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Morphology of acute inflammation MORPHOLOGICAL PATTERNS OF ACUTE INFLAMMATION Dominating pattern: 1. Exudation 2. Necrosis and fibrinous exudation 3. Necrosis 1. DOMINATING PATTERN: EXUDATION Types according to the extent of vascular permeability • Serous inflammation • Fibrinous inflammation • Purulent inflammation • Hemorrhagic inflammation SEROUS INFLAMMATION Exudate: watery, relatively protein-poor fluid, with scanty fibrin. Occurs • On serous membranes (pleura, pericardium, peritoneum, synovium, meninges, conjunctiva) • On respiratory/GI mucosa • In the skin On serous membranes Causes • Immune complexes in systemic lupus erythematosus (SLE): peritonitis, pleurisy, pericarditis termed ”serositis” • Viruses: meningitis, pericarditis, conjuctivitis • Long-term exercise (e.g., long distance running) synovitis Gross features Normally, the serous membrane is smooth and has a glistening surface. In serous inflammation, it becomes reddish and opaque. Shown: acute serous pleurisy Outcome • May heal completely • May transform to fibrinous inflammation Acute serofibrinous peritonitis: the serosal surface of bowels is hyperemic; the bowels adhere to each other via fibrin strands (right: normal serosa) On respiratory/GI mucosa The exudate contains mucous secretions because the mucous glands become stimulated catarrhal inflammation Causes • Allergic reaction (hay fever) – rhinitis with profuse nasal discharge • Viruses - airways: rhinitis, pharyngitis, bronchitis (sore throat, coughing) - small bowels: enteritis (watery diarrhoea) • Cold in children: rhinitis, pharyngitis, bronchitis Gross features The affected mucosa is hyperemic, swollen, and is covered by abundant mucous exudate Outcome of serous infl. on mucosal surfaces • May heal completely • Airways: superinfection with bacteria mucopurulent rhinitis or bronchitis • May be lethal: rotavirus-induced enteritis Special site: larynx Causes of acute serous laryngitis • Infection (Haemophilus influenzae, viruses) • Drugs through allergic mechanisms • Inhalation of toxic gases Gross features: Sudden onset of hyperemia and swelling of mucosa of the vocal cords and epiglottis edema of larynx airway obstruction on occasion, death Edema of larynx induced by adverse (allergic) reaction of an antihypertensive drug administered intravenously in hypertensive crisis. Note marked swelling of laryngeal mucosa which caused upper airway obstruction and death Laryngal edema causing airway obstruction Serous inflammation in the skin Blister: serous exudate accumulates in the epidermis or along the epidermal-dermal junction Vesicle; if larger than 5 mm: bulla Causes • Mechanical irritation (friction), burns • Herpes virus varicellae-induced chickenpox or shingles • Autoimmune: pemphigus Blisters in chickenpox Courtesy of dr. Ildikó Kováts Superinfection with St. aureus: the blisters are filled with pus (pustula) Outcome • May heal completely • Superinfection with St. aureus: the blisters are filled with pus (pustula) sepsis may develop • Lethal: burns involving large areas FIBRINOUS INFLAMMATION Exudate: high content of fibrinogen coagulates into a thick fibrin coating Occurs on serous membranes or in the lungs Causes on serous membranes • Viruses: pleurisy, pericarditis, meningitis • Chronic uremia: pericarditis • Immune complexes in SLE : serositis, arthritis • Irritation: adjacent to pulmonary infarction (pleurisy), myocardial infarction (pericarditis); joints - arthritis Morphology Macro: the serous membrane is opaque and reddish, and is covered by coagulated fibrin Acute fibrinous pericarditis: intense hyperemia, fibrin strands Fibrinous pleurisy Thick strands of fibrin cover the hyperemic visceral pleura Morphology Macro: the serous membrane is opaque and reddish, and is covered by coagulated fibrin Micro: the fibrin appears as homogeneous masses of eosinophilic material Fibrinous pericarditis by LM. The fibrin appears as homogeneous eosinophilic material (left) Outcome • Removed by fibrinolysis heals completely • Abundant fibrin is converted to granulation tissue fibrous strands bridge serous surfaces (adhesions) • Bacterial superinfection purulent inflammation Clinical feature Fibrinous pleurisy or pericarditis friction rub, thoracic pain Fibrinous inflammation of the lungs: lobar pneumonia Causative agent: Streptococcus pneumoniae The entire lobe is affected; the exudate is localized in the alveoli Morphology Macro: the affected lobe is consolidated, resembles to the liver by palpation (hepatisation) Lobar pneumonia. Hepatisation: liver-like consistency because alveoli are packed with fibrin Fibrinous inflammation of the lungs: lobar pneumonia Causative agent: Streptococcus pneumoniae The entire lobe is affected; the exudate is localized in the alveoli Morphology Macro: the affected lobe is consolidated, resembles to the liver by palpation (hepatisation) Micro: fibrin fills the alveolar spaces; days later the exudate turns into purulent Outcome • Heals completely • Complications develop, such as lung abscess • Results in death PURULENT INFLAMMATION General features • Neutrophil granulocytes predominate in the exudate • Causative agents: pus-forming (pyogenic) bacteria, e.g., Staphylococcus, Streptococcus, Neisseria • Pus: viscous, creamy fluid composed of bacteria, viable and dead NGs, debris of liquefied tissues, exuded plasma proteins Sites Skin, deep tissues, preformed cavities, serosal surfaces, airways, and urethra Abscess Liquefactive necrosis-induced cavity filled with pus • Sites: in the skin, perianal region, internal organs, brain, etc. • Deep-seated abscesses have a tendency to break through intramuscular septa. Eventually, the pus reaches a surface, where it is discharged. Sinus tract (fistula): the channel draining the abscess Lung: multiple abscesses as complication of pneumonia Acute abscess: no fibroblastic rim Abscess Liquefactive necrosis-induced cavity filled with pus • Sites: in the skin, internal organs, brain, etc. • Deep-seated abscesses have a tendency to break through intramuscular septa. Eventually, the pus reaches a surface, where it is discharged. Sinus tract (fistula): the channel draining the abscess • Healing: by fibrosis Surgical drainage is often necessary to eliminate abscesses from deep sites Purulent inflammation of the skin: abscesses and cellulitis Frequent in diabetics! Abscesses of skin adnexa Causative agent: Staphylococcus aureus • Folliculitis - suppuration of a hair follicle • Furuncle (boil) - suppuration of a hair follicle + subcutaneous tissue • Carbuncle - suppuration of several hair follicles + subcutaneous tissue Furuncle (boil) Dr. Sándor Husz, SZTE Dermatology Folliculitis on the nose; carbuncle on the face Dr. Sándor Husz, SZTE Dermatology Cellulitis (erysipelas; phlegmon) Caused by Streptococcus pyogenes • The bacteria produce hyaluronidase, which digests dermal connective tissue leading to diffuse spread of bacteria and formation of purulent exudate along the dermis. • Clinical features: rapidly spreading, erythematous cutaneous swelling on the face, or on the body or an extremity in middle-aged persons. The rash has a sharp, well-demarcated, serpiginous border + systemic symptoms: fever and fatigue. • Responds to antibiotics Cellulitis: sharp, erythematous swelling of the skin Courtesy of Erika Varga, MD, Department of Dermatology, SZTE Pus accumulation in preformed cavities: empyema Clinically important Empyema of • gallbladder • paranasal sinuses (maxillary, sphenoidal, ethmoidal, frontal) complication: purulent meningitis • middle ear (purulent otitis media): mainly in children; complication perforation of the tympanic membrane • thorax Empyema of thorax (Pulmonary abscess had ruptured into the pleural cavity) Healing: granulation tissue secondary calcification: callus of pleura Purulent inflammation of serous membranes Acute purulent peritonitis After perforation of an abdominal organ; the peritoneal surface is hyperemic and red, and is covered by creamy exudate Acute purulent meningitis Bacteria reach the subarachnoid space and induce purulent exudation. The exudate is localized in the subarachnoid space; the meningeal vessels are engorged and stand out prominently Outcome Both are frequently lethal In survivors, healing with fibrosis adhesions Purulent peritonitis: the abdominal cavity was filled with more than 2000 ml pus Acute purulent meningitis The exudate is localized in the subarachnoid space, the meningeal vessels are engorged and stand out prominently Purulent inflammation of respiratory mucous membranes • Mucous membranes form a tube, therefore, the exudate may appear distal to the primary site. • The affected mucosa is swollen, red and is covered by mucopurulent or purulent exudate. Acute purulent bronchitis With coughing, the exudate infects other parts of the bronchial tree and alveoli (bronchopneumonia) and also appears as purulent sputum Outcome • May heal completly • May turn into chronic • May result in death Acute purulent tracheobronchitis Acute purulent urethritis in Neisseria gonorrhoeae infection (sexually-transmitted disease, termed gonorrhoea) Complications: purulent inflammation of the prostate, seminal vesicle, epididymis, and testis If untreated: healing by fibrosis infertility Dr. Sándor Husz, SZTE Dermatology HEMORRHAGIC INFLAMMATION Sufficient vascular damage hemorrhages In the bladder: hemorrhagic cystitis, caused by Gram-negative bacteria; the bladder mucosa is swollen, hyperemic and displays focal hemorrhages hematuria Acute hemorrhagic cystitis: the bladder mucosa is swollen, hyperemic and displays focal hemorrhages Hemorrhagic inflammation Sufficient vascular damage hemorrhages In the bladder: hemorrhagic cystitis, caused by Gram-negative bacteria; the bladder mucosa is swollen, hyperemic and displays focal hemorrhages hematuria In the lungs: if influenzavirus infects the alveoli severe alveolar damage hemorrhagic pneumonia; frequently fatal 2) NECROSIS AND FIBRINOUS EXUDATION DOMINATES: PSEUDOMEMBRANOUS INFLAMMATION Pseudomembranous inflammation Pathomechanism: a response of mucous surface to certain bacteria/fungi The surface epithelium becomes necrotic plasma exudates from the submucosal vessels onto the necrotic surface, its fibrinogen content coagulates, and encloses the necrotic epithelium pseudomembrane Pseudomembranous colitis Clostridium difficile infection after antibiotic therapy eradicating normal bacterium flora of the gut Pseudomembranous colitis induced by Clostridium difficile: confluent plaques of yellow fibrin and inflammatory debris adherent to a reddened mucosa Pseudomembranous enterocolitis: in severe cases the small bowels are also affected Clinical features Odorous diarrhoea + septicotoxicosis Outcome • may heal completely • may heal with granulation tissue • may be lethal 3) NECROSIS DOMINATES Comprises • Necrotizing soft tissue infections • Necrotizing pancreatitis • Necrotizing inflammation caused by viruses Necrotizing soft tissue infections • Soft tissues: dermis, subcutis, superficial and deep fasciae, and muscles • Etiology: via trauma or surgical wounds bacteria enter into the soft tissues • Prototype: necrotizing fasciitis; involves the extremities, the perineum and genital area (Fournier’s gangrene) and the abdominal wall • Highly virulent, exotoxin-producing (e.g., Streptococcus) and/or gas producing bacteria (e.g., anaerobs, Clostridium perfringens) proliferate, and the toxins cause thrombosis of the perforating vessels inflammatory necrosis of fascia and surrounding tissues • If gas production is abundant, extensive necrosis of tissues occurs (gas gangrene) Amputated leg because of necrotizing fasciitis Fascia: infiltrated by neutrophils; in part necrotized (bottom) Gram-positive cocci (blue spheres) in the exudate Gas gangrene: necrotizing and gas-producing inflammation of the lower extemity involving the abdominal wall, perineum and scrotum; the gas bubbles detach the epidermis from the underlying tissues Gas gangrene: the gas bubbles accumulated between the epidermis and the underlying tissues Clinical features • Intense pain and swelling of the involved site, the overlying skin is erythematous and warm; myalgia. • Rapid spread reaching 2-3 cm/h septic shock within 24 hours; high mortality rate Necrotizing inflammation of the pancreas • Pancreatic proenzymes become activated within the pancreas • Autodigestion and enzymatic necrosis of parenchyma and vessels • Acute inflammatory reaction acute necrotizinghemorrhagic pancreatitis + systemic inflammatory response sy • Frequently lethal Acute necrotizing-hemorrhagic pancreatitis Enzymatic necrosis in pancreatitis Necrotizing inflammation caused by viruses • Viruses are small intracellular parasites, use host cell metabolism for their replication • Electron microscopy is necessary to visualize them • Certain viruses induce inclusion bodies which can be observed by light microscopy Polyoma virus nephropathy The arrow indicates the characteristic nuclear inclusion body. Polyoma virions in the nucleus of an epithelial cell Cytomegalovirus-induced pneumonia; the infected cells are enlarged, and their nuclei contain a reniform or ovoid inclusion body Pathomechanism of necrosis of virus-infected cells • Viruses can directly lyse cells, eg., respiratory epithelial cells. Cell lysis is a special form of necrosis. E.g., influenzavirus infection • Host CD8+ cytotoxic lymphocytes cause necrosis of virus-infected parenchymal cells: acute viral hepatitis, acute viral myocarditis Influenzavirus infection Epidemic rhinitis and pharyngitis + tracheobronchitis • Grossly: acute catarrhal or serohemorrhagic inflammation with intense intense mucosal hyperemia • LM: necrosis of epithelial cells, lymphocytic and histiocytic infiltration of mucosa, mucus hypersecretion Influenzavirus-induced tracheobronchitis Note intense mucosal hyperemia Influenzavirus infection Epidemic rhinitis and pharyngitis + tracheobronchitis • Grossly: acute catarrhal or serohemorrhagic inflammation with intense intense mucosal hyperemia • LM: necrosis of epithelial cells, lymphocytic and histiocytic infiltration of mucosa, mucus hypersecretion • Clinical features: sudden onset, high fever, myalgias, cough, catarrhal discharge from nose Outcome • Heals completely • Complications: - bacterial superinfection purulent tracheobronchitis; - the virus may infect the alveoli hemorrhagic pneumonia • Lethal in patients with chronic heart disease, elderly people, in immunosuppressed individual Fatal case of viral myocarditis: lymphocytes and mononuclears in the interstitium + myofiber necrosis induced by T-cells (arrow) The majority of lymphocytes are CD8+ cytotoxic T-lymphocytes COMPARISON OF FEATURES OF MICROBIAL AND VIRAL INFECTION Acute inflammation induced by bacteria E.g.: bronchopneumonia Responding cells: neutrophils kill the bacteria + systemic signs: • Fever (IL-1, TNF from neutrophils and macrophages) • Leukocytosis (WBC >12000/ul; qualitatively granulocytosis) • Increase in acute phase proteins COMPARISON OF FEATURES OF MICROBIAL AND VIRAL INFECTION Acute inflammation induced by viruses E.g.: infectious mononucleosis Responding cells: T-lymphocytes eliminate the viruses + systemic signs: • Fever • Leukocytosis (WBC >12000/ul; qualitatively lymphocytosis) • Increase in acute phase proteins