Liver

Gastrointestinal System
Sinusoids are low pressure vascular channels that receive blood from terminal
branches of the hepatic artery and portal vein at the periphery of lobules and
deliver it into central veins. Sinusoids are lined with endothelial cells and flanked
by plates of hepatocytes.
 Fatty liver disease (hepatic lipidosis)
• Fatty liver disease refers to the deposition
and build-up of fat in the liver.
• Fatty liver is a transition phase disease
induced by a negative energy balance in
dairy cows.
• During this period, body fat is mobilized and
transferred to the liver as non-esterified
fatty acids (NEFA) where they are either
metabolized to produce glucose, or if supply
exceeds metabolic capacity, excess becomes
deposited as triacylglycerols.
 Negative energy balance

Fatty liver (hepatic lipidosis) disease is the result of the liver being unable to
cope with the amount of fat entering the liver for metabolism to glucose.
Fat build-up in the liver inhibits metabolic function and induces a negative
cascade of events that often results in death.
Post-mortem diagnosis of a fatty liver (left) and a healthy liver (right)
Enlarged, yellowish pale liver
Photomicrograph of liver of goat with diffuse hepatic lipidosis showing macrovacuoles,
vacuoles pushing the nucleus to one side, signet ring appearance (arrows), infiltration of portal
area with round cells, and congestion of hepatic sinasoides (arrow head).
Photomicrograph of liver of goat with diffuse hepatic lipidosis showing fat droplets stained
orange yellow (Sudan III).
Chronic venous congestion (CVC) , Nutmeg liver
Passive Hyperemia, (Congestion)
• Congestion: it is a passive process which results due to impaired
outflow of venous blood from a tissue
• Obstruction of veins due to thrombi or backward pressure due to
heart failure
Should not be confused with hyperemia
• Hyperemia: is an active process which results due to dilatation of
arterioles and increased inflow of blood as in sites of inflammation.
• Chronic venous congestion is long standing accumulation of
deoxygenated blood and hence there is damage to the tissue.
 Mechanism

Heart Failure

Left heart
Right heart failure
failure

Pressure into
Pressure into venous system
Pulmonary vein

CVC LUNGS CVC LIVER CVC SPLEEN CVC KINDNEYS

• Gross appearance
• Gross
• Liver is larger and wet. Cut section shows congested red centers of hepatic
lobules surrounded by pale colored unaffected peripheral areas. This
appearance is known as nut meg liver. In a long standing case of chronic
venous congestion, there will be increased fibrosis, decreased liver size and
parenchyma is divided into lobules and condition is known as cirrhosis of
liver.
 CVC Liver
• Microscopy
• Central vein and sinusoids are
distended with RBCs. Some areas
of hemorrhage are present.
When these RBCs are
phagocytosed by macrophages,
they are called siderophages.
Central lobular necrosis due to
central vein congestion is seen.
Fatty change is due to hypoxia in
peripheral hepatocytes is also
seen.
Liver centrilobular congestion and necrosis
The liver is firm because of hepatic fibrosis that is most severe in centrilobular areas The
central vein is surrounded by a mild amount of connective tissue from which fine fibrous
septa extend out into the lobule. Note the macrophages containing hemosiderin, the result
of erythrocyte breakdown in this area as a result of chronic congestion.
Cirrhosis is scarring
(fibrosis) of the liver
caused by long-term
liver damage. The scar
tissue prevents the
liver working properly.
Cirrhosis is sometimes
called end-stage liver
disease because it
happens after other
stages of damage from
conditions that affect
the liver, such as
hepatitis.
End-stage liver from a dog .The liver is small, firm, and irregular with nodules of
regenerative parenchyma separated by tracts of fibrous connective tissue.
 Histology showing
cirrhosis with thick
bands of fibrous tissue
replacing the tissue
between portal tracts
(dotted circles). These
fibrous tissue bands
surrounding surviving
hepatocytes and as
these attempt to
regenerate they form
parenchymal nodules.

The hepatocytes also regenerate but are now trapped by fibrous tissue and form nodules. As the fibrous tissue increases in
amount the normal architecture is destroyed, with extensive bridging of fibrous tissue obliterating the normal portal tract to
central vein architecture of the lobule .This pattern is termed cirrhosis
Liver. Hematoxylin and eosin
(H&E). Generalized
disruption of the hepatic
parenchyma, with absence
of lobular pattern.
Hepatocytes appear
aggregated in regeneration
nodules (asterisk) separated
from each other by a very
intense chronic fibrous
reaction in portal spaces
(arrow) and in interlobular
septa.
Liver at a higher
magnification. H&E. Note
the presence of
individualized hepatocytes
(arrowhead) between the
interstitial fibrotic tissue as
well as mononuclear
inflammatory infiltrate.
Inset: bile duct hyperplasia
between fibrotic tissue
(arrow).
 Normally, ammonia is cleared
by liver and kidneys and
metabolized in skeletal
muscle. However, as a result
of liver dysfunction and
portosystemic shunting,
ammonia cannot be cleared
adequately. **Increased
ammonia levels in the plasma
increases metabolism to
glutamine (via glutamine
synthetase) in astrocytes,
which subsequently causes
Why head intracellular swelling and
pressing? edema.
Challenges of High grain diets
• Acute acidosis (Lactic acidosis, Ruminitis)
Liver Abscesses
Abscess, a localized collection of pus in a cavity formed from tissues
that have been broken down by infectious bacteria. The toxins released
by these multiplying bacteria destroy cells and thus trigger an acute
inflammation at the site.
White blood cells collect at the site and break down the dead tissues
and absorb the bacteria by means of phagocytosis.
Thick yellowish pus is formed from the broken-down tissues, the dead
bacteria and leukocytes, and the extracellular fluid that has
accumulated.
 Liver Abscesses
Fusobacterium necrophorum
Normal inhabitant of the rumen of cattle
Its role in ruminal fermentation to metabolize lactic acid

Fusobacterium necrophorum’s ruminal concentration is higher in grain-fed than forage-fed

From the rumen, the organism gains entry into the portal circulation and is trapped in the
liver to cause abscesses

Liver abscesses are often secondary to ruminal acidosis and rumenitis in grain-fed cattle.
Fusobacterium necrophorum.
gram-negative, long, non-
branching filamentous bacillus
Pathogenesis of
liver abscesses in
cattle fed a high-
grain diet.
Liver abscesses: the unseen profit thief
Liver abscesses are a value robber in feedlot cattle
An abscess in the liver is similar to those in other tissues and consists of an infiltrate of
neutrophils, degenerating neutrophils, and necrotic tissue debris.
Peste des petits ruminants (PPR)
Goat plague

Ovine rinderpest
Gross pathological lesions at post-mortem in goats infected with PPR virus. a Necrotic lesions on dental pad; b lesions on
gum and oral cavity; c oro-pharyngeal sections showing necrotic lesions on palatine tonsils and small fibrin deposits on the
base of tongue; d zebra striping in large intestine and e consolidated lungs leading to pneumonia
 BVD
• Bovine viral diarrhea (BVD), also known as mucosal disease.
• Infection is via the oropharyngeal route with primary replication in the
epithelium of the oropharynx and a rapid uptake into the drainage lymph nodes.
Viremia involves infection of lymphocytes giving rise to a leucopenia, and
spreads to other lymphoid tissues, particularly Peyer's patches.
• Leisons:
❖Erosions and ulcers on the buccal mucosa, lower lip, ventral, dorsal and lateral borders of
the tongue, cheeks and gums.
❖The erosions and ulcers extended to pharynx , larynx and esophagus.
❖The rumen and omasum have erosions and ulcers.
❖The Abomasal mucosa is congested, hemorrhagic.
❖The large intestine show erosions and hemorrhages.
❖The payer’s patches are necrotic and sloughed leaving ulcerated mucosa.
❖The lungs are edematous, hemorrhages and show necrosis of lymphocytes.
 Case Study of BVD
• A 14-month-old heifer with a 17-day history of unresponsive bloody diarrhea was
necropsied.
• There were focal, pink-red erosions of the nares and hard palate; ulcers and
fissures of the tongue; and multiple ulcerative lesions of the alimentary canal.
Interdigital skin of both rear limbs was ulcerated and bleeding; and the margins
of the vulva contained red ulcers.
Grossly, there are multiple sharply demarcated ulcers (vertically linear red streaks) and
similar areas covered by diphtheritic membranes (vertically linear yellow-brown streaks).
The cause is the pestivirus of bovine viral diarrhea (BVD).
Bovine viral diarrhea (BVD), ileum, mucosa, cow. Peyer’s patches and the overlying
epithelium are necrotic and covered with suppurative exudate.
Multifocal ulcerative colitis, colon, caused by bovine viral diarrhea (BVD) virus.
Microscopically, there is a focus of necrosis (arrows) of cells of the stratum basale and
stratum spinosum caused by the pestivirus of BVD. H&E stain.
Fig. 12. Oral mucosa; cow.
Mucosal erosions and
intracorneal pustules (arrows).
Fig. 13. Esophagus; cow. Surface
ulceration coated over by
fibrinopurulent exudate (arrow).
Fig. 14. Abomasum; cow. Gastric
glands are dilated and contain
aggregates of neutrophils and
sloughed epithelial cells. Fig. 15.
Small intestine; cow. Crypt
epithelial cells (arrows) and
endothelium lining mucosal
capillaries show
immunoreactivity for BVD
antigen
Parvovirus enteritis (Panleukopenia virus)
• Canine parvovirus is a
highly contagious virus
that commonly causes GI
disease in young,
unvaccinated dogs.
Presenting signs include
anorexia, lethargy,
vomiting, and diarrhea,
which is often
hemorrhagic.
Gross and Microscopic Lesions
• Gross necropsy lesions of canine parvovirus can include:
❖A thickened and discolored intestinal wall
❖Watery, mucoid, or hemorrhagic intestinal contents
❖Edema and congestion of abdominal and thoracic lymph nodes
❖Thymic atrophy
❖In the case of CPV myocarditis, pale streaks in the myocardium
• Histologically
❖ Intestinal lesions are characterized by multifocal necrosis of the crypt
epithelium, loss of crypt architecture, and villous blunting and sloughing.
❖Depletion of lymphoid tissue and bone marrow hypoplasia are also seen.
❖Pulmonary edema, alveolitis, and bacterial colonization of the lungs and liver
may be seen in dogs that died of complicating acute respiratory distress
syndrome, systemic inflammatory response syndrome, endotoxemia, or
septicemia
Dog with severe bloody diarrhea characteristic of severe parvovirus enteritis
Small intestine at necropsy from a dog that died suddenly of parvovirus enteritis. Note the
discoloration of the intestinal wall and fibrin on the serosal surfaces.
Canine parvovirosis in dog. Small intestine: A: very reddish and wrinkled serosa. B:
thickened intestinal wall and mucosae diffusely wrinkled and browned
Normal intestinal villus showing cellular differentiation along the villus. B, Parvovirus-
infected villus showing collapse and necrosis of intestinal villus
C: collapsed intestinal lamina propria, with fusion of the villi, atrophy and disappearance of
crypts, and dilation of the remaining
Photomicrograph of the small intestine of a dog that died of parvovirus enteritis. Villi are
collapsed, and crypt lumina are dilated and filled with necrotic debris