2.respiratory infections
Upcoming SlideShare
Loading in...5

2.respiratory infections






Total Views
Views on SlideShare
Embed Views



0 Embeds 0

No embeds


Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
Post Comment
Edit your comment

2.respiratory infections 2.respiratory infections Presentation Transcript

  • Respiratory Infections
  • Respiratory tract defences
    • Ventilatory flow
    • Cough
    • Mucociliary clearance mechanisms
    • Mucosal immune system
  • Upper respiratory tract infections
    • Rhinitis
      • Rhinovirus, coronavirus, influenza/parainfluenza
      • Non-infective (allergic) rhinitis has similar symptoms (related to asthma)
    • Sinusitis
    • Otitis media
    • Latter 2 have a risk of bacterial superinfection, mastoiditis, meningitis, brain abscess
  • Laryngitis
    • Most commonly upper respiratory viruses
    • Diphtheria
      • C. diphtheriae produces a cytotoxic exotoxin causing tissue necrosis at site of infection with associated acute inflammation. Membrane may narrow airway and/or slough off (asphyxiation)
  • Acute epiglottitis
    • H. influenza type B
    • Another cause of acute severe airway compromise in childhood
  • Pneumonia
    • Infection of pulmonary parenchyma with consolidation
  • Pneumonia
    • Gr. “disease of the lungs”
    • Infection involving the distal airspaces usually with inflammatory exudation (“localised oedema”).
    • Fluid filled spaces lead to consolidation
  • Classification of Pneumonia
    • By clinical setting (e.g. community acquired pneumonia)
    • By organism (mycoplasma, pneumococcal etc)
    • By morphology (lobar pneumonia, bronchopneumonia)
  • Pathological description of pneumonia
  • Organisms
    • Viruses – influenza, parainfluenza, measles, varicella-zoster, respiratory syncytial virus (RSV). Common, often self limiting but can be complicated
    • Bacteria
    • Chlamydia, mycoplasma
    • Fungi
  • Lobar Pneumonia
    • Confluent consolidation involving a complete lung lobe
    • Most often due to Streptococcus pneumoniae (pneumococcus)
    • Can be seen with other organisms (Klebsiella, Legionella)
  • Clinical Setting
    • Usually community acquired
    • Classically in otherwise healthy young adults
  • Pathology
    • A classical acute inflammatory response
      • Exudation of fibrin-rich fluid
      • Neutrophil infiltration
      • Macrophage infiltration
      • Resolution
    • Immune system plays a part antibodies lead to opsonisation, phagocytosis of bacteria
  • Macroscopic pathology
    • Heavy lung
      • Congestion
      • Red hepatisation
      • Grey hepatisation
      • Resolution
      • The classical pathway
  • Lobar pneumonia (upper lobe – grey hepatisation), terminal meningitis
  • Pneumonia – fibrinopurulent exudate in alveoli (grossly “red hepatisation”)
  • Pneumonia – neutrophil and macrophage exudate (grossly “grey hepatisation”)
  • Complications
    • Organisation (fibrous scarring)
    • Abscess
    • Bronchiectasis
    • Empyema (pus in the pleural cavity)
  • Pneumonia – fibrous organisation
  • Bronchopneumonia
    • Infection starting in airways and spreading to adjacent alveolar lung
    • Most often seen in the context of pre-existing disease
  • Bronchopneumonia
  • Bronchopneumonia
    • The consolidation is patchy and not confined by lobar architecture
  • Clinical Context
    • Complication of viral infection (influenza)
    • Aspiration of gastric contents
    • Cardiac failure
    • COPD
  • Organisms
    • More varied – Strep. Pneumoniae, Haemophilus influenza, Staphylococcus, anaerobes, coliforms
    • Clinical context may help. Staph /anaerobes/coliforms seen in aspiration
  • Complications
    • Organisation
    • Abscess
    • Bronchiectasis
    • Empyema
  • Viral pneumonia
    • Gives a pattern of acute injury similar to adult respiratory distress syndrome (ARDS)
    • Acute inflammatory infiltration less obvious
    • Viral inclusions sometimes seen in epithelial cells
  • The immunocompromised host
    • Virulent infection with common organism (e.g. TB) – the African pattern
    • Infection with opportunistic pathogen
      • virus (cytomegalovirus - CMV)
      • bacteria ( Mycobacterium avium intracellulare)
      • fungi (aspergillus, candida, pneumocystis)
      • protozoa (cryptosporidia, toxoplasma)
  • Diagnosis
    • High index of suspicion
    • Teamwork (physician, microbiologist, pathologist)
    • Broncho-alveolar lavage
    • Biopsy (with lots of special stains!)
  • Immunosuppressed patient – fatal haemorrhage into Aspergillus-containing cavity
  • HIV-positive patient CMV (cytomegalovirus) and “pulmonary oedema” on transbronchial biopsy….
  • Special stain also shows Pneumocystis
  • Tuberculosis
    • 22 million active cases in the world
    • 1.7 million deaths each year (most common fatal organism)
    • Incidence has increased with HIV pandemic
  • Tuberculosis
    • Mycobacterial infection
    • Chronic infection described in many body sites – lung, gut, kidneys, lymph nodes, skin….
    • Pathology characterised by delayed (type IV) hypersensitivity (granulomas with necrosis)
  • Tuberculosis (pathogenesis of clinical disease)
    • Virulence of organisms
    • Hypersensitivity vs. immunity
    • Tissue destruction and necrosis
  • Mycobacterial virulence
    • Related to ability to resist phagocytosis.
    • Surface LAM antigen stimulates host tumour necrosis factor (TNF)  production (fever, constitutional symptoms)
  • Organisms
    • M. tuberculosis/M.bovis main pathogens in man
    • Others cause atypical infection especially in immunocompromised host. Pathogenicity due to ability;
      • to avoid phagocytosis
      • to stimulate a host T-cell response
  • Immunity and Hypersensitivity
    • T-cell response to organism enhances macrophage ability to kill mycobacteria
      • this ability constitutes immunity
    • T-cell response causes granulomatous inflammation, tissue necrosis and scarring
      • this is hypersensitivity (type IV)
    • Commonly both processes occur together
  • Pathology of Tuberculosis (1)
    • Primary TB (1st exposure)
      • inhaled organism phagocytosed and carried to hilar lymph nodes. Immune activation (few weeks) leads to a granulomatous response in nodes (and also in lung) usually with killing of organism.
      • in a few cases infection is overwhelming and spreads
  • Pathology of Tuberculosis (2)
    • Secondary TB
      • reinfection or reactivation of disease in a person with some immunity
      • disease tends initially to remain localised, often in apices of lung.
      • can progress to spread by airways and/or bloodstream
  • Tissue changes in TB
    • Primary
      • Small focus (Ghon focus) in periphery of mid zone of lung
      • Large hilar nodes (granulomatous)
    • Secondary
      • Fibrosing and cavitating apical lesion (cancer an important differential diagnosis
  • Primary and secondary TB
    • In primary the site of infection shows non-specific inflammation with developing granulomas in nodes
    • In secondary there are primed T cells which stimulate a localised granulomatous response
  • Primary TB – Ghon Focus
  • Secondary TB
    • Necrosis
    • Fibrosis
    • Cavitation
    • T cell response: CD4 (helper) enhance killing. CD8 (cytotoxic) kill infected cells giving necrosis
  • Granulomatous inflammation with caseous necrosis
  • Acid fast stain – spot the organism (a red snapper)!
  • Complications
    • Local spread (pleura, lung)
    • Blood spread. Miliary TB or “end-organ” disease (kidney, adrenal etc.)
    • Swallowed - intestines
  • The host-organism balance
    • Not all infected get clinical disease
    • Organisms frequently persist following resolution of clinical disease
    • Any diminished host resistance can reactivate (thus 33% of HIV positive are co-infected with TB
  • Secondary TB – rapid death due to miliary disease
  • Miliary white foci – blood spread to lower lobe
  • “ Galloping consumption” – TB bronchopneumonia
  • Decreased immunity – many more organisms on acid fast stain
  • Why does disease reactivate?
    • Decreased T-cell function
      • age
      • coincident disease (HIV)
      • immunosuppressive therapy (steroids, cancer chemotherapy)
    • Reinfection at high dose or with more virulent organism
  • Lung Abscess
    • Localised collection of pus. Central tissue destruction. Lined by granulation tissue/fibrosis (attempted healing)
    • Tumour-like
    • Chronic malaise and fever
  • Lung abscess
    • Organisms:
      • Staphylococcus
      • Anaerobes
      • Gram negatives
    • Clinical contexts:
      • Aspiration
      • Following pneumonia
      • Fungal infection
      • Bronchiectasis
      • Embolic
  • Bronchiectasis
    • Abnormal fixed dilatation of the bronchi
    • Usually due to fibrous scarring following infection (pneumonia, tuberculosis, cystic fibrosis)
    • Also seen with chronic obstruction (tumour)
    • Dilated airways accumulate purulent secretions
  • Bronchiectasis (2)
    • Affects lower lobes preferentially
    • Chronic recurring infection sometimes leads to finger clubbing
  • Complications of bronchiectasis
    • Pneumonia
    • Abscess
    • Septicaemia
    • Empyema
    • “ Metastatic” abscess
    • Amyloidosis
  • Bronchiectasis with chronic suppuration
  • Bronchiectasis
  • Bronchiectasis distal to an obstructing tumour