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Alimentary Canal
Continuous tube
Tube within a tube
Mouth (oral end)
Anus (aboral end)
Function
Acquire nutrients
Digest nutrients Absorb nutrients
Expel non-digestible portion
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Prehension
Fairly complex series of events
Hunger centers in the brain
Higher senses to locate food Lips especially in herbivores
Tongue
Teeth Esophagus
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Digestion
Mouth
Grinding
Salivary enzymes starches
Stomach
Mixing vat
Acidification (monogastrics)
Fermentation (ruminates)
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Digestion
Small intestine
Pancreas
Enzymes
Buffer
Bile
Emulsifies lipids
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Digestion
Carbohydrates
Polysaccharides
Enzymatically broken down to
monosaccharides
Hydrolysis
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Digestion
Proteins
Polypeptides
Enzymatically broken down to amino acids
Hydrolysis
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Digestion
Fats
Triglycerides 3 fatty acids on a glyceride
backbone
Enzymatically broken down to
monoglycerides and fatty acids
Hydrolysis
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Absorption
Ingested fluid
1.5 liters
Secreted fluid
~7 liters
Total fluid
8-9 liters
Not having to pass 9 liters of fecal fluid aday
Priceless
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Absorption
Mostly takes place in the small intestine
Dependant upon surface area
Mucosal folds 3x increase
Villi 10x increase
Microvilli (brush border) 20x increase
Total 600x increase in surface area
~ area of a tennis court
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Absorption
Carbs (monosaccharides)
Active transport
Proteins (amino acids)
Active transport
Fats (monoglycerides and fatty acids)
Micelles diffuse into cell membrane
Reconstituted to tryglycerides in SER Dumped into lacteals as chylomicrons
Travel thru lymphatics and are dumped into the caudal vena
cava
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Dilemma
Nutrients are composed of same materialsas the GI tract
Enzymes/mechanisms that breakdown
nutrients can also affect GI tract Selective absorption
Nutrients kept in
Toxic compounds kept outMost contaminated environment
Up to 10 12 organisms per gram
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Defense mechanisms
Washing
Saliva, mucous, fluid secretion
Flushes bacteria etc. away before they get a
chance to adhere
Keeps cells moist and happy
Prevents buildup of harmful materials
Buffers
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Defense mechanisms
Enzyme control
Secreted in an inactive form
Protein cleavage
pH
Cofactors
Fuse or pin
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Defense mechanisms
Cell turnover
Stratified squamous epithelial cells in upper GI
Mucosal epithelial cells in lower GI
Cells shed from villous tips Crypts form proliferative pool
Cells become more mature as they move up the villi
Average turnover time ~ 3 days
Damage rapidly repaired by sliding of mucosalepithelial cells
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Defense mechanisms
Nutrient sequestration
Fe sequestration
Fe required for bacterial growth
Fe binding proteins
Bacterial response: hemolytic toxins
Competition
Large numbers of normal intestinal flora/fauna Limits niches available for invading organisms
Initial colonization very difficult to unseat
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Defense mechanisms
Acquired immunity Separate (sort of) immune system
GALT
Secretory IgA
Resistant to degradation Blocks uptake of toxic compounds
Very tight control Always bacteria present
Pathogenicity may depend on number or organisms or other
specific circumstances/conditions Always protein antigens present
Under-responsive infection
Over-responsive chronic inflammation IBD, Crohns, ulcerative colitis, PLE, amyloidosis
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Summary
Contradictory function Absorb nutrients/exclude toxins
Digest nutrients, dont digest self
React to pathogens, dont react too much
Effective defense mechanims Constant washing
Rapid turnover
Competition Environmental monitoring
Environmental control
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Clinical Signs
Ptyalism (drooling)
Regurgitation undigested food
Vomiting partially digested food
Diarrhea
Tenesmus
Dehydration not specific for GI disease
Abdominal pain (colic)
Electrolyte abnormalities
Melena digested blood
Hematochezia bloody feces
Cholemesis/hematemesis
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Developmental
Cleft palate
(palatoschesis)
Failure of maxillary
bones to fuse Variably sized defect
in hard palate
May interfere with
nursing, feeding,chronic nasal
infections
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Developmental
Cleft lip/hare lip
Brachygnathia
Superior shortened
maxillae Inferior shortened
mandibles
Prognathism
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Developmental
Dentition
Heterotopic polydontia
Common in horses
Anomalous dentition
Missing or retaineddeciduous teeth
Odontodystrophy
Enamal hypoplasia
Secondary to distemper
virus infection in dogs
Fluorine toxicity,
malnutrition, vitamin A
deficiency
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Traumatic
Fractures
Dislocations
Foreign bodies
Bonesdogs
Linear cats
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Viral Stomatitis: vesicular
stomatitides
Vesicle = small circumscribed elevation of theepidermis/MM containing a serous liquid
Vesicular stomatitides cannot be differentiated
grossly call state or federal vet immediately Foot and mouth disease (Picornavirus) ruminants,
pigs not in US
Vesicular stomatitis (Rhabdovirus) ruminants, pigs,horses in US
Vesicular exanthema (Calicivirus) pigs not in US
Swine vesicular disease (Enterovirus) pigs not inUS
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Oral Cavity Vesicular
Stomatitides
Ruptured vesicle, sheep, FMD
Ruptured vesicles, snout, pig, FMD
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Foot & Mouth, bovine
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Viral Stomatitis: Erosive &
Ulcerative Stomatitides Erosion loss of superficial layers of epidermis
or mucosal membrane
Ulceration loss of all layers of epidermis ormucosal membrane Penetrates the basement membrane
Viral erosive & ulcerative stomatitides BVD-MD
Malignant Catarrhal Fever
Rinderpest Bluetongue
Equine Viral Rhinotracheitis
Felince Calicivirus
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BVD Mucosal Disease
Bovine viral diarrhea virus (BVDV)
Highly contageous
Rarely fatal Fever, diarrhea, mucosal ulcerations,
leukopenia
Multiple serotypes Cytopathic
Non-cytopathic
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BVD Mucosal Disease
Normal disease course
Immunocompetent animal
Subclinical or mild disease
Mucosal disease course Infection during 4th month of gestation
Abortion, fetal mummification, develpmentalanomalies (cerebellar hypoplasia)
Surviving animals Persistent infection
Immunotolerant to virus
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BVD Mucosal Disease
Persistently infected, immunotolerant
animal
Super-infected with a cytopathic strain
Unable to mount effective immune response
Severe ongoing infection
Near 100% fatality rate
Anorexia, bloody diarrhea, fever, mucoid nasaldischarge, ulcerative lesions throughout GI tract
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BVD Mucosal Disease
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Malignant Catarrhal Fever (MCF)
Caused by several different gamma
herpes viruses
Cattle, deer, most other ungulates
Ovine herpes virus 2
North America
Alcelaphine herpes virus 1
Endemic in African wildebeest
Causes disease in zoo ruminants and cattle in
Africa
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Malignant Catarrhal Fever (MCF)
Gross lesion is ulceration of mucosal
surfaces, edema, mucopurulent nasal
discharge, lymphadenopathy
Microscopic lesions
Lymphoid proliferation
Fibrinoid vascular necrosis
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Feline Calicivirus
RNA virus High rates of mutation
Variable virulence
Persistent infections
Minimal clinical signs Virus shed in saliva, nasal
secretions, feces
Clinical signs Ulcers on tongue and foot
pads Conjunctival edema,
edema of face & limbs
Pneumonia in kittens
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Viral Stomatitis: Papular
Stomatitides
Papule small, circumscribed, superficial, solid
elevation of skin or mucous membrane
Pustule visible collection of pus within or
beneath the epidermis or mucous membrane Macule discolored circular area on skin or
mucous membrane that is not elevated above
the surface. Smoking remains of a papule or
pustule
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Bovine Papular Stomatitis
Young cattle 1 month to 2 years old
Parapox virus
Epidermal proliferation
Papules, nodules, macules
Tongue, gingiva, palate, esophagus, rumen,
omasum
Eosinophilic intracytoplasmic inclusions
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Bovine Papular Stomatitis
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Contagious Ecthyma (Orf)
Sheep and lambs, goats, rarely man
Parapox virus
Epidermal proliferation Lips, mouth, teats
Weight loss/poor growth due to pain
Self limiting
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Contagious Ecthyma (Orf)
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Papillomatosis
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Papillomatosis
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Papillomatosis
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Bacterial Stomatitides
Associated with trauma
Feeding, iatragenic, foreign body
Opportunistic normal bacterial inhabitant
Actinobacillus, actinomyces, fusobacterium
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Necrotizing stomatitides
Oral necrobacillosis
Calf diphtheria
Necrotic membrane
Foul breath, anorexia,fever
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Wooden tongue
Actinobacillus
lignieresii
Often associated
w/lingual groove Chronic infection
Severe fibrosis
Wooden tongue
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Wooden tongue
Pyogranulomas
Club-shaped bacterial
colonies
Splendora-Hepli sulfur granules
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Periodontal Disease
Periodontal tissues Gingiva, cementum,
periodontal ligament, alveolarsupporting bone
>85% of dogs and cats 4 yearsand older are affected
Pathogenesis Placque formation
Mucin, slouphed epithelialcells, aerobic gram + bacteria
Mineral salts deposite onplaque
Tartar/calculus
Tartar gingival irritation pH change
Pathogenic gram aerobic& anaerobic bacteriaproliferate beneath gingiva
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Periodontal Disease
Destructive inflammation
forms gingival crevice
Sub-gingival bacteria
continue to proliferate
Deeper pockets ofdestruction
Gingival stroma
Periodontal ligament
Alveolar bone
Tooth loss, bacteremia,
osteomyelitis, bacterial
endocarditis
St f P i d t l Di
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Stages of Periodontal Disease
Stage I gingivitis, gingival edema
Stage II gingivitis, pockets
Stage III stroma loss, deep pockets
Stage IV bone loss, loose teeth
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Inflammatory, non-infectious
Inappropriate immune/inflammatory
response
Self antigen autoimmune
Unknown antigen immune mediated
Generally a problem of small animals
(Dogs and Cats)
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Auto-immune
Considered dermatologic diseases Frequently affect muco-cutaneous junctions
Pemphigus vulgaris Severe, acute or chronic vesicular/bullous disease of humans, dogs,
cats
Flaccid bullae & erosions of muco-cutaneous junctions, oral mucosa,
skin to lesser extent Clinical signs
Salivation, halitosis, mucosal erosion/ulceration
Severity varies greatly
Histology Basal cells remain attached to basement membrane
tomb stone appearance Destruction of acanthocytes (acantholysis)
Lichenoid infiltration of lymphocytes and plasma cells
Scattered neutrophils and eosinophils
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Auto-immune
Bullous pemphigoid
Grossly impossible to
tell from pemphigus
vulgaris
Histology
Subepidermal blister
formation
No acantholysis
Reported in humans,dogs, horses, possible
cases in cats
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Immune Mediated
Feline plasma cell
gingivitis
Raised, erythematous,
proliferative lesion
Glossopalatine arch
Periodontal gingiva
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Immune Mediated
Feline plasma cellgingivitis Histologic appearance
Gingival hyperplasia
Gingival ulceration Large numbers of
plasma cells
Russell bodies
Secondary suppurative
inflammation over areasof ulceration
Increased serumgamma globulin
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Immune Mediated
Eosinophilic ulcer
(Rodent ulcer,
Eosinophilic granuloma
complex)
Chronic superficialulcerative disease of
mucosa and
mucocutaneous junction
Frequently affects upper
lip of cats Siberian huskies
Affected area is thickened,
red, ulcerated
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Immune Mediated
Eosinophilic ulcer
Histologic appearance
Ulcerated surface
Moderate to large
numbers of eosinophilswith macrophages,
lymphocytes, and
plasma cells
Collagenolysis
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Uremic glossitis
Relatively common lesionassociated with renal
failure in dogs and less
commonly in cats
Clinical signs Cyanotic buccal mucosa
Fetid ulceration of tongue
Margins of ulcer swollen
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Uremic glossitis
Histologic appearance
Necrosis of mucosal
epithelium with ulceration
Vascular necrosis of small
arterioles of tongue Ischemic vascular lesion
Pathogenesis poorly
understood
Poor correlation betweenblood ammonia levels
and lesion development
Proliferative and neoplastic oral
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Proliferative and neoplastic oral
lesions
Gingival hyperplasia
Non-neoplastic
proliferation of gingival
tissue
Caused by chronic
inflammation
May be associated with
periodontal disease
Generalized orlocalized
Brachycephalic breeds
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Gingival hyperplasia
Histologic
appearance
Mature fibrous
connective tissue
Hypocellular
May have focal areas
of ulceration and
inflammation
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Epuloides
Fibromatous epulis Fibrous mass arising from
the periodontal ligament
Firm, hard, gray to pink
Similar in appearance to
focal gingival hyperplasia Between teeth or on hard
palate near teeth
Carnasal teeth inbrachycephalic breeds
May mechanicallydisplace the teeth
Attached to the periosteum
Do not invade bone
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Epuloides
Fibromatous epulis
Histologic appearance
Interwoven bundles of
fibroblastic tissue
More cellular thangingival hyperplasia
May have areas of
bone production
Ossifying epulis
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Other tumors of dental origin
Less common than epuli
Ameloblastoma
Dental lamina
Outer enamel epithelium
Odontogenic epithelium
May produce dentin or
enamel matrix
Rare in all species, but less
rare in cattle
Young cattle
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Other tumors of dental origin
Complex odontoma
Fully differentiated dental components
Disorganized, no tooth like structures
Young horses Compound odontoma
Mass containing numerous tooth-like structures
denticles
Young dogs, cattle, and horses Mandibular or maxillary arch
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Oral tumors of non-dental origin
Squamous cell carcinoma Most common oral
neoplasm is cats
Ventral surface of the
tongue, along the
frenulum
Nodular, red-grey mass
Friable
Often ulcerated
Locally invasive
Metastasize to regionallymph nodes
Rarely metastasize to lung
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Squamous cell carcimona
2nd most common oral neoplasmin dogs Usually involves tonsil
Small granular plaque 2-3x sizeof the tonsil
Nodular, firm, white, frequentlyulcerated
Locally invasive Metastasize to regional lymph
nodes
Frequently met to distant sites,especially lung
SCC arising from the gingiva isless likely to met than tonsillarSCC in dogs
Horses & cattle Rare, slow growing, very
destructive, met to regional lymphnodes
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Melanoma
Most common oral tumor in dogs Rare in cats and large animals
Almost always malignant Most have metastasized by the time of dx
More common in males than females More common in pigmented animals
No correlation between degree of pigmentation andbiologic behaviour
Met to lymph nodes, distant organs, especially lungs Median survival time ~ 65 days in untreated animals
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Melanoma
Gross appearance
Nodular, variably
pigmented masses
Anywhere in the oral
mucosa
Invasive and
destructive
May or may not be
ulcerated
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Melanoma
M l
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Melanoma
Microscopicappearance
Variable
Heavily pigmented toamelanotic
Cytologically appear
as round cells
M l
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Melanoma
Fib
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Fibrosarcoma
Can occur in all animals, but usually seenin dogs
3rd most common oral tumor of dogs
~ 25% occur in dogs < 5 yrs of age
Occur in gums around upper molars and in
the cranial of the mandible
Fib
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Fibrosarcoma
Gross appearance Nodular to multi-
nodulare
+/- ulceration
Firm
Local invasion
~ 35% metastasize tolymph nodes
Early pulmonarymetastasis
Fib
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Fibrosarcoma
Histologicappearance
Moderately cellular
Streams of fibroblastic
cells
High mitotic rate
Collagenous extra-
cellular matrix
O t
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Osteosarcoma
Bones of the skull orjaw
Similar in appearance
to fibrosarcoma Bone lysis and
proliferation on
radiographs
R d ll t
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Round cell tumors
Mast cell tumors Discreet mass
Lymphosarcoma
Tonsillar Epitheliotrophic
Plasma cell tumors
Discreet mass
Pleomorphic plasma
cells
S li Gl d
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Salivary Glands
Sialoadenitis = inflammation of salivary gland uncommon in vetmedicine Sialodacryoadenitis (SDA) coronavirus of lab rats
Rabies and canine distemper
Ranula = cystic distention of duct of sublingual or mandibular glands Occurs on floor of mouth alongside the tongue
Cause is unknown Salivary mucocoele (sialocoele) = pseudocyst filled with saliva that
causes inflammation with formation of granulation tissue Possible causes include trauma, foreign body or sialolith
Sialolith = stone in gland or duct Formed from sloughed gland epithelium that becomes surrounded by
mineral Tumors usually derived from glandular/duct epithelium (adenoma,
adenocarcinoma) May also see mesenchymal or mixed tumors including osteosarcoma
S li R l
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Salivary Ranula
Diagnosis of Sialocoele
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Diagnosis of Sialocoele
Aspirate mass with largebore needle Thick fluid that resembles
mucus
Macrophages filled with
vacuoles (ingested mucin)
May also see hematoidin
crystals (from RBC
degradation)
Rx = surgical drainage
and removal of affectedsalivary gland
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E h
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Esophagus
Tube Smooth and striated
muscle
Glands
Mucosal epithelium
Esophagus: developmental
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p g p
anomalies
Developmental anomalies of theesophagus are rare
Segmental aplasia
Esophago-respiratory fistula
Esophageal diverticulae
Hyperkeratosis/squamous metaplasia
Esophagus: traumatic lesions
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Esophagus: traumatic lesions
Obstruction choke
Occurs at areas ofesophageal narrowing
Larynx Thoracic inlet
Base of heart
Diaphragmatic hiatus
Clinical signs Salivation, wretching,
regurgitation,dehydration
Esophagus
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Esophagus
Complications ofchoke
Esophageal rupture
cellulitis, death
Esophageal dilation
mega-esophagus
Ulceration with
subsequent stricture
Common in cattle
Hedge apples
Aspiration pneumonia
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Esophagitis
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p g
Esophageal biopsy fromhorse with 2 month
history of regurgitation
Mucosal ulceration
Marked submucosalinflammation
Disruption of submucosal
glands
Outcome could bestricture or aspiration
pneumonia
Megaesophagus
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Megaesophagus
Dilation of esophagus due to insufficient or uncoordinated peristalsis in themid and cervical esophagus
Observed in humans, cattle, horses, cats, dogs and llamas
Primary clinical sign is regurgitation after ingestion of solid food
May be congenital with onset clinical signs at weaning Persistent right aortic arch (dilation cranial to heart)
Idiopathic denervation in several dog breeds and Siamese cats
May be acquired later in life secondary to: (dilation cranial to stomach) Myasthenia gravis (autoimmune disease against ach receptors at nm jxn)
Autoimmune myositis (inflammation of esophageal wall muscles)
Polyneuritis
Hypoadrenocorticism
Hypothyroidism
Polyradiculoneuropathy Toxins such as botulism, lead, OPs
Parasites such as Toxoplasma gondii and Trypanosoma cruzi
Idiopathic
Megaesophagus
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Persistent right aortic
arch Upper right normal
development of aortic arch
(inset shows normal
embryonic development of
great vessels)
Lower right when embryonicright fourth aortic arch
becomes adult aorta,
esophageal constriction
occurs (inset shows vascular
malformation
Constricting ring formed by rightaortic arch, pulmonary artery, and
ductus arteriosus
Dilation of esophagus occurscranial to heart
Megaesophagus
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Megaesophagus
Megaesophagus
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Megaesophagus
Diagnosis Survey and contrast radiography
Esophagoscopy
T3 and T4 before and after TSH stimulation (R/O
hypothyroidism) Cortisol concentrations with dexamethazone suppression (R/O
hypoadrenalcorticism)
Plasma cholinesterase levels (R/O OP tox)
Antiacetylcholine receptor antibody assay (R/O MG)
Toxoplasma titer
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Megaesophagus
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Esophageal Parasitic Disease
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Esophageal Parasitic Disease
Spirocerca Lupiof canids Nematodes reach esophageal submucosa after they migrate
through the wall of aorta
Form granulomas in wall of intrathoracic esophagus, and
granuloma opens to esophageal lumen allowing eggs to pass
out through feces
Associated clinical problems include dysphagia, aortic
aneurysms, spondylitis, HPO, and esophageal
fibrosarcoma/osteosarcoma
Intermediate host is dung beetle
Dx = thoracic radiography, fecal exam
Rx = ivermectin
Spirocerca lupi
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Spirocerca lupi
Aortic Nodules and Aneurysms
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During the time that parasites are normally in the aorta, or if
parasites are arrested in the aorta during migration, they maycause the formation of small nodules or larger, more diffuse
granulomas and aneurysms which can rupture leading to fatal
extravasation into the abdominal cavity.
y
Epidemiology
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The slide illustrates the general distribution of reported Spirocerca sarcoma in
the Southeast. Incidence of simple Spirocerca infection would follow a similar
distribution. Bailey at Auburn recorded an 8% infection rate in Alabama in a
survey between 1951 and 1963, but only 2% from 1963-1970. Georgia surveysshow less than 1% of the dogs infected. Bailey considered the feeding of
uncooked intestinal tracts of chickens to be a primary source of infection for
dogs . Incidence ofSpirocerca has decreased in recent years due to better care of
dogs, the shift to confinement poultry operations, and reduction of dung beetle
numbers by large scale use of agricultural insecticides.
Egg ofSpirocerca lupi
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Note the small size, thick wall and larvae. A whipworm egg is
also present. Recovery of eggs is dependent on a patent openingto the lumen of the digestive tract and therefore ova are not
consistently found. Spirocerca worms do not live more than a
few years and lesions do not always contain worms at necropsy.
Esophagus: Miscellaneous
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Conditions
Idiopathic muscularhypertrophy of distalesophagus
Seen in horses, no clinicalsignificance
Esophagitis
Often result of trauma
Secondary bacterial infection
Esophageal erosions/ulcers
Reflux, trauma, viral disease
BVD MD in cattle
Papillomas
Ruminant Forestomach
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Rumen papillae Reticulum
epithelial folds
Omasum epithelial
folds
Normal Anatomy
Ruminant Forestomach
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Bloat (ruminal tympany)- Overdistention of rumen and reticulum by gasesproduced during fermentation Primary tympany (legume bloat, frothy bloat)
Following diet change, rumen pH decreases to 5-6, foam forms which blocks cardia andcauses rumen to distend (seen clinically as distended left paralumbar fossa)
Secondary tympany Physical or functional obstruction/stenosis of esophagus leads to eructation failure and
gases accumulate in rumen Esophageal foreign body, vagal nerve dysfunction, lymphosarcoma, etc.
Foreign bodies Hair balls, plant balls
Hardware disease Lead poisoning
Rumenitis Lactic acidosis (Grain overload)
Bacterial secondary to acidosis or mechanical injury
Mycotic secondary to acidosis or antibiotic administration
Lesions due to infarcts caused by fungal vasculitis Primary fungi are Aspergillus, Mucor, Absidia, etc
Miscellaneous Parakeratosis
Vagus indigestion
Ruminant Forestomach - Bloat
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Ruminant Forestomach - Bloat
Post mortemdiagnosis often based
on observing bloat
line which is a line of
demarcation between
the bloodless distal
esophagus and the
congested proximalesophagus at thoracic
inlet
Ruminant Forestomach Foreign
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Bodies
Trichobezoars =hairballs
Hair forms nidus
Phytobezoars =plant balls
Ruminant Forestomach Foreign
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Bodies
Hardware disease Ingestion of baling
wire, nails perforates
through wall of
reticulum (reticulitis)and enters peritoneal
cavity (peritonitis) or
pericardial sac
(pericarditis)
Hardware disease fibrinous pericarditis
Rumenitis (Lactic Acidosis)
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Rumenitis (Lactic Acidosis)
Common disease of cattle that consume excessive readily digestiblecarbohydrates, especially grain (grain overload)
Within 2-6 hours, microbial population of rumen changes to grampositive bacteria (Strep bovis) which results in production of lacticacid
Rumen pH falls below 5 which destroys protozoa, lactate-using
organisms and rumen motility ceases Lactic acid causes chemical rumenitis.
Absorption of lactic acid into bloodstream causes lactic acidosisresulting in cardiovascular collapse (shock), renal failure and death
If survive, may develop bacterial or mycotic rumenitis in severaldays, or liver abscesses (necrobacillosis) or laminitis in several
weeks Dx = check pH of rumen fluid obtained by stomach tube, examine
rumen fluid with microscope ( no protozoa, few gram negative,mostly gram positive bacteria on gram stain)
Grain Overload
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Grain Overload
Reticulitis/Rumenitis
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Reticulitis/Rumenitis
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Mycotic Rumenitis
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Miscellaneous Rumen Conditions
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Ruminal parakeratosis seen in cattle andsheep fed diets with less than 10%roughage
Papillae are enlarged, adhered together andfirm
Affected papillae contain excessive layers ofkeratinized epithelial cells, bacteria and foodmaterial
May alter nutrient absorption, decrease feedefficiency
Miscellaneous Rumen Conditions
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Miscellaneous Rumen Conditions
Vagus Indigestion (chronic indigestion) Seen in cattle and sheep
Gradual development of rumenoreticular and abdominaldistention
Four types recognized based on site of functional obstruction Type I failure of eructation resulting in free-gas bloat, usually due
to inflammatory lesions that involve vagus nerve (hardware disease,pneumonia, etc)
Type II failure of transport from omasum to abomasum via omasalcanal, usually due to abscess in wall of reticulum near vagus(hardware disease), or lymphoma or papilloma blockage
Type III abomasal impaction due to feeding of dry coarseroughage with restricted access to water, especially in winter
Type IV poorly characterized partial forestomach obstruction thatusually occurs during gestation, may be due to enlarging uterusshifting abomasum to more cranial position
Dx definitive may require exploratory left paralumbar fossalaparotomy and rumenotomy
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Abomasal Disorders
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Abomasal Disorders
Abomasal displacement (LDA, RDA)Abomasal volvulus
Abomasal ulcers
Abomasal ImpactionAbomasal inflammation (abomasitis)
Bovine viral diarrhea and mucosal disease
Abomasal parasites Lymphosarcoma
Abomasal Displacements
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Abomasal Displacements
Usually to left side in high producing dairy cattle withinone month of parturition Result of abomasal atony with gas distention and displacement
upward along left abdominal wall
Fundus and greater curvature displaced creating partialobstruction
No interference with blood supply but passage of ingesta slowedleading to chronic partial anorexia
Also see metabolic alkalosis related to sequestration ofchloride in abomasum (HCL production continues)
RDA occurs infrequently but atony, gas production anddisplacement occur as in LDA
Then have rotation (volvulus) of abomasum on its mesenteryresulting in ischemia
Rotation is usually in counterclockwise when viewed from rear
Leads to complete anorexia, necrosis of abomasal wall, shock
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Abomasal Ulcers Seen in adult cattle and calves
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Many etiologic possibilities such asviral disease (BVD, rinderpest, MCF)
Nonviral in dairy cows 6 weeks after
parturition (stress, heavy grainfeeding?)
Nonviral feedlot cattle on high grainrations
Nonviral hand fed dairy calves onmilk replacer that start to eat roughage
Nonviral suckling beef calves ongood summer pasture
Fungal secondary to rumen acidosis.Caused by infarcts due to fungalinvasion and destruction of smallarterioles
Ulcers most common along greatercurvature Type 1 = erosion/ulcer, no hem
Type II = hemorrhagic Type III = perforation/local peritonitis
Type IV = perforation with acute diffuseperitonitis
Perforating Abomasal Ulcer
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e o at g bo asa U ce
Dietary Abomasal Impaction
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Seen in cattle and sheep
fed poor quality,indigestible roughageduring cold weather, canalso be sand if on poorquality pasture with sandy
soil See abomasal atony andchronic dilation
Dehydration, anorexia,alkalosis, and progressive
starvation Abomasal emptyingdefect is an idiopathiccondition in Suffolk sheep
Abomasal Inflammation
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Braxy in sheep and cattle Caused by Clostridium septicum
Hemorrhagic abomasitis with submucosal
emphysema Bacteria produces exotoxin that leads to
toxemia and shock
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Abomasal Parasites
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Haemonchus contor tus common parasite ofsheep and otherruminants
Third stage larvae eaten
on grass enter gastricglands onto surface asadults
Feed on blood serious
anemia andhypoproteinemia (seen assubmandibular andmesenteric edema)
Haemonchus
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Residual damage inabomasal mucosa
caused by third stage
larvae
There is focal
destruction of deep
glands and
lymphocyticinflammation
Abomasal Parasites
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Ostertagiosis Sheep and goats = O.
circumcincta
Cattle = O. ostertagia
Live as larval stages in
gastric glands giving
mucosa a rough and thick
appearance
Chronic inflammation,
mucous cell hyperplasia
and lymphoid nodules
Poor weight gain, diarrhea,
and hypoproteinemia
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Horse Stomach
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Stomach capacity is onlyabout 2.5 gallons
Located on left side ofabdomen beneath ribcage
Junction of distalesophagus and cardia isone-way valve (in but notout) therefore, horses cannot
vomit gastric contents
Celiac artery suppliesblood to stomach
Stomach Colic Conditions
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Gastric dilatationGastric rupture
Gastric impaction
Gastric Ulcer Syndrome (adults/foals)
Gastric parasites
Gastric neoplasia
Gastric Dilatation
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Caused by overeating fermentable foodstuffproducing excessive gas or intestinal obstruction Overeating leads to increase in volatile fatty acids
which inhibit gastric emptying
Obstruction usually in small intestine and fluidaccumulates in stomach
Right dorsal displacement of colon aroundcecum obstructs duodenal outflow
Proximal enteritis-jejunitis leads to gastric fluidbuildup
Gastric Rupture
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p
Stomach rupture is fatal outcome ofuncorrected gastric dilatation
Tear usually occurs along greater
curvatureMost (approximately 2/3) occur secondary
to mechanical obstruction, ileus or trauma
Remaining due to overload or idiopathiccauses
Gastric Impaction
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p
Uncommon cause of colicMay be associated with pelleted feeds,
persimmon seeds, straw, barley, etc
Also associated may be poor dentition,lack or water, rapid eating
Equine Gastric Ulcer Syndrome
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y
Currently recognized EGUS in adults >1 yearof age, in order of decreasing frequency Primary erosion/ulceration of nonglandular
(squamous) mucosa
Primary glandular ulcer disease
Secondary squamous ulceration Currently recognized syndromes in foals
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Gastric fill and contentscomposition in horse allowedfree access to forage
Fill line is not much abovelower esophageal sphincter
Coarser contents layer at topand fine particulates filter tobottom
Upper, coarser mat is furthestaway from acid secretingmucosa and more accessibleto swallowed saliva hashigher pH than more liquid
contents at bottom Bottom contents adjacent to
HCL-producing parietal cells
Normal Gastric Acid Secretion
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Equine Gastric Ulcer Syndrome
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Erosion and/or ulcerationof nonglandular
(squamous) mucosa
Seen as a primary or
secondary condition Seen in adult horses
under intensive training,
any breed
Pathogenesis is poorlyunderstood
EGUS (proposed pathogenesis)*
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Exercise in horsescauses pH change inproximal part of stomach
The more liquid, highlyacidic contents in thelower glandular stomachare squeezed up aroundthe more solid contentsby increased intra-abdominal pressure (redarrows) due to tensing of
abdominal muscles aspart of the movement atfaster gaits
*Merritt, AAEP, 2003
Primary Glandular Ulcer Disease
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Ulceration of glandularmucosa, especially inpyloric region
Causes include NSAIDtoxicity (leads to down
regulation of PGE2production withinglandular mucosa)
Changes in mucosalblood flow andHelicobacter infectionhave not beendemonstrated
Primary Glandular Ulcer Disease
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Multiple sites ofglandular mucosal
ulceration (yellow
arrows) induced by
NSAID toxicity
Squamous mucosa
(upper right) is free of
lesions
Secondary Squamous Ulceration
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Primary lesion commonlyoccurs in duodenum(GDUD) of foals neverseen in horses >1 yearold
In adults may see gastricoutflow obstructioncaused by duodenalstricture reflux?
In adults may also seesecondary to any
condition causingglandular ulcerativegastritis (NSAID)
Secondary Squamous Ulceration
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Endoscopic view ofnormal pyloric sphincterregion (yellow arrow,upper right) in itscommonly open state-this allows for reflux of
duodenal contents Endoscopic view of
severe inflammationaround pyloric canalyellow arrow indicates
mucosal erosion suchlesions can scar andresult in stricture thatreduces gastric emptying
Gastric Ulcer
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Stomach from adultthoroughbred mare
that was unthrifty and
partially anorectic
There are
erosions/ulcers in
both the glandular
and nonglandularportions of the
mucosa
Current Syndromes in Foals (< 1 yr
of age)
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of age)
Gastroduodenal ulcer disease(GDUD) - sucklings and earlyweanlings
Cause is unknown
In early stage of GDUD seeroughened duodenal mucosa
covered with fibrinous plaquecauses some disruption ofgastric emptying with somesecondary squamous erosionand ulceration
May recover after supportiveRx or develop advanceddisease
Advanced GDUD in foals
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Clinical signs include drooling,teeth grinding, periodic boutsof colic especially aftersuckling, and weight loss
If signs persist for a week, mayindicate stricture of duodenum
by inflammation andmechanical obstruction togastric emptying
Barium meal will be retainedlonger than 1 hour
Endoscopy will showerosion/ulceration ofsquamous mucosa of stomachand lower esophagus
Advanced GDUD in Foals
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Endoscopic views of reflux esophagitis
and squamous gastritis that are
commonly seen in foals with chronicGDUD. Lighter islands of tissue in
esophagus are remnants of normal
mucosa. Broken yellow line in stomach
is site of margo plicatus. Severe
ulceration has occurred
Post-mortem finding of 2 distinctstrictures of duodenum (arrows) which
is a serious consequence of GDUD
Primary Erosion/Ulceration of
Squamous Mucosa in Foals
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Squamous Mucosa in Foals
May cause unthriftiness and/or mild colic Etiology and pathogenesis are unknown
Must always rule out partial obstruction of
gastric outflow as after a previouslyunrecognized GDUD
Stress-Related Gastric Ulcers in
Foals
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Foals
Primarily seen in foalssuffering from a severeillness or trauma
May involve down-regulation of PGE2 due to
reduced mucosal bloodflow
Lesions usually confinedto glandular mucosa justadjacent to margoplicatus may be severeenough to perforate
Gastric parasites
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Gastrophilus spp (horse bots) Larvae of bot flies, adult flies are not parasitic and
cannot feed, lay eggs and die
Three species (G. intestinalis lays yellow eggs on
hairs of forelimbs; G. haemorrhoidalis black eggs onhairs of lips; G. nasalis white eggs on hairs of
submaxillary area)
Larvae of all three embed in mucosa of mouth before
passing to stomach, attach to stomach lining by oralhooks, cause mild gastritis, pass out in feces in 8-10
months
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Gastric Parasites
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Habronema (H. muscae, H. microstoma, Draschia megastoma H. microstoma and D. megastoma deposit larvae, but H. muscae lays
eggs containing larvae.
Larvae ingested by housefly or stablefly maggots which develop inmanure
Larval forms develop inside the maggot, becoming infective third stagelarvae at about time adult fly emerges from pupa
Larvae deposited on lips, nostrils and wounds of horses as flies feed iflicked and swallowed, larvae mature in stomach
If larvae in wounds not licked and swallowed, they stay in or aroundwound causing cutaneous habronemiasis
Infected flies can also be eaten by horse
In stomach, H. muscae and H. microstoma are on mucosal surfaceunder layer of mucus cause mild catarrhal gastritis
In stomach, D. megastoma causes granulomas up to 10 cm in diameter Filled with necrotic debris and worms
Covered by epithelium except for small opening for egg passage
Habronema
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Posterior end of
adult Habronema
spp worm
showing spicule
Cutaneous habronemiasis
Nodule in stomach caused by D.
megastoma
Stomach Conditions of Pigs
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Gastric ulcers
Edema disease
Parasites
Pig Gastric Ulcers
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Seen in pigs of all ages butmost common in confinedgrowing pigs (45-90 kg)
Cause unknown but finelyground feed and stress are riskfactors
Lesions occur at parsesophagea and begin as areasof hyperkeratosis, this erodesand later have ulcer.
Pigs can bleed out andproduce tarry stool, or bechronically unthrifty
Edema Disease
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Acute to peracute toxemia caused by severalserotypes of E. coli that are able to produce averotoxin (related to Shigella) now called SLT-IIv(Shiga-like toxin type II variant)
Toxin affects capillaries and small arteriesleading to edema and ischemia in many organs
Usually occurs in young pigs 1-2 weeks afterweaning and affects healthiest animals in a
group We will talk more about this disease later
Edema disease
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Submucosal edema in glandular region
Periocular edema
Edema in stomach wall
Stomach Parasites of Pigs
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Hyostrongylus rubidus(red stomach worm)
Direct life cycle
Seen in grazing pigs
Adults are on mucosal
surface in film of mucus
Larvae are in mucosa and
may cause severe
hypertrophic gastritis with
proliferation of gastric
glands
Stomach Neoplasia
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Cattle lymphosarcoma anywhere inforestomach Usually associated with
BLV
Squamous cell carcinomaof rumen also seen rarely
Horse squamous cellcarcinoma ofnonglandular region of
stomach Pig tumors of stomach
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