Section-07 - Cowmedical

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NECROSIS, GANGRENE AND
POST-MORTEM CHANGES
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Necrosis

Coagulative Necrosis

Caseative Necrosis

Liquifactive Necrosis

Fat Necrosis
Apoptosis
Gangrene
Post Mortem Changes
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Autolysis
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Putrefaction
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Rigor Mortis
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Algar Mortis
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Livor Mortis
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Hypostatic Congestion
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Post Mortem Emphysema
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Post Mortem Clot

Displacement of Organs

Imbibition of Bile
Model Questions
NECROSIS
Local death of tissue /cells in living body is known
as necrosis, It is characterized by the followings.
 Pyknosis is condensation of chromatin
material, nuclei becomes dark, reduced in size
and deeply stained
 Karyorrhexis is fragmentation of nucleus
 Karyolysis is dissolution of nucleus into small
fragments, basophilic granules/fragments.
 Chromatolysis is lysis of chromatin material.
 Necrobiosis is physiological cell death after
completion of its function e.g. RBC after 140
days.
Etiology
 Chronic infections e.g.
tuberculosis.

Systemic fungal infections.
Mycobacterium
Macroscopic features
 Dead tissue looks like milk curd or cottage
cheese.
 Tissue dry, firm, agranular, white/gray/
yellowish in colour
Microscopic features
 Disappearance of cells; no cell details/
architecture.
 Purplish granules on H&E staining, blue
granules from nucleus fragments, red granules
from cytoplasm fragments.
Necrosis is further classified into coagulative,
caseative, liquifactive and fat necrosis which are
different from apoptosis (Fig. 7.1 to 7.3).
LIQUIFACTIVE NECROSIS
Local death of cells/ tissues in living body
characterized by rapid enzymatic dissolution of
cells. The intracellular hydrolases and proteolytic
enzymes of leucocytes play role in dissolution of
cells (Fig. 7.6).
COAGULATIVE NECROSIS
Local death of cells/tissue in living body
characterized by loss of cellular details, while
tissue architecture remains intact (Fig. 7.4).
Etiology
 Infections
 Ischemia
 Mild irritant e.g. toxins/chemical poisons
 Heat, trauma
Etiology
 Pyogenic organisms.
Macroscopic features
 Liquifactive necrosed tissue present in a cavity
“Abscess”.

It contains small/ large amount of cloudy
fluid, which is creamy yellow (Pus).
Macroscopic features
 Organ becomes gray/white in colour, firm,
dense, depressed with surrounding tissue.
Microscopic features
 Cellular out line present, which maintains the
architecture of tissue/ organ.
 Nucleus absent or pyknotic.
 Cytoplasm becomes acidophilic.
Microscopic features
 Areas of liquifactive necrosis stains pink.
 Infilteration of neutrophils
 Sometimes empty spaces but infilteration of
neutrophils at periphery.
CASEATIVE NECROSIS
Local death of cells/tissue in living body; the dead
cells/tissue is characterized by presence of firm, dry
and cheesy consistency. It occurs due to
coagulation of proteins and lipids (Fig. 7.5).
FAT NECROSIS
Local death of adipose cells in living body.
Etiology
 Trauma
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A
Necrosis
Apoptosis
B
F
A
C
G
D
H
E
Fig. 7.1. Diagram showing pathogenesis of necrosis
(A) Normal (B) Pyknosis (C) Karyorrhexis
(D)Karyolysis (E) Chromatolysis and
(F) Apoptosis (G) Blebs and (H) Phagocytosis
B
Fig. 7. 3. Photograph of (A) liver and (B) heart
showing necrosis
A
A
C
B
B
D
Fig. 7.2. Diagram showing necrosis (A) Normal
(B) Coagulative (C) Caseagative and (D)Liquifactive
Fig. 7. 4. Photomicrograph of (A) liver and
(B) Kidney showing coagulative necrosis
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surrounding tissue, resulting in generation of a
local inflammatory response.
Necrosis is the consequence of a passive and
degenerative process while the apoptosis is a
consequence of an active process.
Increased action of enzymes due to leakage of
pancreatic juice.
Starvation
Macroscopic features
 Chalky white mass deposits in organ.
 White opaque firm mass.
Execution of apoptosis requires the coordinated
action of aspartate specific cysteine proteases
(caspases) which are responsible for cleavage of
key enzymes and structural proteins resulting in
death of cell. Apoptosis is triggered by a variety of
signals
which
activate
the
endogenous
endonucleases to cause fragment action of nuclear
DNA into oligonucleosomal size fragments.
Initially, the DNA fragments are large (50-300 Kb)
but are later digested to oligonucleosomal size
(multimers of 180-200 bp). The formation of this
distinct DNA ladder is considered to be a
biochemical hall mark of apoptosis.
Microscopic features
 Adipose cell without nucleus (Fig. 7.7).
 Macrophages giant cells contain fat droplets.
 Presence of lime salts in tissues.
APOPTOSIS
Apoptosis is a finely tuned mechanism for the
control of cell number in animals; the process is
operative during foetal life, tumor regression and in
the control of immune response. Apoptosis plays
an important role in the development and
maintenance of homeostasis and in the maturation
of nervous and immune system. It is also a major
defense mechanism of the body, removing
unwanted and potentially dangerous cells such as
self reactive lymphocytes, virus infected cells and
tumor cells.
There is rounding of nucleus with pyknosis and
rhexis, chromatin coalesces to form a crescent
along the nuclear membrane. Cell fragments to
form blebs, which may have one or more
organelles. Such changes occurs in apoptotic cells
within 20 min of duration.
Most cells in animal have the ability to self destruct
by activation of an intrinsic cellular suicidal
programme when they are no longer needed or are
seriously damaged. The dying cell exhibits
morphological alterations including shrinkage of
cell, membrane blebbing, chromatin condensation
and fragmentation of nucleic acid. Cells under
going apoptosis often fragment into membrane
bound apoptotic bodies that are readily
phagocytosed by macrophages or neighbouring
cells without generating an inflammatory response.
These changes distinguish apoptosis from cell
death by necrosis. Necrosis refers to the
morphology most often seen when cells die from
severe and sudden injury such as ischemia,
sustained hyperthermia or physical and chemical
trauma. In necrosis, there are early changes in
mitochondrial shape and function; cell losses its
ability to regulate osmotic pressure, swells and
ruptures. The contents of the cell are spilled into
Apoptosis is generally synonymously used with
“programmed cell death” but it differs from
programmed cell death as apoptosis cannot be
prevented by cycloheximide or actinomycin D,
rather these chemicals accelerate the process of
apoptosis while programmed cell death is
prevented by these chemicals.
GANGRENE
Necrosis of tissue is followed by invasion of
saprophytes. Gangrene is mainly divided into three
types: Dry, moist and gas gangrene.
DRY GANGRENE
Dry gangrene occurs at extremities like tail, tip of
ears, tip of scrotum, hoof etc. due to necrosis and
invasion of saprophytes. The evaporation of
moisture takes place resulting into dry lesions.
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Fig. 7.5. Photomicrograph showing caseative
necrosis
Fig. 7.9. Photograph of a cow showing gangrene
in udder
Fig. 7.10. Photograph of buffalo calves showing
sloughing of hoofs due to Degnala disease
Fig. 7.6. Photomicrograph showing liquifacticve
necrosis
Fig. 7.7. Photomicrograph Adipose tissue showing
necrosis
Fig. 7.11. Photograph of buffalo calf showing
sloughing of hoofs due to Degnala disease
Fig. 7.8. Photograph buffalo bull showing
dry gangrene at scrotum
Fig. 7.12. Diagram showing moist gangrene
in intestine
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Macroscopic features
 Dry, fragmented crusts like lesions on tail,
scrotum, ear (Fig. 7.8 & 7.9).
 Hoof becomes detached due to necrosis and
gangrene, sloughing, exposing the red raw
surface (Fig. 7.10 & 7.11).
 Blackening of the affected area.
Microscopic features
 Necrosis and invasion of saprophytes in skin of
tail, ear or scrotum.
Fig. 7.13. Photograph showing moist
gangrene in poultry
MOIST GANGRENE
Moist gangrene mostly occurs in internal organs of
body like lungs, intestine, stomach etc. It occurs
due to necrosis and invasion of saprophytes leading
to dissolution of the tissues (Fig 7.12 & 7.13).
Etiology
 Drenching of milk, medicines etc. e.g.
Aspiration pneumonia/ Drenching pneumonia.
 Volvolus/Intussusception or torsion in
intestine.
Macroscopic features
 Greenish or bluish discoloration of the affected
organ.
 Dissolution of affected part into fragments
 Presence of foreign material like milk, fiber,
oil, etc.
Fig. 7.14 Photograph showing gas
gangrene in heifer
Macroscopic features
 Necrosis and invasion of saprophytes
 Presence of foreign material like milk, fibers,
oil etc.
GAS GANGRENE
Gas gangrene occurs in muscles particularly of
thigh muscles of hind legs in heifers in case of
black leg (Black Quarter; B.Q.).
Fig. 7.15 Photomicrograph showing
myositis/gas gangrene
Etiology
 Mycotoxins from fungus Fusarium equiseti
found on paddy straw in low lying areas with
moisture (Degnala disease).
Etiology
 Clostridium chauvei
 Gram positive, rod, anaerobe.
 Produces toxins under anaerobic conditions
which causes disease.
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
Stress, trauma,
animals.
transportation
Putrefaction
Putrefaction is decomposition of tissue after death
by saprophytes leading to production of foul odour.
After autolysis the saprophytes invade from
external environment into the body, multiply and
eventually digest the tissues with their enzymes.
The tissue becomes frazile and produces foul
odour.
predisposes
Macroscopic features
 Oedema of Muscles in affected part
particularly thigh region.
 Blackening of muscles due to production of
H2S by bacteria and its chemical reaction with
iron of free hemoglobin producing iron
sulphide.
 Presence of gas in the area giving crepitating
sound on palpation.
Pseudomelanosis
Pseudomelanosis
is
greenish
or
bluish
discolouration of tissues/ organs after death.
Saprophytes causing putrefaction also produce
hydrogen sulfide which chemically reacts with iron
portion of hemoglobin to produce iron sulfide. Iron
sulfide is a black pigment and produces green, gray
or black shades on combination with other tissue
pigments.
Microscopic features
 Necrosis of muscles
 Presence of Gram positive rod shaped
Clostridia
 Dissolution of muscle fibers due to
saprophytes/ toxins of the organism.
Rigor mortis
Rigor mortis is the contraction and shortening of
muscles after death of animal leading to stiffening
and immobilization of body. It occurs 2-4 hrs after
death and remains till putrefaction sets in. Rigor
mortis begins in cardiac muscles first and then in
skeletal muscles of head and neck with a
progression towards extremities. It is enhanced by
high temperature and increased metabolic activity
before death; while it is delayed by starvation, cold
and cachexia. Rigor appears quickly in case animal
is died due to strychnine poisoning as a result of
depletion of energy source ATP. Muscle fibers
shorten due to contraction and remain in
contraction in the absence of oxygen, ATP and
creatine phosphate. Rigor mortis remains till 20-30
hrs of death, the duration depends on autolysis and
putrefaction. It disappears in same order as it
appeared from head, neck to extremities. It can be
used to determine the length of time after the death
of animal.
POST-MORTEM CHANGES
Alterations in cells/tissues occur after death of
animal. The degree of such alterations and their
speed
depends
upon
the
environmental
temperature, size of animal, species of animal,
external insulation and nutritional state of the
animal. The postmortem changes occurs rapidly in
high environmental temperature, large animal,
fur/wool bearing and fatty animals.
Autolysis
Autolysis is the digestion of tissue by its own
enzymes and is characterized by uniform
destruction of cells without any inflammatory
reaction. After death, a state of hypoxia occurs
leading to decreased ATP. The cell organelles
degenerate and the membrane of lysosomes
dissolved which releases the lysosomal enzymes in
the cell responsible for digestion of cells/tissues.
These enzymes cause disintegration of cell
components into small granules in the cell.
Microscopically, autolysis is characterized by
uniform dead cells without any circulatory changes
and inflammatory reaction.
Algor mortis
Algor mortis is cooling of body. As there is no
circulation of blood after death, which maintains
the body temperature, body becomes cool after
death. However, it takes 2-4 hrs depending on the
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species, environmental temperature and type of
animal.
yellow in colour. Post-mortem clot is uniform in
structure and it does not attach on wall of blood
vessel as thrombus does. In anthrax, postmortem
clot does not appear. Post-mortem clot in formed in
two types: Red or current jelly clot forms when the
components of blood are evenly distributed
throughout the clot. It occurs due to rapid clotting
of blood. The yellow or chicken fat clot occurs
when the components of blood are not distributed
evenly. The ventral position is red and upper
position in yellow due to WBC fibrin and serum. It
occurs due to prolonged coagulation time of blood
leading to sediment of red blood cells.
Livor mortis
Livor mortis is the staining of tissues with
hemoglobin after death of animals. It gives pinkish
discolouration to the tissues.
Hypostatic congestion
Due to gravitational force, the blood is
accumulated in dependent ventral parts of body. It
is helpful in establishment of the state of the body
at the time of death.
Post-mortem emphysema
It occurs due to decomposition by gas producing
organisms including saprophytes. The gas is mainly
accumulated in gastrointestinal tract causing
rupture of the organ.
Displacement of organs
Displacement of internal organs due to rolling of
dead animal. Mainly intestine / stomach and uterus
are affected with displacement which can be
differentiated from antemortem by absence of
passive hyperemia.
Post-mortem clot
It is clotting of blood after death of animal mainly
due to excessive release of thrombokinase from
dying leucocytes and endothelial cells. It is smooth
in consistency and glistening surface with red or
Imbibition of bile
Cholebilirubin present in the gall bladder diffuses
to the surrounding tissues /organs and stains them
with yellow/ greenish pigmentation.
MODEL QUESTIONS
Q. 1.
Fill in the blanks with suitable word(s) to answer the following.
1. ………….. necrosis is caused by Mycobacterium tuberculosis and characterized by …………..
material formed due to coagulation of ………….. and …………..
2. Chromatolysis is the lysis of ………….. material.
3. Necrosis is defined as death of cells/ tissue in ….. body characterized by ……, ….., and ……..
4. Abscess is an example of………….. necrosis caused by ………….. organisms.
5. Fat necrosis occurs by the action of enzymes of …….. and characterized by …….. deposits on
organs.
6. Aspiration pneumonia in calves is an example of ………….. gangrene.
7. Degnala disease is caused by ……… toxins found on paddy straw and characterized by
……….. gangrene.
8. Gas gangrene is caused by ………….. in muscles of heifers and characterized by …………….
………….. and ………….. sound on palpation.
9. Autolysis is ………….. of tissues by ………….. enzymes.
10. Greenish discolouration of tissues after death is known as ………….. as a result of …………..
action and production of ………….. which combines with ………….. of hemoglobin.
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Q. 2.
Write true or false against each statement and correct the false statement.
1. ...........Autolysis is the local death of tissue in living body.
2. ...........Algor mortis is cooling of body after death.
3. ...........necrosis invaded by saprophytes leads to putrefaction.
4. ...........Hypostatic congestion may reveal the time of death of cadavour.
5. ...........Cholebilirubin present in gall bladder diffuses to surrounding tissues is known as
imbibition of bile.
6. ...........Apoptosis is programmed cell death.
7. ...........Karyorrhexis is rounding of cells, which takes a deep stain.
8. ...........In coagulative necrosis, cellular details are maintained.
9. ...........Ischemia may lead to necrosis.
10. ………Fat necrosis is characterized by the presence of creamy yellow liquefied material.
Q. 3.
Write short notes on.
1. Caseative Necrosis
2. Abscess
3. Gas gangrene
Q. 4.
Q. 5.
Define the following.
1. Pyknosis
2. Karyolysis
3. Karyorrhexis
4. Chromatolysis
5. Gangrene
4.
5.
Post-mortem changes
Lysosomal enzymes
6.
7.
8.
9.
10.
Apoptosis
Necrobiosis
Necrosis
Autolysis
Livor mortis
Select appropriate word(s) from four options given against each statement.
1. In liquifactive necrosis………….. cells are present
(a) Monocytes
(b) Lymphocytes
(c) Eosinophils
(d) Neutrophils
2. Programmed cell death is known as ………….. in living body.
(a) Apoptosis
(b) Necrosis
(c) Autolysis
(d) None of the above
3. Chalky white deposits are observed in ………….. necrosis
(a) Coagulative
(b) Liquifactive
(c) Fat
(d) Caseative
4. Gangrene in lungs is an example of ………….. grangrene.
(a) Dry
(b) Moist
(c) Gas
(d)All of the above
5. Degnala disease is an example of ………….. gangrene
(a) Dry
(b) Moist
(c) Gas
(d) None of the above
6. Digestion of cells/tissues by their own enzymes is known as …………..
(a) Necrosis
(b) Autolysis
(c) Gangrene
(d) Putrefaction
7. Greenish discolouration of tissues after death is also known as …………..
(a) Pseudomelanosis (b) Melanosis
(c) Necrosis
(d) Imbibition of bile
8. Algor mortis is the ………….. of body.
(a) Staining with hemoglobin (b) Cooling
(c) Hardening
(d) Softening
9. Rigor mortis remains in body ………….. hrs
(a) 12-15 hrs
(b) 20-30 hrs
(c) 35-48 hrs
(d) 5-10 hrs
10. Lysis of chromatin material is known as …………..
(a) Karyolysis
(b) Karyorhexis
(c) Chromatolysis
(d) Caseation
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