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Pneumonias and Fungal infections

Pneumonias and Fungal infections. Dr.FARHANA ZAKARIA. PNUEMONIA. Defined as acute infection of the lung parenchyma distal to the terminal bronchioles. Pathogenesis. Microorganisms gain entry into the lungs by one of the following routes : Inhalation of microbes present in air

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Pneumonias and Fungal infections

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  1. Pneumonias and Fungal infections Dr.FARHANA ZAKARIA

  2. PNUEMONIA • Defined as acute infection of the lung parenchyma distal to the terminal bronchioles

  3. Pathogenesis • Microorganisms gain entry into the lungs by one of the following routes : • Inhalation of microbes present in air • Aspiration of organisms from the nasopharynx or oropharynx • Hematogenous spread from a distant focus of infection • Direct spread from an adjoining site of infection.

  4. Etiologic classification of pneumonias • BACTERIAL PNEUMONIA • Lobar pneumonia • Bronchopneumonia • VIRAL AND MYCOPLASMAL PNEUMONIA • OTHER TYPES OF PNEUMONIAS • Pneumocystiscarini pneumonia • Legionella pneumonia • Aspiration pneumonia

  5. Anatomical classification • Lobar pneumonia • Broncho pneumonia • Interstitial pneumonia

  6. Bacterial pneumonia • Most common cause of pneumonia

  7. Lobar pneumonia • Is an acute bacterial infection of a part of a lobe , the entire lobe or even two lobes of one or both the lungs • Lower lobes are affected most commonly • Etiology • Pneumococcal pneumonia – more than 90% of all lobar pneumonias are caused by streptococcus pneumoniae . • Is community acquired infection

  8. Staphylococcal pneumonia – staphylococcus aureus causes pneumonia by hematogenous spread of infection. • Streptococcal pneumonia – β-hemolytic streptococci cause pneumonia in severely debilitated elderly patients and in diabetics • Pneumonia by gram-negative aerobic bacteria • Like haemophilus influenza , klebsiella pneumonia, pseudomonas, proteus , E coli , H.influenza.

  9. Morphologic features • Lobar pneumonia can be divided into 4 sequential pathologic phases: • Stage of congestion • Red hepatisation • Grey hepatisation • Resolution

  10. Stage of congestion – initial phase • Represents early acute inflammatory response to bacterial infection and lasts for 1 to 2 days. • Grossly – affected lobe is enlarged , heavy , dark red and congested . • C/S exudes blood-stained frothy fluid

  11. Histologically : • Dilatation and congestion of capillaries in the alveolar walls. • Pale eosinophilic edema fluid in the air spaces • Few red cells and neutrophils in the intra-alveolar fluid. • Numerous bacteria demonstrated in the alveolar fluid by gram’s staining.

  12. Red hepatisation – early consolidation • Lasts for 2 to 4 days • Liver-like consistency of afected lobe on C/S • Grossly: • Affected lobe is red , firm and consolidated • C/S of involved lobe is airless , red-pink , dry , granular and has liver-like consistency • Accompanied by serofibrinous pleurisy.

  13. Histologically , • Edema fluid of preceding stage is replaced by strands of fibrin • Marked cellular exudate of neutrophils and extravasation of red cells • Many neutrophils show ingested bacteria • The alveolar septa are less prominent than in the first stage due to cellular exudation.

  14. Grey hepatisation – late consolidation • This phase lasts for 4 to 8 days • Grossly , the affected lobe is firm and heavy. • C/S is dry, granular and grey in appearance with liver-like consistency . • Change in color from red to grey begins at hilum and spreads towards the periphery . • Fibrinous pleurisy is prominent.

  15. Histologically, • Fibrin strands are dense and more numerous • Cellular exudate of neutrophils is reduced due to disintegration of many inflammatory cells. Red cells are also fewer. • Macrophages begin to appear in the exudate • Cellular exudate is often separated from the septal walls by a thin clear space. • Organisms are less numerous and appear as degenerated forms.

  16. Resolution • This stage begins by 8th to 9th day if no chemotherapy is administered and completed in 1 to 3 weeks. • Grossly , • Previously solid fibrinous constituent is liquefied by enzymatic action , eventually restoring normal aeration in the affected lobe.

  17. Process of softening begins centrally and spreads to periphery. • C/S is grey- red or dirty brown and frothy , yellow , creamy fluid can be expressed on pressing. • Pleural reaction may also show reaction but may undergo organisation leading to fibrous obliteration of pleural cavity.

  18. Histologically , • Macrophages are predominant cells in the alveolar spaces , neutrophils diminish in number. • Granular and fragmented strands of fibrin in the alveolar spaces are seen • Alveolar capillaries are engorged • There is progressive removal of fluid content as well as cellular exudate from the air spaces.

  19. Complications • Organisation • Pleural effusion • Empyema • Lung abscess • Metastatic infection

  20. Bronchopneumonia • Infection of terminal bronchioles that extends into surrounding alveoli resulting in patchy consolidation of lung. • Frequent at extremes of life , as a terminal event in chronic debilitating diseases and as a secondary infection following viral respiratory infections • Common organisms- staphylococci , streptococci , pneumococci , klebsiella pneumonia, haemophilus influenza , pseudomonas.

  21. Gross • Patchy areas of red or grey consolidation affecting one or more lobes , frequently found bilaterally and more often involving lower zones of the lungs . • C/S – dry , granular , firm , red or grey in color , 3 to 4 cms in diameter , slightly elevated over the surface and are often centered around a bronchiole.

  22. Histologically • Acute bronchiolitis • Suppurativeexudate in the peribronchiolar alveoli • Thickening of the alveolar septa by congested capillaries and leucocytic infiltration • Less involved alveoli contain edema fluid.

  23. Fungal infections of lung • More common than tuberculosis in US. • These infections in healthy individuals are rarely serious but in immunosuppressed individuals may prove fatal

  24. Histoplasmosis • Caused by histoplasmacapsulatum • By inhalation of infected dust or bird droppings. • May remain asymptomatic or may produce lesions similar to ghon’s complex.

  25. Coccidioidomycosis • Caused by coccidioidesimmitis , spherical spores • Infection is acquired by close contact with infected dogs. • Lesions consist of peripheral parenchymalgranuloma in the lung

  26. Cryptococcosis • Caused by cryptococcusneoformans which is round yeast having a halo around it due to shrinkage in tissue sections. • Infections occurs by inhalation of pigeon droppings. • Lesions range from small parenchymalgranuloma in the lung to cryptococcal meningitis.

  27. Blastomycosis • Caused by blastomycesdermatitidis. • Result from inhalation of spores in the ground. • May present as ghon’s complex-like lesion , as a pneumonic consolidation , and as multiple skin nodules.

  28. Aspergillosis • Most common fungal infection of the lung caused by aspergillusfumigatus. • Fungus exists as a thin septatehyphae with dichotomous branching and grows best in cool , wet climate. • Result in allergic bronchopulmonaryaspergillosis , aspergilloma and necrotising bronchitis.

  29. Immunocompromised persons develop more serious manifestations of aspergillus infection.

  30. Mucormycosis • Caused by Mucor and Rhizopus. • Pulmonary lesions are especially common in patients with diabetic ketoacidosis.

  31. Candidiasis • Caused by candidaalbicans.- normal commensal in oral cavity, gut and vagina. • Attains pathological forms in immunocompromised host. • Angio-invasive growth of the organism occurs in the airways.

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