Pathogenesis & Host Factors in TB

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Pathogenesis & Host Factors in TB: 

Pathogenesis & Host Factors in TB Dr Gauri P Godbole

Transmission 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 disease

Why 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 tb

Evolution 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 Dissemination

Genesis 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 Caseation

Genesis 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 tubercle

Series 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 yrs

Onset of Sensitivity*: 

Onset of Sensitivity* Tuberculin conversion Erythema nodosum Phlyctenular conjunctivits Pleural effusion Fever

Miliary 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 complex

Some 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 liver

Post 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 factors

Jaundice 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 cirrhosis

Pathogenesis 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