Patterns of Inflammation
* Short duration (minutes-days) with exudation of
fluid & plasma proteins, and emigration of
neutrophils into tissue.
* Longer duration (days-months) with tissue
accumulation of lymphocytes, plasma cells, &
macrophages plus variable proliferation of blood
vessels, fibrosis and necrosis.
Inflammation: essential definitions
Exudation = Escape of fluid, proteins, and blood
cells from vessels into tissues
Exudate = Inflammatory fluid, high protein
concentration and sp.gr. > 1.020
Transudate = Watery fluid, low protein concentration
and sp. gr. < 1.012
Oedema = Excess fluid in tissues & excess fluid
in serous cavities lined by mesothelium
(pleural, pericardial, peritoneal)
Pus = Inflammatory exudate rich in
neutrophils and cell debris
Cardinal Signs of Inflammation
Redness : Hyperaemia.
Warm : Hyperaemia.
Pain : Nerve, Chemical
Swelling : Exudation
Loss of Function: Pain
Function of inflammatory exudates
1-Dilute the invading microorganism and its
2-Bring antibodies through the plasma to the
inflamed area for neutralization.
3-Bring leukocytes that engulf the invading
4-Bring fibrinogen through the plasma, which is
converted, to fibrin mesh, helping in trapping the
microorganism and localize the infection.
5- Initiate the process of repair
* Changes in Vascular Flow and Caliber
* Increased Vascular Permeability
* Extravasation of Leukocytes
• In lumen of blood vessel (3 phases):
• Transmigration of leukocytes
• Migration into interstitium toward injury site by
locomotion along a chemical gradient: Chemotaxis
Filtrate of blood plasma
without changes in endothelial
Few cells,mainly mesothelial
Eg:congestive cardiac failure
Edema of inflamed tissue
associated with increased
Many cells,inflammatory as
well as parenchymal
Eg:purulent exudate such as
More severe injuries and
More greater vascular permeability,
Larger molecules such as
* fibrinogen pass the vascular barrier, and fibrin
is formed and deposited
Exudation of a protein-
rich fluid into a cavity
leads to a transudate. The
fibrin in this fluid can
form a fibrinous exudate
on the surfaces. Here, the
pericardial cavity has been
opened to reveal a
fibrinous pericarditis with
strands of stringy pale
fibrin between visceral
and parietal pericardium.
* A fibrinous exudate is characteristic of
inflammation in the lining of body cavities, such as
the meninges, pericardium and pleura
Fibrinous exudates may be removed by
But when the fibrin is not removed, it
may stimulate the in-growth of
fibroblasts and blood vessels and thus
lead to scarring (organization)
SUPPURATIVE OR PURULENT
Characterized by the production of large amounts
of pus or purulent exudate consisting of
neutrophils, necrotic cells, and edema fluid
Certain bacteria (e.g., staphylococci) produce this
localized suppuration and are therefore referred
to as pyogenic (pus-producing) bacteria
Here is acute
Yellow to tan exudate
fat superiorly, rather
than a smooth,
glistening pale tan
neutrophilic exudate is seen
involving the meninges at
the left, with prominent
There is edema and focal
inflammation in the cortex
to the right.
This acute meningitis is
typical for bacterial
At medium power
neutrophils fill the alveoli
in this case of acute
bronchopneumonia in a
patient with a high fever.
was cultured from
Note the dilated
capillaries in the alveolar
walls from vasodilation
with the acute
It is an acute diffuse suppurative inflammation
caused by streptococci, which secrete
hyaluronidase & streptokinase enzymes that
dissolve the ground substances and facilitate the
spread of infection.
* Areolar tissue; orbit, pelvis, …
* Lax subcutaneous tissue
An ulcer is a local defect of the surface
of an organ or tissue that is produced by
the sloughing (shedding) of
inflammatory necrotic tissue
Ulceration can occur only when tissue necrosis and
resultant inflammation exist on or near a surface
Systemic Effects of Inflammation
Fever is produced in response to Pyrogens
What are pyrogens?
* act by stimulating prostaglandin synthesis in the
vascular and perivascular cells of the hypothalamus.
Bacterial products (called exogenous pyrogens),
stimulate leukocytes to release cytokines such as
IL-1 and TNF (called endogenous pyrogens) that
increase the enzymes (cyclooxygenases) that
convert AA into prostaglandins.
Outcomes of acute inflammation
Fig. 3-24, Pathologic Basis of Disease, 6th ed, WB Saunders, 1999.
Chronic inflammation is inflammation of
prolonged duration (weeks or months) in
which inflammation, tissue injury, and
attempts at repair coexist, in varying
Types of chronic inflammation
1. Chronic non specific inflammation
2. Chronic specific inflammation: It includes
Causes of chronic inflammation
Prolonged acute inflammation or repeated bout of
acute inflammation may lead to the presence of
more mononuclear cells and chronic
Causes of chronic inflammation
Persistent infection by microorganisms that are
difficult to eradicate such as mycobacteria, certain
viruses, fungi and parasites. These often evoke
delayed-type hypersensitivity reaction.
Immune-mediated inflammatory diseases: Include
autoimmune diseases & allergic diseases. May
show mixture of acute and chronic inflammation.
Prolonged exposure to potentially toxic agents,
either exogenous (e.g. silicosis) or endogenous
Morphologically, characterized by:
Infiltration by mononuclear cells i.e. macrophages,
lymphocytes, and plasma cells.
Attempts at healing by connective tissue
replacement of damaged tissue accompanied by
angiogenesis and in particular, fibrosis.
Chronic non specific inflammation
It is seen affecting any organ for a
prolonged period of time.
It is characterized by diffuse infiltration
with mononuclear inflammatory cells.
1. Chronic nonspecific cervicitis
2. Chronic cholecystitis
3. Chronic osteomyelitis
Granulomatous inflammation is the
ditinctive pattern of chronic inflammation.
It is caused by organisms which are difficult
to eradicate and induce immune response
known as delayed hypersensitivity.
Immune reactions usually lead to
development of granuloma, which is a
cellular attempt to contain an offending
Granuloma is a focus of chronic inflammation
consisting of a microscopic aggregation of
macrophages that are transformed into epithelium
like cells- epithelioid cells surrounded by a collar
of mononuclear leukocytes, principally
lymphocytes and occasionally plasma cells.
Frequently, epithelioid cells fuse to form giant
cells, having many nuclei arranged either
peripherally (Langhans-type) or haphazardly
Older granuloma develop an enclosing rim of
fibroblasts and connective tissue.
Chronic Inflammation- Defined as a
prolong process in which tissue destruction
and inflammation occurs at the same time.
Granuloma-Defined as a circumscribed
,tiny,lesion,about 1mm in diameter
,composed predominantly of collection of
modified macrophages called epitheloid
cells and rimmed at the periphery by
Leprosy Mycobacterium leprae AFB in macrophages;
Syphillis Treponema pallidum Gumma(enclosing wall of
histiocytes; plasma cells)
Cat-scratch disease Gram neg bacillus Round or stellate granuloma
Crohn disease Immune reaction against
intestinal bacteria, self
granuloma in the wall of
Sarcoidosis Unknown etiology Noncaseating granulomas
with abundant activated
Foreign body Granuloma with foreign body
type giant cells.
Causative Agent is Bacterium
Gross-Painless mass at jaw cervicofacial,
pulmonary, ileocecal region.
The mas has discharging sinuses draining
yellow sulfur granules with centrsl necrotic
The injured tissue is replaced through regeneration
of native parenchymal cells, by filling of the
defect with fibrous tissue (scarring) or, most
commonly, by a combination of these two
It is formed during the process of repair.
Grossly, pink & granular soft tissue formed at the
surface of the wounds and is characterized by
proliferation of blood vessels & fibroblasts and
with some degree of inflammatory cells infiltrate .
fibroblasts, and a
Pathological aspects of repair
Repair will be abnormal in following
1. Deficient scar formation: Wound
dehiscence (or rupture) and ulceration.
2. Excessive formation of the repair
components: Hypertrophic scar and
3. Formation of contractures.
Hypertrophic scar shows excess amount of
Keloid is overgrowth of scar tissue beyond
the boundaries of original wound healing. It
shows excessive hyalinisation.
• TB (Tuberculosis) is potentially fatal
contagious disease that can affect almost
any part of the body but is mainly an
infection of the lung.
• Tubercle-Round nodule/swelling
• Mycobacterium Tuberculosis from the
• First discovered by Robert KOCH in 1882.
• So called as KOCH BACILLI.
• Although classified as gram positive but its
reaction is weak.
Lung, Ghon complex - In the radiograph and in the photograph, a
calcified, well-circumscribed nodule in the left lung represents an old
healed focus of primary tuberculosis; these are characteristically
peripheral in location. In addition, other calcified nodules can be seen in
the radiograph in the left hilar region -This is a former focus of infection
by TB in draining lymph nodes.
Lung, left, caseous necrosis - Low power
There is a large central area of caseous necrosis, which is seen as
granular pink structureless material with complete destruction of the lung
parenchyma. The caseous material is surrounded by a cellular zone that
contains epithelioid cells and giant cells. These cells are seen at a higher
magnification in the next image. At the periphery, some alveolar spaces
can be seen.
In this higher magnification of the lung lesion, caseous necrosis is seen
as pink granular structureless material that has destroyed the lung
alveoli. Epithelioid cells surrounding the caseous material are
elongated cells with indistinct cell boundaries. Individual epithelioid
cells are difficult to see in this lesion. A large multinucleated giant cell
is clearly visible. The cells with dark round nuclei are lymphocytes.
Lymph node, noncaseating granulomas - Low power. This image is of a
lymph node from a patient with sarcoidosis and is provided here for
comparison with the caseating granulomas of tuberculosis. Each of these
clusters of pink cells is a granuloma composed of interlacing epithelioid
cells and giant cells. Note the absence of caseous necrosis. While
granulomas in sarcoidosis do not have caseous necrosis, it should be
remembered that early lesions in tuberculosis may also have
noncaseating granulomas. .
- Lung, left, acid-fast stain - High power Reddish rods = acid-fast
bacteria (Mycobacterium tuberculosis) seen within an area of caseous
Lung, tuberculosis, secondary (reactivation) - The cavities in the upper
lobes are the pathologic and radiographic findings in secondary, or
reactivation, tuberculosis. The major bronchi have been opened to reveal
mucosal hyperemia, which indicates congestion or inflammation of the
bronchial mucosa. In addition, patchy consolidation is present in the
upper lobe; this may represent either superimposed bronchopneumonia
Spleen, miliary tuberculosis - Gross, cut surface This cut surface of the
spleen shows multiple light tan areas of caseous necrosis, which look
like multiple small abscesses grossly. Miliary tuberculosis may occur in
patients after either primary or secondary (reactivation) tuberculosis
Often due to reactivation or re-infection.
Represents breakdown of immunity
Due to partial immunity.
Load of bacteria to cause this must be relatively large.
MODE OF SPREAD OF EXTRA PULMONARY TB
Bacteria invade pulmonary
vein in vicinity
Bacteria try to
Bones & Joints
It may be Primary or secondary.
Swallowing of sputum in patients with active
tuberculosis causes sec. TB
Most common site - Terminal Ileum
Types Of Intestinal TB:
3. TB Peritonitis
4. TB Lymphadenitis
Mycobacterium avium intracellulare
More common in soil,water,dust and
More seen in AIDS with CD4
Abundant acid fast bacilli seen within
macrophages involve LN,lung,liver,spleen
Granulomas,lymphocytes, tissue destruction
Used for classifying leprosy on basis of
Early reaction: induration within 24 to 48
Delayed granulomatous lesion: After 3 to 4
Pts with tuberculoid leprosy give positive
lepromin test and lepromatous leprosy pts