pathology of the gi tract

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Pathology of the Pathology of the GI tract GI tract Tim Morgan DVM, PhD Tim Morgan DVM, PhD

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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 - PowerPoint PPT Presentation

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Page 1: Pathology of the GI tract

Pathology of the GI tractPathology of the GI tract

Tim Morgan DVM, PhDTim Morgan DVM, PhD

Page 2: Pathology of the GI tract

Alimentary CanalAlimentary Canal

Continuous tubeContinuous tube ““Tube within a tube”Tube within a tube” Mouth (oral end)Mouth (oral end) Anus (aboral end)Anus (aboral end)

FunctionFunction Acquire nutrientsAcquire nutrients Digest nutrientsDigest nutrients Absorb nutrientsAbsorb nutrients Expel non-digestible portionExpel non-digestible portion

Page 3: Pathology of the GI tract

PrehensionPrehension

Fairly complex series of eventsFairly complex series of events Hunger centers in the brainHunger centers in the brain Higher senses to locate foodHigher senses to locate food Lips – especially in herbivoresLips – especially in herbivores TongueTongue TeethTeeth EsophagusEsophagus

Page 4: Pathology of the GI tract

DigestionDigestion

MouthMouth GrindingGrinding Salivary enzymes – starchesSalivary enzymes – starches

StomachStomach Mixing vatMixing vat Acidification (monogastrics)Acidification (monogastrics) Fermentation (ruminates)Fermentation (ruminates)

Page 5: Pathology of the GI tract

DigestionDigestion

Small intestineSmall intestine PancreasPancreas

• EnzymesEnzymes• BufferBuffer

BileBile• Emulsifies lipidsEmulsifies lipids

Page 6: Pathology of the GI tract

DigestionDigestion

CarbohydratesCarbohydrates PolysaccharidesPolysaccharides Enzymatically broken down to Enzymatically broken down to

monosaccharidesmonosaccharides• HydrolysisHydrolysis

Page 7: Pathology of the GI tract

DigestionDigestion

ProteinsProteins PolypeptidesPolypeptides Enzymatically broken down to amino acidsEnzymatically broken down to amino acids

• HydrolysisHydrolysis

Page 8: Pathology of the GI tract

DigestionDigestion

FatsFats Triglycerides – 3 fatty acids on a glyceride Triglycerides – 3 fatty acids on a glyceride

backbonebackbone Enzymatically broken down to monoglycerides Enzymatically broken down to monoglycerides

and fatty acidsand fatty acids• HydrolysisHydrolysis

Page 9: Pathology of the GI tract

AbsorptionAbsorption

Ingested fluidIngested fluid1.5 liters1.5 liters

Secreted fluidSecreted fluid~7 liters~7 liters

Total fluidTotal fluid8-9 liters8-9 liters

Not having to pass 9 liters of fecal fluid a Not having to pass 9 liters of fecal fluid a daydayPricelessPriceless

Page 10: Pathology of the GI tract

AbsorptionAbsorption

Mostly takes place in the small intestineMostly takes place in the small intestine Dependant upon surface areaDependant upon surface area

Mucosal folds Mucosal folds 3x increase 3x increase Villi Villi 10x increase 10x increase Microvilli (brush border) Microvilli (brush border) 20x increase 20x increase Total 600x increase in surface areaTotal 600x increase in surface area

• ~ area of a tennis court~ area of a tennis court

Page 11: Pathology of the GI tract

AbsorptionAbsorption

Carbs (monosaccharides)Carbs (monosaccharides) Active transportActive transport

Proteins (amino acids)Proteins (amino acids) Active transportActive transport

Fats (monoglycerides and fatty acids)Fats (monoglycerides and fatty acids) Micelles diffuse into cell membraneMicelles diffuse into cell membrane Reconstituted to tryglycerides in SERReconstituted to tryglycerides in SER Dumped into lacteals as chylomicronsDumped into lacteals as chylomicrons

• Travel thru lymphatics and are dumped into the caudal vena Travel thru lymphatics and are dumped into the caudal vena cavacava

Page 12: Pathology of the GI tract

DilemmaDilemma

Nutrients are composed of same materials Nutrients are composed of same materials as the GI tractas the GI tract Enzymes/mechanisms that breakdown Enzymes/mechanisms that breakdown

nutrients can also affect GI tractnutrients can also affect GI tract Selective absorptionSelective absorption

Nutrients kept inNutrients kept in Toxic compounds kept outToxic compounds kept out

Most contaminated environmentMost contaminated environment Up to 10 Up to 10 12 12 organisms per gramorganisms per gram

Page 13: Pathology of the GI tract

Defense mechanismsDefense mechanisms

WashingWashing Saliva, mucous, fluid secretionSaliva, mucous, fluid secretion

• Flushes bacteria etc. away before they get a Flushes bacteria etc. away before they get a chance to adherechance to adhere

• Keeps cells moist and happyKeeps cells moist and happy• Prevents buildup of harmful materialsPrevents buildup of harmful materials• BuffersBuffers

Page 14: Pathology of the GI tract

Defense mechanismsDefense mechanisms

Enzyme controlEnzyme control Secreted in an inactive formSecreted in an inactive form

• Protein cleavageProtein cleavage• pHpH• CofactorsCofactors

Fuse or pinFuse or pin

Page 15: Pathology of the GI tract

Defense mechanismsDefense mechanisms

Cell turnoverCell turnover Stratified squamous epithelial cells in upper GIStratified squamous epithelial cells in upper GI Mucosal epithelial cells in lower GIMucosal epithelial cells in lower GI

• Cells shed from villous tipsCells shed from villous tips• Crypts form proliferative poolCrypts form proliferative pool• Cells become more mature as they move up the villiCells become more mature as they move up the villi• Average turnover time ~ 3 daysAverage turnover time ~ 3 days

Damage rapidly repaired by sliding of mucosal Damage rapidly repaired by sliding of mucosal epithelial cellsepithelial cells

Page 16: Pathology of the GI tract

Defense mechanismsDefense mechanisms

Nutrient sequestrationNutrient sequestration Fe sequestrationFe sequestration

• Fe required for bacterial growthFe required for bacterial growth• Fe binding proteinsFe binding proteins• Bacterial response: hemolytic toxinsBacterial response: hemolytic toxins

CompetitionCompetition Large numbers of normal intestinal flora/faunaLarge numbers of normal intestinal flora/fauna

• Limits niches available for invading organismsLimits niches available for invading organisms• Initial colonization very difficult to “unseat”Initial colonization very difficult to “unseat”

Page 17: Pathology of the GI tract

Defense mechanismsDefense mechanisms

Innate immunityInnate immunity Paneth cellsPaneth cells

• Antimicrobial peptidesAntimicrobial peptides• DefensinsDefensins• CathelicidinsCathelicidins• Toll-like receptorsToll-like receptors

NeutrophilsNeutrophils MacrophagesMacrophages

Page 18: Pathology of the GI tract

Defense mechanismsDefense mechanisms Acquired immunityAcquired immunity

Separate (sort of) immune systemSeparate (sort of) immune system GALTGALT Secretory IgASecretory IgA

• Resistant to degradationResistant to degradation• Blocks uptake of toxic compoundsBlocks uptake of toxic compounds

Very tight controlVery tight control• Always bacteria presentAlways bacteria present

Pathogenicity may depend on number or organisms or other Pathogenicity may depend on number or organisms or other specific circumstances/conditionsspecific circumstances/conditions

• Always protein antigens presentAlways protein antigens present• Under-responsive Under-responsive infection infection• Over-responsive Over-responsive chronic inflammation chronic inflammation

IBD, Crohns, ulcerative colitis, PLE, amyloidosisIBD, Crohns, ulcerative colitis, PLE, amyloidosis

Page 19: Pathology of the GI tract

SummarySummary

Contradictory functionContradictory function Absorb nutrients/exclude toxinsAbsorb nutrients/exclude toxins Digest nutrients, don’t digest selfDigest nutrients, don’t digest self React to pathogens, don’t react too muchReact to pathogens, don’t react too much

Effective defense mechanimsEffective defense mechanims Constant washingConstant washing Rapid turnoverRapid turnover CompetitionCompetition Environmental monitoringEnvironmental monitoring Environmental controlEnvironmental control

Page 20: Pathology of the GI tract

Clinical SignsClinical Signs

Ptyalism (drooling)Ptyalism (drooling) Regurgitation – undigested foodRegurgitation – undigested food Vomiting – partially digested foodVomiting – partially digested food DiarrheaDiarrhea TenesmusTenesmus Dehydration – not specific for GI diseaseDehydration – not specific for GI disease Abdominal pain (colic)Abdominal pain (colic) Electrolyte abnormalitiesElectrolyte abnormalities Melena – digested bloodMelena – digested blood Hematochezia – bloody fecesHematochezia – bloody feces Cholemesis/hematemesisCholemesis/hematemesis

Page 21: Pathology of the GI tract

Oral CavityOral Cavity

DevelopmentalDevelopmental TraumaticTraumatic ToxicToxic InflammatoryInflammatory

InfectiousInfectious• Viral, bacterial, fungalViral, bacterial, fungal

AutoimmuneAutoimmune NeoplasticNeoplastic

Page 22: Pathology of the GI tract

DevelopmentalDevelopmental

Cleft palate Cleft palate (palatoschesis)(palatoschesis) Failure of maxillary Failure of maxillary

bones to fusebones to fuse Variably sized defect Variably sized defect

in hard palatein hard palate May interfere with May interfere with

nursing, feeding, nursing, feeding, chronic nasal chronic nasal infectionsinfections

Page 23: Pathology of the GI tract

DevelopmentalDevelopmental

Cleft lip/hare lipCleft lip/hare lip BrachygnathiaBrachygnathia

Superior – shortened Superior – shortened maxillaemaxillae

Inferior – shortened Inferior – shortened mandiblesmandibles

PrognathismPrognathism

Page 24: Pathology of the GI tract

DevelopmentalDevelopmental

DentitionDentition Heterotopic polydontiaHeterotopic polydontia

• Common in horsesCommon in horses Anomalous dentitionAnomalous dentition Missing or retained Missing or retained

deciduous teethdeciduous teeth OdontodystrophyOdontodystrophy

• Enamal hypoplasiaEnamal hypoplasia Secondary to distemper Secondary to distemper

virus infection in dogsvirus infection in dogs

• Fluorine toxicity, Fluorine toxicity, malnutrition, vitamin A malnutrition, vitamin A deficiencydeficiency

Page 25: Pathology of the GI tract

TraumaticTraumatic

FracturesFractures DislocationsDislocations Foreign bodiesForeign bodies

Bones –dogsBones –dogs Linear – catsLinear – cats

Page 26: Pathology of the GI tract

InflammatoryInflammatory

Stomatitis – general termStomatitis – general term Glossitis, gingivitis, pulpitisGlossitis, gingivitis, pulpitis

Infectious diseases of the oral cavityInfectious diseases of the oral cavity ViralViral BacterialBacterial FungalFungal

Page 27: Pathology of the GI tract

Viral Stomatitis: vesicular Viral Stomatitis: vesicular stomatitidesstomatitides

Vesicle = small circumscribed elevation of the Vesicle = small circumscribed elevation of the epidermis/MM containing a serous liquidepidermis/MM containing a serous liquid

Vesicular stomatitides – cannot be differentiated Vesicular stomatitides – cannot be differentiated grossly – call state or federal vet immediatelygrossly – call state or federal vet immediately Foot and mouth disease (Picornavirus) – ruminants, Foot and mouth disease (Picornavirus) – ruminants,

pigs – not in USpigs – not in US Vesicular stomatitis (Rhabdovirus) – ruminants, pigs, Vesicular stomatitis (Rhabdovirus) – ruminants, pigs,

horses – in UShorses – in US Vesicular exanthema (Calicivirus) – pigs – not in USVesicular exanthema (Calicivirus) – pigs – not in US Swine vesicular disease (Enterovirus) – pigs – not in Swine vesicular disease (Enterovirus) – pigs – not in

USUS

Page 28: Pathology of the GI tract

Oral Cavity – Vesicular Oral Cavity – Vesicular

StomatitidesStomatitides

Ruptured vesicle, sheep, FMD Ruptured vesicles, snout, pig, FMD

Page 29: Pathology of the GI tract

Foot & Mouth, bovineFoot & Mouth, bovine

Page 30: Pathology of the GI tract

Vesicular Stomatitides - VSVesicular Stomatitides - VS

Vesicle on teat of cow, VS Ruptured vesicles, coronary band, horse, VS

Page 31: Pathology of the GI tract

Viral Stomatitis: Erosive & Viral Stomatitis: Erosive & Ulcerative StomatitidesUlcerative Stomatitides

Erosion – loss of superficial layers of epidermis Erosion – loss of superficial layers of epidermis or mucosal membraneor mucosal membrane

Ulceration – loss of all layers of epidermis or Ulceration – loss of all layers of epidermis or mucosal membrane mucosal membrane Penetrates the basement membranePenetrates the basement membrane

Viral erosive & ulcerative stomatitidesViral erosive & ulcerative stomatitides BVD-MDBVD-MD Malignant Catarrhal Fever Malignant Catarrhal Fever RinderpestRinderpest BluetongueBluetongue Equine Viral RhinotracheitisEquine Viral Rhinotracheitis Felince CalicivirusFelince Calicivirus

Page 32: Pathology of the GI tract

BVD Mucosal DiseaseBVD Mucosal Disease

Bovine viral diarrhea virus (BVDV)Bovine viral diarrhea virus (BVDV) Highly contageousHighly contageous Rarely fatalRarely fatal Fever, diarrhea, mucosal ulcerations, Fever, diarrhea, mucosal ulcerations,

leukopenialeukopenia Multiple serotypesMultiple serotypes

• CytopathicCytopathic• Non-cytopathicNon-cytopathic

Page 33: Pathology of the GI tract

BVD Mucosal DiseaseBVD Mucosal Disease

““Normal” disease courseNormal” disease course Immunocompetent animalImmunocompetent animal Subclinical or mild diseaseSubclinical or mild disease

Mucosal disease courseMucosal disease course Infection during 4Infection during 4thth month of gestation month of gestation

• Abortion, fetal mummification, develpmental Abortion, fetal mummification, develpmental anomalies (cerebellar hypoplasia)anomalies (cerebellar hypoplasia)

• Surviving animalsSurviving animals Persistent infectionPersistent infection Immunotolerant to virusImmunotolerant to virus

Page 34: Pathology of the GI tract

BVD Mucosal DiseaseBVD Mucosal Disease

Persistently infected, immunotolerant Persistently infected, immunotolerant animalanimal ““Super-infected” with a cytopathic strainSuper-infected” with a cytopathic strain Unable to mount effective immune responseUnable to mount effective immune response Severe ongoing infectionSevere ongoing infection

• Near 100% fatality rateNear 100% fatality rate• Anorexia, bloody diarrhea, fever, mucoid nasal Anorexia, bloody diarrhea, fever, mucoid nasal

discharge, ulcerative lesions throughout GI tractdischarge, ulcerative lesions throughout GI tract

Page 35: Pathology of the GI tract

BVD Mucosal DiseaseBVD Mucosal Disease

Page 36: Pathology of the GI tract

Malignant Catarrhal Fever (MCF)Malignant Catarrhal Fever (MCF)

Caused by several different gamma Caused by several different gamma herpes virusesherpes viruses

Cattle, deer, most other ungulatesCattle, deer, most other ungulates Ovine herpes virus 2Ovine herpes virus 2

• North AmericaNorth America Alcelaphine herpes virus 1Alcelaphine herpes virus 1

• Endemic in African wildebeestEndemic in African wildebeest• Causes disease in zoo ruminants and cattle in Causes disease in zoo ruminants and cattle in

AfricaAfrica

Page 37: Pathology of the GI tract

Malignant Catarrhal Fever (MCF)Malignant Catarrhal Fever (MCF)

Gross lesion is ulceration of mucosal Gross lesion is ulceration of mucosal surfaces, edema, mucopurulent nasal surfaces, edema, mucopurulent nasal discharge, lymphadenopathydischarge, lymphadenopathy

Microscopic lesionsMicroscopic lesions Lymphoid proliferationLymphoid proliferation Fibrinoid vascular necrosisFibrinoid vascular necrosis

Page 38: Pathology of the GI tract

Malignant Catarrhal Fever (MCF)Malignant Catarrhal Fever (MCF)

Page 39: Pathology of the GI tract

Feline CalicivirusFeline Calicivirus

RNA virusRNA virus High rates of mutationHigh rates of mutation Variable virulenceVariable virulence

Persistent infectionsPersistent infections Minimal clinical signsMinimal clinical signs Virus shed in saliva, nasal Virus shed in saliva, nasal

secretions, fecessecretions, feces Clinical signsClinical signs

Ulcers on tongue and foot Ulcers on tongue and foot padspads

Conjunctival edema, Conjunctival edema, edema of face & limbsedema of face & limbs

Pneumonia in kittensPneumonia in kittens

Page 40: Pathology of the GI tract

Viral Stomatitis: Papular Viral Stomatitis: Papular StomatitidesStomatitides

Papule – small, circumscribed, superficial, solid Papule – small, circumscribed, superficial, solid elevation of skin or mucous membraneelevation of skin or mucous membrane

Pustule – visible collection of pus within or Pustule – visible collection of pus within or beneath the epidermis or mucous membranebeneath the epidermis or mucous membrane

Macule – discolored circular area on skin or Macule – discolored circular area on skin or mucous membrane that is not elevated above mucous membrane that is not elevated above the surface. “Smoking remains of a papule or the surface. “Smoking remains of a papule or pustule”pustule”

Page 41: Pathology of the GI tract

Bovine Papular StomatitisBovine Papular Stomatitis

Young cattle 1 month to 2 years oldYoung cattle 1 month to 2 years old Parapox virusParapox virus Epidermal proliferationEpidermal proliferation Papules, nodules, maculesPapules, nodules, macules

• Tongue, gingiva, palate, esophagus, rumen, Tongue, gingiva, palate, esophagus, rumen, omasumomasum

• Eosinophilic intracytoplasmic inclusionsEosinophilic intracytoplasmic inclusions

Page 42: Pathology of the GI tract

Bovine Papular StomatitisBovine Papular Stomatitis

Page 43: Pathology of the GI tract

Contagious Ecthyma (Orf)Contagious Ecthyma (Orf)

Sheep and lambs, goats, rarely manSheep and lambs, goats, rarely man Parapox virusParapox virus Epidermal proliferationEpidermal proliferation

Lips, mouth, teatsLips, mouth, teats Weight loss/poor growth due to painWeight loss/poor growth due to pain Self limitingSelf limiting

Page 44: Pathology of the GI tract

Contagious Ecthyma (Orf)Contagious Ecthyma (Orf)

Page 45: Pathology of the GI tract

PapillomatosisPapillomatosis

PapovavirusPapovavirus Bovine papilloma virusBovine papilloma virus Canine papilloma virusCanine papilloma virus

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

Usually self-limiting lesionsUsually self-limiting lesions

Page 46: Pathology of the GI tract

PapillomatosisPapillomatosis

Page 47: Pathology of the GI tract

PapillomatosisPapillomatosis

Page 48: Pathology of the GI tract

PapillomatosisPapillomatosis

Page 49: Pathology of the GI tract

Bacterial StomatitidesBacterial Stomatitides

Associated with traumaAssociated with trauma Feeding, iatragenic, foreign bodyFeeding, iatragenic, foreign body

Opportunistic normal bacterial inhabitantOpportunistic normal bacterial inhabitant Actinobacillus, actinomyces, fusobacteriumActinobacillus, actinomyces, fusobacterium

Page 50: Pathology of the GI tract

Necrotizing stomatitidesNecrotizing stomatitides

Oral necrobacillosisOral necrobacillosis Calf diphtheriaCalf diphtheria Necrotic membraneNecrotic membrane Foul breath, anorexia, Foul breath, anorexia,

feverfever

Page 51: Pathology of the GI tract

Wooden tongueWooden tongue

Actinobacillus Actinobacillus lignieresiilignieresii

Often associated Often associated w/lingual groovew/lingual groove

Chronic infectionChronic infection Severe fibrosisSevere fibrosis ““Wooden tongue”Wooden tongue”

Page 52: Pathology of the GI tract

Wooden tongueWooden tongue

PyogranulomasPyogranulomas Club-shaped bacterial Club-shaped bacterial

coloniescolonies ““Splendora-Hepli”Splendora-Hepli” ““sulfur granules”sulfur granules”

Page 53: Pathology of the GI tract

Periodontal DiseasePeriodontal Disease Periodontal tissuesPeriodontal tissues

Gingiva, cementum, Gingiva, cementum, periodontal ligament, alveolar periodontal ligament, alveolar supporting bonesupporting bone

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

PathogenesisPathogenesis Placque formationPlacque formation

• Mucin, slouphed epithelial Mucin, slouphed epithelial cells, aerobic gram + bacteriacells, aerobic gram + bacteria

Mineral salts deposite on Mineral salts deposite on plaqueplaque

• Tartar/calculusTartar/calculus Tartar Tartar gingival irritation gingival irritation

• pH changepH change Pathogenic gram – aerobic Pathogenic gram – aerobic

& anaerobic bacteria & anaerobic bacteria proliferate beneath gingivaproliferate beneath gingiva

Page 54: Pathology of the GI tract

Periodontal DiseasePeriodontal Disease

Destructive inflammation Destructive inflammation forms gingival creviceforms gingival crevice

Sub-gingival bacteria Sub-gingival bacteria continue to proliferatecontinue to proliferate

Deeper pockets of Deeper pockets of destructiondestruction

• Gingival stromaGingival stroma

• Periodontal ligamentPeriodontal ligament

• Alveolar boneAlveolar bone

Tooth loss, bacteremia, Tooth loss, bacteremia, osteomyelitis, bacterial osteomyelitis, bacterial endocarditisendocarditis

Page 55: Pathology of the GI tract

Stages of Periodontal DiseaseStages of Periodontal Disease

Stage I – gingivitis, gingival edema

Stage II – gingivitis, pockets

Stage III – stroma loss, deep pockets

Stage IV – bone loss, loose teeth

Page 56: Pathology of the GI tract

Inflammatory, non-infectiousInflammatory, non-infectious

Inappropriate immune/inflammatory Inappropriate immune/inflammatory responseresponse ““Self” antigen – autoimmuneSelf” antigen – autoimmune Unknown antigen – immune mediatedUnknown antigen – immune mediated

Generally a problem of small animals Generally a problem of small animals (Dogs and Cats)(Dogs and Cats)

Page 57: Pathology of the GI tract

Auto-immuneAuto-immune Considered dermatologic diseasesConsidered dermatologic diseases Frequently affect muco-cutaneous junctionsFrequently affect muco-cutaneous junctions Pemphigus vulgarisPemphigus vulgaris

Severe, acute or chronic vesicular/bullous disease of humans, dogs, Severe, acute or chronic vesicular/bullous disease of humans, dogs, catscats

Flaccid bullae & erosions of muco-cutaneous junctions, oral mucosa, Flaccid bullae & erosions of muco-cutaneous junctions, oral mucosa, skin to lesser extentskin to lesser extent

Clinical signsClinical signs• Salivation, halitosis, mucosal erosion/ulcerationSalivation, halitosis, mucosal erosion/ulceration• Severity varies greatlySeverity varies greatly

HistologyHistology• Basal cells remain attached to basement membraneBasal cells remain attached to basement membrane

““tomb stone” appearancetomb stone” appearance• Destruction of acanthocytes (acantholysis)Destruction of acanthocytes (acantholysis)• Lichenoid infiltration of lymphocytes and plasma cellsLichenoid infiltration of lymphocytes and plasma cells• Scattered neutrophils and eosinophilsScattered neutrophils and eosinophils

Page 58: Pathology of the GI tract

Auto-immuneAuto-immune

Bullous pemphigoidBullous pemphigoid Grossly impossible to Grossly impossible to

tell from pemphigus tell from pemphigus vulgarisvulgaris

HistologyHistology• Subepidermal blister Subepidermal blister

formationformation• No acantholysisNo acantholysis

Reported in humans, Reported in humans, dogs, horses, possible dogs, horses, possible cases in catscases in cats

Page 59: Pathology of the GI tract

Immune MediatedImmune Mediated

Feline plasma cell Feline plasma cell gingivitisgingivitis Raised, erythematous, Raised, erythematous,

proliferative lesionproliferative lesion Glossopalatine archGlossopalatine arch Periodontal gingivaPeriodontal gingiva

Page 60: Pathology of the GI tract

Immune MediatedImmune Mediated

Feline plasma cell Feline plasma cell gingivitisgingivitis Histologic appearanceHistologic appearance

• Gingival hyperplasiaGingival hyperplasia• Gingival ulcerationGingival ulceration• Large numbers of Large numbers of

plasma cellsplasma cells Russell bodiesRussell bodies

• Secondary suppurative Secondary suppurative inflammation over inflammation over areas of ulcerationareas of ulceration

Increased serum Increased serum gamma globulingamma globulin

Page 61: Pathology of the GI tract

Immune MediatedImmune Mediated

Eosinophilic ulcer Eosinophilic ulcer (Rodent ulcer, (Rodent ulcer, Eosinophilic granuloma Eosinophilic granuloma complex)complex)

Chronic superficial Chronic superficial ulcerative disease of ulcerative disease of mucosa and mucosa and mucocutaneous junctionmucocutaneous junction

• Frequently affects upper Frequently affects upper lip of catslip of cats

• Siberian huskiesSiberian huskies Affected area is thickened, Affected area is thickened,

red, ulceratedred, ulcerated

Page 62: Pathology of the GI tract

Immune MediatedImmune Mediated

Eosinophilic ulcerEosinophilic ulcer Histologic appearanceHistologic appearance

• Ulcerated surfaceUlcerated surface• Moderate to large Moderate to large

numbers of eosinophils numbers of eosinophils with macrophages, with macrophages, lymphocytes, and lymphocytes, and plasma cellsplasma cells

• CollagenolysisCollagenolysis

Page 63: Pathology of the GI tract
Page 64: Pathology of the GI tract

Uremic glossitisUremic glossitis

Relatively common lesion Relatively common lesion associated with renal associated with renal failure in dogs and less failure in dogs and less commonly in catscommonly in cats

Clinical signsClinical signs Cyanotic buccal mucosaCyanotic buccal mucosa Fetid ulceration of tongueFetid ulceration of tongue

• Margins of ulcer swollenMargins of ulcer swollen

Page 65: Pathology of the GI tract

Uremic glossitisUremic glossitis

Histologic appearanceHistologic appearance Necrosis of mucosal Necrosis of mucosal

epithelium with ulcerationepithelium with ulceration Vascular necrosis of small Vascular necrosis of small

arterioles of tonguearterioles of tongue

Ischemic vascular lesionIschemic vascular lesion Pathogenesis poorly Pathogenesis poorly

understoodunderstood Poor correlation between Poor correlation between

blood ammonia levels blood ammonia levels and lesion developmentand lesion development

Page 66: Pathology of the GI tract

Proliferative and neoplastic oral Proliferative and neoplastic oral lesionslesions

Gingival hyperplasiaGingival hyperplasia Non-neoplastic Non-neoplastic

proliferation of gingival proliferation of gingival tissuetissue

Caused by chronic Caused by chronic inflammationinflammation

• May be associated with May be associated with periodontal diseaseperiodontal disease

Generalized or Generalized or localizedlocalized

Brachycephalic breedsBrachycephalic breeds

Page 67: Pathology of the GI tract

Gingival hyperplasiaGingival hyperplasia

Histologic Histologic appearanceappearance Mature fibrous Mature fibrous

connective tissueconnective tissue HypocellularHypocellular May have focal areas May have focal areas

of ulceration and of ulceration and inflammationinflammation

Page 68: Pathology of the GI tract

EpuloidesEpuloides

Fibromatous epulisFibromatous epulis Fibrous mass arising from Fibrous mass arising from

the periodontal ligamentthe periodontal ligament Firm, hard, gray to pinkFirm, hard, gray to pink

• Similar in appearance to Similar in appearance to focal gingival hyperplasiafocal gingival hyperplasia

Between teeth or on hard Between teeth or on hard palate near teethpalate near teeth

• Carnasal teeth in Carnasal teeth in brachycephalic breedsbrachycephalic breeds

• May mechanically displace May mechanically displace the teeththe teeth

Attached to the periosteumAttached to the periosteum Do not invade boneDo not invade bone

Page 69: Pathology of the GI tract

EpuloidesEpuloides

Fibromatous epulisFibromatous epulis Histologic appearanceHistologic appearance

• Interwoven bundles of Interwoven bundles of fibroblastic tissuefibroblastic tissue

• More cellular than More cellular than gingival hyperplasiagingival hyperplasia

• May have areas of May have areas of bone productionbone production

““Ossifying epulis”Ossifying epulis”

Page 70: Pathology of the GI tract

EpuloidesEpuloides

Acanthomatous epulis Acanthomatous epulis (acanthomatous (acanthomatous ameloblastoma)ameloblastoma) Odontogenic epithelial Odontogenic epithelial

originorigin Rough, cauliflower-like Rough, cauliflower-like

lesionlesion Dental arcade of dogsDental arcade of dogs Locally invasiveLocally invasive

• Invades and destroys Invades and destroys bonebone

• Do NOT metastasizeDo NOT metastasize

Page 71: Pathology of the GI tract

EpuloidesEpuloides

Acanthomatous epulisAcanthomatous epulis Histologic appearanceHistologic appearance

• Highly cellularHighly cellular• Interconnecting Interconnecting

odontogenic epithelial odontogenic epithelial sheets bordered by sheets bordered by columnary to cuboidal columnary to cuboidal cellscells

• Contain numerous, Contain numerous, usually empty, blood usually empty, blood vesselsvessels

Page 72: Pathology of the GI tract

Other tumors of dental originOther tumors of dental origin

Less common than epuliLess common than epuli AmeloblastomaAmeloblastoma

Dental laminaDental lamina Outer enamel epitheliumOuter enamel epithelium Odontogenic epitheliumOdontogenic epithelium May produce dentin or May produce dentin or

enamel matrixenamel matrix Rare in all species, but less Rare in all species, but less

rare in cattlerare in cattle• Young cattleYoung cattle

Page 73: Pathology of the GI tract

Other tumors of dental originOther tumors of dental origin

Complex odontomaComplex odontoma Fully differentiated dental componentsFully differentiated dental components Disorganized, no tooth like structuresDisorganized, no tooth like structures Young horsesYoung horses

Compound odontomaCompound odontoma Mass containing numerous tooth-like structuresMass containing numerous tooth-like structures

• ““denticles”denticles” Young dogs, cattle, and horsesYoung dogs, cattle, and horses Mandibular or maxillary archMandibular or maxillary arch

Page 74: Pathology of the GI tract

Oral tumors of non-dental originOral tumors of non-dental origin

Squamous cell carcinomaSquamous cell carcinoma Most common oral Most common oral

neoplasm is catsneoplasm is cats• Ventral surface of the Ventral surface of the

tongue, along the frenulumtongue, along the frenulum

• Nodular, red-grey massNodular, red-grey mass FriableFriable Often ulceratedOften ulcerated

• Locally invasiveLocally invasive

• Metastasize to regional Metastasize to regional lymph nodeslymph nodes

• Rarely metastasize to lungRarely metastasize to lung

Page 75: Pathology of the GI tract

Squamous cell carcimonaSquamous cell carcimona 22ndnd most common oral neoplasm in most common oral neoplasm in

dogsdogs Usually involves tonsilUsually involves tonsil Small granular plaque Small granular plaque 2-3x size 2-3x size

of the tonsilof the tonsil Nodular, firm, white, frequently Nodular, firm, white, frequently

ulceratedulcerated Locally invasiveLocally invasive Metastasize to regional lymph Metastasize to regional lymph

nodesnodes Frequently met to distant sites, Frequently met to distant sites,

especially lungespecially lung• SCC arising from the gingiva is SCC arising from the gingiva is

less likely to met than tonsillar less likely to met than tonsillar SCC in dogsSCC in dogs

Horses & cattleHorses & cattle Rare, slow growing, very Rare, slow growing, very

destructive, met to regional lymph destructive, met to regional lymph nodesnodes

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MelanomaMelanoma

Most common oral tumor in dogsMost common oral tumor in dogs Rare in cats and large animalsRare in cats and large animals

Almost always malignantAlmost always malignant Most have metastasized by the time of dxMost have metastasized by the time of dx

More common in males than femalesMore common in males than females More common in pigmented animalsMore common in pigmented animals No correlation between degree of pigmentation and No correlation between degree of pigmentation and

biologic behaviourbiologic behaviour Met to lymph nodes, distant organs, especially lungsMet to lymph nodes, distant organs, especially lungs Median survival time ~ 65 days in untreated animalsMedian survival time ~ 65 days in untreated animals

Page 77: Pathology of the GI tract

MelanomaMelanoma

Gross appearanceGross appearance Nodular, variably Nodular, variably

pigmented massespigmented masses Anywhere in the oral Anywhere in the oral

mucosamucosa Invasive and Invasive and

destructivedestructive May or may not be May or may not be

ulceratedulcerated

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MelanomaMelanoma

Page 79: Pathology of the GI tract

MelanomaMelanoma

Microscopic Microscopic appearanceappearance VariableVariable Heavily pigmented to Heavily pigmented to

amelanoticamelanotic Cytologically appear Cytologically appear

as round cellsas round cells

Page 80: Pathology of the GI tract

MelanomaMelanoma

Page 81: Pathology of the GI tract

FibrosarcomaFibrosarcoma

Can occur in all animals, but usually seen Can occur in all animals, but usually seen in dogsin dogs 33rdrd most common oral tumor of dogs most common oral tumor of dogs ~ 25% occur in dogs < 5 yrs of age~ 25% occur in dogs < 5 yrs of age Occur in gums around upper molars and in Occur in gums around upper molars and in

the cranial ½ of the mandiblethe cranial ½ of the mandible

Page 82: Pathology of the GI tract

FibrosarcomaFibrosarcoma

Gross appearanceGross appearance Nodular to multi-Nodular to multi-

nodularenodulare +/- ulceration+/- ulceration Firm Firm

Local invasionLocal invasion ~ 35% metastasize to ~ 35% metastasize to

lymph nodeslymph nodes Early pulmonary Early pulmonary

metastasismetastasis

Page 83: Pathology of the GI tract

FibrosarcomaFibrosarcoma

Histologic Histologic appearanceappearance Moderately cellularModerately cellular

• Streams of fibroblastic Streams of fibroblastic cellscells

High mitotic rateHigh mitotic rate Collagenous extra-Collagenous extra-

cellular matrixcellular matrix

Page 84: Pathology of the GI tract

OsteosarcomaOsteosarcoma

Bones of the skull or Bones of the skull or jawjaw

Similar in appearance Similar in appearance to fibrosarcomato fibrosarcoma

Bone lysis and Bone lysis and proliferation on proliferation on radiographsradiographs

Page 85: Pathology of the GI tract

Round cell tumorsRound cell tumors

Mast cell tumorsMast cell tumors Discreet massDiscreet mass

LymphosarcomaLymphosarcoma TonsillarTonsillar EpitheliotrophicEpitheliotrophic

Plasma cell tumorsPlasma cell tumors Discreet massDiscreet mass Pleomorphic plasma Pleomorphic plasma

cellscells

Page 86: Pathology of the GI tract

Salivary GlandsSalivary Glands SialoadenitisSialoadenitis = inflammation of salivary gland – uncommon in vet = inflammation of salivary gland – uncommon in vet

medicinemedicine Sialodacryoadenitis (SDA) coronavirus of lab ratsSialodacryoadenitis (SDA) coronavirus of lab rats Rabies and canine distemperRabies and canine distemper

RanulaRanula = cystic distention of duct of sublingual or mandibular = cystic distention of duct of sublingual or mandibular glandsglands

Occurs on floor of mouth alongside the tongueOccurs on floor of mouth alongside the tongue Cause is unknownCause is unknown

Salivary mucocoeleSalivary mucocoele (sialocoele) = pseudocyst filled with saliva that (sialocoele) = pseudocyst filled with saliva that causes inflammation with formation of granulation tissuecauses inflammation with formation of granulation tissue

Possible causes include trauma, foreign body or sialolithPossible causes include trauma, foreign body or sialolith Sialolith Sialolith = stone in gland or duct= stone in gland or duct

Formed from sloughed gland epithelium that becomes surrounded by Formed from sloughed gland epithelium that becomes surrounded by mineralmineral

TumorsTumors usually derived from glandular/duct epithelium (adenoma, usually derived from glandular/duct epithelium (adenoma, adenocarcinoma)adenocarcinoma)

May also see mesenchymal or mixed tumors including osteosarcomaMay also see mesenchymal or mixed tumors including osteosarcoma

Page 87: Pathology of the GI tract

Salivary RanulaSalivary Ranula

Page 88: Pathology of the GI tract

Diagnosis of SialocoeleDiagnosis of Sialocoele

Aspirate mass with large Aspirate mass with large bore needlebore needle

Thick fluid that resembles Thick fluid that resembles mucusmucus

Macrophages filled with Macrophages filled with vacuoles (ingested mucin)vacuoles (ingested mucin)

May also see hematoidin May also see hematoidin crystals (from RBC crystals (from RBC degradation)degradation)

Rx = surgical drainage Rx = surgical drainage and removal of affected and removal of affected salivary glandsalivary gland

Page 89: Pathology of the GI tract

Salivary glandSalivary gland

Chronic inflammation of mandibular salivary gland secondary to sialocoele in dog

Sialocoele wall composed of granulation tissue

Page 90: Pathology of the GI tract

EsophagusEsophagus

TubeTube Smooth and striated Smooth and striated

musclemuscle GlandsGlands Mucosal epitheliumMucosal epithelium

Page 91: Pathology of the GI tract

Esophagus: developmental Esophagus: developmental anomaliesanomalies

Developmental anomalies of the Developmental anomalies of the esophagus are rareesophagus are rare Segmental aplasiaSegmental aplasia Esophago-respiratory fistulaEsophago-respiratory fistula Esophageal diverticulaeEsophageal diverticulae Hyperkeratosis/squamous metaplasiaHyperkeratosis/squamous metaplasia

Page 92: Pathology of the GI tract

Esophagus: traumatic lesionsEsophagus: traumatic lesions

ObstructionObstruction ““choke”choke” Occurs at areas of Occurs at areas of

esophageal narrowingesophageal narrowing• LarynxLarynx• Thoracic inletThoracic inlet• Base of heartBase of heart• Diaphragmatic hiatusDiaphragmatic hiatus

Clinical signsClinical signs• Salivation, wretching, Salivation, wretching,

regurgitation, regurgitation, dehydrationdehydration

Page 93: Pathology of the GI tract

EsophagusEsophagus

Complications of Complications of chokechoke Esophageal rupture Esophageal rupture

cellulitis, deathcellulitis, death Esophageal dilation – Esophageal dilation –

mega-esophagusmega-esophagus Ulceration with Ulceration with

subsequent stricturesubsequent stricture• Common in cattleCommon in cattle• Hedge applesHedge apples

Aspiration pneumoniaAspiration pneumonia

Page 94: Pathology of the GI tract

EsophagusEsophagus

Page 95: Pathology of the GI tract

EsophagitisEsophagitis

Esophageal biopsy from Esophageal biopsy from horse with 2 month horse with 2 month history of regurgitationhistory of regurgitation

Mucosal ulcerationMucosal ulceration Marked submucosal Marked submucosal

inflammationinflammation Disruption of submucosal Disruption of submucosal

glandsglands Outcome could be Outcome could be

stricture or aspiration stricture or aspiration pneumonia pneumonia

Page 96: Pathology of the GI tract

MegaesophagusMegaesophagus Dilation of esophagus due to insufficient or uncoordinated peristalsis in the Dilation of esophagus due to insufficient or uncoordinated peristalsis in the

mid and cervical esophagusmid and cervical esophagus Observed in humans, cattle, horses, cats, dogs and llamasObserved in humans, cattle, horses, cats, dogs and llamas Primary clinical sign is regurgitation after ingestion of solid foodPrimary clinical sign is regurgitation after ingestion of solid food May be congenital with onset clinical signs at weaningMay be congenital with onset clinical signs at weaning

Persistent right aortic arch (dilation cranial to heart) Persistent right aortic arch (dilation cranial to heart) Idiopathic denervation in several dog breeds and Siamese catsIdiopathic denervation in several dog breeds and Siamese cats

May be acquired later in life secondary to: (dilation cranial to stomach)May be acquired later in life secondary to: (dilation cranial to stomach) Myasthenia gravis (autoimmune disease against ach receptors at nm jxn)Myasthenia gravis (autoimmune disease against ach receptors at nm jxn) Autoimmune myositis (inflammation of esophageal wall muscles)Autoimmune myositis (inflammation of esophageal wall muscles) PolyneuritisPolyneuritis HypoadrenocorticismHypoadrenocorticism HypothyroidismHypothyroidism PolyradiculoneuropathyPolyradiculoneuropathy Toxins such as botulism, lead, OP’sToxins such as botulism, lead, OP’s Parasites such as Toxoplasma gondii and Trypanosoma cruziParasites such as Toxoplasma gondii and Trypanosoma cruzi Idiopathic Idiopathic

Page 97: Pathology of the GI tract

MegaesophagusMegaesophagus Persistent right aortic Persistent right aortic

archarch Upper right – normal Upper right – normal

development of aortic arch development of aortic arch (inset shows normal (inset shows normal embryonic development of embryonic development of great vessels)great vessels)

Lower right – when embryonic Lower right – when embryonic right fourth aortic arch right fourth aortic arch becomes adult aorta, becomes adult aorta, esophageal constriction esophageal constriction occurs (inset shows vascular occurs (inset shows vascular malformationmalformation

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

• Dilation of esophagus occurs Dilation of esophagus occurs cranial to heartcranial to heart

Page 98: Pathology of the GI tract

MegaesophagusMegaesophagus

Page 99: Pathology of the GI tract

MegaesophagusMegaesophagus

DiagnosisDiagnosis Survey and contrast radiographySurvey and contrast radiography EsophagoscopyEsophagoscopy T3 and T4 before and after TSH stimulation (R/O T3 and T4 before and after TSH stimulation (R/O

hypothyroidism) hypothyroidism) Cortisol concentrations with dexamethazone suppression (R/O Cortisol concentrations with dexamethazone suppression (R/O

hypoadrenalcorticism)hypoadrenalcorticism) Plasma cholinesterase levels (R/O OP tox)Plasma cholinesterase levels (R/O OP tox) Antiacetylcholine receptor antibody assay (R/O MG)Antiacetylcholine receptor antibody assay (R/O MG) Toxoplasma titerToxoplasma titer

Page 100: Pathology of the GI tract

MegaesophagusMegaesophagus

Dilated esophagus anterior to stomach

Page 101: Pathology of the GI tract

MegaesophagusMegaesophagus

Page 102: Pathology of the GI tract

Esophageal Parasitic DiseaseEsophageal Parasitic Disease

Spirocerca LupiSpirocerca Lupi of canids of canids Nematodes reach esophageal submucosa after they migrate Nematodes reach esophageal submucosa after they migrate

through the wall of aortathrough the wall of aorta Form granulomas in wall of intrathoracic esophagus, and Form granulomas in wall of intrathoracic esophagus, and

granuloma opens to esophageal lumen allowing eggs to pass granuloma opens to esophageal lumen allowing eggs to pass out through fecesout through feces

Associated clinical problems include dysphagia, aortic Associated clinical problems include dysphagia, aortic aneurysms, spondylitis, HPO, and esophageal aneurysms, spondylitis, HPO, and esophageal fibrosarcoma/osteosarcoma fibrosarcoma/osteosarcoma

Intermediate host is dung beetleIntermediate host is dung beetle Dx = thoracic radiography, fecal examDx = thoracic radiography, fecal exam Rx = ivermectinRx = ivermectin

Page 103: Pathology of the GI tract

Spirocerca lupiSpirocerca lupi

Page 104: Pathology of the GI tract

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.

Aortic Nodules and Aneurysms

Page 105: Pathology of the GI tract

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.

Epidemiology

Page 106: Pathology of the GI tract

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.

Egg of Spirocerca lupi

Page 107: Pathology of the GI tract

Esophagus: Miscellaneous Esophagus: Miscellaneous ConditionsConditions

Idiopathic muscular Idiopathic muscular hypertrophy of distal hypertrophy of distal esophagusesophagus

Seen in horses, no clinical Seen in horses, no clinical significancesignificance

EsophagitisEsophagitis Often result of traumaOften result of trauma Secondary bacterial infectionSecondary bacterial infection

Esophageal erosions/ulcersEsophageal erosions/ulcers Reflux, trauma, viral diseaseReflux, trauma, viral disease

• BVD MD in cattleBVD MD in cattle PapillomasPapillomas

Page 108: Pathology of the GI tract

Ruminant ForestomachRuminant Forestomach

Rumen papillae Reticulum epithelial folds

Omasum epithelial folds

Normal Anatomy

Page 109: Pathology of the GI tract

Ruminant ForestomachRuminant Forestomach BloatBloat (ruminal tympany)- Overdistention of rumen and reticulum by gases (ruminal tympany)- Overdistention of rumen and reticulum by gases

produced during fermentationproduced during fermentation Primary tympany (legume bloat, frothy bloat)Primary tympany (legume bloat, frothy bloat)

• Following diet change, rumen pH decreases to 5-6, foam forms which blocks cardia 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) and causes rumen to distend (seen clinically as distended left paralumbar fossa)

Secondary tympanySecondary tympany• Physical or functional obstruction/stenosis of esophagus leads to eructation failure and Physical or functional obstruction/stenosis of esophagus leads to eructation failure and

gases accumulate in rumengases accumulate in rumen Esophageal foreign body, vagal nerve dysfunction, lymphosarcoma, etc.Esophageal foreign body, vagal nerve dysfunction, lymphosarcoma, etc.

Foreign bodiesForeign bodies Hair balls, plant ballsHair balls, plant balls Hardware diseaseHardware disease Lead poisoningLead poisoning

RumenitisRumenitis Lactic acidosis (Grain overload)Lactic acidosis (Grain overload) Bacterial – secondary to acidosis or mechanical injuryBacterial – secondary to acidosis or mechanical injury Mycotic – secondary to acidosis or antibiotic administrationMycotic – secondary to acidosis or antibiotic administration

• Lesions due to infarcts caused by fungal vasculitisLesions due to infarcts caused by fungal vasculitis• Primary fungi are Aspergillus, Mucor, Absidia, etc Primary fungi are Aspergillus, Mucor, Absidia, etc

MiscellaneousMiscellaneous ParakeratosisParakeratosis Vagus indigestionVagus indigestion

Page 110: Pathology of the GI tract

Ruminant Forestomach - BloatRuminant Forestomach - Bloat

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

Page 111: Pathology of the GI tract

Ruminant Forestomach – Foreign Ruminant Forestomach – Foreign BodiesBodies

TrichobezoarsTrichobezoars = = hairballshairballs Hair forms nidusHair forms nidus

PhytobezoarsPhytobezoars = plant = plant ballsballs

Page 112: Pathology of the GI tract

Ruminant Forestomach – Foreign Ruminant Forestomach – Foreign BodiesBodies

Hardware diseaseHardware disease Ingestion of baling Ingestion of baling

wire, nails perforates wire, nails perforates through wall of through wall of reticulum (reticulitis) reticulum (reticulitis) and enters peritoneal and enters peritoneal cavity (peritonitis) or cavity (peritonitis) or pericardial sac pericardial sac (pericarditis)(pericarditis)

Hardware disease – fibrinous pericarditis

Page 113: Pathology of the GI tract

Rumenitis (Lactic Acidosis)Rumenitis (Lactic Acidosis) Common disease of cattle that consume excessive readily digestible Common disease of cattle that consume excessive readily digestible

carbohydrates, especially grain (grain overload)carbohydrates, especially grain (grain overload) Within 2-6 hours, microbial population of rumen changes to gram Within 2-6 hours, microbial population of rumen changes to gram

positive bacteria (positive bacteria (Strep bovisStrep bovis) which results in production of lactic ) which results in production of lactic acidacid

Rumen pH falls below 5 which destroys protozoa, lactate-using Rumen pH falls below 5 which destroys protozoa, lactate-using organisms and rumen motility ceasesorganisms and rumen motility ceases

Lactic acid causes chemical rumenitis.Lactic acid causes chemical rumenitis. Absorption of lactic acid into bloodstream causes lactic acidosis Absorption of lactic acid into bloodstream causes lactic acidosis

resulting in cardiovascular collapse (shock), renal failure and deathresulting in cardiovascular collapse (shock), renal failure and death If survive, may develop bacterial or mycotic rumenitis in several If survive, may develop bacterial or mycotic rumenitis in several

days, or liver abscesses (necrobacillosis) or laminitis in several days, or liver abscesses (necrobacillosis) or laminitis in several weeksweeks

Dx = check pH of rumen fluid obtained by stomach tube, examine Dx = check pH of rumen fluid obtained by stomach tube, examine rumen fluid with microscope ( no protozoa, few gram negative, rumen fluid with microscope ( no protozoa, few gram negative, mostly gram positive bacteria on gram stain) mostly gram positive bacteria on gram stain)

Page 114: Pathology of the GI tract

Grain OverloadGrain Overload

Page 115: Pathology of the GI tract

Reticulitis/RumenitisReticulitis/Rumenitis

Page 116: Pathology of the GI tract

RumenitisRumenitis

Page 117: Pathology of the GI tract

Mycotic RumenitisMycotic Rumenitis

Page 118: Pathology of the GI tract

Miscellaneous Rumen ConditionsMiscellaneous Rumen Conditions

Ruminal parakeratosis – seen in cattle and Ruminal parakeratosis – seen in cattle and sheep fed diets with less than 10% sheep fed diets with less than 10% roughageroughage Papillae are enlarged, adhered together and Papillae are enlarged, adhered together and

firmfirm Affected papillae contain excessive layers of Affected papillae contain excessive layers of

keratinized epithelial cells, bacteria and food keratinized epithelial cells, bacteria and food materialmaterial

May alter nutrient absorption, decrease feed May alter nutrient absorption, decrease feed efficiencyefficiency

Page 119: Pathology of the GI tract

Miscellaneous Rumen ConditionsMiscellaneous Rumen Conditions

Vagus IndigestionVagus Indigestion (chronic indigestion) (chronic indigestion) Seen in cattle and sheepSeen in cattle and sheep Gradual development of rumenoreticular and abdominal Gradual development of rumenoreticular and abdominal

distentiondistention Four types recognized based on site of functional obstructionFour types recognized based on site of functional obstruction

• Type I – failure of eructation resulting in free-gas bloat, usually due Type I – failure of eructation resulting in free-gas bloat, usually due to inflammatory lesions that involve vagus nerve (hardware disease, to inflammatory lesions that involve vagus nerve (hardware disease, pneumonia, etc)pneumonia, etc)

• Type II – failure of transport from omasum to abomasum via omasal Type II – failure of transport from omasum to abomasum via omasal canal, usually due to abscess in wall of reticulum near vagus canal, usually due to abscess in wall of reticulum near vagus (hardware disease), or lymphoma or papilloma blockage(hardware disease), or lymphoma or papilloma blockage

• Type III – abomasal impaction due to feeding of dry coarse Type III – abomasal impaction due to feeding of dry coarse roughage with restricted access to water, especially in winterroughage with restricted access to water, especially in winter

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

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

Page 120: Pathology of the GI tract

Stomach and AbomasumStomach and Abomasum

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

Normal horse stomach

Histologic appearance

Page 121: Pathology of the GI tract

Abomasal DisordersAbomasal Disorders

Abomasal displacement (LDA, RDA)Abomasal displacement (LDA, RDA) Abomasal volvulusAbomasal volvulus Abomasal ulcersAbomasal ulcers Abomasal ImpactionAbomasal Impaction Abomasal inflammation (abomasitis)Abomasal inflammation (abomasitis) Bovine viral diarrhea and mucosal diseaseBovine viral diarrhea and mucosal disease Abomasal parasitesAbomasal parasites LymphosarcomaLymphosarcoma

Page 122: Pathology of the GI tract

Abomasal DisplacementsAbomasal Displacements Usually to left side in high producing dairy cattle within Usually to left side in high producing dairy cattle within

one month of parturitionone month of parturition Result of abomasal atony with gas distention and displacement Result of abomasal atony with gas distention and displacement

upward along left abdominal wallupward along left abdominal wall Fundus and greater curvature displaced creating partial Fundus and greater curvature displaced creating partial

obstructionobstruction No interference with blood supply but passage of ingesta slowed No interference with blood supply but passage of ingesta slowed

leading to chronic partial anorexialeading to chronic partial anorexia Also see metabolic alkalosis – related to sequestration of Also see metabolic alkalosis – related to sequestration of

chloride in abomasum (HCL production continues)chloride in abomasum (HCL production continues) RDA – occurs infrequently but atony, gas production and RDA – occurs infrequently but atony, gas production and

displacement occur as in LDAdisplacement occur as in LDA• Then have rotation (volvulus) of abomasum on its mesentery Then have rotation (volvulus) of abomasum on its mesentery

resulting in ischemiaresulting in ischemia• Rotation is usually in counterclockwise when viewed from rearRotation is usually in counterclockwise when viewed from rear• Leads to complete anorexia, necrosis of abomasal wall, shock Leads to complete anorexia, necrosis of abomasal wall, shock

Page 123: Pathology of the GI tract

Right Displaced Abomasum with Right Displaced Abomasum with RotationRotation

Page 124: Pathology of the GI tract

Abomasal UlcersAbomasal Ulcers Seen in adult cattle and calvesSeen in adult cattle and calves Many etiologic possibilities such as Many etiologic possibilities such as

viral disease (BVD, rinderpest, MCF)viral disease (BVD, rinderpest, MCF) Nonviral – in dairy cows 6 weeks after Nonviral – in dairy cows 6 weeks after

parturition (stress, heavy grain parturition (stress, heavy grain feeding?)feeding?)

Nonviral – feedlot cattle on high grain Nonviral – feedlot cattle on high grain rationsrations

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

Nonviral – suckling beef calves on Nonviral – suckling beef calves on good summer pasturegood summer pasture

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

Ulcers most common along greater Ulcers most common along greater curvaturecurvature

Type 1 = erosion/ulcer, no hemType 1 = erosion/ulcer, no hem Type II = hemorrhagicType II = hemorrhagic Type III = perforation/local peritonitisType III = perforation/local peritonitis Type IV = perforation with acute diffuse Type IV = perforation with acute diffuse

peritonitisperitonitis

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Perforating Abomasal Ulcer Perforating Abomasal Ulcer

Page 126: Pathology of the GI tract

Dietary Abomasal ImpactionDietary Abomasal Impaction

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

See abomasal atony and See abomasal atony and chronic dilationchronic dilation

Dehydration, anorexia, Dehydration, anorexia, alkalosis, and progressive alkalosis, and progressive starvationstarvation

Abomasal emptying Abomasal emptying defect is an idiopathic defect is an idiopathic condition in Suffolk sheepcondition in Suffolk sheep

Page 127: Pathology of the GI tract

Abomasal InflammationAbomasal Inflammation

Braxy in sheep and cattleBraxy in sheep and cattle Caused by Caused by Clostridium septicumClostridium septicum Hemorrhagic abomasitis with submucosal Hemorrhagic abomasitis with submucosal

emphysemaemphysema Bacteria produces exotoxin that leads to Bacteria produces exotoxin that leads to

toxemia and shocktoxemia and shock

Page 128: Pathology of the GI tract

BVD-MDBVD-MD Pestivirus that has cattle as primary host but Pestivirus that has cattle as primary host but

most even-toed ungulates are susceptiblemost even-toed ungulates are susceptible Two biotypes – noncytopathic and Two biotypes – noncytopathic and

cytopathic (effect in cultured cells)cytopathic (effect in cultured cells) All age cattle are susceptibleAll age cattle are susceptible Persistently infected cattle are natural Persistently infected cattle are natural

reservoir – noncytopathic virus transmitted reservoir – noncytopathic virus transmitted in utero, therefore infected at birth and in utero, therefore infected at birth and infection lasts for lifeinfection lasts for life

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

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

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

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

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

Page 129: Pathology of the GI tract

Abomasal ParasitesAbomasal Parasites

Haemonchus contortusHaemonchus contortus – common parasite of – common parasite of sheep and other sheep and other ruminantsruminants

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

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

Page 130: Pathology of the GI tract

HaemonchusHaemonchus

Residual damage in Residual damage in abomasal mucosa abomasal mucosa caused by third stage caused by third stage larvaelarvae

There is focal There is focal destruction of deep destruction of deep glands and glands and lymphocytic lymphocytic inflammationinflammation

Page 131: Pathology of the GI tract

Abomasal ParasitesAbomasal Parasites

OstertagiosisOstertagiosis Sheep and goats = Sheep and goats = O. O.

circumcinctacircumcincta Cattle = Cattle = O. ostertagiaO. ostertagia Live as larval stages in Live as larval stages in

gastric glands giving gastric glands giving mucosa a rough and thick mucosa a rough and thick appearanceappearance

Chronic inflammation, Chronic inflammation, mucous cell hyperplasia mucous cell hyperplasia and lymphoid nodulesand lymphoid nodules

Poor weight gain, diarrhea, Poor weight gain, diarrhea, and hypoproteinemiaand hypoproteinemia

Page 132: Pathology of the GI tract

Abomasal LymphosarcomaAbomasal Lymphosarcoma

Lymphosarcoma can Lymphosarcoma can be primary, metastatic be primary, metastatic or multicentric in or multicentric in originorigin

In cattle, often caused In cattle, often caused by bovine leukemia by bovine leukemia virusvirus

Page 133: Pathology of the GI tract

Horse StomachHorse Stomach

Stomach capacity is only Stomach capacity is only about 2.5 gallonsabout 2.5 gallons

Located on left side of Located on left side of abdomen beneath rib abdomen beneath rib cagecage

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

therefore, horses cannot therefore, horses cannot vomit gastric contents vomit gastric contents

Celiac artery supplies Celiac artery supplies blood to stomachblood to stomach

Page 134: Pathology of the GI tract

Stomach Colic ConditionsStomach Colic Conditions

Gastric dilatation Gastric dilatation Gastric ruptureGastric rupture Gastric impactionGastric impaction Gastric Ulcer Syndrome (adults/foals)Gastric Ulcer Syndrome (adults/foals) Gastric parasitesGastric parasites Gastric neoplasiaGastric neoplasia

Page 135: Pathology of the GI tract

Gastric DilatationGastric Dilatation

Caused by overeating fermentable foodstuff Caused by overeating fermentable foodstuff producing excessive gas or intestinal obstructionproducing excessive gas or intestinal obstruction Overeating leads to increase in volatile fatty acids Overeating leads to increase in volatile fatty acids

which inhibit gastric emptyingwhich inhibit gastric emptying Obstruction usually in small intestine and fluid Obstruction usually in small intestine and fluid

accumulates in stomachaccumulates in stomach Right dorsal displacement of colon around Right dorsal displacement of colon around

cecum – obstructs duodenal outflowcecum – obstructs duodenal outflow Proximal enteritis-jejunitis leads to gastric fluid Proximal enteritis-jejunitis leads to gastric fluid

buildup buildup

Page 136: Pathology of the GI tract

Gastric RuptureGastric Rupture

Stomach rupture is fatal outcome of Stomach rupture is fatal outcome of uncorrected gastric dilatationuncorrected gastric dilatation

Tear usually occurs along greater Tear usually occurs along greater curvaturecurvature

Most (approximately 2/3) occur secondary Most (approximately 2/3) occur secondary to mechanical obstruction, ileus or traumato mechanical obstruction, ileus or trauma Remaining due to overload or idiopathic Remaining due to overload or idiopathic

causescauses

Page 137: Pathology of the GI tract

Gastric ImpactionGastric Impaction

Uncommon cause of colicUncommon cause of colic May be associated with pelleted feeds, May be associated with pelleted feeds,

persimmon seeds, straw, barley, etcpersimmon seeds, straw, barley, etc Also associated may be poor dentition, Also associated may be poor dentition,

lack or water, rapid eating lack or water, rapid eating

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Equine Gastric Ulcer SyndromeEquine Gastric Ulcer Syndrome Currently recognized EGUS in adults >1 year Currently recognized EGUS in adults >1 year

of age, in order of decreasing frequencyof age, in order of decreasing frequency Primary erosion/ulceration of nonglandular Primary erosion/ulceration of nonglandular

(squamous) mucosa (squamous) mucosa Primary glandular ulcer diseasePrimary glandular ulcer disease Secondary squamous ulcerationSecondary squamous ulceration

Currently recognized syndromes in foals <1 Currently recognized syndromes in foals <1 year of age, in order of decreasing frequencyyear of age, in order of decreasing frequency Gastroduodenal ulcer disease (GDUD)Gastroduodenal ulcer disease (GDUD) Primary erosion/ulceration of squamous mucosaPrimary erosion/ulceration of squamous mucosa NSAID-induced ulcer disease (primary glandular ulcer NSAID-induced ulcer disease (primary glandular ulcer

disease as for adults)disease as for adults)

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Normal Equine Stomach FillNormal Equine Stomach Fill Gastric fill and contents Gastric fill and contents

composition in horse allowed composition in horse allowed free access to foragefree access to forage

Fill line is not much above Fill line is not much above lower esophageal sphincterlower esophageal sphincter

Coarser contents layer at top Coarser contents layer at top and fine particulates filter to and fine particulates filter to bottombottom

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

Bottom contents adjacent to Bottom contents adjacent to HCL-producing parietal cells HCL-producing parietal cells

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Normal Gastric Acid Secretion Normal Gastric Acid Secretion

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Equine Gastric Ulcer SyndromeEquine Gastric Ulcer Syndrome

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

Seen as a primary or Seen as a primary or secondary conditionsecondary condition

Seen in adult horses Seen in adult horses under intensive training, under intensive training, any breedany breed

Pathogenesis is poorly Pathogenesis is poorly understoodunderstood

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EGUS (proposed pathogenesis)EGUS (proposed pathogenesis)**

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

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

*Merritt, AAEP, 2003

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Primary Glandular Ulcer DiseasePrimary Glandular Ulcer Disease

Ulceration of glandular Ulceration of glandular mucosa, especially in mucosa, especially in pyloric regionpyloric region

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

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

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Primary Glandular Ulcer DiseasePrimary Glandular Ulcer Disease

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

Squamous mucosa Squamous mucosa (upper right) is free of (upper right) is free of lesionslesions

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Secondary Squamous UlcerationSecondary Squamous Ulceration

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

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

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

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Secondary Squamous UlcerationSecondary Squamous Ulceration

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

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

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Gastric UlcerGastric Ulcer

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

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

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Current Syndromes in Foals (< 1 yr Current Syndromes in Foals (< 1 yr of age)of age)

Gastroduodenal ulcer disease Gastroduodenal ulcer disease (GDUD) - sucklings and early (GDUD) - sucklings and early weanlingsweanlings

Cause is unknownCause is unknown In early stage of GDUD see In early stage of GDUD see

roughened duodenal mucosa roughened duodenal mucosa covered with fibrinous plaque – covered with fibrinous plaque – causes some disruption of causes some disruption of gastric emptying with some gastric emptying with some secondary squamous erosion secondary squamous erosion and ulcerationand ulceration

May recover after supportive May recover after supportive Rx or develop advanced Rx or develop advanced diseasedisease

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Advanced GDUD in foalsAdvanced GDUD in foals Clinical signs include drooling, Clinical signs include drooling,

teeth grinding, periodic bouts teeth grinding, periodic bouts of colic especially after of colic especially after suckling, and weight losssuckling, and weight loss

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

Barium meal will be retained Barium meal will be retained longer than 1 hourlonger than 1 hour

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

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Advanced GDUD in FoalsAdvanced GDUD in Foals

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 Primary Erosion/Ulceration of Squamous Mucosa in FoalsSquamous Mucosa in Foals

May cause unthriftiness and/or mild colicMay cause unthriftiness and/or mild colic Etiology and pathogenesis are unknownEtiology and pathogenesis are unknown Must always rule out partial obstruction of Must always rule out partial obstruction of

gastric outflow as after a previously gastric outflow as after a previously unrecognized GDUDunrecognized GDUD

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Stress-Related Gastric Ulcers in Stress-Related Gastric Ulcers in FoalsFoals

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

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

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

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Gastric parasitesGastric parasites

Gastrophilus spp (horse bots)Gastrophilus spp (horse bots) Larvae of bot flies, adult flies are not parasitic and Larvae of bot flies, adult flies are not parasitic and

cannot feed, lay eggs and diecannot feed, lay eggs and die Three species (G. intestinalis – lays yellow eggs on Three species (G. intestinalis – lays yellow eggs on

hairs of forelimbs; G. haemorrhoidalis – black eggs on hairs of forelimbs; G. haemorrhoidalis – black eggs on hairs of lips; G. nasalis – white eggs on hairs of hairs of lips; G. nasalis – white eggs on hairs of submaxillary area)submaxillary area)

Larvae of all three embed in mucosa of mouth before Larvae of all three embed in mucosa of mouth before passing to stomach, attach to stomach lining by oral passing to stomach, attach to stomach lining by oral hooks, cause mild gastritis, pass out in feces in 8-10 hooks, cause mild gastritis, pass out in feces in 8-10 monthsmonths

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Horse BotsHorse Bots

Large numbers of larvae attached to gastric mucosa

Adult bot fly

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Gastric ParasitesGastric Parasites Habronema (H. muscae, H. microstoma, Draschia megastomaHabronema (H. muscae, H. microstoma, Draschia megastoma

H. microstoma and D. megastoma deposit larvae, but H. muscae lays H. microstoma and D. megastoma deposit larvae, but H. muscae lays eggs containing larvae.eggs containing larvae.

Larvae ingested by housefly or stablefly maggots which develop in Larvae ingested by housefly or stablefly maggots which develop in manuremanure

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

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

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

Infected flies can also be eaten by horseInfected flies can also be eaten by horse In stomach, H. muscae and H. microstoma are on mucosal surface In stomach, H. muscae and H. microstoma are on mucosal surface

under layer of mucus – cause mild catarrhal gastritisunder layer of mucus – cause mild catarrhal gastritis In stomach, D. megastoma causes granulomas up to 10 cm in diameterIn stomach, D. megastoma causes granulomas up to 10 cm in diameter

• Filled with necrotic debris and wormsFilled with necrotic debris and worms• Covered by epithelium except for small opening for egg passage Covered by epithelium except for small opening for egg passage

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HabronemaHabronema

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 PigsStomach Conditions of Pigs

Gastric ulcersGastric ulcers Edema diseaseEdema disease ParasitesParasites

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Pig Gastric UlcersPig Gastric Ulcers Seen in pigs of all ages but Seen in pigs of all ages but

most common in confined most common in confined growing pigs (45-90 kg)growing pigs (45-90 kg)

Cause unknown but finely Cause unknown but finely ground feed and stress are risk ground feed and stress are risk factorsfactors

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

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

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Edema DiseaseEdema Disease

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

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

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

We will talk more about this disease laterWe will talk more about this disease later

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Edema diseaseEdema disease

Submucosal edema in glandular region

Periocular edema

Edema in stomach wall

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Stomach Parasites of PigsStomach Parasites of Pigs

Hyostrongylus rubidus Hyostrongylus rubidus (red stomach worm)(red stomach worm)

Direct life cycleDirect life cycle Seen in grazing pigsSeen in grazing pigs Adults are on mucosal Adults are on mucosal

surface in film of mucussurface in film of mucus Larvae are in mucosa and Larvae are in mucosa and

may cause severe may cause severe hypertrophic gastritis with hypertrophic gastritis with proliferation of gastric proliferation of gastric glands glands

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Stomach NeoplasiaStomach Neoplasia

Cattle – lymphosarcoma Cattle – lymphosarcoma – anywhere in – anywhere in forestomachforestomach

Usually associated with Usually associated with BLVBLV

Squamous cell carcinoma Squamous cell carcinoma of rumen also seen rarelyof rumen also seen rarely

Horse – squamous cell Horse – squamous cell carcinoma of carcinoma of nonglandular region of nonglandular region of stomachstomach

Pig – tumors of stomach Pig – tumors of stomach very rarevery rare