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 appearanceMicroscopic

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 AbscessCellullitis Cause: Staphylococcus AureusGroup A Streptococci The organism secretes: coagulase enzymeFibrinolysin Hyaluronidase It is localized inflammationIt is diffuse Central zone of necrosisExtensive necrosis Pus: rapid formation, thick and yellowSlow 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 E- mediated 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.