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Premium member Presentation Transcript Pathogenesis & Host Factors in TB: Pathogenesis & Host Factors in TB Dr Gauri P GodboleTransmission to Disease: Transmission to Disease Droplet nuclei Control measures – ventilation, UV rays, masks 25 – 50 % rate of infection even in household contacts Small proportion develop diseaseWhy so ?: Why so ? May not reach individual May not multiply & infect ?? Viability Potentially infective dose Infection to disease ? Defn. : reaction of human tissues to presence & multiplication of M tbEvolution of Primary infection: Evolution of Primary infection First infection with M tb is primary infection. Lung : first organ involved M tb in alveolus – neutrophils & alveolar macrophages Multiplication of bacilli – site of entry – parenchymal ( Ghon’s ) focus – Ghon’s complex DisseminationGenesis of the Tubercle: Genesis of the Tubercle 0 hrs : serous exudate & neutrophils 48 hrs : monocytes & macrophages Upto 2 wks : macrophage* & then giant cells ; lymphocytes appear 2 nd month : sudden increase in lymphocytes CaseationGenesis of Typical Tubercle: Genesis of Typical Tubercle Stage I : activated macrophage ingests and kills MTb Stage II : early tubercle – macrophages increase – symbiosis Stage III : 3 wks tubercle Stage IV : enlarging tubercleSeries of Battles – Host Vs Invader: Series of Battles – Host Vs Invader 1.Inhaled MTb – multiply - elimination by macrophages 2.Small caseous lesions – progress - heal- no XR lesion - stabilise – no XR lesion 3.Larger caseous lesions – heal or stabilise - grow & empty into blood/lymph 4.Liquefaction of caseous lesion – bronchial tree Independent battles in each lesion.Balance of Tissue destruction & Bacillary elimination: Balance of Tissue destruction & Bacillary elimination CMI Caseation Liquefaction Extracellular growth In solid caseum, tubercle bacilli may survive, but do not multiply.Fate of Primary Complex: Fate of Primary Complex Progression to progressive primary Healing by fibrosis Fibrosis to calcification Calcification to ossification Calcification to resorption Viable organisms persist*Walgren’s Time Table: Walgren’s Time Table Stage 1 : Primary Complex * Stage 2 : Miliary / disseminated : 6 mths Stage 3 : Pleural effusion* : 1 year Stage 4 : Bronchogenic : post primary Skeletal : 3 yrs Genito urinary : 5 - 15 yrsOnset of Sensitivity*: Onset of Sensitivity* Tuberculin conversion Erythema nodosum Phlyctenular conjunctivits Pleural effusion FeverMiliary Dissemination from Primary Complex: Miliary Dissemination from Primary Complex Parenchymal focus in lungs – Lymph node – Thoracic duct – Right heart – both lungs Primary complex – Pulmonary veins – Left Heart – Aorta – 1. all organs 2. bronchial arteries – lungs Fate as for primary complexSome terms for localised foci: Some terms for localised foci Simon’s focus : apical* primary-lungs Weigart’s focus : subintimal focus Rich’s focus : subcortical focus* Puhl’s focus : in cerebellum Ashman’ focus : deep apical lesion Simond’s focus : in liverPost Primary Pulmonary TB: Post Primary Pulmonary TB Endogenous exacerbation of old Simon’s focus Continuation of primary infection into progressive primary Reinfection – exogenous Marfan’s observation : well healed scars of cervical lymphadenitis rarely developed pulmonary TB‘First successful implant’ hypothesis: ‘First successful implant’ hypothesis A.Virulent tubercle bacilli - vulnerable region via a bacillemia in first infection: 1. low risk of infection 2. low incidence of vaccination 3. low sensitization to environmental mycobacteria 4. high incidence of high virulent isolates B. Bacilli - vulnerable region via the airway- repeated episodes of infection ( probability of a first implant low) 1. high risk of infection 2. high incidence of vaccination 3. sensitization to environmental mycobacteria 4. high incidence of low virulent isolates,Disease after Infection: Disease after Infection Genetic Factors : Europeans,Asians,Jews; Negroes ; height Physiological Factors : Age extremes ; puberty ; males > 35 yrs ; pregnancy & parturition Environmental Factors : Nutrition ; Housing conditions ; Occupation Alcoholism Smoking Steroids & immunosuppressives Other Diseases Psychological factors Immunological factorsJaundice in TB patients: Jaundice in TB patients Drug induced Primary Tb : granulomatous hepatitis ; miliary ; porta hepatis LNs ; CBD stricture ; abscess Unrelated causes : ALD; Hepatitis A/B/C ; primary biliary cirrhosisPathogenesis of Hemoptysis in TB: Pathogenesis of Hemoptysis in TB Rasmussen’s aneurysms Intense allergic response Broncholith Calcification Endobronchial lesion AV aneurysms Bronchiectasis Fungal colonisation of cavity You do not have the permission to view this presentation. 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