Granuloma (TB) PDF

L10 patho Granuloma (TB) Tuberculosis: chronic infective granuloma caused by mycobacterium tuberculosis;tubercle bacilli (human and bovine). -Mycobacterium tuberculosis non-motile a...

L10 patho Granuloma (TB) Tuberculosis: chronic infective granuloma caused by mycobacterium tuberculosis;tubercle bacilli (human and bovine). -Mycobacterium tuberculosis non-motile acid and alcohol fast, very resistant organism, but easily killed by sunlight The pathological changes depend upon the chemical structure of the bacteria which are formed of three components (The bacilli are formed of three chemical components): a) A lipid fraction: the capsule. b) A protein fraction: the body of the organism called tuberculoprotein. The pathogenicity of the organism depends mainly upon the antigenic nature of the tuberculoprotein. c) A small polysaccharide fraction Predisposing factors  Poverty, malnourishment, poor living conditions.  lack of medical care or any debilitating or immunosuppressive conditions. Route of infection  Inhalation: is the commonest method.  Ingestion: of raw milk contaminated with bovine (mycobacterium bovis) or human bacilli, infect the tonsils or the intestine.  Skin inoculation: by handling infected materials as infected meat. This method is not common. Tubercle formation Type IV hypersensitivity Polysaccharide fraction of the tubercle bacilli attracts the neutrophil leucocytes within few hours that lack lipase The lipid fraction of the capsule attracts the macrophages after the first day phagocytose the free bacilli(epitheloid cells) The bacilli are partially digested with the release of tuberculoprotein stimulates a cell mediated immune response within 10 days 1|Page  L10 patho Macroscopic picture The tubercle is of microscopic size.  Tubercles fuse with one another to form small rounded grossly visible gray follicles 1-2 millimeters in diameter.  When caseation occurs the lesion appears pale yellow and cheesy in consistency. Pathogenesis Tissue reaction in tuberculosis  A proliferative reaction: composed mainly of inflammatory cells.  An exudative reaction: showing excess inflammatory fluid exudate Fate of tubercle High immunity:  small foci are completely fibrosed.  Large foci are capsulated by fibrous tissue and its central caseating part shows dystrophic calcification. Living bacteria may remain in the lesion Low immunity:  Direct spread  Lymphatic spread  Blood spread  Intracanalicular spread TRUE OR FALSE Tubercle is formed by Type II hypersensitivity reaction false 2|Page  L10 patho Pulmonary tuberculosis Difference Primary TB Secondray TB nature Infection for first time Reinfection (2nd time) Age Children (childhood TB) Adult (Adulthood TB) Hypersensitivity&immmunity Not yet developed Developed Tissue reaction proliferative Exudative sites Tonsil, lung intestine, skin Anywhere Lymph node Always affected Not usually affected Primary pulmonary tuberculosis first infection of the lung with tubercle bacilli -frequent in children. -Infection is by inhalation of the human bacilli Pathological features: (The primary pulmonary complex) triad of: a) Ghon's focus :at the periphery of the lung underneath the pleura b) Tuberculous lymphangitis c) Tuberculous lymphadeniti Ghon's focus: Is an initial tuberculous lung lesion. Grossly:  it is a yellowish lesion.  1-1.5 mm in diameter.  It is commonly subpleural.  It occurs anywhere in the lung, most frequently at the lower aspect of the upper lobes or the upper aspect of the lower lobes. Microscopically: It consists of several adjacent caseating tubercles. Tuberculous lymphangitis: A chain of tubercles along the course of lymphatic vessels ----- appear beaded. Tuberculous lymphadenitis: The hilar lymph nodes are enlarged , soft and the cut surface is pale yellow ,and show caseating tubercles. - Caseation may be marked and the nodes become matted forming a "cold abscess 3|Page  L10 patho Fate of Primary pulmonary complex Healing infection is mild and the resistance is good. * small lesion heals by complete fibrosis. * bigger one heals by dystrophic calcification. Spread 1-Direct spread : tuberculous pneumonia, pleurisy. 2- Haematogenous spread: Small number of bacilli: Destroyed, Moderate number: (isolated organ tuberculosis) Large number of bacilli: Miliary tuberculosis 3- Encapsulation and reactivation Secondary pulmonary tuberculosis Tuberculous infection that arises in a previously sensitized individual infected with lowered immunity Infection: Exogenous: inhalation of human bacilli. Endogenous: Reactivation of a capsulated primary focus. Pathological features: start at the apex of the lung ,Commonly the right, small tuberculous focus. Course The dose and virulence of bacteria State of immunity and hypersensetivity 1-Regression : fibrotic tuberculosis 2-Progression: A- Chronic fibrocaseous pulmonary tuberculosis : moderate immumity & hypersensitvity. B- Bronchopneumonia & Acute caseous pneumonia (acute fatal) * Large dose of virulent bacteria * High hypersensitivity. * Low immunity Tuberculous bronchopneumonia The caseous necrosis is extensive, and cavitation is prominent Intestinal tuberculosis a) primary intestinal tuberculosis b) secondary intestinal tuberculosis Primary intestinal tuberculosis Due to ingestion of bovine bacilli in milk, forming a primary complex usually at the terminal ileum. Pathology (A primary intestinal complex) 1- Intestinal lesions: tubercles in the payer's patches at the terminal ileum (minimal ulcers) 2- Tuberculous lymphangitis. 3-Tuberculous lymphadenitis: (tabes mesentaris). 4|Page  L10 patho Fate 1- Localization. 2-Spread: a) Direct and lymphatic: this leads to tuberculous peritonitis. b) Hematogenous spread leading to isolated organ or miliary tuberculosis. Secondary intestinal tuberculosis Aetiology: Due to swallowing infected sputum in patients with chronic fibrocaseous tuberculosis. Pathological features: mainly in the terminal ileum and adjacent caecum Caseous necrosis and erosion of the covering mucosa results in tuberculous ulcers: * These ulcers are multiple.. * Their edges are ragged and undermined. * Their floors are yellowish, caseous and soft. * In the terminal ileum, they are transversely arranged (girdle ulcers)heal by fibrosis Complications: 1-Intestinal hemorrhage. 2-Intestinal fistula. 3-Perforation of the ulcers leads to septic peritonitis. 4-Spread of infection: a-Direct and lymphatic leading to tuberculous peritonitis. b-Blood spread leads to isolated organ or miliary tuberculosis. 5-Fibrosis leads to intestinal obstruction. 6-Secondary amyloidosis CHOOSE Tuberculous ulcer has A. Everted egde B. Sharp edge C. Undermined edge D. rolled edge 5|Page