Pathology of the gi tract
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Pathology of the GI tract - PowerPoint PPT Presentation

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Pathology of the GI tract. Tim Morgan DVM, PhD. 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. Prehension. Fairly complex series of events

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Pathology of the gi tract l.jpg

Pathology of the GI tract

Tim Morgan DVM, PhD

Alimentary canal l.jpg
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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  • 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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  • Mouth

    • Grinding

    • Salivary enzymes – starches

  • Stomach

    • Mixing vat

    • Acidification (monogastrics)

    • Fermentation (ruminates)

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  • Small intestine

    • Pancreas

      • Enzymes

      • Buffer

    • Bile

      • Emulsifies lipids

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  • Carbohydrates

    • Polysaccharides

    • Enzymatically broken down to monosaccharides

      • Hydrolysis

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  • Proteins

    • Polypeptides

    • Enzymatically broken down to amino acids

      • Hydrolysis

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  • Fats

    • Triglycerides – 3 fatty acids on a glyceride backbone

    • Enzymatically broken down to monoglycerides and fatty acids

      • Hydrolysis

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Ingested fluid

1.5 liters

Secreted fluid

~7 liters

Total fluid

8-9 liters

Not having to pass 9 liters of fecal fluid a day


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  • 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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  • 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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  • Nutrients are composed of same materials as the GI tract

    • Enzymes/mechanisms that breakdown nutrients can also affect GI tract

  • Selective absorption

    • Nutrients kept in

    • Toxic compounds kept out

  • Most 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 mucosal epithelial 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

  • Innate immunity

    • Paneth cells

      • Antimicrobial peptides

      • Defensins

      • Cathelicidins

      • Toll-like receptors

    • Neutrophils

    • Macrophages

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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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  • Contradictory function

    • Absorb nutrients/exclude toxins

    • Digest nutrients, don’t digest self

    • React to pathogens, don’t 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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Oral Cavity

  • Developmental

  • Traumatic

  • Toxic

  • Inflammatory

    • Infectious

      • Viral, bacterial, fungal

    • Autoimmune

  • Neoplastic

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  • 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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  • Cleft lip/hare lip

  • Brachygnathia

    • Superior – shortened maxillae

    • Inferior – shortened mandibles

  • Prognathism

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  • Dentition

    • Heterotopic polydontia

      • Common in horses

    • Anomalous dentition

    • Missing or retained deciduous teeth

    • Odontodystrophy

      • Enamal hypoplasia

        • Secondary to distemper virus infection in dogs

      • Fluorine toxicity, malnutrition, vitamin A deficiency

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  • Fractures

  • Dislocations

  • Foreign bodies

    • Bones –dogs

    • Linear – cats

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  • Stomatitis – general term

    • Glossitis, gingivitis, pulpitis

  • Infectious diseases of the oral cavity

    • Viral

    • Bacterial

    • Fungal

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Viral Stomatitis: vesicular stomatitides

  • Vesicle = small circumscribed elevation of the epidermis/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 in US

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Oral Cavity – Vesicular Stomatitides

Ruptured vesicle, sheep, FMD

Ruptured vesicles, snout, pig, FMD

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Vesicular Stomatitides - VS

Ruptured vesicles, coronary band, horse, VS

Vesicle on teat of cow, VS

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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 or mucosal 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, develpmental anomalies (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 nasal discharge, ulcerative lesions throughout GI tract

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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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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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  • Papovavirus

    • Bovine papilloma virus

    • Canine papilloma virus

  • Papillomas (warts) on mucosa of mouth, esophagus, rumen (cattle)

  • Usually self-limiting lesions

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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, alveolar supporting bone

  • >85% of dogs and cats 4 years and older are affected

  • Pathogenesis

    • Placque formation

      • Mucin, slouphed epithelial cells, aerobic gram + bacteria

    • Mineral salts deposite on plaque

      • Tartar/calculus

    • Tartar  gingival irritation

      • pH change

        • Pathogenic gram – aerobic & anaerobic bacteria proliferate beneath gingiva

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Periodontal Disease

  • Destructive inflammation forms gingival crevice

  • Sub-gingival bacteria continue to proliferate

    • Deeper pockets of destruction

      • Gingival stroma

      • Periodontal ligament

      • Alveolar bone

  • Tooth loss, bacteremia, osteomyelitis, bacterial endocarditis

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Stages of Periodontal Disease

Stage I – gingivitis, gingival edema

Stage III – stroma loss, deep pockets

Stage II – gingivitis, 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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  • 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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  • 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 cell gingivitis

    • Histologic appearance

      • Gingival hyperplasia

      • Gingival ulceration

      • Large numbers of plasma cells

        • Russell bodies

      • Secondary suppurative inflammation over areas of ulceration

    • Increased serum gamma globulin

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Immune Mediated

  • Eosinophilic ulcer (Rodent ulcer, Eosinophilic granuloma complex)

    • Chronic superficial ulcerative 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 eosinophils with macrophages, lymphocytes, and plasma cells

      • Collagenolysis

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Uremic glossitis

  • Relatively common lesion associated 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 between blood ammonia levels and lesion development

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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 or localized

    • 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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  • 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 in brachycephalic breeds

      • May mechanically displace the teeth

    • Attached to the periosteum

    • Do not invade bone

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  • Fibromatous epulis

    • Histologic appearance

      • Interwoven bundles of fibroblastic tissue

      • More cellular than gingival hyperplasia

      • May have areas of bone production

        • “Ossifying epulis”

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  • Acanthomatous epulis (acanthomatous ameloblastoma)

    • Odontogenic epithelial origin

    • Rough, cauliflower-like lesion

    • Dental arcade of dogs

    • Locally invasive

      • Invades and destroys bone

      • Do NOT metastasize

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  • Acanthomatous epulis

    • Histologic appearance

      • Highly cellular

      • Interconnecting odontogenic epithelial sheets bordered by columnary to cuboidal cells

      • Contain numerous, usually empty, blood vessels

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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 regional lymph nodes

      • Rarely metastasize to lung

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Squamous cell carcimona

  • 2nd most common oral neoplasm in dogs

    • Usually involves tonsil

    • Small granular plaque  2-3x size of the tonsil

    • Nodular, firm, white, frequently ulcerated

    • Locally invasive

    • Metastasize to regional lymph nodes

    • Frequently met to distant sites, especially lung

      • SCC arising from the gingiva is less likely to met than tonsillar SCC in dogs

  • Horses & cattle

    • Rare, slow growing, very destructive, met to regional lymph nodes

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  • 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 and biologic behaviour

  • Met to lymph nodes, distant organs, especially lungs

  • Median survival time ~ 65 days in untreated animals

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  • Gross appearance

    • Nodular, variably pigmented masses

    • Anywhere in the oral mucosa

    • Invasive and destructive

    • May or may not be ulcerated

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  • Microscopic appearance

    • Variable

    • Heavily pigmented to amelanotic

    • Cytologically appear as round cells

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  • Can occur in all animals, but usually seen in 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 ½ of the mandible

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  • Gross appearance

    • Nodular to multi-nodulare

    • +/- ulceration

    • Firm

  • Local invasion

  • ~ 35% metastasize to lymph nodes

  • Early pulmonary metastasis

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  • Histologic appearance

    • Moderately cellular

      • Streams of fibroblastic cells

    • High mitotic rate

    • Collagenous extra-cellular matrix

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  • Bones of the skull or jaw

  • Similar in appearance to fibrosarcoma

  • Bone lysis and proliferation on radiographs

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Round cell tumors

  • Mast cell tumors

    • Discreet mass

  • Lymphosarcoma

    • Tonsillar

    • Epitheliotrophic

  • Plasma cell tumors

    • Discreet mass

    • Pleomorphic plasma cells

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Salivary Glands

  • Sialoadenitis = inflammation of salivary gland – uncommon in vet medicine

    • 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

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Diagnosis of Sialocoele

  • Aspirate mass with large bore 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 affected salivary gland

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Salivary gland

Chronic inflammation of mandibular salivary gland secondary to sialocoele in dog

Sialocoele wall composed of granulation tissue

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  • Tube

    • Smooth and striated muscle

    • Glands

    • Mucosal epithelium

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Esophagus: developmental anomalies

  • Developmental anomalies of the esophagus are rare

    • Segmental aplasia

    • Esophago-respiratory fistula

    • Esophageal diverticulae

    • Hyperkeratosis/squamous metaplasia

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Esophagus: traumatic lesions

  • Obstruction

    • “choke”

    • Occurs at areas of esophageal narrowing

      • Larynx

      • Thoracic inlet

      • Base of heart

      • Diaphragmatic hiatus

    • Clinical signs

      • Salivation, wretching, regurgitation, dehydration

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  • Complications of choke

    • Esophageal rupture  cellulitis, death

    • Esophageal dilation – mega-esophagus

    • Ulceration with subsequent stricture

      • Common in cattle

      • Hedge apples

    • Aspiration pneumonia

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  • Esophageal biopsy from horse with 2 month history of regurgitation

  • Mucosal ulceration

  • Marked submucosal inflammation

  • Disruption of submucosal glands

  • Outcome could be stricture or aspiration pneumonia

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  • Dilation of esophagus due to insufficient or uncoordinated peristalsis in the mid 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, OP’s

    • Parasites such as Toxoplasma gondii and Trypanosoma cruzi

    • Idiopathic

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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 embryonic right fourth aortic arch becomes adult aorta, esophageal constriction occurs (inset shows vascular malformation

      • Constricting ring formed by right aortic arch, pulmonary artery, and ductus arteriosus

      • Dilation of esophagus occurs cranial to heart

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  • 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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Dilated esophagus anterior to stomach

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Esophageal Parasitic Disease

  • Spirocerca Lupi of 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

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Aortic Nodules and Aneurysms

During the time that parasites are normally in the aorta, or if parasites are arrested in the aorta during migration, they may cause the formation of small nodules or larger, more diffuse granulomas and aneurysms which can rupture leading to fatal extravasation into the abdominal cavity.

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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 surveys show 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 of Spirocerca 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.

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Egg of Spirocerca lupi

Note the small size, thick wall and larvae. A whipworm egg is also present. Recovery of eggs is dependent on a patent opening to 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.

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Esophagus: Miscellaneous Conditions

  • Idiopathic muscular hypertrophy of distal esophagus

    • Seen in horses, no clinical significance

  • Esophagitis

    • Often result of trauma

    • Secondary bacterial infection

  • Esophageal erosions/ulcers

    • Reflux, trauma, viral disease

      • BVD MD in cattle

  • Papillomas

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Ruminant Forestomach

Normal Anatomy

Rumen papillae

Reticulum epithelial folds

Omasum epithelial folds

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Ruminant Forestomach

  • Bloat (ruminal tympany)- Overdistention of rumen and reticulum by gases produced during fermentation

    • Primary tympany (legume bloat, frothy bloat)

      • Following diet change, rumen pH decreases to 5-6, foam forms which blocks cardia and causes 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

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Ruminant Forestomach - Bloat

  • Post mortem diagnosis often based on observing bloat line which is a line of demarcation between the bloodless distal esophagus and the congested proximal esophagus at thoracic inlet

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Ruminant Forestomach – Foreign Bodies

  • Trichobezoars = hairballs

    • Hair forms nidus

  • Phytobezoars = plant balls

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Ruminant Forestomach – Foreign 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

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Rumenitis (Lactic Acidosis)

  • Common disease of cattle that consume excessive readily digestible carbohydrates, especially grain (grain overload)

  • Within 2-6 hours, microbial population of rumen changes to gram positive bacteria (Strep bovis) which results in production of lactic acid

  • 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 acidosis resulting in cardiovascular collapse (shock), renal failure and death

  • If survive, may develop bacterial or mycotic rumenitis in several days, 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)

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Miscellaneous Rumen Conditions

  • Ruminal parakeratosis – seen in cattle and sheep fed diets with less than 10% roughage

    • Papillae are enlarged, adhered together and firm

    • Affected papillae contain excessive layers of keratinized epithelial cells, bacteria and food material

    • May alter nutrient absorption, decrease feed efficiency

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Miscellaneous Rumen Conditions

  • Vagus Indigestion (chronic indigestion)

    • Seen in cattle and sheep

    • Gradual development of rumenoreticular and abdominal distention

    • 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 omasal canal, 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 coarse roughage with restricted access to water, especially in winter

      • Type IV – poorly characterized partial forestomach obstruction that usually occurs during gestation, may be due to enlarging uterus shifting abomasum to more cranial position

    • Dx – definitive may require exploratory left paralumbar fossa laparotomy and rumenotomy

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Stomach and Abomasum

  • Similar function and response to injury among ruminant abomasum and simple-stomached animals

Normal horse stomach

Histologic appearance

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Abomasal Disorders

  • Abomasal displacement (LDA, RDA)

  • Abomasal volvulus

  • Abomasal ulcers

  • Abomasal Impaction

  • Abomasal inflammation (abomasitis)

  • Bovine viral diarrhea and mucosal disease

  • Abomasal parasites

  • Lymphosarcoma

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Abomasal Displacements

  • Usually to left side in high producing dairy cattle within one month of parturition

    • Result of abomasal atony with gas distention and displacement upward along left abdominal wall

    • Fundus and greater curvature displaced creating partial obstruction

    • No interference with blood supply but passage of ingesta slowed leading to chronic partial anorexia

    • Also see metabolic alkalosis – related to sequestration of chloride in abomasum (HCL production continues)

    • RDA – occurs infrequently but atony, gas production and displacement occur as in LDA

      • Then have rotation (volvulus) of abomasum on its mesentery resulting 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

  • Many etiologic possibilities such as viral disease (BVD, rinderpest, MCF)

  • Nonviral – in dairy cows 6 weeks after parturition (stress, heavy grain feeding?)

  • Nonviral – feedlot cattle on high grain rations

  • Nonviral – hand fed dairy calves on milk replacer that start to eat roughage

  • Nonviral – suckling beef calves on good summer pasture

  • Fungal – secondary to rumen acidosis. Caused by infarcts due to fungal invasion and destruction of small arterioles

  • Ulcers most common along greater curvature

    • Type 1 = erosion/ulcer, no hem

    • Type II = hemorrhagic

    • Type III = perforation/local peritonitis

    • Type IV = perforation with acute diffuse peritonitis

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Seen in cattle and sheep fed poor quality, indigestible roughage during cold weather, can also be sand if on poor quality pasture with sandy soil

See abomasal atony and chronic dilation

Dehydration, anorexia, alkalosis, and progressive starvation

Abomasal emptying defect is an idiopathic condition in Suffolk sheep

Dietary Abomasal Impaction

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Abomasal Inflammation roughage during cold weather, can also be sand if on poor quality pasture with sandy soil

  • 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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BVD-MD roughage during cold weather, can also be sand if on poor quality pasture with sandy soil

  • Pestivirus that has cattle as primary host but most even-toed ungulates are susceptible

  • Two biotypes – noncytopathic and cytopathic (effect in cultured cells)

  • All age cattle are susceptible

  • Persistently infected cattle are natural reservoir – noncytopathic virus transmitted in utero, therefore infected at birth and infection lasts for life

  • Clinical disease and reproductive failure in cattle in contact with persistently infected cattle

  • Acute and chronic MD are highly fatal forms of BVD seen in persistently infected cattle that become infected with cytopathic biotype (from non-CPE mutation, other cattle or MLV vaccine)

  • Acutely, see erosions/ulcers throughout GI tract especially over Peyer’s patches, necrosis of lymphoid tissue, interdigital skin lesions

  • Chronically, see intermittent diarrhea and gradual wasting with lesions similar to acute but less severe

  • Dx = require diagnostic lab support – paired serum samples with 4 fold rise in titer, PCR, virus isolation (submit lymph node, spleen, gut lesions)

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Abomasal Parasites roughage during cold weather, can also be sand if on poor quality pasture with sandy soil

  • Haemonchus contortus – common parasite of sheep and other ruminants

  • Third stage larvae eaten on grass – enter gastric glands – onto surface as adults

  • Feed on blood – serious anemia and hypoproteinemia (seen as submandibular and mesenteric edema)

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Residual damage in abomasal mucosa caused by third stage larvae

There is focal destruction of deep glands and lymphocytic inflammation


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Ostertagiosis larvae

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

Abomasal Parasites

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Abomasal Lymphosarcoma larvae

  • Lymphosarcoma can be primary, metastatic or multicentric in origin

  • In cattle, often caused by bovine leukemia virus

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Horse Stomach larvae

  • Stomach capacity is only about 2.5 gallons

  • Located on left side of abdomen beneath rib cage

  • Junction of distal esophagus and cardia is one-way valve (in but not out)

    • therefore, horses cannot vomit gastric contents

  • Celiac artery supplies blood to stomach

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Stomach Colic Conditions larvae

  • Gastric dilatation

  • Gastric rupture

  • Gastric impaction

  • Gastric Ulcer Syndrome (adults/foals)

  • Gastric parasites

  • Gastric neoplasia

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Gastric Dilatation larvae

  • Caused by overeating fermentable foodstuff producing excessive gas or intestinal obstruction

    • Overeating leads to increase in volatile fatty acids which inhibit gastric emptying

  • Obstruction usually in small intestine and fluid accumulates in stomach

  • Right dorsal displacement of colon around cecum – obstructs duodenal outflow

  • Proximal enteritis-jejunitis leads to gastric fluid buildup

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Gastric Rupture larvae

  • Stomach rupture is fatal outcome of uncorrected gastric dilatation

  • Tear usually occurs along greater curvature

  • Most (approximately 2/3) occur secondary to mechanical obstruction, ileus or trauma

    • Remaining due to overload or idiopathic causes

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Gastric Impaction larvae

  • Uncommon cause of colic

  • May be associated with pelleted feeds, persimmon seeds, straw, barley, etc

  • Also associated may be poor dentition, lack or water, rapid eating

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Equine Gastric Ulcer Syndrome larvae

  • Currently recognized EGUS in adults >1 year of 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 <1 year of age, in order of decreasing frequency

    • Gastroduodenal ulcer disease (GDUD)

    • Primary erosion/ulceration of squamous mucosa

    • NSAID-induced ulcer disease (primary glandular ulcer disease as for adults)

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Normal Equine Stomach Fill larvae

  • Gastric fill and contents composition in horse allowed free access to forage

  • Fill line is not much above lower esophageal sphincter

  • Coarser contents layer at top and fine particulates filter to bottom

  • Upper, coarser mat is furthest away from acid secreting mucosa and more accessible to swallowed saliva – has higher pH than more liquid contents at bottom

  • Bottom contents adjacent to HCL-producing parietal cells

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Equine Gastric Ulcer Syndrome larvae

  • Erosion and/or ulceration of nonglandular (squamous) mucosa

  • Seen as a primary or secondary condition

  • Seen in adult horses under intensive training, any breed

  • Pathogenesis is poorly understood

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EGUS (proposed pathogenesis) larvae*

  • Exercise in horses causes pH change in proximal part of stomach

  • The more liquid, highly acidic contents in the lower glandular stomach are squeezed up around the more solid contents by increased intra-abdominal pressure (red arrows) due to tensing of abdominal muscles as part of the movement at faster gaits

*Merritt, AAEP, 2003

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Primary Glandular Ulcer Disease larvae

  • Ulceration of glandular mucosa, especially in pyloric region

  • Causes include NSAID toxicity (leads to down regulation of PGE2 production within glandular mucosa)

  • Changes in mucosal blood flow and Helicobacter infection have not been demonstrated

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Primary Glandular Ulcer Disease larvae

  • Multiple sites of glandular mucosal ulceration (yellow arrows) induced by NSAID toxicity

  • Squamous mucosa (upper right) is free of lesions

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Secondary Squamous Ulceration larvae

  • Primary lesion commonly occurs in duodenum (GDUD) of foals – never seen in horses >1 year old

  • In adults may see gastric outflow obstruction caused by duodenal stricture – reflux?

  • In adults may also see secondary to any condition causing glandular ulcerative gastritis (NSAID)

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Endoscopic view of normal pyloric sphincter region (yellow arrow, upper right) in its commonly open state- this allows for reflux of duodenal contents

Endoscopic view of severe inflammation around pyloric canal – yellow arrow indicates mucosal erosion – such lesions can scar and result in stricture that reduces gastric emptying

Secondary Squamous Ulceration

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Gastric Ulcer arrow, upper right) in its commonly open state- this allows for reflux of duodenal contents

  • Stomach from adult thoroughbred mare that was unthrifty and partially anorectic

  • There are erosions/ulcers in both the glandular and nonglandular portions of the mucosa

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Current Syndromes in Foals (< 1 yr of age) arrow, upper right) in its commonly open state- this allows for reflux of duodenal contents

  • Gastroduodenal ulcer disease (GDUD) - sucklings and early weanlings

  • Cause is unknown

  • In early stage of GDUD see roughened duodenal mucosa covered with fibrinous plaque – causes some disruption of gastric emptying with some secondary squamous erosion and ulceration

  • May recover after supportive Rx or develop advanced disease

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Clinical signs include drooling, teeth grinding, periodic bouts of colic especially after suckling, and weight loss

If signs persist for a week, may indicate stricture of duodenum by inflammation and mechanical obstruction to gastric emptying

Barium meal will be retained longer than 1 hour

Endoscopy will show erosion/ulceration of squamous mucosa of stomach and lower esophagus

Advanced GDUD in foals

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Advanced GDUD in Foals bouts of colic especially after suckling, and weight loss

Endoscopic views of reflux esophagitis and squamous gastritis that are commonly seen in foals with chronic GDUD. 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 distinct strictures of duodenum (arrows) which is a serious consequence of GDUD

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Primary Erosion/Ulceration of Squamous Mucosa in Foals bouts of colic especially after suckling, and weight loss

  • May cause unthriftiness and/or mild colic

  • Etiology and pathogenesis are unknown

  • Must always rule out partial obstruction of gastric outflow as after a previously unrecognized GDUD

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Stress-Related Gastric Ulcers in Foals bouts of colic especially after suckling, and weight loss

  • Primarily seen in foals suffering from a severe illness or trauma

  • May involve down-regulation of PGE2 due to reduced mucosal blood flow

  • Lesions usually confined to glandular mucosa just adjacent to margo plicatus – may be severe enough to perforate

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Gastric parasites bouts of colic especially after suckling, and weight loss

  • 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 on hairs 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 oral hooks, cause mild gastritis, pass out in feces in 8-10 months

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Horse Bots bouts of colic especially after suckling, and weight loss

Large numbers of larvae attached to gastric mucosa

Adult bot fly

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Gastric Parasites bouts of colic especially after suckling, and weight loss

  • 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 in manure

    • Larval forms develop inside the maggot, becoming infective third stage larvae at about time adult fly emerges from pupa

    • Larvae deposited on lips, nostrils and wounds of horses as flies feed – if licked and swallowed, larvae mature in stomach

    • If larvae in wounds not licked and swallowed, they stay in or around wound causing cutaneous habronemiasis

    • Infected flies can also be eaten by horse

    • In stomach, H. muscae and H. microstoma are on mucosal surface under 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

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Habronema bouts of colic especially after suckling, and weight loss

Posterior end of adult Habronema spp worm showing spicule

Cutaneous habronemiasis

Nodule in stomach caused by D. megastoma

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Stomach Conditions of Pigs bouts of colic especially after suckling, and weight loss

  • Gastric ulcers

  • Edema disease

  • Parasites

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Pig Gastric Ulcers bouts of colic especially after suckling, and weight loss

  • Seen in pigs of all ages but most common in confined growing pigs (45-90 kg)

  • Cause unknown but finely ground feed and stress are risk factors

  • Lesions occur at pars esophagea and begin as areas of hyperkeratosis, this erodes and later have ulcer.

  • Pigs can bleed out and produce tarry stool, or be chronically unthrifty

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Edema Disease bouts of colic especially after suckling, and weight loss

  • Acute to peracute toxemia caused by several serotypes of E. coli that are able to produce a verotoxin (related to Shigella) now called SLT-IIv (Shiga-like toxin type II variant)

  • Toxin affects capillaries and small arteries leading to edema and ischemia in many organs

  • Usually occurs in young pigs 1-2 weeks after weaning and affects healthiest animals in a group

  • We will talk more about this disease later

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Edema disease bouts of colic especially after suckling, and weight loss

Periocular edema

Submucosal edema in glandular region

Edema in stomach wall

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Stomach Parasites of Pigs bouts of colic especially after suckling, and weight loss

  • 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

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Stomach Neoplasia bouts of colic especially after suckling, and weight loss

  • Cattle – lymphosarcoma – anywhere in forestomach

    • Usually associated with BLV

    • Squamous cell carcinoma of rumen also seen rarely

  • Horse – squamous cell carcinoma of nonglandular region of stomach

  • Pig – tumors of stomach very rare