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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