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Digestive System
The affections of digestive system are among the
most common in veterinary medicine. The gastrointestinal tract diseases are
common due to relatively easy entrance to the body by pathogens. The digestive
system troubles are usually not serious and usually transit. Vomiting, anorexia,
diarrhea, colic, tympany, impaction and constipation are seen associated with
troubles in digestive system affection.
Developmental anomalies
Anomalies occur infrequently in domestic animals. Anomalies include facial
clefts, harelip, cleft palate (palatoschisis) (Fig. 1),
agnathia (Fig. 2)
brachygnathia, micrognathia, prognathia and glossoschisis.
Fig.
1: Buccal
cavity showing fissure in hard palate (palatoschisis).
Fig.
2: Lamb
showing agnathia.
Cleft
lip (chelioschisis):
It
affects the upper lip and represented by presence of fissure.
Cleft
palate (palatoschisis):
It is open cleft between the oral and nasal cavities. The newborn animals with
cleft palate drip milk from their nostrils during nursing, whereas older animals
develop respiratory affection and pneumonia.
Inflammatory processes
The
inflammation of buccal cavity and its contents resulted from exposure to
different irritant are common. Those irritants may cause a diffuse inflammation
of the buccal cavity (stomatitis) (Fig 3)
, or a localized inflammation. The
localized inflammation of gingival (gingivitis), tissue surrounded the teeth
(periodontitis), pharynx (pharyngitis), tongue (glossitis), tonsils
(tonsillitis) or lips (chelitis).
Fig.
3: Buccal
cavity showing stomatitis represented by congested, erosion or ulcerated mucous
membrane.
Gingivitis
Most
cases result from bacterial infection follow either trauma, poor oral hygiene or
various immunodeficient states.
Macroscopic picture
The
gingival bleeds easily, erythematous and edematous (Fig. 4).
Fig.
4: Gingivitis
characterized by inflamed gingiva.
Microscopic picture
The
gingival connective tissue shows congested blood vessels and infiltrated with
neutrophils and lymphocytes.
The
overlying gingival epithelium may be ulcerated or hyperplastic.
Stomatitis
1. Catarrhal stomatitis
It is a
mild superficial acute inflammation of oral mucosa. It is caused by mild
irritant as trauma, chemical and infectious agents.
Macroscopic picture
The
buccal mucosa shows redness, swelling and covered with grayish or brownish gray
mucous. The living animal express pain and difficult prehension and mastication
•Bacterial decomposition of food results in a fetid odor.
Microscopic picture
•Dilatation of the submucosal blood vessels beside infiltration of the submucosa
by inflammatory cells and hyperplasia of lymphoid tissue of soft palate tonsils,
and pharynx.
•
Desquamation of the epithelial lining which covered with mucus and bacteria.
Sequelae:
Catarrhal stomatitis usually heals rapidly when the cause is stopped.
2. Vesicular stomatitis
Vesicular stomatitis usually associated with viral diseases, thermal or chemical
agents
Causes
1-
Viral diseases as foot and mouth disease, infectious vesicular stomatitis and
herpes virus.
2-
Thermal and chemical agents.
Macroscopic picture
Vesicles containing clean fluid are seen on oral
mucosa (lips, tongue, gums, dental pad and hard palate).
The
size are varies and filled with clear fluid
Rupture
of vesicles leaving an erosion or ulcer (Fig. 5).
Fig.
5: Dental pad showing ruptured vesicle in case of
vesicular stomatitis.
Microscopic picture
The affected epithelial cells show vacuolar and
hydropic degenerations. The fluid from several degenerated cells coalesces with
each other to form vesicles.
Some
vesicles may be rupture by mouth movement, leaving erosions with intact
germinal basal layer (Fig. 6).
Fig.
6: Erosion of the tongue showing desquamation of the
epithelium with congested blood vessels and inflammatory cells in lamina
propria. H&E.
Sequelae
It is a
mild inflammation, so if the cause is removed healing is usually occur
EROSION
It is
represented by loss of superficial layers of an epithelial covering or lining
with intact basal layer. It associated with acute inflammation in the underlying
propria.
ULCER
It is
focal loss of the lining or covering epithelium and the base of the ulcer lies
in the underlying propria. Ulcers are vary in size and shape (Figs 7& 8). Their
The ulcer edges tend to be elevated and healing occurred by scar formation (Fig.
9).
Fig.
7: Buccal cavity,
dental bad showing ulcer of the
tongue characterized by
focal
loss of the lining or covering epithelium and the base of the ulcer lies in the
underlying propria.
Fig.
8: Buccal cavity, Tongue showing ulcer
characterized by
focal
loss of the lining or covering epithelium and the base of the ulcer lies in the
underlying propria.
Fig.
9: Buccal cavity, tongue showing healed ulcer.
3. Suppurative stomatitis
It
occurs associated with wound infected with pyogenic microorganisms.
The
inflammation may be focal or diffuse. The inflamed oral tissue shows redness and
swelling. The pus are usually removed by movement of food leaving erosion or
ulcer (Fig. 10).
Fig.
10: Tongue
showing suppurative inflammation of tongue due to actinobacillosis characterized
by colonies in center, radiating clubs and surrounded with neutrophils. H&E
4. Fibrinous stomatitis
It
occurs with severe irritation where the principle constituent of exudate is
fibrin.
It is
usually associated with necrosis and ulceration of oral epithelium.
5. Necrotic stomatitis
It may
be diffuse associated with chemical and thermal agent or focal associated with
foreign bodies, sharp teeth and bacterial infection as Fusiform necrophorum.
It is
usually associated with necrosis and ulceration of oral epithelium.
Macroscopically,
focally slight swollen gray, yellow or brown oral mucosa surrounded by red zone.
Ulcer may be resulted from removal of necrotic tissue by mouth movement (Fig.
11).
Ulcer may be round, oval or irregular in shape and vary in size
Microscopically, the oral mucosa shows coagulative necrosis infiltrated and
separated by inflammatory cells (Fig. 12).
Fig.
11:Tongue
showing necrotic glossitis.
Fig.12:Tongue
showing necrotic inflammation characterized by complete desquamation of the
epithelial lining with exposed lamina propria. H&E.
Necrosis
All types of necrosis can involve the oral
structures. All of them can associate with specific infections.
Disturbance in pigmentation
Black
pigmentation
(Melanotic pigmentation) is observed in the buccal mucosa especially in dogs.
Moreover in lead toxicosis a blue black line is a usually seen on gum of
animals.
In case of
jaundice, yellow coloration of oral mucosa is seen.
Disturbance of growth
Atrophy
of gums
of dogs
and cats with age are noticed.
Hyperplasia and hyperkeratosis:
are
seen in buccal cavity of bovine poisoned with chlorinated naphthaline. The
lesions are usually seen on the mucosa of the tongue, lips and other buccal
surfaces.
Disturbance in circulation
Congestion and edematous swelling
of the tongue and buccal mucosa are specific lesions of blue tongue of sheep.
Cyanotic buccal mucosa with ulceration
is common in uremic dogs and cats.
Hyperemia
occurs in association with inflammation.
Hemorrhage
is a result of mechanical injury.
Edema
is associated with hypoproteinemia in parasitic infection.
Neoplasm of the oral cavity
Viral
papilloma
occurs frequently in the oral cavity of dogs, cattle and rabbit. It may be
disappears if not removed surgically within 1-3 months. Epulis is a
benign neoplasm derived from connective tissue or periodontal ligament.
Classification
1. Fibromatous epulis
It
consists of mass of stellate fibroblasts surrounded by dense fibrillar collagen
and covered by intact gingival epithelium.
2. Acanthomatous epulis
It
similar to fibromatous epulis but, contains sheets or cords of stratified
squamous epithelium (Fig. 13).
3-Ossification epulis
It
similar to fibromatous epulis, but in addition contains either irregular island
of osteoid or mineralized bone or a cellular eosinophilic cemmentum or
dentin-like structure.
Malignant melanoma
is common in dog and rare in others (Fig.14).
Fibrosarcoma
is
common in dog and cat .
Osteosarcoma
occurs in bone of upper and lower jaws.
Lymphosarcoma,
Mast cell tumors and granular cell tumor are observed.
Squamous cell carcinoma
occurs in any species. It is the most common malignancy of the oral cavity of
cats and dogs (Fig. 15).
Fig.
13: Buccal cavity of cattle showing acanthomatous epulis characterized by
presence of epithelial cords in fibrous stroma. H&E
Fig.
14: Buccal cavity, jaw showing melanoma.
Fig.
15: Oral cavity of dog showing squamous cell carcinoma characterized by keratin
in center surrounded by flattened malignant cells in center and polyhedral in
periphery (cell nest). H&E.
Tonsils
Anatomically the tonsils consists of either distinct paired, nodular (dog and
cat) or diffuse (pig, cow and horse) aggregates of lymphoid tissue situated at
the opening of oropharynx.
The
discrete nodular tonsils of human, dogs and cats have crypts lined by stratified
squamous epithelium that extend into the parenchyma of organ.
Tonsilitis
It is also
common in swine. Tonsilitis is easily detected in dogs and cats.
Causes
It
occurs when pathogenic bacteria as
Streptococcus, Staphylococcus,
Corynebacterium pyogenes, Erysipelothrix rhusiopathiae and spherophorus
necrophorus are
colonize the tonsillar crypts and induce an acute inflammation.
Inflammation of the tonsils is common particularly in dogs suffering canine
distemper, and infectious canine hepatitis.
Macroscopic picture
Suppurative
tonsilitis is usual type, but others type of inflammation as serous, catarrhal
and the necrotic types are observed.
•
Tonsils appear swollen and hyperemic.
• The
crypt will exude a purulent white yellow exudate. Also the surface of tonsils
may covered by some exudate.
•
Painful swelling of mandibular lymph nodes is observed.
Microscopic picture
Tonsils
show follicular hyperplasia.
Tonsil
crypts are filled with desquamated epithelium, bacteria and inflammatory cells,
mainly neutrophils, in suppurative one.
Neoplasms
Several
type of tumors are recorded including squamous cell carcinoma are recorded
Dental anomalies
1. Dentigerous cysts
It is
epithelial lined cystic structures in bone or soft tissue of jaw. Usually, the
cysts are lined by stratified squamous epithelium and they often filled with
keratin. Occasionally fragments of poorly formed tooth within dentigerous cyst
(Fig. 16).
2. Segmental enamel hypoplasia
The enamel of tooth is produced by specialized
cells called ameloblasts. The ameloblasts are susceptible to injury by poisons
as fluorine, drugs as tetracycline and viruses as canine distemper.
Causes
The causes
include cachectic diseases, malnutrition, intoxicosis, and infectious diseases
Exposure to poisons or viruses prior to or during enamel development.
Macroscopically,
affected teeth have defects in enamel that result in exposure of underlying
dentin giving the teeth a mottled appearance (Fig. 17).
3. Anodontia
is lack
of tooth development.
4. Oligodontia
is development of fewer teeth than normal.
5. Polydontia
is the
presence of supernumerary teeth.
Degenerative dental diseases
1. Dental attrition
It is
the wearing away of dental structure as a result of poor masticatory function,
or oral cavity conformation.
2. Dental caries
It is
characterized by digestion of the inorganic matrix of enamel and dentin
demineralization. Dental caries results from bacterial metabolites with
production of acids and enzymes, which lead to demineralization and destruction
of dental matrices
(Fig. 18).
Fig.
16: Buccal
cavity showing dentigerous cyst.
Fig. 17: Teeth
showing segmental enamel hypoplasia.
Fig.
18:Teeth
showing segmental enamel hypoplasia.
Fig.
19:
Gross picture of dental caries. The enamel becomes dull, white and pocked. The
exposed dentine becomes brownish black.
Macroscopically, the enamel becomes dull, white and pocked. The exposed dentine
becomes brownish black.
3. Dental plaque
It is
accumulated non-mineralized bacterial mass, food particles, desquamated
epithelium adhered to tooth surface.
4. Dental calculus (Dental tartar)
It is
the mineralization of dental plaque by utilizing calcium of saliva. It consists
of calcium phosphate in dog and calcium carbonate in horse.
It
causes mechanical irritation and persistent inflammation of gums.
5. Cemmentum hyperplasia.
It lead to very long teeth due
to pushing the tooth out.
6. Pigmentation of the
teeth usually
involves dentine or cement about the root. Reddish brown of dentine may be
observed in pulpal hemorrhage or inflammation. Yellowish coloration is noticed
in icterus.
Congenital porphyria
is a condition recorded in calves and swine, which stain the dentine red
in young animals (pink tooth) and dark brown in adults.
Inflammation of teeth and periodentium
Pulpitis
It is
the inflammation of vascular part of the tooth (pulp).
The
causes are usually bacteria and enter through enamel defect or via blood.
It may
lead to osteomyelitis
Periodontitis
It is
the inflammation of tissue around teeth.
It may
be superficial (gingivitis) or deep (pyorrhea).
Salivary
glands
Sialoadenitis
It is
the inflammation of salivary glands. It is rare in domestic animals.
It is usually suppurative.
Causes
Bacterial which enter the gland through the salivary duct or through extension
as in strangles.
Viral
infections as rabies, distemper and malignant catarrhal fever.
Trauma and vitamin A deficiency.
The
infections occur through salivary ducts by extension or through blood.
Ptylism is
the increased salivary secretion. The caseous may be poisoning or associated
with stomatitis (Fig. 19).
Cysts
It
occurs due to obstruction of the salivary ducts by foreign bodies.
Its fluid content is usually viscid grayish-yellow or brownish, clear or turbid
and odorless. In dog and cow a cyst
frequently observed in sublingual duct, located in frenulum of tongue is
referred to as a ranula (Fig. 20).
Sialoliths (salivary calculi)
• It
is a rare disorder of cattle, horse and dog.
• It is a calcium
concretions which formed either in duct or in the gland itself as a result of
chronic inflammation which provides desquamated cells as a minute nidus upon
which calcium salts precipitate. When the duct is occluded for long periods, a
cyst may be formed in salivary duct and followed by gland atrophy.
Fig.
19:Cattle
showing ptylism.
Fig.
20: Buccal cavity, sublingual ranula cyst.
Pharyngitis usually accompanies stomatitis. Pharyngitis is seen in the course of
several diseases including Anthrax in pig and dog and calf diphtheria.
Pharyngitis may be suppurative, catarrhal or diphtheretic. The soft palate is
red and swollen besides tonsilitis are noticed.
Esophagus is a muscular tube that extends from pharynx down ad through diaphragm
to the stomach. The esophagus has physiologic high-pressure zones at either end
that act as sphincters. The upper cricopharyngeal sphincter prevent entry of air
and pharyngeal contents in the esophagus except during swallowing and the lower
esophageal (cardiac sphincter) prevents reflex into the esophagus of acidic
cardiac juice.
Aplasia
and hypoplasia
are common and usually involve that portion of the esophagus in the region of
the heart. Hypoplasia of the esophagus with epithelial defect is a common cause
of choke.
Disorders of esophagus can be categorized into one of three types; inflammatory
degenerative lesions, obstructive lesions or motility disorders.
Obstructive and functional disorders
1. Cricopharyngeal achalasia
It is a
disorder due to inadequate relaxation of the upper esophageal sphincter
recognized infrequency in canine and characterized by dysphagia and
regurgitation of food. Grossly, deformity of cricopharyngeal muscle is seen.
Microscopically, fibrosis, atrophy, regeneration and phagocytosis are recorded.
2. Megaesophagus (esophageal achalasia)
Generalized or segmental dilatation of the esophagus results from neuromuscular
disorders that impair esophageal motility .
Megaesophagus has been described in dogs, cats, foal and human and can be
congenital or acquired.
a. Congenital megaesophagus
It is an congenital disorder recorded in dogs. It
has also been described in cats.
Affected puppies and kittens usually suckle normally but after weaning
regurgitate solid food shortly after swallowing.
The
pathogenesis of this condition is poorly understood, but it has been speculated
that there is a delay in the maturation of esophagus nervous innervation.
Macroscopic picture
The
affected esophagus was dilated and flaccid esophagus, two to three time normal
is seen. Sometimes the dilatation is uniform, but in other is quite to
eccentric. The dilated portion usually contains fetid fluid.
Microscopic picture
There
is no reduction in the number of myenteric ganglial cells in the wall of
esophagus.
b. Acquired megaesophagus
Causes
It
occurs in adult dogs secondary to any defect in neural reflex involved in
swallowing and normal function of esophagus musculature.
A
variety of central and peripheral nervous system disorders include canine
distemper, other viral encephalitis, neoplasms, peripheral neuritis, bilateral
vagus nerve damage, lead poisoning, botulism and myasthenia gravis.
Myasthenia gravis
It is
reported in dogs and cats.
The
pathogenesis of this condition is due to develop autoantibodies to nicotinic
acetylcholine receptors, which interfere with neuromuscular innervation.
The
affected dogs develop generalized muscular weakness followed by signs of
megaesophagus.
3. Choke
Partial
obstruction of the esophagus, particularly in dogs, leads to vomition of
consumed food. Before it reaches the stomach. The food causes distention of the
esophageal portion above the obstruction with formation of an esophageal
diverticulum, ectasia or perforation.
Causes
1. Pressure produced by enlarged lymph nodes, tumor ad abscess.
2. Congenital vascular ring anomalies and esophageal hypoplasia.
3. Potato, turnips or small ears of corn is the
frequent causes in ruminants, but accumulation and germination of grains in
horse.
4.
Dogs and cats are
usually choked by sharp pieces of bone which lodge mostly in the thoracic
esophagus.
Macroscopically,
the esophagus shows distention of the esophageal portion above the obstruction
(Figs 21 & 22).
.
Sequelae
1. Local gangrene with sapremia and toxemia which kill the animal in few days.
2. Tympany in ruminant due to prevents regurgitation of gas.
3-Partial obstruction lead to formation of esophageal diverticulum ectasia or
perforation.
4. Esophageal abscess (Fig. 23).
Fig. 21:
the esophagus shows distention of the esophageal portion above the obstruction.
Fig. 22:
Gross picture of esophageal choke.
Fig.
23: Esophagus showing esophageal abscess
represent by replacement of esophageal wall by pus. H&E.
Diverticulum is
asymmetrical and unilateral sac-like dilatation.
Ectasia
is a uniform spindle or cylindrical-shaped dilatation.
Hyperplasia and hyperkeratosis
of the epithelial lining of the esophagus is seen in poisoning with chlorinated
naphthaline in cattle (Fig 24).
Fig.
24: Esophagus showing microscopic picture of hyperkeratosis characterized by
thickened stratum corneum. H&E.
Metaplasia of the
esophageal lining of the esophageal glands of chicken may be caused by vitamin A
deficiency.
Aplasia
and hypoplasia are
frequent.
Neoplasms of the esophagus
are rare. The lesions caused by Spirocerca lupi in dogs may change to
fibrosarcoma or osteogenic sarcoma.
Ingluvies (crop of birds)
Impaction,
necrosis and inflammation (ingluvitis) occur (Figs 25 & 26)
. The later may be
catarrhal or ulcerative. Pendulous crop with fluid contents is frequent in
turkeys.
Diverticulum is a symmetrical and unilateral sac like dilatation.
Fig. 25:
Crop showing
ingluvitis
represented by dilatation of blood vessels, leukocytic infiltration and edema in
lamina propria besides erosion in mucosa.
H&E.
Fig. 26: Gingivitis
due to candidacies showing Candida hyphae stained with PAS.
Esophagitis
The
inflammation of esophagus is infrequent due to the strong stratified squamous
epithelial lining.
Causes
1. Trauma.
2. Caustic chemical and reflex gastric acid.
3. Infection with parasites (tricmoniasis, Congylonemiasis and Spirocercosis),
mycotic as (candidiasis) and viral (bovine viral diarrhea).
Esophagitis may be catarrhal, fibrinous, suppurative and necrotic (Figs 27 & 28).
Reflux esophagitis
It is a
form of chemical esophagitis due to reflex of gastric acid and pepsin from
stomach into the lower portion of esophagus.
Macroscopic picture
The
affected part is hyperemic and contain linear erosion and ulceration.
Microscopic picture
1. Epithelial erosion or ulceration and proliferation of adjacent epithelial lining
to repithelization of damaged area.
2. Capillary dilatation and polymorph nuclear leukocytes are seen in lamina propria
beside fibroblast proliferation.
3. In
chronic case fibrosis is a Sequelae.
Sequelae
Fibrosis which, contract and lead to stenosis of esophagus (Fig. 29)
and
esophageal chock and diverticulum are recorded.
Fig.
27: Esophagus showing necrotic esophagitis represented by necrosis of epithelial
lining and congestion, edema and inflammatory cells in lamina propria. H&E.
Fig. 28: Esophagus
showing ulcerative esophagitis represented by complete desquamation of
epithelial mucosal lining beside congestion, edema and inflammatory cells in
lamina propria. H&E.
Fig. 29:
Gross picture of esophageal stenosis.
Parasites
Several parasites can be seen in the wall of esophagus such as
Tricmoniasis, Congylonemiasis, Sarcocyst (Fig. 30)
and Spirocercosis (Fig.
31).
Fig.
30: Gross picture of esophageal
wall showing sarcocyst represented by presence of white nodules in the
esophageal serosa.
Fig. 31:
Esophagus
showing microscopic picture of Spirocerca lupi adult worms in fibrous tissue nodule
infiltrated with inflammatory cells. H&E.
The
rumen, reticulum and omasum are called forestomach. They
act as a large tank
lined by keratinized stratified squamous
epithelium (without secretory function) and function as a large fermentation chamber where digestion of plant
material occurs by some bacteria and protozoa and synthesize several
vitamins.
Physical influence
1. Perforation
occurs usually in reticulum but infrequently in rumen. It may be:
1. External perforation
It is
most commonly in rumen as result of insertion of trocars and knives to relieve
tympany.
2. Internal perforation (Traumatic reticulitis)
It
occurs in bovine species due to they don’t have highly sensitive prehensile
organ as lips and tongue nor a discriminating sense of taste.
Cattle
swallow metallic objects such as nails, screws, and pieces of wire that have
been carelessly left in their feeding areas. Most foreign bodies always remain
in the reticulum by the folds of its mucosa. The foreign body penetrates the
reticulum by the help of its movement, abdominal pressure, pressure of uterus
and during parturition (Figs 32 & 33 )
. At the point of penetration at first there
is hemorrhage. After that the migration of foreign body through the wall of
rumen causes an inflammatory tract filled with pus and food and surrounded by
granulation tissue.
Fig.
32:
Traumatic reticulitis, sharp foreign body is seen on the rumenal serosa.
Fig. 33:
Reticulum showing traumatic reticulitis with the presence of foreign body
penetrating the reticulum mucosa.
When
the foreign body reaches the serosa, a local fibrinous peritonitis is produced
and adhesion occurs between reticulum and other viscera.
After
leaving the reticulum the foreign body penetrate the diaphragm, pericardial sac,
heart, lung or spleen lead to abscess formation.
2. Rupture of rumen
may occurs due to mechanical injury from outside or over distention from inside.
3. Dilatation of forestomach (Tympany or Bloat)
it is Over accumulation
of large quantities of gas (methane,
CO2 CO, H2S) in the lumen of rumen.
Causes
1.
It may be due to
excessive gas production during fermentation process, 2-Interference
with normal eructation as by chock.
Classification of tympany
a. Frothy or primary tympany
In this
case the gas is dispersed
or trapped in the form of small bubbles in
rumenal fluid. Agents responsible for foaming are suspected to be
Saponins and some plant proteins are responsible for formation of foam.
Secondary tympany or free gas tympany
It
results from physical obstruction of esophageal or pharyngeal passageways or
pressure upon the esophagus by tumor, abscess and swollen lymph node.
It is
develop gradually and often are chronic.
Death
results from forward displacement of the diaphragm which limit the respiratory
capacity and also the expanded rumen compress the abdominal viscera and occlude
the caudal vena cava, which result in anorexia. Moreover, absorption of toxic
gases as carbon monoxide, carbon dioxide and hydrogen sulfide is another cause
of death.
Lesions
1. Distended rumen and marked forward displacement of diaphragm that compress the
lungs into the anterior portion of thorax are seen.
2. The
abdominal viscera appeared pale.
3. The
rumenal content will contain small bubbles of gas, clotted blood or free gas.
4. Numerous hemorrhages are present on the serosa, trachea, heart and bronchial
lymph nodes.
4. Atony or rumen impaction
It is
the tightly impacted rumen with undigested food leading to weakness of ruminal
muscle. After few hors ruminal contraction becomes weak or stops. There is a
little or no gas in rumen.
Lesions
1- Thin
easily folded wall of the rumen are seen besides the ruminal content has fetid
odor. Atrophy of the ruminal muscles with acute toxic hepatitis resulted from
absorption of toxic product are seen (cause of death).
5. Ruminal acidosis, rumenitis and ulcer
These
condition represent successive stages often associated with sudden changes of
diet from a low energy ration to highly fermentable carbohydrates as grain and
bread.
Pathogenesis
Ingestion of excessive quantities of highly fermentable carbohydrate which
fermented by normal ruminal flora and bound with production of volatile fatty
acids which lead to decrease ruminal pH.
At pH
5.0 the normal Gram-negative bacteria and protozoa of rumen die, with overgrowth
of streptococcus which produce large quantities of lactic acid leading to
decrease of ruminal pH to level than so which in turn kill off streptococcus.
At this
point, the acid loving lactobacillus acidophilus rapidly proliferate with the
ruminal contents and death occurs when pH drops below 4.5.
During
the sequence of chemical changes described above, the musculature of rumen and
reticulum lose their tone and ability to contract due to effect of increased
level of volatile fatty acids which interact epithelial receptors in ruminal and
reticulum mucosa and inhibit contraction through vagovagal reflex.
The
over production of lactic acid by streptococci lead to chemical rumenitis and
reticulitis with damage and loss of epithelial.
Moreover, increase lactic acid concentration lead to increase osmotic pressure
of the ingesta, which attract water and electrolytes from blood leading to
clinical dehydration, hemoconcentration, an urea and shock.
Postmortem findings
1. The
ruminal content is thick in consistency with fetid odor.
2. Swollen ruminal papillae, cytoplasmic vacuolization, erosion or ulcer are seen
(Fig 34 &35).
Fig. 34:
Rumen
showing complete desquamation of the epithelial lining with infiltration of the
lamina propria with inflammatory cells. H&E.
Fig. 35:
Rumen showing necrotic rumenitis and ulcer which heal by scar formation.
3. The
lamina propria shows infiltration with neutrophils.
4. The
necrotic areas slough and become re-repithelization which is usually white in
contrast to the normal black epithelium.
Parasites
Several
parasites are seen in the rumen such as paramphistomiasis, hemonchosis and
oestertagiasis (Fig 36)
Fig. 36: Rumen
showed parasites (paramphistomum) in the lumen besides erosion of the mucosa and
inflammatory cells in lamina propria. H&E.
Omasum
The
omasum and esophageal groove is seldom the site of important pathologic
processes.
Pyogranuloma caused actinobacillosis may be seen.
Neoplasms of the forestomach.
Papilloma and squamous cell carcinoma and lymphosaroma are recorded.
Stomach
The
abomasum of ruminants is essentially similar in anatomic structure and
physiologic function to the glandular stomach of monogastric animals.
Pyloric stenosis and hypertrophy
Functional pyloric stenosis occurs sometimes in young dogs and characterized
clinically by delayed gastric emptying which lead to vomiting and poor growth.
In some
cases, there is grossly hypertrophy of pyloric muscle, but in other cases is
only function disorder of the gastric sphincter.
Gastric
dilatation and torsion.
Acute
distension of stomach
with gas occurs in several species mainly in dog.
Acute
dilatation
characterized clinically by discomfort, abdominal pain, marked distension of
abdomen and reluctance to move.
Cause
The
cause is generally unknown but predisposing causes may be parturitions,
overeating, pica, abdominal surgery and trauma.
Sequelae
The
gastric dilatation lead to torsion, mechanical obstruction of caudal vena cava
and portal vein besides decrease cardiac output which lead to arterial
hypotension, cellular catabolism increase and decrease renal function.
Macroscopic picture
1.
Greatly enlarged stomach, distended with gas and ingesta.
2.
Torsion may be result in twisting of the gastrosplenic omentum.
3. Severe congestion of veins and organs of caudal aspect of the body.
4. Stomach may be ruptured and spilling its content into the peritoneal cavity.
5. The
cranial aspect of the body is ischemic.
6. Liver is pale and spleen in congested.
7. Petechae and ecchymosis may be seen in serous membrane.
8.
Acute
dilatation in horse lead to stomach rupture. Rabbit may also affected. The
disorders has been reported in swine.
Displacement of abomasum
It is
the displacement of abomasum from its ventral and right-sided position in the
anterior abdomen to the left side displacing the rumen to the right.
Cause
It may
be due to atony and gaseous distension of abomasum (Fig. 37)
associated with
feeding ration containing high proportions of concentrates rather than roughage.
Also following recent parturition.
Clinical signs
include anorexia, depression, dehydration and distended abdomen particularly
protrusion of left paralumber fossa.
If the
displacement isn’t corrected immediately, the condition is fetal.
mpaction
It
occurs in stomach as the result of rapid ingestion of an excessive amount of
ground feed, grains without adequate water consumption (Fig. 38).
It is
especially serious in horse even without gaseous fermentation, which is usually
absorbed. Circulatory disturbances and shock may be fatal in few hours.
Fig. 37:
Gross picture of abomasum
displacement.
Fig. 38:
Gross picture of abomasum
showing impaction.
Abomasitis
Inflammation of abomasum is similar to gastritis. Catarrhal, hemorrhagic,
eosinophilic, lymphocytic abomasitis are noticed. Erosion may be seen associated
with abomasitis as in case of bovine viral diarrhea (Fig. 39)
.
Moreover ulcerative abomasitis also recorded in cattle (Fig. 40)
.
Fig. 39: Abomasum
showing necrotic abomasitis represented by necrosis in the rumenal mucosa
besides infiltration of lamina propria with inflammatory cells. H&E.
Fig.
40: Necrotic
abomasitis due to mucor infection. The lamina propria showing thrombus and
fibrinous inflammation. H&E.
Parasites
• A
wide variety of parasites may infest the stomach.
•
Gastrophilus spp. larvae, Habroonema spp., and Draschia spp. are seen in horse.
•
Haemonchus spp., Ostertagia spp. and Trichostrongylus spp. are recorded in
ruminant.
•
Physaloptera spp. and Ganthostoma are seen in dogs and cats.
Gastritis
Inflammation
of the stomach is called gastritis which is frequent in all domestic animals.
It may
be primary mostly due to ingestion of toxic substances or secondary to an
infection as canine distemper, hog cholera and viral diarrhea. Clinically, it is
characterized by pain, anorexia and vomiting. It is usually catarrhal or
hemorrhagic, but suppurative and fibrinous inflammation occurs.
1) Acute
catarrhal gastritis
It is common
type of mild gastritis occurs several viral, parasitic and physical agents.
Lesions of
catarrhal gastritis include a diffusely red , and thick mucosa covered with a
gray tenacious mucus. Hemorrhages may be present on the ridges.
The affected
mucous membrane is usually edematous and eroded. The fundus usually presents
Causes
Physical or chemical agents besides infectious agents as in case of canine
distemper, feline enteritis and parasitic gastritis are common causes.
Macroscopic picture
1. Reddening and thickening of gastric mucosa are seen.
2.
Increase in mucus secretion is observed.
Microscopic picture
1. Hyperemia, desquamated epithelium beside leukocytic infiltration is seen.
2. Hyperplasia of minute mucosal lymphoid nodules
is noticed.
2)
Chronic catarrhal gastritis
• It
reported with Haemonchus contortus.
• The
hyperplastic lymphoid tissue seen grossly as small white mucosal nodules.
3)
Acute hemorrhagic gastritis
Causes
1-Infectious agents as leptospirosis in dog and Clostridium septicum (Braxy) in
sheep are common causes.
2-
Uremia and arsenic poison.
Macroscopic picture
Deep
reddening of gastric mucosa is seen beside presence of blood on the surface of
mucosa and mix with content which turned to brown black due to effect of gastric
acid (Fig. 41).
Fig. 38: Stomach
showing hemorrhagic gastritis. H&E.
Microscopic picture
The
predominant type of exudate is erythrocytes beside congested capillaries,
leukocytic infiltration and desquamated epithelium. Inflammatory edema and
fibrinous exudate may be seen.
Fig. 41: Gross picture of hemorrhagic gastritis in uremic dog.
4)
Lymphocytic gastritis
It is
seen in dog and cats associated with infection by Heliobacter and H. pylori.
5)
Eosinophilic gastritis
It is
characterized by the predominant type of exudate is eosinophils. Moreover, it
causes chronic fibrotic gastritis. Mostly it associated with larva migrans in
dog.
Hemorrhages
The
hemorrhagic areas appear brown, not red because of the action of the gastric
juices on hemoglobin.
Ulcer
It is a
result of deep necrosis and usually acute. It is now recognized in most domestic
species.
Foreign bodies
Concretions
as hairball in cat stomach
(piliconcretions) and food balls (phytoconcretions) are frequent in cattle and
swine. Moreover, rubber ball in dog stomach
is recorded. The small ones may obstruct the pylorus, duodenum or the esophagus
during regurgitation.
Neoplasm of stomach
Adenocarcinoma, adenomatous polyps, undifferentiated carcinoma, squamous cell
carcinoma, leiomyoma and leiomyosarcoma are recorded.
The
intestine protect it self from enzymes and injures by mucus secreted by mucous
gland.
Enteritis
It is
inflammation of intestinal tract. Gastroenteritis is the inflammation involves
the entire tract. Moreover, the inflammation confined to special part can give
specific name as duodenitis, jejunitis, typhlitis or cectis and proctitis.
Acute
enteritis may confirm to any one of the five types of oxidative acute
inflammation. Sub acute and chronic inflammations are by no mean rare.
The
whole small intestine and large intestine may be uniformly inflamed.
Causes
Viral,
bacterial, parasitic or metabolic and nutritional diseases may cause enteritis.
1. Viral
infection: enteritis usually associated with several viral infections such as
cattle plague, malignant catarrhal fever, bovine viral diarrhea and feline
enteritis
2. Enteritis
is also noticed in the course of several bacterial diseases such as salmonellosis, Pasteurellosis, necrobacillosis and Johne's disease
3-Several
parasites induced enteritis during their infections as ascariasis (Fig. 42),
Coccidiosis (Fig.
43)
, oesophagostomiasis.
Fig.
42: Intestine showing
parasitic enteritis due to presence of adult ascarid
worm. The intestine showing necrotic mucosa and leukocytic infiltration. H&E.
Fig. 43:
Cecum showing
hemorrhagic enteritis. The bloody intestinal content
due to coccidiosis.
4. Enteritis
also associated with metabolic disorders as uremia
5. Physical
agents as spoilage and coarse food, beside chemicals and poisonous substances an
induce enteritis.
Pathogenesis of enteritis
Enteritis
may occurs in the course of several diseases or due to sudden changes in food,
which lead to disturbs the activity of non pathogenic microorganisms and changed
it to pathogenic one. The microorganisms colonize a new portion and produce
enteritis.
Moreover,
the young age (particularly those deprived from colostrum) is more susceptible
to enteritis than old one due to they do not have enough antibodies.
Enteritis
affects the intestinal function leading to passage of food with out complete
digestion or absorption. The undigested foods in intestine is consider a
suitable media for bacterial growth, which produce toxins leading to toxemia or
invade blood resulting in septicemia. Moreover, hypersensitivity to certain kind
of food such as milk may produce enteritis particularly in young calves.
Enteritis
due physical agents is noticed in region where the flow of the ingesta is
reduced, as around the ileocecal valve. But the chemical agents produce their
effect on posterior portions of the intestinal tract where those chemicals
become concentrated after most of the water is reabsorbed.
Classification of enteritis
Enteritis
can be classified into acute and chronic enteritis. Moreover, acute enteritis is
exudative and classifies into the following.
1. Catarrhal enteritis
It is an
acute inflammation of the intestine where the predominant constituent of the
exudate is mucus.
Causes
The cause is
usually mild as chemical intoxication, many
infectious agent and parasites and physical agent as coarse food.
Macroscopic picture
1. The
intestinal content contain a creamy white thick mucus.
2. The
intestinal wall become swollen, red and thick.
Microscopic picture
Vascular and
exudative reactions of inflammation are observed in the intestinal mucosa.
Numerous goblet cells, congested blood
vessels and leukocytic infiltration are seen (Figs. 44 & 45).
Fig. 44: Intestine
showing catarrhal enteritis represented by increase number of goblet cells,
congested blood vessels besides leukocytic infiltration. H&E.
Fig. 45: Intestine
showing catarrhal enteritis represented by increase number of goblet cells,
congested blood vessels besides leukocytic infiltration. H&E.
2. Hemorrhagic enteritis
It is an
acute inflammation of the intestine where the predominant constituent of the
exudate is erythrocyte. It is usually localized.
Causes
Locally
destructive endotoxin or exotoxin or by highly virulent infection as anthrax,
lamb dysentery S. typhimurium and Shigella. Also virus as canine and feline
parvovirus.
Macroscopic picture
The animal
usually dies of septicemia, shock or fatal hemorrhage.
The
intestinal content is mixed with blood (brownish in anterior portion and bright
red in posterior portion) (Fig. 46 ).
The
intestinal wall is hemorrhagic and thickened.
Microscopic picture
The vascular
and exudative reactions are evident.
Extravasated erythrocytes and inflammatory cells in intestinal wall (Fig 47).
Fig.
46: Intestine showing hemorrhagic enteritis.
Fig.
47: Microscopic picture of hemorrhagic enteritis characterized by extravasations
of erythrocytes, necrotic epithelial lining and inflammatory cells. H&E
3:-
Purulent inflammation
It is inflammation of the intestine which the predominant type of exudate is pus
Causes
It is
due to pyogenic microorganisms associated with mechanical injuries as foreign
body or helminthes as hook worms.
Macroscopic picture
It is
characterized by presence of pus mixed with ingesta beside congestion and
swollen mucosa.
Microscopic picture
The
intestinal mucosa infiltrated with dead and life neutrophils beside congested
blood vessels.
4:-
Acute fibrinous enteritis
It is an acute
inflammation of the intestine where the predominant constituent of the exudate
is fibrin.
Causes
1. Severe chemical agent as mercuric chloride and arsenic.
2. Infectious agents as Salmonella enteridis, Escherichia coli and Salmonella
Macroscopic picture
The
intestinal mucosa is covered by yellowish gray fibrinous membrane and the lumen
contains ropes of fibrin (Fig. 48).
The
intestinal mucosa is usually eroded, congested and edematous.
Microscopic picture
The
intestinal mucosa covered with fibrin mixed with inflammatory cells and necrotic
epithelium.
The
intestinal mucosa shows necrotic epithelium, congested blood vessels and
infiltration with neutrophils.
Fig. 48: Intestine
showing gross picture of fibrino-necrotic enteritis.
5. Necrotic enteritis
It is the
inflammation of the intestine associated with an extensive necrosis of the
intestinal mucosa.
Causes
The cause is
usually a severe chemical, bacterial (salmonellosis), viral (cattle plague) or
parasitic disease (coccidiosis) and. Nutritional deficiency (Vitamin B and
protein).
Macroscopic picture
The cardinal
signs of inflammation are seen besides necrosis of the intestinal mucosa.
Microscopically, congested blood vessels and leukocytic infiltration besides
necrosis of the epithelial lining are noticed (Fig. 49 ).
Fig. 49:
Necrotic enteritis showing necrosis of the mucosa and
infiltration of the lamina propria with H&E
6. Lymphocytic-plasmocytic enteritis
It is
the most common idiopathic inflammatory bowel disease of dog and cat and
associated with chronic diarrhea and vomiting.
Progressive weight loss, hypoproteinemia, ascites and peripheral edema are
noticed in severely affected animal.
Microscopically,
extensive infiltration of lamina propria by lymphocytes and plasma cells are
noticed beside fusion and atrophy of intestinal villi.
Crypt
may be hypertrophied and filled with mucus.
7. Eosinophilic enteritis
It is a chronic gastroenteritis
occurs in dog and cat and associated with repeated episodes of diarrhea and
peripheral eosinophilia.
Causes
The
cause is unknown but it may be as immediate reaction to some antigen. It may be
associated with parasitic infestation.
Microscopically,
eosinophils, mast cells and macrophages infiltrate the mucosa, submucosa and
tunica muscularis. Caseous necrosis surrounded by eosinophils is noticed (Fig.
50).
Fig.
50: Intestine
showing eosinophilic infiltration due to presence of Schistosoma eggs. The
Schistosoma eggs are seen in the intestinal serosa and surrounded with
eosinophils, fibrous tissue and macrophages. H&E.
8. Chronic proliferative enteritis
It is
seen with those granulomatous diseases involving intestine as partuberculosis
(Johne’s disease, tuberculosis, Hjarre’s disease in fowl).
Macroscopic picture
The diameter
of the intestine is increased and its wall is thickened (Fig. 51)
. The thickened
mucosa is usually yellowish-white, ridged and covered with a layer of mucus.
The intestinal wall is thickened and covered
with mucus. The intestinal content is watery.
Microscopic picture
Chronic inflammation is
proliferative, so the intestinal wall is infiltrating with inflammatory cells
particularly lymphocyte and plasma cells, fibroblasts and macrophages resulting
in thickening of the mucosa (Fig. 52).
It is
varies and characteristic for each disease. Mucinous degeneration of intestinal
epithelium is seen. The crypts become atrophied or cystic.
Fig.
51:
Intestine showing gross picture of chronic enteritis characterized by
thickened intestinal wall in case of John's disease.
Fig.
52: Chronic
enteritis characterized by infiltration of chronic inflammatory cell in the
lamina propria. H&E.
Circulatory disturbances
Active
hyperemia either
physiological during digestion or pathological during enteritis are seen.
Acute passive congestion
may be caused by a
sudden interference with the venous outflow as in case of strangulation.
Chronic
passive congestion
of the intestine is associated with chronic general passive congestion and with
liver diseases.
Thrombosis of the
anterior mesenteric arteries is frequent in horses where the cause is the larvae
of strongylus vulgaris. Moreover, aneurysm of the thrombosed anterior mesenteric
arteries may occur (Fig. 53).
Hemorrhage in the
intestine is associated with acute inflammation, septicemic diseases, poisoning,
infarction, passive hyperemia and mechanical injuries (Fig. 54).
Fig. 53:
Microscopic picture of anterior mesenteric artery showing thrombosis represented
by large eosinophilic mass attached to the arterial wall. H&E.
Fig. 54:
Microscopic picture intestine showing intestinal hemorrhage represented by
extravagation and accumulation of the erythrocytes in intestinal lumen.
H&E.
Perforation
It may
be caused by gunshot, parasites and ulcers.
Sequelae
1. Rapid perforation causes acute peritonitis and death.
2. Slow
perforation causes localized peritonitis, adhesion and abscess.
Rupture
It
occurs due to trauma and lead to death.
Intestinal obstruction
The
small intestine becomes completely obstructed by foreign bodies such as rubber
balls, nipples or nuts in dogs or hairball (pilicon cretion) in cats.
Strangulated hernias intussusception portion, volvulus and torsion cause
complete obstruction in any species.
Volvulus
It is
passing of loop of intestine through a tear in the mesentery (Fig. 55).
Fig. 55: Intestine
showing
passing of loop of intestine through a tear in the mesentery (volvulus)
Torsion
It is
the rotation of intestine around its long axis.
Intussusception
It
occurs due to excessive peristaltic motility forces a segment of intestine
inside the segment just below it (Fig. 56).
The
result of volvulus, torsion, intussusception are passive congestion, hemorrhage,
necrosis and gangrene. The animal dies from toxemia.
Fig. 56:
Intestine
showing segment of intestine inside the segment just below it (intussusception).
Hernia
It is
the abnormal protrusion of the viscera or its covering through an abnormal
opening in the wall of body cavity.
Hernia
consist of hernial sac consists of peritoneum covered by skin, hernial ring and
hernial contents.
Types
Several
types depend upon their location as inguinal, umbilical and diaphragmatic
hernias are observed.
Eversion
It is
turning outward of the rectum through anal canal opening.
Intestinal emphysema
Numerous gas vesicles are seen in the wall of small intestine, mesentery lymph
nodes is slaughtered swine and sheep.
Neoplasm of small intestine
Adenoma, Adenocarcinoma, leiomyoma and leiomyosarcoma, lipoma, lymphosarcoma and
mast cell tumors are recorded.
The cecum
Impaction of the cecum
It is often fetal in horse. It occurs when old
animal switch from soft food to coarse rations (dry roughage).
Grossly,
the cecum becomes atonic and distended to unbelievable dimension with undigested
food.
Tympany
of cecum
is the form of alimentary bloating in horse.
Intussusception
rarely
occurs in dog and cats.
The colon
Congenital and hereditary anomalies
1. Megacolon
It
occurs in dog and mice due to absence of myenteric ganglia distal to the dilated
portion.
2. Duplication of colon
It
occurs in dogs where the colon was equally duplicated from the cecum to colon.
3. Atrasia coli
It is
the absence of colon.
The rectum and anus
Atrasia
ani
is the failure of development of anal opening (Fig. 57).
Prolapse of rectum
is occurs in all species but more in swine and cattle (Fig. 58).
Fig. 57:
Gross picture of atrasia
ani (Absence of anal opening).
Fig. 58:
Gross picture of prolaps
of rectum.
Liver and biliary tract
Liver is the
largest complex organ with numerous vital functions
Liver has smooth capsular surface, which contain red brownish friable
tissue. The liver is seen by light microscope to be divided into many
traditional functional lobules with the shape of an irregular pyramidal
hexahedron (classic anatomic lobules).
Central
vein is present in the center of lobule. The hepatocytes are large, with a
central round nucleus and abundant cytoplasm. The hepatocytes are arranged in
hepatic cords separated by hepatic sinusoids. The liver cells are separated from
sinusoids by a narrow space (space of disse). Kupffer cells are present in the
sinusoids scattered among endothelial cells. Around the periphery of each lobule
are four to five portal tracts, composed of terminal branches of hepatic artery,
portal vein and bile ducts, which embedded in connective tissue
Liver has
two blood supplies, which are the hepatic artery and the portal vein.
The blood supplies to the liver parenchyma.
About 30 to 40% is provide by terminal branch of hepatic artery, and the
remainder by the portal vein branch. Blood flows from the portal veins
and their branch through the hepatic sinusoids where it is mixed with arterial
blood, derived from branches of the hepatic artery and drains through the
central veins of hepatic lobules and joins the posterior vena cava via the
hepatic vein. It is clear that the blood in sinusoids flows from periphery
towards center of the hepatic lobules,
The
biliary system begins at the biliary canaliculi (which are small channels lined
by the complex microvilli of hepatocytes), which drain into interlobular bile
ducts (canals of hering), which drain into bile duct in the portal tract.. The
bile in canaliculi flows from the center of hepatic lobule towards periphery.
Liver
is characterized by its great ability to regenerate. If three quarters of dog’s
liver is removed the original mass will be restored with six to eight weeks.
Hepatic failure
The
liver failure occurs only when there is extensive liver destroying over 80% of
the organ.
Acute
liver failure
is
results from acute liver necrosis caused by viral hepatitis, toxic drugs and
chemicals, and characterized by jaundice, hypoglycemia, bleeding tendency,
electrolyte and acid base disturbance, hepatic encephalopathy, elevation of
serum hepatic enzymes (LDH, AST, ALT).
Chronic
liver failure
is usually result from cirrhosis, which associated with progressive necrosis of
liver cells fibrosis, and nodular regeneration and it characterized by edema,
bleeding, portal hyperplasia, hepatic encephalopathy, hepatorenal syndrome, and
endocrine changes caused by disorder metabolism of certain hormones.
Hepatic encephalopathy
It is
clear that there is association between the hepatic diseases and nervous signs
or symptoms.
Pathogenesis
Impaired hepatic function allows various exogenous and endogenous metabolites to
enter circulation, which are responsible for signs and lesions of hepatic
encephalopathy. Elevated level of ammonia is considered the principle offending
metabolites (liver converts ammonia to urea).
Causes
1- It
associated with acute or chronic hepatic failure.
2-
Portosystemic shunt that allows the portal blood to by-pass the liver.
Signs
Blindness, abdominal movement, convulsion, coma and death are seen.
Lesions
The
liver shows massive necrosis or fibrosis. The brain shows edema, neuronal
necrosis and swelling, astrocytes degeneration.
Hepatorenal syndrome
It is
appearance of renal failure in patients with severe liver diseases.
Congenital
defects
1-Intrahepatic congenital cyst
It
observed in liver due to lack of outlet of primitive bile duct or connection
with the main biliary system (Fig. 64).
Fig.
59:
Gross picture of intrahepatic congenital cyst.
2. Atrasia of extrahepatic bile duct
resulting in biliary
cirrhosis.
3. Congenital portal systemic vascular shunts
It
occurs due to persistence of ducts venosus or connection between portal vein and
caudal vena cava (Fig. 60 ).
Fig. 60:
Microscopic picture of congenital portal systemic shunt.
Disturbance in growth
Atrophy
may be local as
caused by pressure of tumor, abscess or parasitic cyst, or general as occurs in
deficiency and cachectic diseases as well as old age and starvation:
Hypertrophy of hepatocytes
may be compensatory or due to some poisons.
Hyperplasia of hepatic cells
Ts common as a regenerative process. It may be diffuse or focal. The latter may
form multiple nodules throughout the liver. Moreover, hyperplasia of the
epithelial lining of bile duct (Fig. 61) is seen with hepatic coccidiosis in
rabbit.
Fig. 61:
Liver showing microscopic picture of bile duct hyperplasia
characterized by proliferation and folding of epithelial lining. H&E
Circulatory
disorders
Passive congestion
It may
be either acute (Fig. 62 )
or chronic (Fig. 63)
. Passive congestion is due to
reduction in blood flow through hepatic vein or vena cava, heart or lungs. The
liver is cyanotic in acute form and nutmeg appearance in chronic cases.
Active
hyperemia
is associated with systemic infection or abscess.
Fig.
62:
Gross picture of acute passive congestion of the liver. The liver is
dark red in color.
Fig. 63:
Gross picture of chronic passive congestion of liver showing dark
red center surrounded with yellowish areas.
Acquired portosystemic shunt
It
follows chronic liver diseases leading to portal hypertension. The liver shows
numerous tortuous connections between the portal vein and systemic veins.
Telangiectasis
It is the
dilatation of functioning blood vessels anywhere.
It is indicate focal greatly dilated sinusoids within any part of hepatic
lobules. The hepatic cells between lobules are partially or completely
disappeared.
Telangiectasis may results from over distention of the hepatic cells with
glycogen, which is eroded and replaced by blood (saw
dust). Such erosion may be promoted by absorption of hydrogen sulfide
from the gut.
Macroscopically, dark red spots of irregular shape and diameter are seen.
Microscopically, endothelial-lined cavities communicating with portal
capillaries and central veins are seen (Fig. 64). Moreover, the hepatic cells
between the dilated sinusoids are partially or completely absent.
Anemia
is associated with general anemia and lead to various retrogressive changes.
Hemorrhage
is observed in dog and cats due to hepatic rupture (Fig. 65).
Thrombosis of hepatic
vessels is common with hepatitis (Fig. 66 ).
Infarction of the liver
is usually caused by hepatitis, which impaired portal and hepatic circulation as
caused by bacillary hemoglobinuria in cattle and sheep.
Fig.
64:
Liver of cattle showing telangiectasis represented by dilated blood
spaced filled with erythrocytes. H&E.
Fig.
65:
Gross picture of ecchymotic hemorrhage.
Fig.
66: Liver showing microscopic picture of hemorrhage
represented by replacement of hepatic parenchyma with erythrocytes.
H&E.
Fig.
67: Liver showing intravascular eosinophilic mass (Thrombus)
attached to the wall of inflamed blood vessels. H&E.
Degeneration and deposition
Fatty liver
The
accumulation of fat or triglycerides in cytoplasm of hepatocytes known as fatty
liver is recorded (Fig. 68)
. Hepatic lipidosis or fatty change is one of the most
common lesions encountered.
Glycogen
Hepatocytes normal contain glycogen. Abnormal accumulation of glycogen is seen
in diabetes mellitus and glycogen storage diseases.
Sawdust
liver is another
condition in the liver of fattened healthy animals.
Macroscopically, numerous
yellowish foci of 1-2mm scattered throughout the liver, as if the organ is
sprinkled with sawdust. Microscopically areas of coagulative necrosis of the
hepatic cells surrounded with neutrophils and lymphocytes are seen.
Fig.
68:
Liver showing fatty changes represented by the presence of clear
vacuoles in the cytoplasm of hepatic cells pushing nucleus to one
side. H&E
Amyloidosis
Amyloid
infiltration is seen in liver either primary or secondary (Fig. 72 )
.
Fig.
69:
Liver of mice showing pale eosinophilic structureless materials
(amyloid) under the endothelial lining of hepatic sinusoids. H&E.
Pigment
Bile
pigments
are seen in association with cholestasis.
Lipofuscin
is common in liver of old animal.
Hemosiderin
is accumulated in kupffer’s cell and hepatocytes in case of increase destruction
of erythrocytes (Fig.s 73)
.
Melanosis
is occasionally seen in liver.
Fig.
70:
Spleen showing sidrocytes containing golden yellow
pigment (hemosiderin). H&E
Hepatic degeneration and necrosis
The
liver respond to injury takes so many ways. One feature of responds to many
diseases is necrosis.
Several toxic substances reach the liver through its double blood supply due to
its detoxifying role, thus liver is liable to be damaged. The extent of hepatic
damage depends upon the state of nutrition of liver cells, the dose of the toxin
and the period of exposure.
Causes
Several
injuries can reach to the liver through its double blood supply and cause
degeneration and necrosis.
1. Nutritional deficiencies particularly of sulfur containing amino acids (as methionine, cystine), vitamins (as tocopherols), choline and trace elements as
selenium.
2. Poisons
which may be chemicals as chloroform, carbon tetrachloride and phosphorus or
toxins of plant origin as senecio alkaloids, and saponins and fungal toxins as
aflatoxin.
3. Parasites
as migrating larvae of nematodes and trematodes and Fascioliasis (Fig. 71).
Fig.
71: Liver of mice showing hepatitis due to presence of
ascarid larva. H&E.
4. Several
types of pathogenic bacteria and their toxins cause hepatic damage as
Salmonella, Corynebacterium pyogenes and Bacillus necrophorus.
5. Several
viral diseases cause hepatic damage as in infectious canine hepatitis, Rift
valley fever and in Equine rhinopneumonitis,
The
hepatic necrosis is usually coagulative in type and recognized macroscopically
by pyknosis and acidophilic cytoplasm follow by disappearance of cells. Caseous
or liquifactive necrosis may seen in liver with granulomatous diseases and
abscess.
According to location, necrosis may take several different patterns.
A. Focal necrosis
Small
necrotic area or foci of sublobular size appear here and there as sawdust liver
of cattle which seen frequently by meat inspectors (Figs 72 & 73).
Fig.
72: Liver showing focal coagulative necrosis. H&E
Fig.
73:
Liver showing focal
coagulative necrosis. H&E
B. Zonal necrosis
It is characterized by necrosis of hepatocytes
restricted to a particular part of lobules.
1. Centrolobular
necrosis characterized by necrosis of hepatocytes nearest or entirely circle the
central vein. It is usually seen in hypoxic condition such as passive congestion
and anemia.
2. Midzonal
necrosis affects the hepatocytes half ways between the periphery and center of
lobule. It is usual form of necrosis.
3. Periportal
necrosis is characterized by necrosis of hepatocytes surrounding the portal
areas. It is seen associated with blood borne poison as phosphorus poisoning.
4. Paracentral
necrosis is characterized by wedge-shaped with apex at central vein and base at
the portal area. It is seen associated with occlusion of terminal branches of
portal vein as Rift valley fever.
Disassociation of liver cells
It is
one of characteristic feature of certain diseases (particularly leptospirosis)
where the liver cells detached from one to another (individualized) and somewhat
rounded and the cytoplasm become more acidophilic.
Hepatitis
It is
the inflammation of the liver parenchyma. The inflammation of bile duct is
called cholangitis while cholangiohepatitis that is common in the biliary system
but extend into liver parenchyma. Moreover, Portal hepatitis is refer to
inflammation of hepatic parenchyma around the portal area and infiltrate the
portal area with inflammatory cells.
Acute hepatitis
In
acute hepatitis, vascular feature of inflammation (dilatation of arterioles,
venules and lymphatics may be present in portal areas). Leukocytes present in
portal areas and sinusoid (neutrophils in bacterial, lymphocytes and plasma
cells in viral). Degenerative changes in hepatocytes including swelling,
apoptosis, and necrosis are seen (Figs 74&75).
Fig.
74: Liver showing focal lymphocytic aggregation. H&E.
Fig.
75: Liver showing hepatitis represented by infiltration of
hepatic parenchyma with inflammatory cells besides congested bepatic
sinusoids. H&E.
If the
animal survives, necrotic tissue is removed by phagocytic cells and replaced by
regenerating parenchyma or fibrous scar, but if the antigen persists an abscess
or granuloma may form.
Chronic hepatitis
It is
characterized by infiltration of the hepatic parenchyma and mainly portal areas
by lymphocytes and plasma cells (portal hepatitis). Increased fibrous connective
tissue in portal areas with proliferation of bile ducts is seen. Moreover, with
progression, the fibrosis extends from the portal area to the central vein
(pseudolobulation).
Chronic
hepatitis may include focal necrosis with association of macrophages and few
neutrophils along with fibrous (chronic active hepatitis) (Fig 76) which is
progressive and lead to cirrhosis. Certain species of bacteria and fungi are
particularly resistant to killing by phagocytic cells and are capable of
inducing chronic inflammation and granuloma.
Fig.
76: liver showing active chronic hepatitis represented by fibrous connective
tissue infiltrated with eosinophils and , macrophages, lymphocytes. H&E.
Causes and forms of hepatitis
The
causes usually blood borne infection, because the liver receives both arterial
blood via hepatic artery and venous blood from gastrointestinal tract via portal
vein. It can either primary or part of systemic process. Infection also can give
access to the liver by ascending through biliary system or by direct extension
through the peritoneal cavity.
1.
Infectious hepatitis
It
caused by infectious agents as bacteria, virus or parasitic (Figs 77 &
78).
Bacterial causes of hepatitis include Clostridium novyi (black disease),
Clostridium hemolyticum (bacillary hemoglobinurea). Also, it associated with
leptpspirosis, salmonellosis and necrobacillosis. Corynebacterium pyogenes is a
common cause of suppurative hepatitis in cattle.
Viral
causes of hepatitis including infectious canine hepatitis, rift valley fever,
and yellow fever and generalized herpesvirus infection.
Protozoal infections include coccidiosis, leishmaniasis and amoebiasis. Metazoan
parasites induced hepatitis through migration of larvae, which lead to necrosis,
inflammation and fibrosis as Ascaris, sum, Strongylus in horse and Cysticercus
tenuicollis. Moreover, Capilaria hepatica and Echinococcus replaced the hepatic
parenchyma. Liver flukes including Fasciola hepatica, F. gigantica, Dicrocoelium
dendriticum damage the liver through larval migration and the presence of adults
within the bile ducts and hepatic parenchyma. Fungal diseases as histoplasmosis.
Fig. 77 :
Liver showing hepatitis
due to infestation with Cysticercus fasciolaris cyst. H&E.
Fig.
78:
Liver showing infectious hepatitis characterized by coagulative
necrosis surrounded by line of defense. H&E.
2-Toxic
or non infectious hepatitis
It is
inflammation of liver due to exposure to many drugs and toxins. In some cases it
characterized by cell death after suffering cloudy swelling and fatty changes.
In other types, it is accompanied by acute and chronic inflammation.
Pathogenesis
By the
way of portal vein, the liver is the first organ to receive substance from the
gastrointestinal tract so, it is the first organ expose to ingested toxins or
toxins formed in intestinal tract.
In
liver there are two principle mechanisms
a. Direct toxicity to hepatic cells during detoxify and removal of toxic
substances.
b. Conversion of xenobiotic to toxin as in aflatoxins and carbon tetrachloride.
Causes
1. Chemical poisons as copper, arsenic and phosphorus.
2. Mycotoxins as aflatoxin.
3. Plant poisons as snecio.
4. Metabolic poisons are those produced during disease as gastroenteritis, metritis.
The
picture is vary according to the affected toxins. The liver is usually mottled,
congested and enlarged first. Later on the liver appears small in size and
yellow in color due to necrosis and fatty change (acute yellow atrophy)
or become red and small due to necrosis and congestion and hemorrhages (acute
red atrophy). Finally, fibrosis, biliary hyperplasia and parenchyma
regeneration are noticed.
Microscopic picture
1. Degenerative changes and necrosis of hepatocytes are seen.
2. Congestion of central veins, hepatic sinusoids and portal blood vessels in
addition to fibroblast proliferation.
3. Inflammatory cells usually absent, but in some cases lymphocytic infiltration
are seen in portal areas.
4. In
chronic hepatitis, hepatocyte regeneration, fibrosis and cirrhosis are seen.
Response of liver to injury
1.
Regeneration
The
liver has regenerative capacity, so if the animal survive massive necrosis,
parenchyma regeneration without scaring are noticed as long as the reticulin
frame-work of the affected portion remain intact. The liver regenerate as much
as 80% of its mass without apparent ill. A prolonged regeneration often results
in nodular proliferation with architecturally distorted liver.
2. Fibrosis
It
occurs with necrosis and destruction of hepatocytes and Reticulin frame. Also
when necrosis is more than regenerative capacity of liver. Chronic cholangitis
(Fig. 79) can produce fibrosis that is most pronounced in portal area. Also, it
observes in chronic hypoxia usually in centrolobular area.
Fig.
79:
Liver of mice showing chronic cholangitis characterize by bile duct
hyperplasia surround by fibrous tissue proliferation. H&E.
3. Biliary hyperplasia
A
variety of causes can results in proliferation of new bile ducts within the
portal areas (Fig.s 80).
Fig. 80:
Liver of mice showing bile duct hyperplasia represented by newly
formed bile ductules. H&E.
Cirrhosis (End stage liver)
It is a
serious disease of the liver characterized by massive replacement of the hepatic
parenchyma by fibrous tissue and nodules of regenerating hepatocytes, which lead
to hepatic failure. Cirrhosis may be:
1. Portal cirrhosis
It
occurs following massive destruction of hepatic parenchyma and Reticulin
network. All the liver elements are showed regeneration, which lead to nodular
hepatocytes, distortion of organs with fibrous tissue and anastomosis between
hepatic artery and central vein with more necrosis and cirrhosis.
Macroscopic picture
The
affected liver is small, firm nodular (Figs 81 & 82)
. Ascites is usually present.
Jaundice is seen at the terminal stage. Microscopically hepatic nodules formed
from regenerating hepatocytes without central vein and surrounded by small
branches of central vein and hepatic artery (arteriovenous shunt) which lead to
ischemia and necrosis (Figs 87& 88).
Fig. 81:
Gross picture of liver cirrhosis. The liver is small in size and
nodular.
Fig.
82.
Gross picture of liver cirrhosis. The liver is small in size and
nodular.
Fibrous
connective tissue proliferation which start from the portal areas and extend
between the lobules (interlobular cirrhosis) are seen.
Moreover, the fibrous tissue enters the lobule and surrounded group of
hepatocytes (intralobular cirrhosis. The fibrous tissue is infiltrated with
lymphocytes and plasma cells. Blood vessels may accompany those fibrous strands
and connect the portal and central vein.
Fig.
83:
Liver of mice showing portal cirrhosis represented by massive
replacement of hepatic parenchyma by fibrous tissue. H&E.
Fig.
84:
Liver of mice showing portal cirrhosis represented by massive
replacement of hepatic parenchyma by fibrous tissue stained blue with Mason
Trichrom.
2. Biliary cirrhosis
Macroscopically, liver is hard, enlarged with smooth surface hepatic tissue is
yellowish green (jaundice appear early). Bile duct may be thickened white and
calcified. Microscopically, numerous newly formed bile ductules with thickened
wall. The bile ducts surrounded by thick bands of fibrous tissue which extend
between lobules and cause pressure atrophy of hepatocytes (Figs 85 &
86).
Fig. 85:
Liver of cattle showing biliary cirrhosis characterize by
proliferation of portal fibrous connective tissue which extend in
between hepatic cords besides hyperplasia of bile ducts. H&E
Fig. 86:
Liver of cattle showing biliary cirrhosis due to presence of
adult fasciola worm in bile duct and characterize by proliferation
of portal fibrous connective tissue which extend in between hepatic
cords besides hyperplasia of bile ducts. H&E
Special forms of cirrhosis
3. Glissonian cirrhosis
It
resembles portal cirrhosis but restricted to short area under the capsule.
Central cardiac cirrhosis
It
characterized by increase amount of fibrin tissue around central vein in chronic
venous congestion.
Pigment cirrhosis
It
occurs with hemochromatosis.
Parasitic cirrhosis
It
occurs in association with parasites as fascioliasis and Schistosomiasis (Fig.
87).
Fig.
87:
Liver of mice showing parasitic cirrhosis due to presence of
Schistosoma eggs. H&E
Effect of cirrhosis
1. Ascites with biliary cirrhosis due to increase portal hypertension.
2. Hepatic failure of synthesis prothrombin (defect in clotting) or protein
(edema).
3. Failure to detoxify toxins and hormones as estrogen which lead to atrophy of
testes and disappearance of secondary sexual characters of male.
The
presence of fibrous tissue in liver is progressive process that means stimulate
proliferation of a new fibrous tissue even with cause removal.
Neoplasm of liver
Hepatoma, hepatocellular carcinoma (Fig. 88)
, cavernous and hemangiosarcoma are
primary hepatic tumors.
Fig.
88:
Liver showing gross picture of hepatocellular carcinoma.
Gall bladder and bile duct
Cholangitis
is inflammation of bile ducts (Fig. 89 )
but cholecystitis is inflammation
of gall bladder (Fig. 90 & 91)
. Cholangitis and cholecystitis are usually catarrhal
or serous.
Cholelithiasis is the
formation of cholelith or gallstone. It is rare in domestic animals.
Fig.
89:
Liver showing chronic cholangitis represented by hyperplasia of
epithelilal lining and infiltration of the portal area with chronic
inflammatory cells and fibrous tissue. H&E
Fig.
90:
Gall bladder showing acute cholecystitis.
Fig.
91: Microscopic picture of hemorrhagic cholecystitis
characterized by erosion of epithelial lining, extravagation of
erythrocytes and inflammatory cells. H&E.
Peritonitis
Most
cases of peritonitis result from infectious agents Parasitic, bacterial and
viral) (Fig. 92)
. It may be localized in dogs and ruminant or generalized in
equine.
The
principle routes by which infectious agents enter to the peritoneal cavity are
surgical incision through abdomen rupture or perforation of stomach, intestine
and uterus or via blood stream in certain specific infection as feline
infectious peritonitis.
Acute peritonitis
It is
characterized by great amount of fluid in abdominal cavity. The exudates may be
fibrinous (Fig. 93 ), supportive or hemorrhagic.
Chronic peritonitis
It is
characterized by diffuse or localized thickening of peritoneum (Figs 94 &
95)
.
Fig.
92:
Mesenteric blood vessels contain adult Schistosoma worms (Parasitic
peritonitis)
Fig.
93: Peritoneum showing acute fibrinous peritonitis.
Fig.
94: Peritoneum of cattle shoed chronic nodular
peritonitis.
Fig.
95: Microscopic picture of tuberculous peritonitis
characterized by nodules consist from central casseation surrounded
with epithelioid cells, macrophages and finally fibrous tissue. H&E.
Chylous ascites
It
occurs due to injury of thoracic duct and accumulation of chyle in abdominal
cavity.
Neoplasm
Mesotheloma and lipoma are recorded.
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