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Pulmonary Infections
This document discusses various pulmonary infections including viruses, bacteria, fungi, and their classifications. It describes bronchopneumonia as a patchy pneumonia localized around bronchioles and surrounding alveoli. Lobar pneumonia involves consolidation of an entire lobe and is often caused by pneumococcus. Interstitial pneumonia shows inflammation predominantly in alveolar walls. The document outlines etiologies, pathogenesis, histopathology, and clinical features of different pulmonary infections.
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Introduction to pulmonary infections including types: viruses, mycoplasma, bacteria, and fungi.
Classification based on etiologic agent (e.g., pneumococci), host reaction, and anatomical distribution.
Bacterial pneumonia due to lung invasion, impaired clearing mechanisms affect defenses and lead to infections.
Factors such as chronic diseases, immunologic deficiencies, and immunosuppressive treatments affect individual resistance.
Terminology related to consolidation patterns differentiating bronchopneumonia and lobar pneumonia.
Gross and microscopy pathology revealing patchy consolidation in bronchopneumonia with inflammatory responses.
Potential complications of bronchopneumonia including lung abscesses and spread to surrounding structures.
General description and common clinical signs of bronchopneumonia, highlighting symptoms and pathophysiology.
Definition, etiology, and pathogenesis of lobar pneumonia, characterized by larger infection areas within the lobe.
Microscopic features of lobar pneumonia showing widespread consolidation and associated inflammatory response.
Comparison highlighting symptoms, affected populations, causative organisms, and recovery outcomes.
Different types of pneumonia syndromes including community-acquired, atypical, and aspiration pneumonia.
Common causes of community-acquired atypical pneumonia including mycoplasma and various viruses.
Lung abscess characteristics, causes, and conditions that may lead to its formation in individuals.
Common causes of pulmonary infiltrates in immunocompromised hosts leading to diffuse or focal infiltrates.
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Pulmonary Infections
- 1. Pulmonary Infections Dr.CSBR.Prasad, M.D.
- 2. Pulmonary infections • VirusesInterstitial Pneumonias • Mycoplasma • Bacterial Bronchopneumonia Lobar pneumonia. • Fungal
- 3. Pulmonary infections • InterstitialPneumonia • Atypical Pneumonia • Viral Pneumonia • Bronchopneumonia • Lobar pneumonia.
- 4. Classification 1. Etiologic agentPneumococcal Staphylococcal 2. Nature of host reaction Suppurative Fibrinous 3. Anatomic distribution Lobular (bronchopneumonia) Lobar Interstitial
- 5. Bacterial pneumonia • Bacterialinvasion of the lung parenchyma evokes exudative solidification (consolidation) of the pulmonary tissue known as bacterial pneumonia.
- 6. Pathogenesis Defence mechanisms 1. Filtering function of nasopharynx 2. Mucociliary action of lower air passages 3. Phagocytosis and elimination by alveolar MØ
- 7. Pneumonia results when…. 1.Clearing mechanisms are impaired 2. Resistance of the host in general is lowered.
- 8. Clearing mechanism interference 1.Lossor suppression of cough reflex 2.Injury to the mucociliary apparatus 3.Interference with phagocytic action of alveolar MØ. 4.Pulmonary congestion and edema 5.Accumulation of secretions
- 9. Clearing mechanism interference 1-Loss or suppression of cough reflex coma, anesthesia, neuromuscular disorders, drugs / chest pain, aspiration of gastric contents, Systemic sclerosis
- 10. Clearing mechanism interference 2.Injuryto 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. Clearing mechanism interference 3.Interference with phagocytic action of alveolar MØ. Alcohol, Tobacco smoke, Anoxia, intoxication.
- 12. Clearing mechanism interference 4.Pulmonary congestion and edema CHF Hypostatic pulmonary edema.
- 13. Clearing mechanism interference 4.Accumulation of secretions Cystic fibrosis Bronchial obstruction Foreign bodies, Pul. fibrosis, Tumors
- 14. Factors affecting resistanceof individual 1. Chronic diseases 2. Immunologic deficiency 3. Immunosuppressive treatment 4. Leukemia 5. Unusually virulent infections.
- 15. Terminology • If theconsolidation 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. Bronchopnemonia • Patchy consolidation of lung . • Centered around the terminal bronchiole • Common in extremes of age - infancy/old age • An extension of bronchitis / bronchiolitis.
- 17. Etiology of bronchopneumonia Any pathogen • staphylococci, • streptococci, • pneumococci, • haemophilus influenza, • pseudomonas aeroginosa, • coliform bacteia.
- 18. Gross pathology – bronchopneumonia 1. Patchy distribution in ONE LOBE 2. 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 inflammation 4. Confluence produces – lobar pneumonia.
- 19. Microscopy of bronchopneumonia •Suppurative exudation involving, bronchi, bronchioles and adjacent alveolar spaces - PMN • Central necrosis • Abscess - fibrosis – resolution.
- 25. This slice oflung with bronchopneumonia. Find a row of subpleural centrilobular nodules. Find rosettes (2 are marked). Find tree-in-bud patterns (1 is marked).
- 29. Complications of bronchopneumonia 1. Lung abscess 2. Spread to pleural cavity – empyema 3. Spread to pericardial cavity-suppurative pericarditis. 4. Bacteremia – metastatic abscesses.
- 30. Bronchopneumonia General Patchy pneumonia that is localized, often to the Description bronchioles and surrounding alveoli. One or more of the following symptoms: coughing, chest pains, fever, blood-streaked Clinical 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 and Histopathology adjacent alveoli. FOCAL destruction of alveolar walls (you can see normal parenchyma in other areas adjacent
- 31. Lobar pneumonia Definition: It’s anacute 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.
- 32. Etiology and pathogenesis •Pneumococci ( streptococcus pneumoniae) 1,3,7 and 2 type 3 is virulent form Staphylococci, Streptococci Gram negative: Pseudomonas, Proteus, Klebsiella, Haemophilus influenzae.
- 33. Pathogenesis of lobarpneumonia • Exudate spread through pores of Kohn • Mucoid encapsulation- protection from phagocytosis. (Pneumococcus, Klebsiella, Hemophilus) Which disease is associated with recurrent infections by capsulated organisms?
- 34.
- 41. Microscopy of lobarpneumonia • Wide spread fibrinosuppurative consolidation of large areas and even whole lobes of lung. • Serous exudation • Vascular engorgement • Fibrinocellular exudation - resolution / organisation.
- 46. Comparison of bronchopneumoniavs. lobar pneumonia Bronchopneumonia Lobar Pneumonia Location 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 alveoli Spread of infection consolidation is patchy Whole lobe becomes consolidated Susceptible 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.
- 47. Pneumonia syndromes 1. Community acquired acute pneumonia 2. Community acquired atypical pneumonia 3. Nosocomial pneumonia 4. Aspiration pneumonia 5. Chronic pneumonia 6. Necrotizing pneumonia & lung abscess 7. Pneumonia in immunocompromised host
- 48. Community acquired acute pneumonia • Sterptococcus pneumoniae • Moraxella • Haemophilus influenza • Legionella
- 49. Community acquired atypical pneumonia • Mycoplasma pneumonia • Chlamydia species • Viruses --- RSV, parainfluenza, Influenza A and B. Adenovirus, SARS
- 50.
- 51. Nosocomial pneumonia •Gram negative rods • Staph aureus.
- 52. Aspiration pneumonia Anaerobic oral flora
- 54. Chronic pneumonia • Nocardia,Actinomycosis • Granulomatous: Mycobacterium TB, Atypical mycobacteria, Histoplasma, coccidides. Note: Chronic bacterial pneumonias are usually caused by obstrution of the bronchus supplying the region involved. It’s most common in the part of a lung obstructed by a bronchogenic carcinoma.
- 55. Necrotizing pneumonia & lung abscess • Anaerobic organisms • Staph aureus
- 56. Four stages 1. Stage of congestion 2. Stage of red hepatization 3. Stage of grey hepatization 4. Stage of resolution.
- 57. Stage of congestion • Represents bacterial infection • Lasts for 24 hrs • Vascular engorgement • Intraalveolar fluid with few PMN + bacteria • Grossly: heavy, boggy, red and subcrepitant.
- 59. Stage of redhepatization • Neutrophils + fibrin precipitation • Red cell extravasation • Exudate confluence - obscures pulmonary architecture • Grossly: Lung appears distinctly red, firm airless with liver like consistency.
- 61. Stage of greyhepatization • Accumulation of fibrin • Disintegration of WBCs and RBCs. • Clear zone adjacent to alveolar septa. • Grossly: grayish brown dry surface. • Spread to pleural cavity – empyema.
- 63. Stage of resolution •Progressive enzymatic digestion to produce granular semifluid debris - resorbed. • Ingestion by MØ -- coughed up . • Gross: normal lung • Pleura: fibrous thickening.
- 64. Complications of lobarpneumonia 1. Abundant mucinous secretion 2. Abscess formation 3. Organization of exudate. 4. Bacterial dissemination.
- 66. Clinical features oflobar pneumonia 1. Rusty sputum 2. X-ray opaque shadows 3. Limitation of breath sounds 4. Bronchial breath sounds. 5. Fever.
- 67. Viral / Mycoplasmapneumonia • 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.
- 68. Etiology of PAP • Mycoplasma pneumonia • RSV • Influenza virus type A & B • Adenovirus • Rhinovirus • Rubeola • Varicella • Chlamydia • Coxiella burnetti (Q fever)
- 69. Morphology of PAP •Patchy, may involve whole lobe unilateral / bilateral. • Red blue, congested, subcrepitant • No obvious consolidation • Pleura – normal.
- 70. 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.
- 73.
- 74.
- 75. Microscopy of PAPcontd., 1- Bacterial infection- Ulcerative bronchitis Bronchiolitis. 2- Herpes virus, varicella –Necrosis. Giant cells Intranuclear inclusions.
- 76. Clinical features ofPAP • Dry hacking cough • Lab: elevated cold agglutinin titres in mycoplasma pneumonia.
- 77. Lung abscess • Localsuppurative process within in the lung characterised by necrosis (liquifactive necrosis) of lung tissue. • Common in males.
- 78. Etiology of lungabscess • Any pathogen • Staphylococcus aureus • Gram negative organisms • Anaerobic Bacteroides Fusobacterium
- 79. Etiology contd., 1. Aspiration of infective material 2. Antecedent primary bacterial infection 3. Septic embolism 4. Neoplastic 5. Miscellaneous 6. Primary cryptogenic
- 80. Aspiration of infectivematerial • Coma • Alcoholism • Anesthesia • Sinusitis • Gingivodental sepsis
- 81. Antecedent primary bacterial infection • Post pneumonic Staph aureus Klebsiella • Bronchiectasis
- 82. Septic embolism • Thrombophlebitis •Infective endocarditis
- 83. Neoplastic • Secondary toinflammation by obstruction.
- 85. Miscellaneous • Direct trauma •Esophagus, spine, diaphragm, pleura etc.,
- 86. Morphology of lungabscess • 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.
- 94. Causes of pulmonaryinfiltrates in immunocompromised hosts Diffuse infiltrates Focal infiltrates Common Common CMV, P.carinii, Drugs GN rods, Staph.aureus Aspergillus, Candida, Malignancy UNCOMMON UNCOMMON Bacteria, Aspergillus, Cryptococcus, Mucor, P.carinii, Cryptococcus, Malignancy Legionella pneumophila.
- 95. E N D gotoChronic Bronchitis