Pathology II Systems pathology PATHOLOGY OF THE ALIMENTARY SYSTEM II ESOPHAGUS Anomalies Atresia • Lack of development of the esophageal lumen (seen sporadically) Achalasia • Esophageal motility disorders are termed achalasiaÆsequential contractility of the esophagus is defectiveÆ regurgitation Æ weight loss Cricopharyngeal Achalasia o Presentation Rare condition of dogs (terriers, cocker spaniels, miniature poodles); noted after weaning/before 6 months of age Dysphagia, regurgitationÆgagging and choking behavior o Pathogenesis Congenital disorder (neurological) of upper esophageal sphincter (cricopharyngeal musculature) Æ failure to relax May occur as an acquired condition Æacquired canine achalasiaÆ variable abnormality of cricopharyngeal musculature Megaesophagus (esophageal ectasia) o Presentation Described in dogs, cats, horses, cows, ferrets and new world camelids Dilation of the esophagus due to insufficient or uncoordinated peristalsis Regurgitation after ingestion of solid food Æ may not be identified until after weaning Animals may develop aspiration pneumonia o Pathogenesis Causes range from: • Innervation or denervation disorders • Partial physical obstruction/stenosis secondary to inflammation • Idiopathic Congenital megaesophagus • Partial blockage of lumen by persistent right fourth aortic arch Æthe aorta, pulmonary artery, and ductus arteriosus form a ring around trachea and the esophagus, preventing full dilation of esophagus Æ specifically dilates esophagus cranial to heart • Idiopathic denervation of esophagus (great Danes, Irish Setters, miniature schnauzers, Labrador retrievers, wire-haired fox terriers, Shar-peis, Newfoundlands, Siamese cats) Acquired megaesophagus • Humans Æ failure of opening of cardiac sphincter • Domestic species Æ primary lesion of esophagus o Idiopathic 1 | Page
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Pathology II Systems pathology
PATHOLOGY OF THE ALIMENTARY SYSTEM II
ESOPHAGUS
Anomalies
Atresia • Lack of development of the esophageal lumen (seen sporadically)
Achalasia • Esophageal motility disorders are termed achalasia sequential contractility of the esophagus is
defective regurgitation weight loss Cricopharyngeal Achalasia
o Presentation Rare condition of dogs (terriers, cocker spaniels, miniature poodles); noted after
weaning/before 6 months of age Dysphagia, regurgitation gagging and choking behavior
o Pathogenesis Congenital disorder (neurological) of upper esophageal sphincter (cricopharyngeal
musculature) failure to relax May occur as an acquired condition acquired canine achalasia variable abnormality of
cricopharyngeal musculature
Megaesophagus (esophageal ectasia) o Presentation
Described in dogs, cats, horses, cows, ferrets and new world camelids Dilation of the esophagus due to insufficient or uncoordinated peristalsis Regurgitation after ingestion of solid food may not be identified until after weaning Animals may develop aspiration pneumonia
o Pathogenesis Causes range from:
• Innervation or denervation disorders • Partial physical obstruction/stenosis secondary to inflammation • Idiopathic
Congenital megaesophagus • Partial blockage of lumen by persistent right fourth aortic arch the aorta,
pulmonary artery, and ductus arteriosus form a ring around trachea and the esophagus, preventing full dilation of esophagus specifically dilates esophagus cranial to heart
• Idiopathic denervation of esophagus (great Danes, Irish Setters, miniature schnauzers, Labrador retrievers, wire-haired fox terriers, Shar-peis, Newfoundlands, Siamese cats)
Acquired megaesophagus • Humans failure of opening of cardiac sphincter • Domestic species primary lesion of esophagus
o Idiopathic
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o Secondary to polymyositis, myasthenia gravis, hypothyroidism, esophagitis, recurrent gastric dilation
o Lead and thallium toxicosis
Parasitic Diseases Few diseases of clinical importance; may be noted as incidental findings
Gongylonema spp.
o Nematodes reside beneath esophageal mucosa in ruminants, pigs, horses, primates, occasionally rodents
o Thin, red, serpentine, 10-15cm length; intermediate hosts are cockroaches and dung beetles
Gasterophilus spp. o Fly larvae that attach to gastric and distal esophageal mucosa of equids by oral hooks; eggs are laid on
skin, activated by warmth and moisture of licking o Burrow into oral mucosa, molt, migrate along esophagus; eventually detach, shed in feces
Hypoderma lineatum
o Larva of warble fly of ruminants; migrate to esophageal adventitia, then to subcutaneous tissues of the back
Spirocerca lupi
o Esophageal parasite of canids; occur in warm climates intermediate hosts are dung beetles paratenic hosts are rodents, chickens, reptiles
o Reach esophageal submucosa after migrating through aortic wall a passage forms between the granuloma containing parasite and esophageal lumen ova pass into alimentary tract feces
o Clinical presentation Dysphagia, aortic aneurysm, hemothorax May induce formation of esophageal fibrosarcoma or osteosarcoma Vertebrae adjacent to aortic granulomas spondylosis deformans
Sacrcocystis gigantea
• White protozoal cysts up to 1 cm long beneath the mucosa originating in the muscle. Seen in sheep, they are of no clinical significance
Miscellaneous Esophageal Lesions/Conditions
Idiopathic Muscular Hypertrophy of the Distal Esophagus
o Incidental lesion in horses and pigs, usually of no clinical significance o Marked increased in the thickness of the smooth muscle in the muscularis (distal esophagus); rarely
plays a role in esophageal impaction Dilation of the Esophageal Glands of Aged Dogs
o Incidental lesion in dogs, may be quite spectacular; surface “erosions” are actually mucosal elevations filled with mucus; may vary in numbers, usually only few millimeters in diameter; overlying mucosa is smooth and shiny
Esophageal Erosions and Ulcers
o Relatively common, have a variety of causes: Reflux of stomach acid “acid reflux esophagitis” Ingestion of caustics Improper use of stomach tubes – linear scraping of crests of longitudinal folds of mucosa Infectious disease (BVD)
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Leukoplakia
o Discrete, flat, white mucosal elevations (epithelial plaques) in esophagus and stomach of no clinical significance
o May be mistaken with lesions of thrush or neoplasia Choke
o Esophageal obstruction secondary to stenosis or blockage of various causes; often occur in anatomic locations in which esophageal dilation is restricted (dorsal to larynx, thoracic inlet, base of heart, diaphragmatic hiatus)
o Most commonly results from ingestion of overlarge bodies; if present for more than 2 days circumferential pressure necrosis stricture formation
o May relate to poor dentition in older animals – incomplete mastication esophageal impaction o May also relate to neoplastic or inflammatory lesions of esophagus, extraesophageal obstruction
Neoplasia
Esophageal Squamous Cell Carcinoma
Rare; reported in cats and horses Bracken fern (Pteridium aquilinum) consumption has been implicated as a potential cause
Dysphagia, regurgitation, proximal esophageal dilation, weight loss; palpable esophageal mass if cervical Generally are not identified early as they grow lumenally
*Other esophageal neoplasia may include papillomas, leiomyomas, fibrosarcomas (See Spirocerca lupi) and lymphosarcoma RUMEN, RETICULUM, OMASUM
• Generally relate to disorders of rumen motility and rumen flora • Abrupt alterations in diet altered activity/population constituents
o May result in a spectrum of changes from ruminal acidosis tympany • Mucosa may become inflamed with acid pH of contents bacterial and mycotic overgrowth • Reticulum may trap foreign bodies as they leave esophagus local irritation – penetration
Bloat
o Overdistension of rumen/reticulum by gases produced during fermentation o Approximately 50% mortality; hereditary predisposition may occur
1. Primary Bloat
o Known as legume bloat, dietary bloat, frothy bloat o Presentation
1-3 days after animals begin a new diet; predisposed by certain feedstuffs, including alfalfa, ladino clover, grain concentrates
Clinical signs include a distended left paralumbar fossa, distended abdomen, increase HR/RR, decreased ruminal movements, sudden death
o Pathogenesis Legumes promote formation of stable foam; nonvolatile acids of legume and ruminal
fermentation lower pH to 5-6 Foam physically blocks cardia, prevents eructation; death occurs due to compression of
diaphragm, reduced size of pleural cavity, respiratory failure, increased intrathoracic pressure decreased venous return to heart
o Gross lesions Generalized congestion cranial to thoracic inlet; bloat line (pale distal esophagus, congested
proximal esophagus) Identification of foamy ruminal contents may be difficult as foam may collapse after death
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2. Secondary Bloat
o Results from physical or functional obstruction or stenosis of esophagus failure to eructate o May result from
o Collection/accumulation of foreign material in rumen, reticulum o Trichobezoars (hair balls) often seen in bottle-fed calves o Phytobezoars (plant balls) excess of dietary indigestible roughage o Ingestion of metallic objects (wire, nails) may result in perforation of reticulum reticulitis,
o Rumenitis is often considered synonymous with lactic acidosis synonymous with grain overload carbohydrate engorgement chemical rumenitis
o Triggered by sudden dietary change to easily fermented feed/change in feed volume (often associated with sudden weather changes)
o Pathogenesis Normal microflora rich in cellulolytic Gram-negative bacteria Change to highly fermentable feeds promotes growth of Gram-positive bacteria
(Lactobacillus spp., Streptococcus bovis) produce lactic acid pH drops <5 (normal 5.5-7) acidic pH inhospitable to normal microflora, damages rumen mucosa increased free fatty acids ruminal atony
Death often within 24 hours, mortality rates range from 25-90%; results from: • Dehydration secondary to increased osmotic effect of ruminal solutes – fluid efflux
into rumen • Systemic acidosis (absorption of lactate from rumen) • Circulatory collapse
o Gross lesions Ruminal contents are watery, acidic, often contain grain Necrosis of ruminal epithelium Animals surviving episodes may have pale stellate scars in the ruminal mucosa
Bacterial Rumenitis
o Occurs secondary to lactic acidosis, mechanical ruminal trauma o Bacteria may colonize rumen wall, may translocate to portal circulation liver
Arcanobacterium pyogenes – common isolate from liver abscesses Fusobacterium necrophorum – necrobacillosis in the liver
Mycotic Rumenitis
o Occurs secondary to lactic acidosis, mechanical trauma, antibiotic treatment o Reduction of normal rumen flora proliferation of fungi invasion of vessels round infarctive
lesions in mucosa o Fungal vasculitis and thrombosis; some may translocate in portal circulation hematogenous spread
to placenta (mycotic placentitis) abortions o Common offenders include Aspergillus, Mucor, Rhizopus, Absidia, Mortierella spp. o Candidiasis – uncommon; incidental finding at necropsy
o Morphology of rumen papillae is determined by dietary fibre content (longer/larger in high roughage diets)
o Hard, brown, often clumped ruminal papillae; of no clinical consequence; occurs in animals fed <10% roughage
Ruminal Papillomas
o Viral-induced; in some countries may relate to ingestion of bracken fern Vagus Indigestion
o Damage to vagus nerve Functional outflow obstruction in forestomachs Functional pyloric stenosis
o Causes include inflammation of the vagus nerve due to: Traumatic reticuloperitonitis Live abscesses Abomasal volvulus Bronchopneumonia Many cases are idiopathic
o Results in ruminoreticular distension
Mechanical Outflow Obstruction o May result from lymphosarcoma, papilloma, foreign body
Parasitic Diseases
Paramphistomiasis
• Fluke infestation of the ruminant forestomach (Paramphistomum, Calicophoron, Cotylophoron) • Usually of no clinical significance, however heavy infestations in the small intestine can cause
hypoproteinemia, anemia and death • Intermediate host is a snail
STOMACH/ABOMASUM
• Protective features o Gastric motility o Foveolar mucus protective mucus layer over mucosa o Secretory IgA o Acid luminal pH o Effective pyloric sphincter
Mechanical Abnormalities
Gastric Dilation/Volvulus
o Presentation Occurs in various species, most common in dogs (particularly large, deep-chested breeds) as
an acute syndrome Not to be mistaken for simple gastric dilation in puppies associated with overeating
o Pathogenesis Recurrent gastric dilation (overfeeding, postprandial exercise, hereditary factors)
stretching and relaxation of gastrohepatic ligament gastric rotation vascular compression decreased venous outflow, hypoxia
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Gastric hypoxemia, acid-base imbalance, obstruction of pylorus and cardia, increase intragastric pressure antiperistaltic waves followed by atony, ischemia cardiac arrhythmia shock
Decreased portal venous return pancreatic ischemia release of myocardial depressant factor cardiac collapse, death
Predisposing factors • Source of distending gas (not well understood – C. perfringens in feed, from
digestion, from aerophagia), fluid, feed • Obstruction of cardia preventing eructation/emesis • Obstruction of pylorus
o Gross lesions Splenic displacement, twisted esophagus (generally stomach rotates clockwise relative to
ventrodorsal axis when viewed from ventrum, 180˚-360˚ degrees)
Abomasal Displacement o Presentation
Most commonly to the left; may occur on right; abomasum normally resides on xiphoid process and ventral abdominal midline
Left-sided • Generally nonfatal disease of high-producing dairy cattle after parturition (increased
feed uptake, hypocalcaemia, cranial shifting of the rumen and abomasum during pregnancy)
• May occur with strenuous exercise • Leads to partial obstruction of abomasal flow
Right-sided • 15% of abomasal displacements; 20% lead to volvulus • Most common in peri and postparturient cows and calves
Displacements lead to abdominal pain, abomasal tympany, anorexia, elevated heart rate, depressed peristalsis, lack of feces
Acute Gastric Dilation/Rupture
o Presentation Common as terminal event in horses with intestinal obstruction/displacement; may occur as a
sequel to ingestion of highly-fermentable feeds/grain, or behavioral stereotypies such as cribbing and aerophagia
• In some countries, may occur due to grass sickness dysautonomia (association with C. perfringens type A enterotoxin)
Occurs in nonhuman primates (associated with C. perfringens overgrowth)
Chronic Gastric Dilation o Usually secondary to other disease
difficult parturition, transport fatigue, metabolic disorders, vagal indigestion Partial to complete anorexia, lack of normal contraction sounds, enlarged gas cap and
distended abdomen, reduced motility, scant feces Lesions are few, consist of enlarged stomach, abnormal volume/character of feed residue
Gastric Impaction
o Pathogenesis
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May result from thoracic lesions (pneumonia, pleuritis, lymphadenopathy, lymphosarcoma) causing damage to the vagal nerves
Excessive roughage, hairballs, foreign bodies Abomasal emptying defect idiopathic condition of Suffolk sheep (form of acquired
dysautonomia?)
Inflammatory Diseases
Gastritis and Abomasitis o Must be distinguished from simple hyperemia and petechiae (non specific agonal lesions)
Gastritis o Often associated with vomiting, dehydration, metabolic acidosis o Pathologic changes include necrosis, hemorrhage, edema, erosions, ulcerations, increased mucus
Braxy (Hemorrhagic/Emphysematous Abomasitis) o Presentation
Sheep and cattle, most common in UK, Europe, seen occasionally in North America (cooler climates)
o Pathogenesis Infection with Clostridium septicum (factors initiating bacterial invasion are unknown) Lesions and death due to exotoxemia
o Gross lesions Mucosal hemorrhage and submucosal emphysema
Embolic Gastric Infarction in Swine
o Occurs in septicemic conditions • Salmonellosis (Salmonella spp.) • Swine Dysentery (Brachyspira hyodysenteriae) • Glasser’s Disease (Haemophilus parasuis) • Colibacillosis (E. coli)
o Pathogenesis Bacterial emboli lodge in the submucosal gastric vessels thrombosis, infarction, ulceration Similar lesions occur with some mycotoxins (Fusarium spp.)
Common isolates include Histoplasma capsulatum (dogs), rarely Mycobacterium tuberculosis
Wall of stomach becomes progressively thickened, stomach becomes less functional Numerous infiltrative macrophages; plasma cells, lymphocytes, fibroblasts, variable numbers
of neutrophils, eosinophils, multinucleated giant cells Causative organisms can be demonstrated with special stains (PAS, Acid Fast)
Eosinophilic Gastritis
o Presentation Rare, occurs in most species; studied mostly in dogs, cats, humans Three forms are recognized
1. Focal eosinophilic gastritis 2. Diffuse eosinophilic gastritis 3. Scirrhous eosinophilic gastritis of dogs and cats
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o Pathogenesis Focal eosinophilic gastritis
• Eosinophil infiltration in response to trapped nematode larvae • Dogs Toxocara canis migration (puppy infected by T. canis in milk/feed/feces
larvae remain in tissues for years, attract eosinophils) • Tissue reaction to larvae results in epithelial cell hyperplasia and polyp-like
proliferation of the antral mucosa pyloric obstruction
Diffuse eosinophilic gastritis • Assumed to be a hypersensitivity reaction (offending antigen is unknown) • In many cases there is peripheral eosinophilia
Scirrhous eosinophilic gastritis of dogs and cats
• Infiltrates of eosinophils in mucosa, submucosa, extensively through muscle layers; may be present segmentally in intestine, colon
• Dogs some small/medium arterioles of submucosa have medial necrosis, intimal proliferation, eosinophilic perivasculitis
• Eosinophilic infiltrate followed by fibroplasias of lamina propria, submucosa, muscle layers
• Regional lymph nodes are enlarged with infiltrates of eosinophils and lymphoid hyperplasia
Hypertrophic or Hyperplastic Diseases
Hypertrophic Gastritis • Described in dogs, horses, primates, rodents o Pathogenesis
Believed to result from retention of gastric fluid and reflux of intestinal bile Similar mucosal glandular changes are seen in immune-mediated lymphoplasmacytic gastritis
of dogs Associated with gastric nematode Nochtia nocti in primates Associated with Habronema spp. and Trichostrongylus axei in horses Thickened rugae resulting from hyperplasia of gastric glands
Chronic Giant Hypertrophic Gastropathy
o Presentation Basenji, beagle, boxer, bull terriers, others more rarely Weight loss, diarrhea, vomiting, hypoproteinemia
o Pathogenesis Etiology unknown Chronic gastritis results in increased mucosal permeability to serum proteins protein-
losing gastropathy Mucosa is hyperplastic, and hypertrophic
Ulcers and Erosions
Ulcer
• Mucosal defect in which entire epithelial thickness (including basement membrane) is lost • Partial-thickness epithelial loss is an erosion
o Acute ulcers shallow, often with soft hyperemic margins; occur in diffusely congested mucosa
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o Chronic ulcers deeper, lack hyperemic rim, have indurated, fibrotic margins; crater often lined by grey-tan fibrinopurulent membrane
Perforating Ulcer penetration through remaining tissue layers into peritoneal cavity
Presentation
o Dog vomiting, variable appetite, abdominal pain, anemia, occasionally weight loss o Foals abdominal pain, bruxism, salivation, gastric reflux, dorsal recumbency o Cattle partial or complete anorexia, decreased milk production, melena o Any species hematemesis, melena
Pathogenesis o Theories regarding ulcer development in animals relate to an imbalance between acid production and
mucosal protection as a result of: Local disturbances or trauma to mucosal epithelial barrier due to:
• back-flush of bile salts from duodenum • ingestion of lipid solvents (alcohol)
Normal or high gastric acidity Local disturbances in blood flow resulting in ischemia Steroid and NSAID-induced depression of prostaglandin formation or concentration
decreased secretion of phospholipids which are protective o Helical organisms and gastric ulcers
Strong association between helical bacterium and gastric ulcers in humans However gastric Helicobacter-like organisms are readily identified in dogs and cats
association has not been established • More than 90% of cats are infected with Helicobacter spp. (H. felis, H, heilmannii)
Abomasal Ulcers
o Vary from subclinical to fatal In calves
• Dietary changes o Substitution of roughage for milk/replacer, often associated with stress
• Mechanical irritation of abomasum by roughage Dairy cattle associated with heavy grain feeding (lactic acidosis) at time of parturition
Gastric Ulcers in Pigs Occur in pigs fed finely ground grain or pelleted feed Relates to fermentation of sugars in the feed by commensal bacteria (Lactobacillus and
Bacillus spp.), and the stress of confinement rearing Limited to stratified squamous portion of gastric mucosa surrounding cardia Can cause exsanguination
Gastric Ulcers in Dogs and Cats
o Generally idiopathic o Ulcers can occur in islet cell tumors producing gastrin (Zollinger-Ellison syndrome) and mast cell
tumors Release histamine into blood stream, which binds to receptors on parietal cells ↑ HCl
secretion
Gastric Ulcers in horses o Foals
Idiopathic; may be associated with NSAID administration as in other species
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o Common in competitive and performance horses o Ulcerative gastritis in horses associated to cantharidin toxicity (Blister beetles in alfalfa hay)
Miscellaneous Diseases and Conditions
Uremic Gastritis
• Typically occurs in carnivores as a result of chronic renal disease • In ungulates, is a rare condition associated with obstructive renal disease (post renal uremia) • Characterized by mineralization of glands, vessels, and interstitium of gastric mucosa • May result in ulcer formation
Gastric amyloidosis
• Occasionally present in cases of systemic amyloidosis • Reported in Siamese and Abyssinian cats, bats, goats, rhesus monkeys, sheep and Siberian tigers
Pyloric Stenosis
• May be due to an anatomic problem or an inability of pyloric sphincter to function properly (congenital or acquired)
• Most common in brachycephalic dogs, Siamese cats, horses and humans • Recognized in recently weaned animals by projectile vomiting, enlargement of stomach, retention of
gastric residue
Giant Hypertrophic Pyloric Gastropathy • Lesion seen in older small-breed dogs • The cause is unknown • The lesion may resemble carcinoma grossly • Microscopically there is marked foveolar and glandular hyperplasia, hypertrophy of smooth muscle,
small mucosal erosions/ulcerations and a variable degree of lymphoplasmacytic infiltrate *Not to be confused with ***Chronic Giant Hypertrophic Gastropathy*** (see above)
Parasites
Horses o Equine Bots (Gasterophilus nasalis and Gasterophilus intestinalis)
Commonly seen in animals on inadequate anthelminthic regimes Both parasites attach to mucosa via anterior pinchers; pass in feces as larvae, pupate, develop
into flies G. intestinalis colonizes stratified portion of stomach G. nasalis colonizes glandular portion of stomach May cause gastric ulcers
o Draschia megastoma
Found in brood pouches in glandular mucosa adjacent to margo plicatus Adults in cysts of submucosal nodules release eggs through pore passed in feces,
consumed by fly that serves as intermediate host Cause raised parasitic nodules in gastric mucosa; may cause gastric ulcers
o Habronema muscae and H. majus Found on the mucosa, can cause mild ulceration
o Trichostrongylus axei Catarrhal gastritis
Ruminants
o Haemonchosis (Haemonchus contortus) Common in ruminant abomasums (+++lambs)
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Adults on abomasal surface measure 2-3cm; females are red and white blood-filled intestine and white uterus (barber pole worm)
Acquired on pasture grasses as third-stage larvae enter abomasum, encyst in gastric glands in hypobiotic state develop to adult stage move out to surface eggs pass in feces
Parasite feeds on blood can cause anemia, hypoproteinemia subcutaneous submandibular edema, pale mucous membranes and organs, stunted growth, liquid feces
o Ostertagiasis (Ostertagia circumcincta in sheep, goats, Ostertagia ostertagia in cattle)
Most important parasitic disease of cattle and small ruminants in temperate climates Often associated with coinfection with Trichostrongylus spp. within other GI locations (small
intestine) Combined parasitism low weight gains, inappetence, diarrhea; later stages
hypoproteinemia, ventral edema Direct life cycle similar to Haemonchus spp.; reside as third, fourth, fifth stage larvae in
gastric glands of abomasum Heavy infestation abomasal mucosa takes on appearance of Moroccan leather
(multinodular) due to mucous cell hyperplasia, lymphoid nodules in submucosa Microscopically abomasitis typified by chronic lymphoplasmacytic inflammation with
some eosinophils, increased globular leukocytes; decrease in number of parietal and chief cells, hyperplasia of mucous cells
Nematodes are small (1.5cm long), brown, smaller than H. contortus Pigs
o Hyostrongylosis (Hyostrongylus rubidus) Red, threadlike nematodes “Thin sow syndrome” Similar lesion to Ostertagiasis; mucosa is thickened, catarrhal, cobblestoned Microscopically, there is mucous metaplasia of parasitized and adjacent glands; chronic cases
with lymphoid follicles
Carnivores (dogs and cats) Most are incidental findings
o Gnathostomiasis (Gnathostoma spp.) Form submucosal granulomatous nodules that can exceed 5cm diameter Heavy infections can be significant as may cause disturbances in motility, vomition and if
nodules are ruptured peritonitis
o Ollulaniasis (Ollulanus tricuspis) Minute nematode approximately 0.8mm long Rarely cause
o Physaloptera spp. Not infrequently found in the stomach on endoscopic examination, or at necropsy May be responsible for vomiting Adult worms appear similar to ascarids; generally attach by anterior hooks to proximal
duodenal mucosa at gastric valve Intermediate hosts are coprophagous beetles
Neoplasia
Leiomyoma, leiomyosarcoma
Benign smooth muscle tumor Lymphosarcoma
o May be primary, metastatic, or multicentric o Cattle often caused by Bovine leukosis virus; predilection for abomasum, right atrium, uterus
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Squamous Cell Carcinoma o Derived from stratified squamous (esophageal) portion of stomach o Relatively common in horse originate in pars esophagea
Glandular Neoplasms (Adenomas, Adenocarcinomas) o Occur in all species; most common in dog, cat o Adenocarcinoma Highly malignant, metastasize early, implants in the abdominal cavity
INTESTINE Normal Mucosal Architecture Small intestine • Crypts of Lieberkuhn progenitor cell population
o Daughter cells differentiate, and move out of from the crypt to the villus o Crypt cells secrete electrolyte, fluid and mucus
• Villus o Epithelium gradually differentiates as it moves up villus o Distal 2/3 functional absorptive enterocytes o Epithelial turnover about 2-7 days depending on species and age of animal; cells programmed
to move up and off villus Cecum and colon • No villi, but low ridges; glands containing progenitor and mucus cells PATHOGENIC MECHANISMS IN THE INTESTINE Ischemic Disease • Reduced blood flow due to any cause shock or vascular obstruction results in hypoxia and loss of surface epithelium within minutes
o Crypt epithelium is more resistant to hypoxia and may survive several hours • Reflow to mucosa may compound damage by production of free radicals "reperfusion injury" • Most common cause of ischemia is vascular obstruction, which may be due to arterial spasm or
damage, embolism, or obstruction of venous outflow Villus Atrophy • Three basic pathogenetic mechanisms based on equilibrium between rate of epithelial cell production
and rate of surface cell loss, and plasticity of the lamina propria
a) Damage to progenitor cell population in crypts o Radiation (hence term “radiomimetic”, mimicking the effect of radiation) o Toxins any mitotic poison, eg. cyclophosphamide, vincristine o Ischemia of sufficient duration to damage crypt epithelium o Viruses panleukopenia, canine parvovirus, bovine virus diarrhea
Coccidia that develop in and destroy crypt epithelium
b) Primary exfoliation of surface cells/increased turnover o Damage to surface cells (Rotavirus, Coronavirus, some coccidia, transient ischemia) o Villi contract o Within 2-3 days, compensatory hyperplasia of proliferative compartment in crypts repairs cell loss and
mucosal architecture returns to normal, if animal survives period of malabsorption/diarrhea
c) Primary crypt cell hyperplasia/failure of differentiation/increased turnover o Intestinal hypersensitivity o Chronic inflammation nematodes, Johne's disease, Giardia o T-cell-mediated cytokines from lymphocytes stimulate increased proliferation of progenitor cells in
crypts emergent cells differentiate poorly and are lost from surface by apoptosis more rapidly than
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normal, resulting in villus atrophy Erosive, Ulcerative and Necrotizing Lesions of Intestinal Mucosa Simple erosion
o Surface epithelium is damaged but the inflammatory reaction in the lamina propria is not severe o Plasma protein loss may occur, but if progenitor cell population is intact, repair will ensue rapidly if the
insult is removed Hemorrhagic enteritis
• Severe damage to superficial blood vessels Intestinal adenomatosis (Lawsonia intracellularis in pigs), coccidiosis, some clostridial
toxemias Fibrinous enteritis
o Severe acute inflammatory lesions resulting in substantial vascular damage, permeability and fibrin effusion into the lumen, with local diffuse erosion or ulceration of the mucosa
o May produce a diphtheritic membrane, cast salmonellosis, intestinal adenomatosis, mucosal disease, swine dysentery, coccidiosis, and others
Necrotic enteritis o Coagulation or caseous necrosis of mucosa, with minimal or peripheral inflammatory response in early
stages clostridial toxins C. perfringens Granulomatous enteritis
o Chronic inflammatory reactions in the lamina propria, with accumulation of macrophages, giant cells, plasma cells, possibly granuloma formation
o Mycobacterium, Histoplasma, Prototheca, other rare intracellular agents Diarrhea
• Defined as secretion of abnormally fluid feces accompanied by an increased volume of feces and an increased frequency of defecation
• Diarrhea mechanisms (not mutually exclusive): o Secretory Due to an excess of secretion over absorption of fluid (resulting from derangement of
normal secretory and absorptive mechanisms) Example Bacterial enterotoxins (reduce water absorption and increase water secretion)
o Malabsorption Osmotic retention of water in the lumen, commonly results from villus atrophy o Effusion Increased permeability of the mucosa leading to increased movement of fluid and
solutes to the lumen o Hypermotility not a primary mechanism in domestic animals
• Additionally, there are non-intestinal causes of diarrhea (pancreatic insufficiency, pancreatitis, chronic
renal failure and others) • The main consequence of diarrhea is dehydration and this can result in hypovolemia hemoconcentration
Embryonic cells in the lumen fail to break down o Generally named for the part of bowel occluded (atresia ani, atresia coli)
Meckel’s Diverticulum
• Remnant of omphalomesenteric duct near terminal ileum; represents the stalk of the yolk sac Megacolon
• Large usually fecal-filled colon • Seen in dogs, pigs, overo foals • May be caused by a congenital lack of submucosal and/or myenteric plexuses secondary to failed migration
of neuroblasts from neural crest • Affected overo foals fail to pass meconium, develop colic, and die • May also develop secondary to atresia ani, or acquired damage to colonic innervations (traumatic)
Intestinal Obstruction
Enterolithiasis
• Arab horses predisposed associated with diets containing large quantities of phosphorus and magnesium • Most commonly struvite-derived (ammonium magnesium phosphate) • Generally lodge at pelvic flexure, transverse colon
Impaction
• Presence of aggregated ingesta that fails to move along the intestinal tract o Common in horses following anthelminthic administration (ascarid impaction) o Cecal impaction in old horses with poor dentition, high roughage diet, debility; ingestion of sand
Stricture • Can result from penetrating or non-penetrating wounds • Or due to vascular injury rectal strictures in pigs with salmonellosis thrombosis of the cranial
hemorrhoidal artery and lack of collateral circulation Intussusception
• Telescoping of one intestinal segment (intussusceptum) into another segment (intussuscipiens) • Generally unknown etiology, thought associated with irritability and hypermotility; presence of foreign
bodies, neoplasms, some parasites (Oesophagotomum spp. nodular worm of sheep) o Dogs granulomas, surgical exposure/manipulation, hypertrophied lymphoid nodules, linear
foreign bodies, ascarids o Cats foreign bodies, adenocarcinomas o Cattle abscesses, tumors o Horses ascarids, parasitic granulomas, verminous arteritis, neoplasia; ileocecal/ cecocecal/
ceocolic intussusceptions associated with Anoplocephala perfoliata
Paralytic Ileus (adynamic ileus) • Nonmechanical hypomotility resulting in functional obstruction of the bowel • The gut is not “paralyzed” but because of continuous nerve discharge becomes refractory • May result from peritonitis, shock, severe painful stimuli, states of abnormal metabolism, toxemia,
electrolyte imbalance hypocalcemia/hypomagnesemia/hypokalemia, vitamin B deficiency, uremia, tetanus, diabetes mellitus, lead poisoning
• May occur with surgical manipulation/handling – sympathetic nerve inhibition (Adynamic ileus)
Intestinal Displacements
Internal Herniation
• Displacements of intestine through normal or pathologic foramen in the abdominal cavity. Occur most commonly in horses
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o Mesenteric tear entrapment o Epiploic foramen entrapment potential space (dorsal border formed by caudate lobe of
liver, caudal vena cava; ventral border formed by right pancreatic lobe, gastropancreatic ligament, portal vein; cranial border is hepatoduodenal ligament; caudal border is junction of pancreas and mesoduodenum) proposed that caudal liver lobe atrophies in older animals enlarges foramen intestinal loops enter and become incarcerated/strangulated
External Herniation • Formed when a hernial sac (pouch of parietal peritoneum) penetrates outside the abdominal cavity
o Can be umbilical, ventral, diaphragmatic, hiatal, inguinal, scrotal, perineal Perineal old male dogs with prostate gland enlargement
• If not accompanied by peritoneal pouch eventrations
Volvulus and Torsion • Volvulus twisting of the intestine on its mesenteric axis • Torsion rotation of organ along its long axis
Both result in vascular obstruction and ischemic injury (edema congestion hemorrhage necrosis) Intestinal strangulation due to pedunculated lipomas
• Most common in horses, can occur in dogs • Lipomas wrap around the mesentery and strangle the intestine infarction
Nephrosplenic Entrapment
• Left dorsal displacement of left dorsal or left ventral segments of large colon between spleen and left body wall
• Occurs over nephrosplenic ligament between left kidney, spleen; cause is unknown
Miscellaneous Diseases and Conditions Cecal/Large Intestinal Rupture
• Most common in postparturient mares; can also result from impaction and as a complication of anesthesia; site vary; mechanisms unknown
Diverticula
• Epithelium-lined cavities that are derived from mucosal epithelium and extend through muscularis mucosae, submucosa, muscularis, often reaching serosa; may reach peritoneum; may rupture
• Muscular hypertrophy of tunica muscularis associated with diverticulosis recorded in young Yorkshire pigs, Romney Marsh and Hampshire sheep
Muscular Hypertrophy of the Distal Ileum
• Idiopathic condition of horse, pig; generally incidental finding, may lead to impaction/rupture of ileum or can be asymptomatic
• In horses may affect ileum, progress proximal to jejunum may result from work hypertrophy proximal to damaged/stenotic ileocecal valve; can be associated with diverticula
• In cats seen in conjunction with hypereosinophilic syndrome Hemomelasma ilei
• Variably sized pink to black plaques located in the antimesenteric serosal surface of the ileum (can be anywhere in the intestines)
• Attributed to larval migration of Strongylus spp. (usually S. edentatus) ; however parasites not seen in the lesion (cause unknown)
Leiomyometaplasia (Intestinal lipofuscinosis)
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• “Brown dog gut” Accumulation of lipofuscin in the lysosomes of smooth muscle cells of the tunica muscularis (Vit E deficiency, chronic enteric or pancreatic disease)
Intestinal amyloidosis
• As a result of systemic amyloidosis
Toxins • Phosphorus, arsenic, bracken fern (cattle), mercury, oak, copper, nitrate, thallium • Blister beetles (Cantharidin blister causing substance) most common in horses sloughing of the
epithelium of stomach and small intestine and urinary bladder. May cause myocardial necrosis • Corticosteroids colonic perforation in dogs, delayed GI healing (decrease cell turnover, decreased
mucus, increased gastrin increased acid) • NSAIDs right dorsal colitis in horses (necrosis, ulcers, massive edema submucosal rupture)
Vascular diseases of the intestines
Verminous arteritis
• Strongylus vulgaris (4th stage larva) present in the wall of the cranial mesenteric artery-arteritis aneurisms mural thromboses bowel infarction
Lymphangiectasia (Lacteal dilation) • Most common cause of protein losing enteropathy in dogs • Clinical signs include diarrhea, steatorrhea, hypoproteinemia and ascites • Can be due to a congenital developmental disorder of the lymphatic vessels or acquired (lymph vessel
obstruction) caused by granulomatous or neoplastic diseases • Inherited in some breeds? • Most cases are idiopathic
Diseases of the intestinal epithelium
Diseases of the absorptive enterocytes
• Loss of enterocytes lining the intestinal villi (infectious agents have a tropism for these cells) o Loss of enterocytes results in temporary villous atrophy maldigestion, malabsorption o Lost enterocytes are replaced by maturing cells migrating from the crypts (crypts are not
• Loss of cells capable of rapid mitosis (undifferentiated crypt cells) • Impaired regeneration of the epithelium • Agents that target crypt cells are called “radiomimetic agents” target rapidly dividing cells • Diseases are often more severe and can be fatal
Diseases of the microvilli-glycocalyx • Diseases that target the microvilli and glycocalyx
Examples • Attaching and effacing E.coli
Other diseases • Diseases in which the targets are unknown or nonspecific • Separation of apical junctional complexes (tight junctions)
Diseases of the lamina propria
1. Infiltrative/Inflammation: Chronic inflammation/cellular infiltration resulting in physical impairment of mucosal diffusion with disruption of overlying epithelium increased permeability
a. Canine histiocytic ulcerative colitis (Boxer colitis) b. Johne’s disease (Mycobacterium paratuberculosis) c. Amyloidosis d. Lymphoma
2. Necrotizing: Necrosis of gut associated lymphoid tissue and extension to the overlying epithelium • BVD • Rhodococcus equi
3. Vascular changes and lymphangiectasia: Idiopathic or secondary to obstruction of flow
Diseases due to specific pathogens Viral diseases
Virus Disease Species Rotavirus (ds RNA) (*species specific rotavirus)
-Reduction of colostral antibodies -Virus is cytolytic -Cause disease in association with other pathogens -Diarrhea + dehydration+weakness -Sloughing of villous cells shortening and fusion of villi
Calves (1st wks of life) Piglets (up to 7 wks of life) Foals-
Coronavirus (ss RNA)
1. Calfhood enteritis -Enteritis and colitis -Crypt lumens contain cell debris and crypts may be hyperplastic -Lamina propria and draining lymph nodes contain an increased number of inflammatory cells 2. Transmissible gastroenteritis in pigs 3. Feline enteric coronavirus -Generally a mild, self-limiting disease, but cases of fatal enteritis have been reported -Degeneration and loss of jejunal enterocytes
Calves Pigs Cats
Adenoviral enteritis (*species specific adenovirus)
-Enteritis with amphophilic IN/IB in villous enterocytes -Villous blunting and fusion -Systemic disease (respiratory, liver, kidneys)
Ruminants, pigs and horses (arabs-CID)
Bacterial
E.coli Enterotoxic -Secretory diarrhea (enterotoxin induced) -NaCl is secreted into the intestinal lumen and water is drawn into the intestines -Yellow, watery pasty diarrhea -Bacteria present in the luminal surface of the
Calves, piglets (2-3 days-old)
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enterocytes Septicemic -Lack of passive immunity
-Enteritis, fibrinous arthritis, serositis, meningitis, white spotted kidneys
Calves, lambs, foals
Edema disease -Enterotoxemic colibacillosis of pigs (Bacterial enterotoxin verotoxin) -Associated to changes in feed at weaning -Generalized vascular endothelial damage, edema of gastric submucosa, focal symmetric encephalomalacia
Pigs (6-14 wks)
Post weaning colibacilosis
-Hemolytic E.coli -Similar to enterotoxic with secretory diarrhea and no intestinal lesions
Attaching and effacing -Bacterial attachment to host cells -Dilated fluid filled intestines
Calves, pigs, lambs, rabbits
Mucoid enteropathy -Copious mucus in the cecum, colon and feces Rabbits Salmonella spp.
• Enteroinvasive bacteria all species are pathogenic • Survive and multiply within phagocytic cells (granulomatous inflammation) • Produce disease via enterotoxins and endotoxins • Organism colonizes small intestine, colon, lymph nodes and gall bladder
Clinical presentation
Peracute Salmonella septicemia -Fibrinoid necrosis of blood vessels, wide spread petechiation and cyanosis (DIC) -Younger animals are at greater risk -Fibrinous polyserositis may be present
Chronic enteric salmonellosis -Ulceration and necrosis of the cecum and colon (button ulcers), rectal strictures (due to vascular thrombosis)
Cattle, pigs, horses
Clostridial enteritis
Clostridium perfringens A α toxin
1. Necrotic enteritis in birds 2. Enterotoxemia of calves and lambs 3. Necrotizing enterocolitis of piglets 4. Canine hemorrhagic enteritis 5. Equine colitis (?) 6. Lincomycin associated enteritis
B α, β, ε toxins
1. Lamb dysentery 2. Hemorrhagic enteritis in calves and foals 3. Hemorrhagic enterotoxemia of lambs
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C α, β toxins
1. Necrotic enteritis of birds 2. Hemorrhagic enterotoxemia of neonatal farm animals 3. Struck of sheep
D α, ε toxins
1. Pulpy kidney in lambs 2. Enterocolitis in goats
E α and ι
1. Enteritis in rabbits 2. Enterotoxemia of calves and lambs
Clostridium piliforme Tyzzer’s disease 1. Foals < 6 wks of age Clostridium difficile Colitis X- Pseudomembranous colitis, piglets and horses Clostridium colinum Quails- Ulcerative colitis Clostridium spiroforme Rodents and rabbits-enterotoxemia
Campylobacteriosis
• Proliferative segmental enteropathy in a variety of species (dogs, cats, sheep, cattle) • Gram- , motile, obligate intracellular bacteria • Dogs Puppies <3 months of age watery mucoid diarrhea • Microscopically surface erosions and proliferation of cryptal enterocytes with the presence of bacteria in
the apical cytoplasm of infected cells • Important in poultry and in food safety as are considered an emerging zoonotic disease
Mycobacterial enteritis
• Mycobacterium tuberculosis, M. avium intracellulare and M. bovis • Bacteria are ingested, taken up by M cells of the GALT in the distal ileum • Characterized by a roughened, rugae-like appearance of the intestine • Granulomatous lymphadenopathy sometimes with mineralization and necrosis
Protozoa
o Cryptosporidium attach to superficial epithelial cells of the small intestine and can cause acute diarrhea in calves, lambs, kids and foals
Intestinal Diseases of Carnivores
Bacterial Enteritis
• May be superimposed on viral disease panleukopenia in cats, CPV and distemper in dogs • Uncommon cause of clinical illness or death • Rarely, significant g-negative infection occurs Salmonella, Shigella, Yersinia • Transient asymptomatic Salmonella infection may be relatively common in dogs • Cases/outbreaks of enteric/septicemic salmonellosis (S. typhimurium, some multidrug resistant) reported in
cats • Salmonella carriage and disease associated with raw-meat-based diets in dogs and cats • Zoonotic potential
Camyplobacter jejuni
• Non-fatal diarrhea (dogs, cattle, sheep, cats) • Associated with superficial erosive colitis • Potentially zoonotic • High proportion of asymptomatic carriers?
Clostridial Gastroenteritis
• Acute-chronic diarrhea in dogs, including canine hemorrhagic gastroenteritis and canine intestinal hemorrhage syndrome
• Pathogenesis C. perfringens/C. difficile overgrowth enterotoxemia local diffusion of necrotizing
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toxin into mucosa • Milder cases loss of superficial epithelium villus atrophy/malabsorption with diarrhea • Severe cases necrosis of superficial mucosa with hemorrhagic gastroenteritis • Acute onset of vomition and diarrhea (bloody) • If severe and hemorrhagic reduced plasma volume DIC
Gross lesions • Loops of dark red congested bowel (segmental or extensive) and involve any level • Frank blood in the lumen; mucosa a deep reddish black • Must be differentiated on clinico/pathologic grounds from: canine parvovirus, anticoagulant toxicity,
• Three clinical syndromes originally described: o Generalized Neonatal pups < 2 weeks of age, death occurs by 10 days of age o Cardiac form Pups 2-8 weeks that can cause sudden death from cardiac arrhythmias die
by 5 months of age from chronic myocardial fibrosis and resultant cardiac arrhythmias o Leukopenia/enteritis Common form in pups 8 weeks and older
Vomiting, anorexia, pyrexia, dehydration, lethargy, bloody diarrhea Leukopenia, with relative or absolute lymphopenia, hypoproteinemia, and anemia
Gross lesions Leukopenic/enteric form
o Segmental to diffuse hemorrhagic gastroenteritis with mucoid/bloody intestinal contents and fibrinous serosal exudate
o Peyer's patch necrosis o Enlarged, congested, edematous mesenteric lymph nodes o Semiliquid, yellow-gray bone marrow o Thymic atrophy
Myocardial form o Pale streaks in myocardium, pale, flabby o Pulmonary edema with white frothy fluid in trachea and bronchi
Microscopically Severe necrohemorrhagic gastroenteritis; crypt necrosis; blunting; fusion; basophilic intranuclear inclusion bodies in enterocytes (rare), necrosis and depletion of lymphoid tissues; bone marrow depletion; focal myocardial necrosis with intranuclear basophilic inclusion bodies in cardiomyocytes Feline Panleukopenia • Parvovirus tropism for mitotic cells pathogenesis related to proliferating cell populations • Lymphoid, hemopoietic organs; progenitor cells of the gut; and cerebellum of late prenatal or early
postnatal kittens (causing cerebellar dysplasia/hypoplasia) • Clinical signs are dehydration, depression and vomiting • Clinical pathology panleukopenia Gross lesions
o Flaccid, segmentally reddened intestine; serositis o Cerebellar hypoplasia o Thymic atrophy; lymph node edema o Pale bone marrow with semi-fluid consistency
• Microscopically Intestine - patchy to extensive destruction of crypt epithelium, flattened crypt cells, villus atrophy and erosion, fibrinous exudates; basophilic intranuclear inclusion bodies in enterocytes (early infection); involuted Peyers patches
• Cerebellar hypoplasia with thinning of layers and loss of granular cells and Purkinje cells
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Minute parvovirus of canids CPV-1
• Causes myocarditis, respiratory disease and intestinal enterocyte hyperplasia with eosinophilic to amphophilic intranuclear inclusion bodies---****no crypt necrosis******
Canine Coronavirus Infection • Causes generally nonfatal enteritis in puppies • A hemorrhagic form with extensive colitis has been reported • Virus replicates in cytoplasm of mature enterocytes on the apical two-thirds of the villi, resulting in villus
atrophy • Colitis can occur, but principal disease signs and pathogenicity related to small intestinal lesions Gross lesions • Dilated intestinal loops filled with watery, yellow-green feces, congested mucosa • Microscopically villus blunting and fusion
Rotavirus
• Very rare in young puppies; usually non-fatal
Parasitic diseases Small intestine Toxocara/Toxascaris • Lumen dwelling, feed on digesta; low pathogenic potential • Heavy infestations may compete for nutrients animal runts or pot-bellied • Rarely can cause intestinal, bile or pancreatic duct obstruction and rupture Hookworm • Dogs Ancylostoma caninum (zoonotic) and Uncinaria • Blood sucking parasites iron loss anemia, hypoproteinemia • Colostral infection may result in significant (60-100) numbers in young puppies with prepatent infection
death • Pallor, hydropericardium, ascites, blood in intestine Strongyloides spp. • Rare; mammary transmission, skin penetration; young dogs • Very small - burrow in epithelium, may penetrate crypts and into lamina propria, rarely to submucosa and
regional lymph nodes • Chronic inflammatory infiltrate in lamina propria malabsorption, protein loss, diarrhea, wasting Giardia spp.
• Common in puppies and kittens (zoonotic) • Protozoa attaches to the brush border interfering with membrane digestion/absorption especially of CHO
malabsorption, diarrhea, usually not life threatening Coccidiosis • Isospora spp. • If severe malabsorptive diarrhea in puppies or kittens • May cause hemorrhagic enteritis Large intestine Trichuris vulpis
• Cecum; in large numbers in dogs may involve the colon, in which case it may become pathogenic • Burrows in the epithelium erosion of epithelium, chronic inflammation in lamina propria, focal
or extensive exudation and effusion, perhaps with blood
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Trichomoniasis
Tritrichomonas foetus ● Large bowel diarrhea in cats ● Mild to moderate colitis w/ microabscessation.
Other intestinal diseases
Malabsorption/Protein-losing enteropathies
• Problem in dogs especially; relatively uncommon in cats • Pathogenesis and etiologies poorly defined • May involve fat and CHO malabsorption and/or protein loss • Usually manifest as chronic small bowel diarrhea, wasting and possible hypoproteinemia • Biopsy of small intestine is essential for confirmatory pathologic diagnosis, classification of the lesion and
prognosis
Pathogenetic mechanisms
• Excess accumulation of inflammatory cells, including macrophages, lymphocytes, plasma cells and eosinophils in the lamina propria
• The epithelium usually seems intact, but may be transiently discontinuous and can be ulcerative • Villi are often moderately atrophic and stumpy, probably due to increased rate of epithelial turnover,
related to chronic immunoinflammatory reactions in lamina propria a) Eosinophilic gastroenteritis
• May involve stomach, small intestine and colon - infiltrate has heavy eosinophil component; vomition if stomach involved
b) Lymphocytic-plasmacytic enteritis • Chronic inflammatory cell infiltration in the lamina propria (lymphocytes and plasma cells) • Preneoplastic ???
Mucosal colitis • Lesions confined to mucosa and lamina propria • Foul smelling intermittently diarrheic feces, wasting associated with loss of colonic function and protein loss
Idiopathic mucosal colitis
• Cause of large bowel diarrhea • Majority of cases have no known etiology, and are characterized by patchy congestion, hemorrhage and
thickening of the mucosa, associated with histologic lesions of erosion of superficial mucosa, expansion of proliferative compartment in the glands, and an increased mixed inflammatory cell component in the mucosa
• Occasionally one type of cell dominates "eosinophilic" or "lymphocytic-plasmacytic" (no etiologic or prognostic connotation)
• Treatment is symptomatic Transmural colitis • Rare regional enteritis of the colon, involving mucosa, submucosa, muscularis, and regional nodes in extreme
cases
Granulomatous or Histocytic ulcerative colitis • Boxer dogs, usually under 2 yrs (but has been reported in other breeds) • Descending colon and rectum usually, but process may involve entire length of gut and stomach • Thickened corrugated mucosa, punctate erosions and ulcers which may become confluent • Histologic confirmation by presence of large macrophages, containing PAS+ granules among the chronic
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inflammatory infiltrate which may extend to the regional lymph nodes • Erosion, ulceration and chronic inflammation resulting in loss of colonic function, plasma loss and some
hemorrhage explain the signs of diarrhea with some blood, wasting • Cause unknown - rare similar cases occur in other breeds, without PAS+ granules in histiocytes • May also be rare cases of ulcerative/granulomatous transmural colitis due to Entamoeba histolytica,
Prototheca (algae-like organisms), Histoplasma capsulatum, and in cats, submucosal vasculitis (FIP-associated?), all of which must be diagnosed histologically
Feline ulcerative colitis ● Similar to Boxer colitis ● Colonic erosion and ulceration
Citrobacter freundii colitis
● Pups and immunocompromised dogs ● Potential zoonosis ● Bacteremia, septicemia and hemorrhagic enterocolitis with mucohemorrhagic diarrhea
Salmon poisoning
● Neorickettsia helminthoeca ● Consumption of salmon with trematode fluke Nanophyetus salmincola 6-8 days = febrile, depressed,
oculonasal discharge, severe diarrhea, vomiting, anorexia, splenomegaly
Wheat-sensitive enteropathy of Irish setters ● Hereditary, like gluten-sensitive enteropathy in humans
Canine senile gastrointestinal amyloidosis
● Amyloid located in and around vessels of submucosa and muscular layers in gut and mesentery ● Cause unknown, not clinical
Intestinal Diseases of Pigs
Bacterial Enteritis Gut edema • Weaned pigs growers, feeders • Enterotoxigenic E. coli (0138, 0139, 0141), often same strains as postweaning colibacillosis; fimbrial
attachment (F18) to enterocytes facilitates colonization • Shigatoxin released by bacteria in gut and absorbed to produce disease no enteritis • Toxin causes arteriolar degeneration in vessels with endothelial receptors edema and fibrinoid necrosis • of vessel walls; hence tissue ’targeting“ of edema to particular sites • Necropsy diagnosis edema of gastric submucosa, mesentery of spiral colon, slight subcutaneous edema of
throat, inguinal areas; usually no hemorrhages Enterocolitis and septicemia/ endotoxemia in weaned pigs
• Gram-negative organisms - E. coli (post weaning colobacillosis) and Salmonella spp. (S. typhimurium and S.cholerasuis)
• Establish in gut and some strains may enter circulation septicemia with signs associated with endotoxemia Pathogenesis of Endotoxemia Endotoxin = lipopolysaccharide of cell wall of Gram (-) bacteria interacts with LPS binding protein in plasma
bound LPS binds to CD14 receptor on macrophage interacting with the “toll-like receptor“ TLR-4 release of effector cytokines TLR-4 engagement on endothelial cells endothelial activation/prothrombotic state
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Signs
• Blue discoloration of skin, gangrene of ears due to capillary dilation, congestion and microvascular thrombosis infarction if animal survives acute episode; pulmonary congestion and edema
• Obligate intracellular curved gram-negative bacterium that colonizes enterocytes in the ileum, cecum, and colon of several species and causes proliferative enteritis
• Porcine proliferative enteropathy encompasses four histomorphologically distinct syndromes o Porcine Intestinal Adenomatosis (PIA) uncomplicated condition in young growing
animals Nodular or polypoid masses; expansion, elongation, and branching of crypts; numerous mitoses; absent goblet cells; crypt abscesses; open or vesiculate nuclei with basophilic cytoplasm; atrophy of surrounding villi
o Necrotic Enteritis (NE) progression of PIA coagulative necrosis of adenomatous epithelium with inflammation
o Regional Ileitis (RI) progression of NE thickened intestine “hosepipe gut”; may result in stricture
o Proliferative Hemorrhagic Enteropathy (PHE) occurs in pigs > 4 months old; this may be an acute manifestation of PIA Abundant fluid blood, intestinal clots and fibrin casts within lumen and no discernible points of hemorrhage; thickened edematous ileum with a cerebriform pattern; pale skin
Four hypotheses are postulated as the mechanism by which L. intracellularis induces the prominent epithelial hyperplasia
o Regulation of cell differentiation or apoptosis genes o Production of a mitogenic agent o Wound healing response to bacterially induced damage o Alteration of normal growth factor receptor-signalling mechanisms
Swine dysentery (Brachyspira hyodysenteriae)
• Acute to chronic disease, mainly of weaned pigs (7-16 weeks) • Bacteria invades intestinal crypts and disrupts colonic epithelium progressive erosion of superficial
epithelium excess mucus production edema and hemorrhage pseudomembrane production death from dehydration and bacterial toxemia ( toxins hemolysin and lipooligosaccharide)
• Lesions in the large intestine fibrinonecrotic pseudomembranous colitis with a granular, hyperemic mucosa in advanced cases mucus, fibrin and blood in the lumen in chronic cases
• Highly contagious disease in pigs < 10 days of age • Virus destroys villi loss of intestinal surface area malabsorption diarrhea • Vomiting and profuse yellow watery diarrhea, rapid weight loss • Disease in feeder pigs and sows
o Inapparent or mild fever, inappetance, diarrhea o Agalactia in affected sows
Intestinal parasitism
Isospora suis
• Disease in 5-15 day age group
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• Infection early in life replication of asexual and sexual stages in villus epithelium excess surface cell loss villus atrophy with erosion and exudation necrotic enteritis due to overgrowth by colonic anaerobes (severe cases)
Ascaris suum
• Usually found in the upper small intestine pathogenicity poorly defined • Larval migration induces lesions in the liver (“milk spots”) and the lungs
Oesophagostomum spp.
• Usually found in the large intestine mild, subclinical disease
Differential Diagnosis
• Diarrhea in young piglets o Transmissible gastroenteritis (TGE) o Isospora spp. o Rotavirus o Clostridium perfringens type C and C. difficile o Salmonella spp.
• For hemorrhagic enteritis in pigs o Clostridium perfringens type C o Swine dysentery (Brachyspira hyodysenteriae ) o Escherichia coli in post weanling pigs o Acute enteric salmonellosis o Lawsonia intracellularis (PHE)
Other Intestinal emphysema
• Gas-filled cystic spaces in the intestinal wall • Rare, incidental finding in healthy swine at slaughter • Pathogenesis unknown Clostridium perfringens and E. coli have been isolated from lesions, but not
consistently
Intestinal Diseases of Ruminants
Bacterial Enteritis Salmonellosis • Animals over 2-4 weeks of age • Manifests as enteropathic/invasive/septicemic S. typhimurium, S. dublin, S. muenster • Peracute minimal intestinal lesions with septicemia, or hemorrhagic/fibrinohemorrhagic enteritis • Chronic cases may have focal or extensive diphtheritic membranes or fibrin casts in small intestine and/or
colon, with enlarged mesenteric nodes, and signs of septicemia Clostridial enterotoxemias (Clostridium perfringens)
• Syndromes a) Hemorrhagic enteritis of neonates - up to 3 weeks of age - Types B,C,E b) Pulpy Kidney C. perfringens Type D • Lambs, goats, rarely calves on good feed - grass or feedlot • Sudden death with or without diarrhea - carcass in good condition
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• Toxin causes endothelial damage edema, may be clear pericardial fluid effusion; also may cause mild epithelial necrosis
• Rapid decomposition - hence "pulpy kidney" • Focal symmetrical encephalomalacia (FSE) necrosis of basal ganglia, thalamus and subcortical white
matter = causing nervous signs in lingering or surviving sheep Mycobacterium avium paratuberculosis (Johnes disease)
• Cattle over 2 years of age chronic diarrhea and wasting • Sheep, goats and deer also usually not as severe but can be a clinical problem, though with minimal
diarrhea • Signs associated with establishment of acid fast M. a. paratuberculosis in macrophages in the lamina
propria of the intestine, especially ileum, also cecum, colon • Accumulation of macrophages and giant cells can be extensive, and associated with subtotal villus atrophy
protein losing enteropathy "transmural regional enteritis" granulomatous reaction extending to the submucosa, lymphatics and regional lymph nodes.
• Wasted cachectic carcass, evidence of diarrhea; enlarged mesenteric lymph nodes (may be caseous necrosis in sheep & goats; may mineralize in goats); lymphangitis; thick transverse folds of mucosa in affected areas, especially ileum, possibly cecum and colon
• Acid fast bacilli in macrophages in sections or impressions of the mucosa or ileocecal mesenteric lymph node
Viral Enteritis
Bovine viral diarrhea
• Acute, highly contagious, worldwide disease of cattle that results in enteric and respiratory disease and associated reproductive loss
• Flaviviridae, genus Pestivirus • Can infect sheep, goats and pigs (+ rhinoceros, giraffe and eland)
o Two biotypes, cytopathic (CP) and noncytopathic (NCP) NCP strains are associated with acute bovine virus diarrhea, BVD-induced
thrombocytopenia, abortions, and teratogenic events CP strains produce mucosal disease
• BVD is immunosuppressive and predisposes animals to secondary infections • Bovine Virus Diarrhea
o Most BVDV infections in immunocompetent, nonpregnant cattle are subclinical o Clinical disease usually occurs in seronegative, immunocompetent cattle from 6-months to 2-years
old • Transplacental infections
o 50-100 days of gestation Fetal death, abortion, mummification o 100-150 days of gestation Congenital defects (microencephaly, cerebellar hypoplasia,
o If the calf survives a NCP infection prior to 125 days of gestation, it may develop immunotolerance and persistent infection (mucosal disease)
• Mucosal disease (MD) o In utero infection (prior to day 125) w/ noncytopathic strain immune tolerance and persistent
infection infection w/ cytopathic strain mucosal disease erosions and ulcerations of mouth, tongue, esophagus, oral and ruminal papillae, abomasum, cecum/colon, Peyer's patches swollen, necrohemorrhagic, +/- diphtheritic membranes; erosive-ulcerative interdigital dermatitis and coronitis
Malignant catarrhal fever
• Gamma herpesvirus in the genus rhadinovirus • Causes lymphoproliferation, vasculitis, and erosive to ulcerative mucosal lesions
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• Affects numerous species of cervids and bovids • Four forms
o Wildebeest-associated (WA-MCF): Alcelaphine herpesvirus-1; primarily in Africa, but also in zoos and wild animal parks
o Sheep-associated (SA-MCF): Ovine herpesvirus-2; worldwide; one of most serious diseases in farmed deer in New Zealand, Australia, and Britain
o White-tailed deer herpesvirus (MCF-WTD): Newly recognized form that is highly virulent in White-tailed deer; closely related to the above viruses; reservoir unknown
o Caprine herpesvirus-2 in association with naturally occurring malignant catarrhal fever in captive Sika deer
Blue tongue and epizootic hemorrhagic disease (EHD) • Bluetongue clinical in sheep, white-tailed deer, usually subclinical in cattle, but may cause clinical disease • EHD clinical in white-tailed deer, pronghorn antelope, mild disease in cattle can occur • Closely related orbiviruses clinically and pathologically inseparable • Viral damage to vascular endothelium DIC infarction of epithelia congestion and erosion of muzzle,
nasal, tongue and reticulorumenal mucosa leading to ulceration Winter dysentery • Diarrhea/dysentery of juvenile-adult cattle; occasionally fatal • Coronavirus infection of colonic surface and cryptal epithelium • Rarely presents for necropsy; if it does: fibrino-hemorrhagic/hemorrhagic colitis grossly • Major differential diagnoses: salmonellosis, coccidiosis, bovine adenovirus enteritis, BVD • Laboratory diagnosis: demonstration of viral antigen in colonic epithelium in association with crypt necrosis
Intestinal parasitism Strongyloides and Trichostrongylus spp.
• Burrow in the epithelium at the base of villi, inducing villus atrophy • Disease is associated with malabsorption, protein-losing enteropathy • Nematodirus and Cooperia coil around or between villi, do not burrow, and cause a generally less severe
villus atrophy than the above Coccidiosis
• Significant coccidia in goats and [sheep] E. arloingi [E. bakuensis], E. christenseni [E. ahsata], and E. • nina-kohl-yakimovae [E. ovinoidalis] • In cattle E. bovis and E. zuernii may be pathogenic • Significant disease may occur late during the prepatent period, before oocysts are passed, but coccidiosis
should not be a problem in lambs and kids under 3 weeks of age, and is rare in calves under several months of age
Differential Diagnosis
• Chronic diarrhea in adult cattle o M. paratuberculosis o Bovine viral diarrhea o Salmonellosis o Intestinal parasites (coccidiosis, gastrointestinal helminthiasis) o Malnutrition; neoplasia (lymphosarcoma; chronic reticulopericarditis)
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Intestinal Diseases of Horses
Bacterial Enteritis FOALS Rhodococcus equi • Foals to several months of age • Organism may enter the body via the respiratory tract or gut resides and multiplies in macrophages, but
stimulates a substantial accumulation of neutrophils pyogranulomatous inflammation abscesses • If the respiratory route is primary, severe anteroventral purulent bronchopneumonia with abscessation occurs • Exudate containing organisms is coughed up and swallowed and 2% intestinal lesions may develop (intestinal
lesions may be primary) • Gross lesions rarely small intestine, commonly cecum and color raised craterous ulcerated areas 1-3 cm in
diameter, often at sites of submucosal lymphoid follicles • Mesenteric lymph nodes may be massively involved and obliterated by large abscesses
Actinobacillus equuli
• Cause of septicemic "shigellosis" in young foals
Lawsonia intracellularis • Sporadically associated with adenomatosis, causing fatal protein-losing enteropathy charcterized by
hypoproteinemia, dependent edema, weight loss and sometimes diarrhea, in foals and young horses OLDER HORSES
• Primary small bowel disease in mature horses is rare, being limited to Lawsonia intracellularis infection in younger animals, mentioned above, occasional cases of granulomatous enteritis of usually unknown etiology, and to intestinal lymphosarcoma
• Disease manifests as protein-losing enteropathy/malabsorption with wasting and sometimes diarrhea Salmonellosis • S. typhimurium especially • Typhlocolitis any age horse • Complete spectrum from peracute septicemia to chronic enterocolitis, diarrhea and wasting • Peracute, acute severe typhilitis and colitis - edema of mesenteric attachments, dark blood-stained fluid
content, red edematous mucosa possibly with erosions overlain by fibrin • Subacute chronic fibrinous typhlitis and colitis • Chronic Salmonellosis should be considered in mature animals with chronic diarrhea and/or wasting Clostridial typhlocolitis (Colitis "X")
• Peracute to acute disease, usually profuse diarrhea without blood, though some die too quickly to scour • Sometimes antibiotic (Tetracycline, Lincomycin) associated • Mucosa of cecum and colon deeply congested, edematous, perhaps some fibrin; submucosa, serosa • Dehydration, lesions typical of endotoxemic shock in other organs • Etiology unclear/variable. Probably related to dysbacteriosis, with associated proliferation of toxigenic
Clostridium spp. (including probably C. perfringens and C. difficile)
NSAIDs-Associated "Enterocolitis" • Phenylbutazone, flunixin meglumine are associated with a syndrome of ulcerative glossitis/stomatitis,
gastric
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• Ulcerative enteritis, ulcerative colitis (right dorsal colitis), renal papillary necrosis. Probably ischemic, related to prostaglandin E inhibition
Potomac Fever "Equine monocytic ehrlichiosis"
• Neorickettsia (Ehrlichia) risticii • Oral ulceration, ulcerative gastritis, hyperemia/hemorrhage/ulceration in colon • Organism very difficult to demonstrate in tissue of dead animals microscopically; not cultured - PCR
diagnosis
Intestinal parasitism Anoplocephala perfoliata
• Small and large intestine (ileocecal orifice) rarely pathogenic - if so, ulcerative lesions in proximal cecum protein loss and wasting
• Associated with spasmodic colic, ileocecal intussusception, possibly ileal muscular hypertrophy Strongyloides westeri • Foals, rarely clinical; burrows in epithelium of villi, crypts in upper small intestine. May lead to villus atrophy,
malabsorption, plasma protein loss, diarrhea Parascaris equorum • Essentially nonpathogenic with exception of potential for obstruction in heavy infestations, especially after
anthelminthic therapy Large strongyles • Lesions associated with migration S. vulgaris especially (Haemomelasma ilei)
Small strongyles • Cyathostomins larval development in mucosa of cecum, colon, possibly associated with diarrhea, plasma
protein loss, especially when hypobiotic larvae emerge (Ostertagia-like, in spring). Adults probably essentially nonpathogenic
Coccidia (Eimeria leuckarti) • Develop in lamina propria of small bowel non-pathogenic
Trichomonas • Probably not pathogenic; merely opportunists reflecting markedly altered large bowel flora/fauna
Intestinal neoplasia • Relatively uncommon • Depression, anorexia, weight loss, swollen abdomen, abdominal mass, intestinal obstruction. Large or small
bowel diarrhea if widely infiltrative, with blood if colonic; obstruction if causes stricture or occupies lumen Benign • Leiomyomas (most common) • Benign mucosal polyps (rare)
Malignant Intestinal adenocarcinoma
• Duodenum, colon, rectum mainly small intestine (ileum especially) • May cause scirrhous serosal thickening, stenosis, obstruction and associated anterior dilatation, may
ulcerate, metastasize to mesenteric lymph nodes and liver
Polypoid tubulopapillary (or papillotubular) rectal adenomas and adenocarcinomas • Epithelial tumors that can arrange in acinar structures and papillary projections • More common in dogs • Several cm in diameter are relatively commonly encountered within a few centimeters cranial to the anal
margin
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Leiomyosarcoma • Malignant tumor with some areas of recognizable smooth muscle differentiation
Gastrointestinal stromal tumor • Malignant tumor presumed to originate from primitive mesenchymal cells capable of pluripotential
differentiation (smooth muscle, neural or dual) Lymphosarcoma References
