Pulmonary Infections


Published on

Target: UG medical students.

Published in: Health & Medicine
  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Pulmonary Infections

  1. 1. Pulmonary Infections Dr.CSBR.Prasad, M.D.
  2. 2. Pulmonary infections• Viruses Interstitial Pneumonias• Mycoplasma• Bacterial Bronchopneumonia Lobar pneumonia.• Fungal
  3. 3. Pulmonary infections• Interstitial Pneumonia• Atypical Pneumonia• Viral Pneumonia• Bronchopneumonia• Lobar pneumonia.
  4. 4. Classification1. Etiologic agent Pneumococcal Staphylococcal2. Nature of host reaction Suppurative Fibrinous3. Anatomic distribution Lobular (bronchopneumonia) Lobar Interstitial
  5. 5. Bacterial pneumonia• Bacterial invasion of the lung parenchyma evokes exudative solidification (consolidation) of the pulmonary tissue known as bacterial pneumonia.
  6. 6. PathogenesisDefence mechanisms 1. Filtering function of nasopharynx 2. Mucociliary action of lower air passages 3. Phagocytosis and elimination by alveolar MØ
  7. 7. Pneumonia results when….1. Clearing mechanisms are impaired2. Resistance of the host in general is lowered.
  8. 8. Clearing mechanism interference1.Loss or suppression of cough reflex2.Injury to the mucociliary apparatus3.Interference with phagocytic action of alveolar MØ.4.Pulmonary congestion and edema5.Accumulation of secretions
  9. 9. Clearing mechanism interference1- Loss or suppression of cough reflex coma, anesthesia, neuromuscular disorders, drugs / chest pain, aspiration of gastric contents, Systemic sclerosis
  10. 10. Clearing mechanism interference2.Injury to the mucociliary apparatus impairment of ciliary function destruction of ciliated epithelium cigarette smoke, hot/corrossive gas inhalation, viral diseases, immotile cilia syndrome, Cystic fibrosis
  11. 11. Clearing mechanism interference3. Interference with phagocytic action of alveolar MØ. Alcohol, Tobacco smoke, Anoxia, intoxication.
  12. 12. Clearing mechanism interference4. Pulmonary congestion and edema CHF Hypostatic pulmonary edema.
  13. 13. Clearing mechanism interference4. Accumulation of secretions Cystic fibrosis Bronchial obstructionForeign bodies, Pul. fibrosis, Tumors
  14. 14. Factors affecting resistance of individual 1. Chronic diseases 2. Immunologic deficiency 3. Immunosuppressive treatment 4. Leukemia 5. Unusually virulent infections.
  15. 15. Terminology• If the consolidation is patchy and centered around the terminal bronchiole the patient is said to have bronchopneumonia.• If the consolidation involves the whole of one or more lobes, the disease is called lobar pneumonia.• When the inflammation is predominantly in the alveolar walls with only secondary changes in the alveoli, the condition is termed interstitial pneumonitis.
  16. 16. Bronchopnemonia• Patchy consolidation of lung .• Centered around the terminal bronchiole• Common in extremes of age - infancy/old age• An extension of bronchitis / bronchiolitis.
  17. 17. Etiology of bronchopneumonia Any pathogen • staphylococci, • streptococci, • pneumococci, • haemophilus influenza, • pseudomonas aeroginosa, • coliform bacteia.
  18. 18. Gross pathology – bronchopneumonia1. Patchy distribution in ONE LOBE2. Multiple, bilateral, and basal 3 to 4 cms, slightly elevated dry granular grey red to yellow with poor delimitation at margins.3. Foci of consolidated areas of acute suppurative inflammation4. Confluence produces – lobar pneumonia.
  19. 19. Microscopy of bronchopneumonia• Suppurative exudation involving, bronchi, bronchioles and adjacent alveolar spaces - PMN• Central necrosis• Abscess - fibrosis – resolution.
  20. 20. This slice of lung withbronchopneumonia.Find a row of subpleuralcentrilobular nodules.Find rosettes (2 are marked).Find tree-in-bud patterns (1is marked).
  21. 21. Complications of bronchopneumonia 1. Lung abscess 2. Spread to pleural cavity – empyema 3. Spread to pericardial cavity-suppurative pericarditis. 4. Bacteremia – metastatic abscesses.
  22. 22. BronchopneumoniaGeneral Patchy pneumonia that is localized, often to theDescription bronchioles and surrounding alveoli. One or more of the following symptoms: coughing, chest pains, fever, blood-streakedClinical Signs sputum, chills, and difficulty in breathing. Signs of pulmonary congestion Inhalation of organisms.Pathophysiology Scarring if alveoli destroyed. Patchy distribution in and around small airways Dense acute inflammatory exudate of PMNs, fibrin and blood in bronchi, bronchioles andHistopathology adjacent alveoli. FOCAL destruction of alveolar walls (you can see normal parenchyma in other areas adjacent
  23. 23. Lobar pneumoniaDefinition:It’s an acute bacterial infection of a large portion of a lobe or of an entire lobe, which tends to occur at any age but relatively uncommon in infancy and old age.
  24. 24. Etiology and pathogenesis• Pneumococci ( streptococcus pneumoniae) 1,3,7 and 2 type 3 is virulent form Staphylococci, StreptococciGram negative: Pseudomonas, Proteus, Klebsiella, Haemophilus influenzae.
  25. 25. Pathogenesis of lobar pneumonia• Exudate spread through pores of Kohn• Mucoid encapsulation- protection from phagocytosis. (Pneumococcus, Klebsiella, Hemophilus) Which disease is associated with recurrent infections by capsulated organisms?
  26. 26. Alveolar StructurePores of Kohn
  27. 27. Microscopy of lobar pneumonia• Wide spread fibrinosuppurative consolidation of large areas and even whole lobes of lung.• Serous exudation• Vascular engorgement• Fibrinocellular exudation - resolution / organisation.
  28. 28. Comparison of bronchopneumonia vs. lobar pneumonia Bronchopneumonia Lobar PneumoniaLocation 1. often bilateral large area, even whole lobe involvement 2. basal (i.e. lower lobes)Route of infection spreads from bronchioles to nearby both alveoli and bronchioles alveoliSpread of infection consolidation is patchy Whole lobe becomes consolidatedSusceptible group infants, elderly Adults especially alcoholics and vagrants.Causative Organism Dependent on circumstances Often caused by Pneumococcus or predisposing to infection(i.e. Klebsiella. nosocomial or community acquired)Recovery If treated, recovery usually involves If treated promptly, many recover with focal organisation of lung by lungs returning to normal structure and fibrosis. functioning by resolution. In other cases the exudate in alveoli is organised, leading to lung scarring and permanent lung dysfunction.Notes Patients who are immobile develop Patient are severely ill and usually retention of secretions; thus, most associated bacteriemia. commonly involves the lower lobes.
  29. 29. Pneumonia syndromes1. Community acquired acute pneumonia2. Community acquired atypical pneumonia3. Nosocomial pneumonia4. Aspiration pneumonia5. Chronic pneumonia6. Necrotizing pneumonia & lung abscess7. Pneumonia in immunocompromised host
  30. 30. Community acquired acute pneumonia• Sterptococcus pneumoniae• Moraxella• Haemophilus influenza• Legionella
  31. 31. Community acquired atypical pneumonia• Mycoplasma pneumonia• Chlamydia species• Viruses --- RSV, parainfluenza, Influenza A and B. Adenovirus, SARS
  32. 32. RSV
  33. 33. Nosocomial pneumonia • Gram negative rods • Staph aureus.
  34. 34. Aspiration pneumonia Anaerobic oral flora
  35. 35. Chronic pneumonia• Nocardia, Actinomycosis• Granulomatous: Mycobacterium TB, Atypical mycobacteria, Histoplasma, coccidides.Note: Chronic bacterial pneumonias are usually caused byobstrution of the bronchus supplying the region involved.It’s most common in the part of a lung obstructed by abronchogenic carcinoma.
  36. 36. Necrotizing pneumonia & lung abscess• Anaerobic organisms• Staph aureus
  37. 37. Four stages1. Stage of congestion2. Stage of red hepatization3. Stage of grey hepatization4. Stage of resolution.
  38. 38. Stage of congestion• Represents bacterial infection• Lasts for 24 hrs• Vascular engorgement• Intraalveolar fluid with few PMN + bacteria• Grossly: heavy, boggy, red and subcrepitant.
  39. 39. Stage of red hepatization• Neutrophils + fibrin precipitation• Red cell extravasation• Exudate confluence - obscures pulmonary architecture• Grossly: Lung appears distinctly red, firm airless with liver like consistency.
  40. 40. Stage of grey hepatization• Accumulation of fibrin• Disintegration of WBCs and RBCs.• Clear zone adjacent to alveolar septa.• Grossly: grayish brown dry surface.• Spread to pleural cavity – empyema.
  41. 41. Stage of resolution• Progressive enzymatic digestion to produce granular semifluid debris - resorbed.• Ingestion by MØ -- coughed up .• Gross: normal lung• Pleura: fibrous thickening.
  42. 42. Complications of lobar pneumonia 1. Abundant mucinous secretion 2. Abscess formation 3. Organization of exudate. 4. Bacterial dissemination.
  43. 43. Clinical features of lobar pneumonia 1. Rusty sputum 2. X-ray opaque shadows 3. Limitation of breath sounds 4. Bronchial breath sounds. 5. Fever.
  44. 44. Viral / Mycoplasma pneumonia• Primary atypical pneumonia (PAP)• Acute febrile respiratory disease characterized by patchy inflammatory changes in the lungs, largely confined to alveolar septa and pulmonary interstitium.• Atypical – lacks alveolar exudate.
  45. 45. Etiology of PAP• Mycoplasma pneumonia• RSV• Influenza virus type A & B• Adenovirus• Rhinovirus• Rubeola• Varicella• Chlamydia• Coxiella burnetti (Q fever)
  46. 46. Morphology of PAP• Patchy, may involve whole lobe unilateral / bilateral.• Red blue, congested, subcrepitant• No obvious consolidation• Pleura – normal.
  47. 47. Microscopy of PAP• Interstitial inflammatory reaction• Alveolar septa widened, edematous, L,Hi,pl cells.• Alveoli are free of exudate. NO EXUDATE.• Intraalveolar proteinacious material, cellular exudate.• Characteristic PINK HYALINE EMEMBRANE LINING alveolar damage similar to ARDS.
  48. 48. CMV
  49. 49. RSV
  50. 50. Microscopy of PAP contd.,1- Bacterial infection- Ulcerative bronchitis Bronchiolitis.2- Herpes virus, varicella –Necrosis. Giant cells Intranuclear inclusions.
  51. 51. Clinical features of PAP• Dry hacking cough• Lab: elevated cold agglutinin titres in mycoplasma pneumonia.
  52. 52. Lung abscess• Local suppurative process within in the lung characterised by necrosis (liquifactive necrosis) of lung tissue.• Common in males.
  53. 53. Etiology of lung abscess• Any pathogen• Staphylococcus aureus• Gram negative organisms• Anaerobic Bacteroides Fusobacterium
  54. 54. Etiology contd.,1. Aspiration of infective material2. Antecedent primary bacterial infection3. Septic embolism4. Neoplastic5. Miscellaneous6. Primary cryptogenic
  55. 55. Aspiration of infective material • Coma • Alcoholism • Anesthesia • Sinusitis • Gingivodental sepsis
  56. 56. Antecedent primary bacterial infection • Post pneumonic Staph aureus Klebsiella • Bronchiectasis
  57. 57. Septic embolism• Thrombophlebitis• Infective endocarditis
  58. 58. Neoplastic• Secondary to inflammation by obstruction.
  59. 59. Miscellaneous• Direct trauma• Esophagus, spine, diaphragm, pleura etc.,
  60. 60. Morphology of lung abscess• mm to 5 to 6 cms• Common on right side, mostly single.• In pneumonia / bronchiectasis – Multiple, basal, diffusely scattered.• Cavity with or without suppurative debris• Contd infection-large fetid, green black multilocular cavity with poor margins• GANGRENE OF LUNG.
  61. 61. Causes of pulmonary infiltrates in immunocompromised hosts Diffuse infiltrates Focal infiltratesCommon CommonCMV, P.carinii, Drugs GN rods, Staph.aureus Aspergillus, Candida, MalignancyUNCOMMON UNCOMMONBacteria, Aspergillus, Cryptococcus, Mucor, P.carinii,Cryptococcus, Malignancy Legionella pneumophila.
  62. 62. E N Dgoto Chronic Bronchitis