1. TUBERCULOSIS

2. Cell Wall Lipoarabinomannan(LAM) Inhibits macrophage activation by interferon-gamma. Virulent Factors

3. Pathogenesis

4. Polymorphism in the NRAMP 1 gene NRAMP1 Transmembrane protein in lysosomes Pumps Ca++ out of lysosome May inihibit growth by Limiting availability of ions needed by bacteria Susceptiblity Gene

5. Stimulate macrophages to kill TB bacteria Stimulates formation of phagolysosome in infected macrophages Stimulates expression of NO synthase Nitric oxide ( destroy bacterial cell wall to DNA ) Differantiation of macrophages  Epitheloidhistiocytes Halts infection Mature TH1

6. TB Granuloma

7. Clinical Features

8. Secondary Disseminated Tuberculosis.

9. Ghon complex

10. Slowly progressive infection Low Communicability Affecting the skin & peripheral nerves Disabling deformity Most are contained in the skin Likely transmitted by aerosols from lesions in the Upper Respiratory Tract  Hematogenous  grows only in relatively Cool Tissues of the skin & Extremities Leprosy

11. Virulence factor

12. Leprosy

13. Leprosy- immune response

14. Paucibacillary Leprosy Have dry , scaly, skin lesions Lack sensation , Asymmetric peripheral nerve involvement Have TH1 response Normal immune response Granuloma containing less microbe Damage neurons Production of IL-2 & IFN- g Lepromin skin test is strongly (+) T cell response – Delayed Hypersensitivity rxn to lepromin Tuberculoid Leprosy

15. Lepromatous Leprosy- Multibacillary