
      • Diffuse, Interstitial pneumonia of insidious onset
      • Commonly due to Pneumocystis carinii (jirovecii) (PCP)
    • Acute leukaemia:
      • Focal pneumonia of insidious onset
      • Fever, productive cough
      • Often due to Aspergillus fumigatus
    • Bone marrow transplantation
      • Severe, diffuse, interstitial pneumonia
      • Often due to cytomegalovirus

Complications of pneumonia

  • Abscess formation
    • Pathogenesis:
      • Aspiration of infective material or gastric acid (most common)
        • Possibly due to impaired consciousness
      • Caused by certain bacteria associated with bronchopneumonia (esp. SA, Klebsiella pneumoniae, type 3 pneumococcus)
      • Septic embolism – of infective endocarditis or teeth gums
      • Airway obstruction
      • Penetrating injury to the lungs
      • Spread from adjacent organs
      • Haematogenous spread to the lung
        • Empyema formation
        • A sinus into the pleural space is formed, pus collects and enters the pleural cavity
  • Disseminated infection
    • Eg: meningitis, septic arthritis, infective endocarditis
    • Septic shock and multiple organ failure
  • Respiratory failure
  • Organisation of exudate – process of granulation – fibrous growth into exudate
    • Thus causes loss of gas exchange in the lungs