Chronic granulomatous inflammation


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Chronic granulomatous inflammation

  1. 1. Chronic Granulomatous Inflammation Prepared by: Rana Ahsan Javed Roll No. 255 3rd Year MBBS
  2. 2. Chronic Inflammation► Definition:  Inflammation of prolonged duration in which active inflammation, tissue injury and the healing proceed simultaneously  Endogenous (Atherosclerosis)► Causes:► Persistent Infections  Ex. Treponema palladium (causative organism of syphilis)  Organism of low toxicity and evoke an immune reaction = delayed hypersensitivity► Prolonged Exposure to toxic Agents,  Exogenous (Silicosis)► Autoimmunity  Ex. Autoimmune diseases
  3. 3. Definition:► Granulomatous inflammation is a distinctive pattern of chronic inflammatory reaction► It is a protective response to chronic infection or foreign material, preventing dissemination and restricting inflammation.► Some autoimmune diseases such as rheumatoid arthritis and Crohns disease are also associated with granulomas.
  4. 4. Granuloma:► Epithelioid cells fuse to form giant cells containing 20 or more nuclei.► The nuclei arranged either peripherally (Langhans-type giant cell ) or► haphazardly (foreign body-type giant cell).► These giant cells can be found either at the periphery or the center of the granuloma.
  5. 5. Granulomatous inflammation► Types of Granulomatous Inflammation► 1. Immune granulomas  Caused by insoluble particles that are capable of inducing a cell- mediated immune response  Macrophages are transformed into Epitheloid cells and multinucleate giant cells  Examples: ► Bacteria  Tuberculosis *** (high incidence due to drug resistant stains)  Leprosy ► Parasites  Schistosomiasis (3 types) ► Fungi  Histoplasmosis  Blastomycosis
  6. 6. Histoplasmosis Granuloma
  7. 7. Granulomatous inflammation2. Foreign Body Granulomas Don’t incite either an inflammatory or immune response. Epitheloid cells and giant cells are apposed to the surface and encompass the foreign body. The foreign body is usually found in the center of the granuloma. Examples: Metal/Dust Berylliosis Silicosis Foreign body Splinter Suture
  8. 8. ► 3. Sarcoidosis  Bad systemic disease, probably autoimmune disease  Etiologic agent is unknown
  9. 9. Sarcoidosis Granuloma.
  10. 10. Infectious causes:► Bacteria  Tuberculosis  Leprosy► Parasites  Schistosomiasis► Fungi  Histoplasmosis  Blastomycosis► Metal/Dust  Berylliosis  Silicosis
  11. 11. Foreign body aspiration Berrylliosis
  12. 12. ► Granuloma: bacilli are inhaled by droplets► Bacteria are phagocytosed by alveolar macrophages► After amassing substances that they cannot digest, macrophages lose their motility, accumulate at the site of injury and transform themselves into nodular collections; the Granuloma► A localized inflammatory response recruits more mononuclear cells► The granuloma consists of a kernel of infected macrophages surrounded by foamy macrophages and a ring of lymphocytes and a fibrous cuff (containment phase)► Containment usually fails when the immune status of the patient changes; the granuloma caseates,
  13. 13. ► 2-10micrometer in length.► Struntrually gram positive but also containslarge amount of lipids in the cell wall:making them acid fast.► No toxins► No spores► Obligate Aerobic► Elicit granulomatous inflammation.
  14. 14. TUBERCULOSIS► Primary TB► SecondaryTB► Progressive pulmonary TB► Miliary TB
  15. 15. ► PATHOGENESIS► The course of tuberculosis depends on age and immune competence AND total burden of the organisms► Tuberculous Infection : refers to growth of the organism in a person,whether there is symptomatic disease or not.► Active Tuberculosis ; refers to infection manifested by tissue destruction-----symptomatic disease.
  16. 16. Multiplication of the organism inside thealveolar macrophage processing& presentation of the antigen onthe surface A clone of sensitized T-cells proliferate,produce gamma INT. Activation of themacrophages(augmenting their capacity to kill
  17. 17. Clinical and pathologic implications of primary tuberculosis1] Development of resistance to the infection.2] The foci of scarring may harbor viable bacilli for life and act as a nidus for reactivation.3] The disease may develop into progressive primary tuberculosis in immunocompro- mised patients such as AIDS patients, elderly, and malnourished children.
  18. 18. Tuberculin Test► It is a classic example of delayed hypersensitivity.► The tuberculin reaction, is produced by the intracutaneous injection of tuberculin, a protein-lipopolysaccharide component of the tubercle bacillus.
  19. 19. Gram stain Most bacteriaAcid fast stain Mycobacteria, nocardiae (modified)Silver stains Fungi, legionellae, pneymocytosisPeriod acid-Schiff Fungi, amebaeMucicarmine CryptococciGiemsa Campylobacteria, leishmaniae, malaria, parasitesAntibody probes Viruses, rickettsiaeCulture All classesDNA probes Viruses, bacteria, protozoaPolarizingmicroscope Foreign body