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THE DIGESTIVE SYSTEM Oral cavity Developmental anomalies .Anomalies occur infrequently in domestic animals .Cleft lip (chelioschisis): affects the upper lip Cleft palate (palatoschisis): is an open cleft between the oral and nasal cavities. The newborn animals with cleft palate drip milk from their nostrils during nursing, whereas older .animals develops respiratory affection and pneumonia Inflammatory processes The inflammation of oral cavity may be diffuse (stomatitis) or localized inflammation of gingival (gingivitis), tissue surrounded the teeth (periodontitis), pharynx (pharyngitis), ).tongue (glossitis), tonsils (tonsillitis) or lips (chelitis


Gingivitis Most cases result from bacterial infection follow either trauma, poor oral hygiene or various immunodeficient states. Macroscopic picture The gingiva bleeds easily, erythematous and edematous. Microscopic picture • The gingival connective tissue shows congested blood vessels and infiltrated with neutrophils and lymphocytes. •The overlying gingivial epithelium may be ulcerated or hyperplastic.


Stomatitis 1- Catarrhal stomatitis It is a mild 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 mucus. •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. •Desquamation of the epithelial lining which covered with mucus and bacteria.


Vesicular stomatitis- 2 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. Rupture of vesicles leaving an erosion or ulcer. Microscopic picture •The affected epithelial cells show vacuolar and hydropic degenerations. The degenerated cells coalesce with each other to form vesicles. •Some vesicles may be rupture leaving erosions with intact germinal basal layer.


Suppurative stomatitis- 3 •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. 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. The necrotic areas may .removed leaving ulcer Microscopically, the oral mucosa shows coagulative necrosis • infiltrated and separated by inflammatory cells


Neoplasm of the oral cavity Viral papilloma occurs in dogs, cattle and rabbit. Oral and labial mucosa. 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, contain sheets or cords of stratified squamous epithelium. 3-Ossification epulis It similar to fibromatous epulis, but in addition contains either irregular island of osteoid or mineralized bone or acellular eosinophilic cemmentum or dentin-like structure


Squamaous cell carcinoma occurs in any species. It is the most common malignancy of the oral cavity of cats and .dogs Malignant melanoma is common in dog and rare in others. 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.


Tonsillitis Causes It occurs when pathogenic bacteria as staphylococci colonize the tonsillar crypts and induce an acute inflammation. Macroscopic picture • 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. Microscopic picture • Tonsils show follicular hyperplasia. • Tonsils crypts are filled with desquamated epithelium, bacteria and inflammatory cells mainly neutrophils is suppurative


Dental pathology Dental anomalies 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. Segmental enamel hypoplasia NB: 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 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. Anodontia is lack of tooth development. Oligodontia is development of fewer teeth than normal. Polydontia is the presence of supernumerary


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 dermineralization. Dental caries results from bacterial metabolites with production of acids and enzymes, which lead to demineralization and destruction of dental matrices. Macroscopically, the enamel becomes dull, white and pocked. The exposed dentine becomes brownish black. Dental plaque It is accumulated non mineralized bacterial mass, food particles, desquamated epithelium adhered to tooth surface. 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.


Inflammation of teeth and periodentium Pulpitis •It is the inflammation of vascular part of the tooth (pulp). •The cause is 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. Causes -Bacterial 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


Cysts •It occurs due to obstruction of the salivary ducts by foreign bodies. The fluid content is odorless, grayish white or brownish and clear or turbid. • In dog and cow a cyst frequently observed in sublingual duct, located in frenulum of tongue is referred to as a ranula. 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. Neoplasm of salivary gland The neoplasm of salivary glands are uncommon in domestic animals. Adenoma and adenocarcinoma


Pharynx Pharyngitis usually accompanies stomatitis. Pharyngitis are seen in the course of several diseases including Anthrax in pig and dog and calf diphtheria. Esophagus Esophagus is a muscular tube that extend 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. 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(sphincter spasm) 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.Cardiac achalasia is spasm of the cardiac oesophageal sphincter which treated surgically (cardiomyotomy) or by injection of Botuline toxins in oesopgagial muscle 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 inherited disorder in several breeds of 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 •Prominently 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 contain 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 It is complete or partial obstruction of the esophagus. Causes 1- Enlarged lymph nodes, tumor ad abscess. 2- Congenital vascular ring anomalies and esophageal hypoplasia. 3- Potato, turnips or small ears of corn in ruminants and accumulation and germination of grains in horse. 4- Sharp pieces of bones in dog and cat. Macroscopically, the esophagus shows distention of the esophageal portion above the obstruction. Sequalae 1- Local gangrene with sapremia and toxemia which kill the animal. 2- Tympany in ruminant due to prevent regurgitation of gas. 3-Partial obstruction lead to formation of esophageal diverticulum ectasia or perforation.


.Diverticulum is a symmetrical and unilateral sac like dilatation Ectasia is a uniform spindle or clyndrical shaped dilatation. 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. Eosinophilic esophagitis is an inflammatory condition in which the wall of the esophagus becomes filled with large numbers of eosinophils Eosinophilic esophagitis affects both children and adults. For unknown reasons, men are more commonly affected than women, and it is most commonly found among young boys and men 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 polymorphonuclear leukocytes in lamina propria beside fibroblasts proliferation. 3-In chronic cases fibrosis is a sequelea. Sequalae Fibrosis which contract and lead to stenosis of esophagus and esophageal chock and diverticulum. Neoplasm of esophagus Papilloma, squamous cell carcinoma, and fibrosarcoma are recorded. Crop of birds .Impaction, necrosis and inflammation (ingluvitis) occur


Forestomach of ruminants The rumen, reticulum and omasum are called forestomach. They have no secretory function. They are lined by keratinized stratified squamous epithelium and function as a large fermentation chamber where digestion of plant material occur by some bacteria and protozoa. 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 doesn’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 penetrate the reticulum by the help of its movement, abdominal pressure, pressure of uterus and during paruration. At the point of penetration at first there is hemorrhage. After that the migration of foreign body through the wall of reticulum causes an inflammatory tract filled with pus and food and surrounded by granulation tissue.


When the foreign body reachs 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. Atony of rumen may result from serious nerve involvement or by pressure on nerve by abscess. 2- Rupture of rumen may occurs due to mechanical injury from outside or over distention from inside. 3- Dilatation of forestomach (Tympany,tympanites or Bloat) it is the excessive quantities of gas in the lumen of rumen. Causes 1- Interference with normal eructation as by chock. 2-Over production of gas during fermentation process. Classification of tympany a) Frothy or primary tympany In this case the gas is dispersed in the form of small bubbles in rumenal fluid.It is acute ,occure suddenly and mostly fatal.It is due to either feeding on large quantity of green succulent legumes as clover or alfilfa or sudden change from dry ration to green ration.The pathogenesis depend on excessive gas production due to colonization of ruminal bacteria on the chloroplast of the green legumes,denaturation of the soluble protein of the chloroplast by the ruminal acidity,such denaturated protein act as foam-stabilizer.morovere plant pectines increase the surface tension of the ruminal fluid.additionally,the green plants lacke the stacks or stems which enhance the ruminal expulsive movement.in contrast plant lipids act as anti-foaming b) Secondary tympany or free gas tympany It results from physical obstruction of esophageal or pharyngeal passage ways or pressure upon the esophagus by tumor, abscess and swollen lymph node.


.It is develop gradually and often are chronic or intermittent Death which is common in primry type or in the secondry type of complete obstruction,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 anoxia. 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. 2- The abdominal viscera appear pale. 3- The ruminal 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. 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. 2-The ruminal content has fetid odor. 3-Atrophy of the ruminal muscles. 4-Acute toxic hepatitis is seen (cause of death).


Ruminal acidosis, rumenitis and ulcer- 5 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 whch 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 dehydraton, hemoconcentration, anuria 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. 3-The lamina propria shows infiltration with neutrophils. 4-The necrotic areas slough and showed reepithelization which is usually white in contrast to the normal black epithelium. Omasum The omasum and esophageal groove are seldom the site of important pathologic processes. Pyogranulom 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 parturation, overeating, pica, abdominal surgery and trauma. Sequelae It lead to torsion. •Mechanical obstruction of caudal vena cava and portal vein. •Cardiac output is decreased 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 omintum. 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. -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 associated with feeding ration containing high proportions of concentrates rather than roughage. • Also following recent parturation. • 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. Impaction It occurs in stomach as the result of rapid ingestion of an excessive amount of ground feed, grains without adequate water consumption. It is especially serious in horse even without gaseous fermentation, which is usually absorbed. Circulatory disturbances and shock may be fatal in few hours. 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 dog and cat


Gastritis • It is the inflammation of stomach. • 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. 1) Acute catarrhal gastritis Causes 1- Physical or chemical agents. 2- Infectious agents as in case of canine distemper, feline enteritis and parasitic gastritis. Macroscopic picture 1- Reddening and thickening of gastric mucosa. 2- Increase in mucus secretion. Microscopic picture 1- Hyperemia, desquamated epithelium beside leukocytic infiltration are seen. 2- Hyperplasia of minute mucosal lymphoid nodules. 2) Chronic catarrhal gastritis • It reported with Haemonchus contortus. • The hyperplastic lymphoid tissue seen grossly as small white mucosal nodules.


Acute hemorrhagic gastritis) 3 Causes 1-Infectious agent as leptospirosis in dog and Clostridium septicum (Braxy) in sheep. 2- Uremia and arsenic poison. Macroscopic picture 1- Deep reddening of gastric mucosa. 2- Presence of blood on the surface of mucosa and mix with content which turned to brown black due to effect of gastric acid. 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. 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 cause chronic fibrotic gastritis. Mostly it associated with larva migrans in dog.


Hemorrhages Large and small hemorrhages may occur in the gastric mucosa. Hemorrhage producing infection involve the gastric mucosa are hog cholera, anthrax and leptospirosis. Ulcer It is a result of deep necrosis and usually acute. It is now recognized in most domestic species. Foreign bodies Rubber ball in dog stomach, hair balls in cat stomach are seen. Sand in horse, cattle and sheep raised on sandy land. Neoplasm of stomach Adenocarcinoma, adenomatous polyps, undifferentiated carcinoma, squamous cell carcinoma and leiomyoma and leiomyosarcoma are recorded.


Small intestine Enteritis It is inflammation of any part of intestinal tract. Gastroenteritis is the inflammation involve the entire tract. Other terminology may be used when inflammation more than one part as duodenitis, jejunitis, typhlitis or cectis and proctitis. Acute enteritis may confirm to any one of the five types of exudative acute inflammation. Subacute and chronic inflammation are by no mean rare. The whole small intestine and large intestine may be uniformly inflamed or perhaps localized. 1) Catarrhal enteritis Causes 1- Chemical intoxication. 2- Many infectious agent and parasites. 3- Physical agent as coarse food. Macroscopic picture 1- The intestinal content contain mucus. 2- The intestinal wall become swollen, red and thick. Microscopic picture Numerous goblet cells, congested blood vessels and leukocytic infiltration are seen.


Hemorrhagic enteritis) 2 Causes Locally destructive endo or exotoxin or by highly virulent infection as anthrax, S. typhimurium and Shigella. Also virus as canine and feline parvo virus. Macroscopic picture • The intestinal content is mixed with blood (brownish in anterior portion and bright red in posterior portion). • The intestinal wall are hemorrhagic and thickened. Microscopic picture • Extravasated erythrocytes and inflammatory cells in intestinal wall. 3) Purulent inflammation Causes It is due to pyogenic microorganisms associated with mechanical injuries as foreign body or helminth parasite 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.


Acute fibrinous enteritis) 4 Causes 1- Severe chemical agent as mercuric chloride and arsenic. 2- Infectious agents as Salmonella enteritidis, Escherichia coli and Salmonella cholera suis. Macroscopic picture • The intestinal mucosa is covered by yellowish gray fibrinous membrane. • The intestinal mucosa is usually eroded, congested and edematous. Microscopic picture 1- The intestinal mucosa covered with fibrin mixed with inflammatory cells and necrotic epithelium. 2- The intestinal mucosa shows, necrotic epithelium, congested blood vessels and infiltration with neutrophils. 5) 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, ascitis 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


Eosinophilic enteritis) 6 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 an immune reaction to some antigen. Microscopically, the mucosa, submucosa and tunica muscularis are infiltrated by eosinophils, mast cells and macrophages. Caseous necrosis surrounded by eosinophils is noticed. 7) Chronic proliferaive enteritis It is seen with those granulomatous diseases involving intestine as partuberculosis (Johne’s disease, tuberculosis, Hjarre’s disease in fowl). Macroscopic picture • The intestinal wall is thickened and covered with mucus. • The intestinal content is watery. Microscopic picture • It is varies and characteristic for each disease. •Mucinous degeneration of intestinal epithelium and infiltration of tunica propria with macrophages, lymphocytes, plasma cells and fibroblasts are seen. •The crypt become atrophied or cystic.


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 hair ball (piliconcretion) in cats and phytolith in hores and ruminents. Strangulated hernias intussusception portion, volvulus and torsion cause complete obstruction in any species. Volvulus It is twisting of intestine ,may be due to passing of loop of intestine through a tear in the mesentry. 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. The result of volvulus, torsion, intussusception are passive congestion, hemorrhage, necrosis and gangrene. The animal die from toxemia.


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 hernieal contents. Types Several types depend upon their location as inguinal, umbilical and diaphragmatic hernia(hiatus) are observed. Eversion(prolaps) It is turning outward of the rectum through anal canal opening. Intestinal emphysema Numerous gas vesicles are seen in the wall of small intestine, mesentry and esentirc lymph nodes is slaughtered swine and sheep Neoplasm of small intestine Adenoma, adenocarcinomal ,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 ration (dry roughage). Grossly, the cecum become atonic and distended to unbelievable dimensinon with undigested food. Tympanites of cecum is the form of alimentary bloating in horse. Intussusception rarely occurs in dog and cats.

The colon Congenital and hereditary anomalies

Megacolon It occurs in dog and mice due to absence of myenteric ganglia distal to the dilated portion.

Duplication of colon It occurs in dogs where the colon was equally duplicated from the cecum to colon.

Atrasia coli It is the absence of colon.

The rectum and anus Atrasia ani: It is the failure of development of anal opening. Prolapse of rectum: it occurs in all species but more in swine and cattle. Peritoneum Peritonitis • Most cases of peritonitis result from infectious agents. It may be localized in dogs and ruminant or generalized in equine. • The principle routes by which infectious agants enter to the peritoneal cavity are: 1) Surgical incision through abdomen. 2) Rupture or perforation of stomach, intestine and uterus. 3) 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 exudate may be fibrinous, suppurative or hemorrhagic Chronic peritonitis It is characterized by diffuse of localized thickening of peritoneum. Hydroperitoneum, ascitis Accumulation of watery fluid in peritoneal cavity is called hydroperitoneum but in non inflammatory fluid is called Ascitis. Ascitis occurs as a part of generalized edema. Ascitis morphologically results from chronic passive congestion of portal venous system especially with hepatic cirrhosis. Chylous ascitis It occurs due to injury of thoracic duct and accumulation of chyle in abdominal cavity. Neoplasm Mesotheloma and lipoma are recorded.


Liver and biliary tract Liver is seen by light microscope or even by necked eye to be divided into many lobule with the shape of an irregular pyramidal hexahedron (classic anatomic lobules). At the center of anatomic lobules is the central vein (smallest branch of hepatic vein). The lobule is made of interconnecting plate of hepatocytes separated by endothelium lined sinusoids. Individual hepatocytes are large, with a central round nucleus and abundant cytoplasm. 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. The biliary system begins at the biliary canaliculi (which are small channels lined by the complex microvilli of hepatocytes), which drain into interlobular bile duct (canals of hering), which drain into bile duct in the portal tract. 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. The blood supply to the liver parenchyma flows from the portal triads to the central veins. About 30 to 40% is provide by terminal branch of hepatic artery, and the remainder by the portal vein branch. 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.


Normal Liver


Hepatic failure The liver failure occurs only when there is extensive liver destruction ,over 80% of the organ. Acute liver failure It results from acute liver necrosis caused by viral hepatitis, toxic drugs and chemicals, and characterized by: (1) Jaundice. (2) Hypoglycemia. (3) Bleeding tendency. (4) Electrolyte and acid base disturbance. (5) Hepatic encephalopathy. (6) Elevation of serum enzymes (LDH, AST, ALT). Chronic liver failure It usually result from cirrhosis, which associated with progressive necrosis of liver cells fibrosis, and nodular regeneration and it characterized by: (1) Edema. (2) Bleeding. (3) Portal hyperplasia.and portal hypertension (4) Hepatic encephalopathy. (5) Hepatorenal syndrome. (6) Endocrine changes caused by disorder metabolism of certain hormones.


Hepatic encephalopathy It is clear that there are 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 hepatoencephalopathy. Elevated level of amonia is considered the principle offending metabolites (liver converts ammonia to urea). Causes 1- It associated with acute or chronic hepatic failure. 2- Porto-systemic shunt which allow the portal blood to by-pass the liver. Signs Blindness, abdominal movement, convulsion, coma and death. 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 Congenital defects aren’t common. Intrahepatic congenital cyst It observed in liver due to lack of outlet of primitive bile duct or connection with the main biliary system.


Atrasia of extrahepatic bile duct It will lead to biliary cirrhosis. Congenital portal- systemic vascular shunts It occurs due to persistence of ducts venosus or connection between portal vein and caudal vena cava. Circulatory disorders Passive congestion It may be either acute or chronic. 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. Acquired porto-systemic shunt It follow chronic liver diseases leading to portal hypertension. The liver shows numerous tortuous connection between the poral vein and systemic veins. Telangiectasis It is greatly dilated sinusoids within any part of hepatic lobules. The hepatic cells between lobules are partially or completely disappeared. Telangiectasis is observed in cattle without clinical significance. Telangiectasis may results from foci of necrosis termed saw dust. Anemia: It is associated with general anemia and lead to various retrogressive changes. Hemorrhage: It is observed in dog and cats due to hepatic rupture. Thrombosis of hepatic vessels is common with hepatitis. Infarction of the liver is usually caused by hepatitis which impaired portal and hepatic circulation as caused by bacillary hemoglobinuria in cattle and sheep.


Degeneration and deposition Fatty liver The accumulation of fat or triglycerides in cytoplasm of hepatocytes known as fatty liver. 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. Amyloid Amyloid infiltration are seen in liver either primary or secondary. 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. Melanosis is occasionally seen in liver. Hepatic necrosis The liver responds to injury takes so many ways. One feature of responds to many diseases is necrosis. The hepatic necrosis is usually coagulative in type and recognized microscopically 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 forms.


a) Focal necrosis Where small necrotic area or foci of sublobular size appear here and there as saw dust liver of cattle which seen frequently by meat inspectors. It occurs in well fattened young cattle which appear in perfect health. Macroscopically, the liver shows several or many yellowish foci of necrosis as granules of saw dust scattered over the liver. Microscopically, they consist of collection of hepatic cells in state of coagulative necrosis surrounded and mixed with neutrophils and lymphocytes. 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. Paracentral necrosis is characterized by wedge-shaped with apex at central vein- 4 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. N.B.: •The inflammation of bile duct is called cholangitis while cholangiohepatitis ,inflammation of the the bilary system which extend into liver parenchyma. •Portal hepatitis, which 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. •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 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. • With progression, the fibrosis extend 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 tissue (chronic active hepatitis) 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. 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 gain access to the liver by ascending through biliary system or by direct extension through the peritoneal cavity.


Infectious hepatitis- 1 It caused by infectious agents as bacteria, virus or parasitic. 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, yellow fever and generalized herpesvirus infection. And HVCandB in human Protozoal infections include coccidiosis, leishmaniasis and amoebiasis. Metazoan parasites due to migration of larvae which lead to necrosis, inflammation and fibrosis as Ascaris sum. Strongylus in horse and Cysticercus tenuicollis in sheep and cattle. Capilari 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.

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 or 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(chemicals that are forign to the biological system) to toxin as in aflatoxins and carbon tetrachloride.

Causes 1- Chemical poisons as copper, arsenic and phosphorus ccl4 and others. 2-Mycotoxins as aflatoxin. 3- Plant poisons as snecio. 4-Metabolic poisons are those produced during disease as gastroenteritis, metritis. Macroscopically,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 colour due to necrosis and fatty change (acute yellow atrophy) or become red and small due to necrosis and congestion and hemorrhage (acute red atrophy). Finally, fibrosis, biliary hyperplasia and paranchymal 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, hepatocytes 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, parenchymal 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 fram. Also when necrosis is more than regenerative capacity of liver. •Chronic cholangitis can produce fibrosis that is most pronounced in portal area. •Also, it observe in chronic hypoxia usually in centrolobular area. 3- Biliary hyperplasia A variety of causes can results in proliferation of new bile ducts within the portal areas usually accompanied by fibrosis which is extended to the hepatic lobules.


)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 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(no energy to cells). Macroscopic picture •The affected liver is small, firm nodular. •Ascites is usually present. Jaundice is seen at the terminal stage. Microscopic picture 1- 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. 2- Fibrous connective tissue proliferation which start from the portal areas and extend between the lobules (interlobular cirrhosis.monolobular or multilobular). 3- Moreover, the fibrous tissue enter the lobule and surrounded group of hepatocytes (intralobular cirrhosis or pericelular cirrhosis. 4- The fibrous tissue is infiltrated with lymphocytes and plasma cells. Blood vessels may accompany those fibrous strands and connect the portal and central vein


Biliary cirrhosis- 2 Macroscopic picture 1- Liver is hard, enlarged with smooth surface. 2-Hepatic tissue is yellowish green (jaundice appear early). 3- Bile duct may be thicked white and calcified. Microscopic picture 1- Numerous newly formed bile ductules with thickened wall. Compressing the surrounding hepatocytes 2- The bile ducts surrounded by thick bands of fibrous tissue which extend between lobules and cause pressure atrophy of hepatocytes. Special forms of cirrhosis Glissonian cirrhosis It resemble 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. Pigmentary cirrhosis It occurs with hemochromatosis. Parasitic cirrhosis It occurs in association with parasites as fasioliasis and schistosomiasis Effect of cirrhosis 1- Ascites with portal 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.(feminization) The presence of fibrous tissue in liver is progressive process that means stimulate proliferation of a new fibrous tissue even with cause removal4-anemia due to lack of erythropiotien and toxic depression of bon marrow


Neoplasm of liver Hepatoma, hepatocellular carcinoma, cavernous hemangioma and hemangiosarcoma are primary hepatic tumors. Gall bladder and bile duct •Cholangitis is inflammation of bile ducts. • Cholecystitis is inflammation of gall bladder. • Cholangitis and cholecystitis are usually catarrhal or serous. Cholelithiasis It is the formation of cholelith or gall-stone. It is rare in domestic animals.


The Digestive System