MORPHOLOGY OF ACUTE INFLAMMATION

Transcription

1 MORPHOLOGY OF ACUTE INFLAMMATION

2 Morphological patterns of acute inflammation Dominating pattern 1. Exudation 2. Necrosis and fibrinous exudation 3. Necrosis

3 1. DOMINATING PATTERN: EXUDATION Subtypes Serous Fibrinous Purulent Hemorrhagic

4 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

5 On serous membranes Causes Immune complexes in systemic lupus erythematosus (SLE): peritonitis, pleurisy, pericarditis termed serositis Viruses: meningitis, pericarditis, conjuctivitis Extensive exercise (e.g., long distance running) synovitis

6 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

7 Outcome May heal completely May transform to fibrinous inflammation

8 Acute serofibrinous peritonitis: the serosal surface of bowels is hyperemic; the bowels adhere to each other via fibrin strands (right: normal serosa)

9 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

10 Outcome of serous infl. on mucosal surfaces May heal completely Airways: superinfection with bacteria mucopurulent rhinitis or bronchitis May be lethal: rotavirus-induced enteritis

11 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

12 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

13 Laryngal edema causing airway obstruction

14 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

15 Blisters in chickenpox Superinfection with St. aureus: the blisters are filled with pus (pustula) Courtesy of dr. Ildikó Kováts

16 Outcome May heal completely Superinfection with St. aureus sepsis may develop Lethal: burns involving large areas

17 FIBRINOUS INFLAMMATION Exudate: high content of fibrinogen coagulates into a thick fibrin coating Occurs on serous membranes or in the lungs

18 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

19 Morphology Macro: the serous membrane is opaque and reddish, covered by coagulated fibrin Micro: the fibrin appears as homogeneous masses of eosinophilic material

20 Acute fibrinous pericarditis: intense hyperemia, fibrin strands

21 Fibrinous pleurisy Thick strands of fibrin cover the hyperemic visceral pleura

22 Fibrinous pericarditis by LM. The fibrin appears as homogeneous eosinophilic material (left)

23 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

24 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

25 Lobar pneumonia. Hepatisation: liver-like consistency because alveoli are packed with fibrin

26 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

27 Sites Skin, deep tissues, preformed cavities, serosal surfaces, airways, and urethra

28 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

29 Lung: multiple abscesses as complication of pneumonia

30 Acute abscess: no fibroblastic rim

31 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

32 Furuncle (boil) Dr. Sándor Husz, SZTE Dermatology

33 Folliculitis on the nose; carbuncle on the face Dr. Sándor Husz, SZTE Dermatology

34 Cellulitis (erysipelas) 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 (phlegmonous inflammation). 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

35 Cellulitis: sharp, erythematous swelling of the skin Courtesy of Erika Varga, MD, Department of Dermatology, SZTE

36 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

37 Empyema of thorax (Pulmonary abscess had ruptured into the pleural cavity) Healing: granulation tissue secondary calcification: callus of pleura

38 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 multiply and induce purulent exudation in the subarachnoid space The meningeal vessels are engorged and stand out prominently Outcome Both are frequently lethal In survivors, healing with fibrosis adhesions

39 Purulent peritonitis: the abdominal cavity was filled with more than 2000 ml pus

40 Acute purulent meningitis The exudate is localized in the subarachnoid space, the meningeal vessels are engorged and stand out prominently

41 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.

42 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

43 Acute purulent tracheobronchitis

44 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

45 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

46 Acute hemorrhagic cystitis: the bladder mucosa is swollen, hyperemic and displays focal hemorrhages

47 2) NECROSIS AND FIBRINOUS EXUDATION DOMINATES: PSEUDOMEMBRANOUS INFLAMMATION

48 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

49 Pseudomembranous colitis Clostridium difficile infection after antibiotic therapy eradicating normal bacterium flora of the gut

50 Pseudomembranous colitis induced by Clostridium difficile: confluent plaques of yellow fibrin and inflammatory debris adherent to a reddened mucosa

51 Pseudomembranous enterocolitis: in severe cases the small bowels are also affected

52 Clinical features Odorous diarrhea + septicotoxicosis Outcome may heal completely may heal with granulation tissue may be lethal

53 3) NECROSIS DOMINATES Comprises Necrotizing soft tissue infections Necrotizing pancreatitis Necrotizing inflammation caused by viruses

54 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

55 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)

56 Amputated leg because of necrotizing fasciitis

57 Fascia: infiltrated by neutrophils; in part necrotized (bottom)

58 Gram-positive cocci (blue spheres) in the exudate

59 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

60 Gas gangrene: the gas bubbles accumulated between the epidermis and the underlying tissues

61 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

62 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

63 Acute necrotizing-hemorrhagic pancreatitis

64 Enzymatic necrosis in pancreatitis

65 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

66 Polyoma virus nephropathy The arrow indicates the characteristic nuclear inclusion body

67 Polyoma virions in the nucleus of an epithelial cell

68 Cytomegalovirus-induced pneumonia; the infected cells are enlarged, and their nuclei contain an inclusion body

69 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

70 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

71 Influenzavirus-induced tracheobronchitis Note intense mucosal hyperemia

72 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

73 Fatal case of viral myocarditis: lymphocytes and mononuclears in the interstitium + myofiber necrosis induced by T-cells (arrow)

74 The majority of lymphocytes are CD8 + cytotoxic T-lymphocytes

75 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

76 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