Your SlideShare is downloading. ×
  • Like
2.respiratory infections
Upcoming SlideShare
Loading in...5
×

Thanks for flagging this SlideShare!

Oops! An error has occurred.

×

Now you can save presentations on your phone or tablet

Available for both IPhone and Android

Text the download link to your phone

Standard text messaging rates apply

2.respiratory infections

  • 608 views
Published

 

Published in Education , Health & Medicine
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Be the first to comment
No Downloads

Views

Total Views
608
On SlideShare
0
From Embeds
0
Number of Embeds
0

Actions

Shares
Downloads
44
Comments
0
Likes
1

Embeds 0

No embeds

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
    No notes for slide

Transcript

  • 1. Respiratory Infections
  • 2. Respiratory tract defences
    • Ventilatory flow
    • Cough
    • Mucociliary clearance mechanisms
    • Mucosal immune system
  • 3. 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
  • 4. 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)
  • 5.  
  • 6. Acute epiglottitis
    • H. influenza type B
    • Another cause of acute severe airway compromise in childhood
  • 7. Pneumonia
    • Infection of pulmonary parenchyma with consolidation
  • 8. Pneumonia
    • Gr. “disease of the lungs”
    • Infection involving the distal airspaces usually with inflammatory exudation (“localised oedema”).
    • Fluid filled spaces lead to consolidation
  • 9. Classification of Pneumonia
    • By clinical setting (e.g. community acquired pneumonia)
    • By organism (mycoplasma, pneumococcal etc)
    • By morphology (lobar pneumonia, bronchopneumonia)
  • 10. Pathological description of pneumonia
  • 11. Organisms
    • Viruses – influenza, parainfluenza, measles, varicella-zoster, respiratory syncytial virus (RSV). Common, often self limiting but can be complicated
    • Bacteria
    • Chlamydia, mycoplasma
    • Fungi
  • 12. Lobar Pneumonia
    • Confluent consolidation involving a complete lung lobe
    • Most often due to Streptococcus pneumoniae (pneumococcus)
    • Can be seen with other organisms (Klebsiella, Legionella)
  • 13. Clinical Setting
    • Usually community acquired
    • Classically in otherwise healthy young adults
  • 14. 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
  • 15. Macroscopic pathology
    • Heavy lung
      • Congestion
      • Red hepatisation
      • Grey hepatisation
      • Resolution
      • The classical pathway
  • 16. Lobar pneumonia (upper lobe – grey hepatisation), terminal meningitis
  • 17. Pneumonia – fibrinopurulent exudate in alveoli (grossly “red hepatisation”)
  • 18. Pneumonia – neutrophil and macrophage exudate (grossly “grey hepatisation”)
  • 19. Complications
    • Organisation (fibrous scarring)
    • Abscess
    • Bronchiectasis
    • Empyema (pus in the pleural cavity)
  • 20. Pneumonia – fibrous organisation
  • 21. Bronchopneumonia
    • Infection starting in airways and spreading to adjacent alveolar lung
    • Most often seen in the context of pre-existing disease
  • 22. Bronchopneumonia
  • 23. Bronchopneumonia
    • The consolidation is patchy and not confined by lobar architecture
  • 24. Clinical Context
    • Complication of viral infection (influenza)
    • Aspiration of gastric contents
    • Cardiac failure
    • COPD
  • 25. Organisms
    • More varied – Strep. Pneumoniae, Haemophilus influenza, Staphylococcus, anaerobes, coliforms
    • Clinical context may help. Staph /anaerobes/coliforms seen in aspiration
  • 26. Complications
    • Organisation
    • Abscess
    • Bronchiectasis
    • Empyema
  • 27. 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
  • 28. 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)
  • 29. Diagnosis
    • High index of suspicion
    • Teamwork (physician, microbiologist, pathologist)
    • Broncho-alveolar lavage
    • Biopsy (with lots of special stains!)
  • 30. Immunosuppressed patient – fatal haemorrhage into Aspergillus-containing cavity
  • 31. HIV-positive patient CMV (cytomegalovirus) and “pulmonary oedema” on transbronchial biopsy….
  • 32. Special stain also shows Pneumocystis
  • 33. Tuberculosis
    • 22 million active cases in the world
    • 1.7 million deaths each year (most common fatal organism)
    • Incidence has increased with HIV pandemic
  • 34. 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)
  • 35. Tuberculosis (pathogenesis of clinical disease)
    • Virulence of organisms
    • Hypersensitivity vs. immunity
    • Tissue destruction and necrosis
  • 36. Mycobacterial virulence
    • Related to ability to resist phagocytosis.
    • Surface LAM antigen stimulates host tumour necrosis factor (TNF)  production (fever, constitutional symptoms)
  • 37. 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
  • 38. 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
  • 39. 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
  • 40. 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
  • 41. 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
  • 42. 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
  • 43. Primary TB – Ghon Focus
  • 44. Secondary TB
    • Necrosis
    • Fibrosis
    • Cavitation
    • T cell response: CD4 (helper) enhance killing. CD8 (cytotoxic) kill infected cells giving necrosis
  • 45. Granulomatous inflammation with caseous necrosis
  • 46. Acid fast stain – spot the organism (a red snapper)!
  • 47. Complications
    • Local spread (pleura, lung)
    • Blood spread. Miliary TB or “end-organ” disease (kidney, adrenal etc.)
    • Swallowed - intestines
  • 48. 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
  • 49. Secondary TB – rapid death due to miliary disease
  • 50. Miliary white foci – blood spread to lower lobe
  • 51. “ Galloping consumption” – TB bronchopneumonia
  • 52. Decreased immunity – many more organisms on acid fast stain
  • 53. 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
  • 54. Lung Abscess
    • Localised collection of pus. Central tissue destruction. Lined by granulation tissue/fibrosis (attempted healing)
    • Tumour-like
    • Chronic malaise and fever
  • 55. Lung abscess
    • Organisms:
      • Staphylococcus
      • Anaerobes
      • Gram negatives
    • Clinical contexts:
      • Aspiration
      • Following pneumonia
      • Fungal infection
      • Bronchiectasis
      • Embolic
  • 56. 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
  • 57. Bronchiectasis (2)
    • Affects lower lobes preferentially
    • Chronic recurring infection sometimes leads to finger clubbing
  • 58. Complications of bronchiectasis
    • Pneumonia
    • Abscess
    • Septicaemia
    • Empyema
    • “ Metastatic” abscess
    • Amyloidosis
  • 59. Bronchiectasis with chronic suppuration
  • 60. Bronchiectasis
  • 61. Bronchiectasis distal to an obstructing tumour