2.respiratory infections

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2.respiratory infections

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