Pathology Inflammation-2 By Prof. Dr. SALAH FAYED Inflammation-2 • Suppurative inflammation: characterized by: – Dense infiltration by neutrophils (PNLs). – Rapid liquefaction of necrotic tissue. – Pus formation. Types: • Localized (abscess). • Diffuse (cellulitis). Inflammation-2 Abscess: • Definition: – Localized area of suppurative inflammation. • Causative organisms: – Many bacteria, but the most common is Staphylococcus Aureus, which produces coagulase enzyme. • Site: any organ or tissue. Inflammation-2 • Morphology of an abscess: – Central area of necrosis. – Pus (yellowish fluid composed of proteins and dead cells) in the cavity. – Peripheral pyogenic membrane (the limiting layer of the cavity of an abscess). – Granulation tissue. Skin abscess Diagram for gross appearance Microscopic Inflammation-2 Furuncle: • Small abscess in a hair follicle or sebaceous gland. • The commonest sites are: – Face. – Neck. – Axilla. Furuncle, gross appearance Inflammation-2 Carbuncle: • Multi-locular abscess with multiple sinuses discharging pus. • Usually occurs in patients with diabetes mellitus. • Site: usually the back of the neck. Carbuncle, in the back of the neck Inflammation-2 • Fate of an abscess: – If evacuated, healing occurs by minimal fibrosis. – If not evacuated, complications may occur as: • Ulcer: area without covering epithelium. • Sinus: blind tract connecting the abscess cavity to the surface. • Fistula: tract connecting between two cavities or surface and cavity, e.g. gastro-colic fistula and peri-anal fistula. Inflammation-2 Cellulitis: • Diffuse suppurative inflammation. • Occurs in loose subcutaneous tissue. • The causative organisms: most commonly group A streptococcus hemolyticus. • The organism secretes: – Fibrinolysin. – Hyaluronidase enzyme. Cellulitis Differences between abscess and cellulitis Abscess Cause: Staphylococcus Aureus Cellullitis Group A Streptococci The organism secretes: coagulase enzyme Fibrinolysin Hyaluronidase It is localized inflammation It is diffuse Central zone of necrosis Extensive necrosis Pus: rapid formation, thick and yellow Slow formation, thin and contains RBCs Inflammation-2 Non suppurative inflammation: • Catarrhal inflammation: – Mild inflammation of mucous membranes. – There is excess mucus secretion. – Examples are: • Rhinitis. • Gastritis. • Colitis. – If bacterial infection occurs, the secretion becomes muco-purulent. Catarrhal inflammation, rhinitis Inflammation-2 • Serous inflammation: – There is serous exudate with low fibrin content. – Examples are: • Blisters of superficial burns. • Herpes simplex infection. Herpes simplex Inflammation-2 • Serofibrinous inflammation: – There is serous fluid & fibrin secretion. – Occurs in serous and synovial membranes. – Examples: • Pericarditis, • Pleurisy, • Arthritis. Inflammation-2 • Fibrinous inflammation: – Characterized by excess fibrin secretion. – The causative organism: Pneumococci. – The best example: • Lobar pneumonia (fibrinious exudate fills the alveoli). Lobar pneumonia Inflammation-2 • Hemorrhagic inflammation: – Presence of large number of RBCs in the exudate due to vascular damage: – Examples: • Plague. • Anthrax. Inflammation-2 • Membranous inflammation: – There is severe damage to the mucosa. – Examples: • Diphtheria. • Bacillary dysentery. Inflammation-2 • Necrotizing inflammation: – There is severe tissue damage by the virulent organisms. – Examples: • Necrotizing fasciitis. • Necrotizing pharyngitis. Inflammation-2 • Allergic inflammation: – The exudate is serous or serofibrinous. – There is excess eosinophils. – Examples: • Bronchial asthma. • Urticaria. Inflammation-2 Chronic inflammation: • Causes of chronic inflammation: – May follow acute inflammation. – Persistence of the agent. – Infections with certain organisms: • • • • Some viral infections. Mycobacteria (TB and Leprosy). Parasitisc infestations (e.g. Schistosomiasis). Some fungal infections. Inflammation-2 – Auto-immune diseases. – Response to a foreign material. – Response to a malignant tumor. Inflammation-2 Important cells in chronic inflammation: • Macrophages: – Monocytes of blood, the most commonly present during inflammation . – Other cells derived from the tissues: • • • • • Histiocytes of connective tissue. Alveolar macrophages. Kupffer cells of the liver. Osteoclasts of the bone. Microglia of the brain. Inflammation-2 – Chemotactic factors for monocytes: • • • • C5a, MCP-1, PDGF, TGF-β. – Macrophages secrete a wide variety of active products “monokines”. Inflammation-2 • Lymphocytes: – B cells and plasma cells. – T cells. – They secrete chemokines (lymphotaxin). Inflammation-2 • Eosinophils: – Have a role in parasitic infections and Ig Emediated reactions. – Secrete eosinophilic chemokines (eotaxin). – Its granules contain major basic protein (MBP), toxic to parasites. Inflammation-2 • Basophils: – Tissue-based basophils are called mast cells. – They are present in high numbers in the lung and skin. – Play an important role in Ig E mediated reactions. – Secrete histamine. Inflammatio-2 • Morphology of chronic inflammation: – The reaction is more proliferative than exudative. – The cellular reaction is pleomorphic, containing: • Macrophages. • Lymphocytes. • Plasma cells, etc. – The arterioles, gradually show thick wall and narrow lumen. – Fibrosis is a common feature. Chronic inflammation, microscopic Inflammation-2 • Chronic granulomatos inflammation: – It is special type of chronic inflammation with a distinctive histologic appearance. – Characterized by granuloma formation. Inflammation-2 • Composition of a granuloma: – Epithelioid cells: derived from macrophages by the effect of INF-γ, closely backed large cells with abundant cytoplasm (epithelial-like). – Giant cells formed by fusion of epithelioid cells: • Langhan’s type with peripheral arrangement of nuclei. • Foreign body type with central nuclei. – Lymphocytes and plasma cells. Granulomatous inflammation, microscopic Inflammation-2 • Granulomatous diseases: – Tuberculosis. – Syphilis. – Leprosy. – Fungal infections. – Parasitic infections. – Foreign body reaction. – Sarcoidosis.