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Pathology of the GI tract

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

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

  2. 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

  3. Prehension • Fairly complex series of events • Hunger centers in the brain • Higher senses to locate food • Lips – especially in herbivores • Tongue • Teeth • Esophagus

  4. Digestion • Mouth • Grinding • Salivary enzymes – starches • Stomach • Mixing vat • Acidification (monogastrics) • Fermentation (ruminates)

  5. Digestion • Small intestine • Pancreas • Enzymes • Buffer • Bile • Emulsifies lipids

  6. Digestion • Carbohydrates • Polysaccharides • Enzymatically broken down to monosaccharides • Hydrolysis

  7. Digestion • Proteins • Polypeptides • Enzymatically broken down to amino acids • Hydrolysis

  8. Digestion • Fats • Triglycerides – 3 fatty acids on a glyceride backbone • Enzymatically broken down to monoglycerides and fatty acids • Hydrolysis

  9. Absorption 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 Priceless

  10. Absorption • Mostly takes place in the small intestine • Dependant upon surface area • Mucosal folds  3x increase • Villi  10x increase • Microvilli (brush border)  20x increase • Total 600x increase in surface area • ~ area of a tennis court

  11. Absorption • Carbs (monosaccharides) • Active transport • Proteins (amino acids) • Active transport • Fats (monoglycerides and fatty acids) • Micelles diffuse into cell membrane • Reconstituted to tryglycerides in SER • Dumped into lacteals as chylomicrons • Travel thru lymphatics and are dumped into the caudal vena cava

  12. Dilemma • 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

  13. 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

  14. Defense mechanisms • Enzyme control • Secreted in an inactive form • Protein cleavage • pH • Cofactors • Fuse or pin

  15. 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

  16. 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”

  17. Defense mechanisms • Innate immunity • Paneth cells • Antimicrobial peptides • Defensins • Cathelicidins • Toll-like receptors • Neutrophils • Macrophages

  18. 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

  19. Summary • 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

  20. 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

  21. Oral Cavity • Developmental • Traumatic • Toxic • Inflammatory • Infectious • Viral, bacterial, fungal • Autoimmune • Neoplastic

  22. Developmental • Cleft palate (palatoschesis) • Failure of maxillary bones to fuse • Variably sized defect in hard palate • May interfere with nursing, feeding, chronic nasal infections

  23. Developmental • Cleft lip/hare lip • Brachygnathia • Superior – shortened maxillae • Inferior – shortened mandibles • Prognathism

  24. Developmental • 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

  25. Traumatic • Fractures • Dislocations • Foreign bodies • Bones –dogs • Linear – cats

  26. Inflammatory • Stomatitis – general term • Glossitis, gingivitis, pulpitis • Infectious diseases of the oral cavity • Viral • Bacterial • Fungal

  27. 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

  28. Oral Cavity – Vesicular Stomatitides Ruptured vesicle, sheep, FMD Ruptured vesicles, snout, pig, FMD

  29. Foot & Mouth, bovine

  30. Vesicular Stomatitides - VS Ruptured vesicles, coronary band, horse, VS Vesicle on teat of cow, VS

  31. 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

  32. BVD Mucosal Disease • Bovine viral diarrhea virus (BVDV) • Highly contageous • Rarely fatal • Fever, diarrhea, mucosal ulcerations, leukopenia • Multiple serotypes • Cytopathic • Non-cytopathic

  33. 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

  34. 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

  35. BVD Mucosal Disease

  36. 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

  37. Malignant Catarrhal Fever (MCF) • Gross lesion is ulceration of mucosal surfaces, edema, mucopurulent nasal discharge, lymphadenopathy • Microscopic lesions • Lymphoid proliferation • Fibrinoid vascular necrosis

  38. Malignant Catarrhal Fever (MCF)

  39. 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

  40. 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”

  41. 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

  42. Bovine Papular Stomatitis

  43. 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

  44. Contagious Ecthyma (Orf)

  45. Papillomatosis • Papovavirus • Bovine papilloma virus • Canine papilloma virus • Papillomas (warts) on mucosa of mouth, esophagus, rumen (cattle) • Usually self-limiting lesions

  46. Papillomatosis

  47. Papillomatosis

  48. Papillomatosis

  49. Bacterial Stomatitides • Associated with trauma • Feeding, iatragenic, foreign body • Opportunistic normal bacterial inhabitant • Actinobacillus, actinomyces, fusobacterium

  50. Necrotizing stomatitides • Oral necrobacillosis • Calf diphtheria • Necrotic membrane • Foul breath, anorexia, fever

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