Pathology of the GI tract

Presentation on theme: "Pathology of the GI tract"— Presentation transcript:

1 Pathology of the GI tract
Tim Morgan DVM, PhD

2 Alimentary Canal Continuous tube Function “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 Stomach Grinding Salivary enzymes – starches
Mixing vat Acidification (monogastrics) Fermentation (ruminates)

5 Digestion Small intestine Pancreas Bile Enzymes Buffer
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 Secreted fluid Total 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) Proteins (amino acids)
Active transport Proteins (amino acids) 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 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 Competition 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 Neutrophils
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 Effective defense mechanims
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 Neoplastic
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 Prognathism
Superior – shortened maxillae Inferior – shortened mandibles Prognathism

24 Developmental Dentition Heterotopic polydontia Anomalous dentition
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 Mucosal 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 Persistent infections Clinical signs
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

51 Wooden tongue Actinobacillus lignieresii
Often associated w/lingual groove Chronic infection Severe fibrosis “Wooden tongue”

52 Wooden tongue Pyogranulomas Club-shaped bacterial colonies
“Splendora-Hepli” “sulfur granules”

53 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

54 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

55 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

56 Inflammatory, non-infectious
Inappropriate immune/inflammatory response “Self” antigen – autoimmune Unknown antigen – immune mediated Generally a problem of small animals (Dogs and Cats)

57 Auto-immune Considered dermatologic diseases
Frequently affect muco-cutaneous junctions Pemphigus vulgaris Severe, acute or chronic vesicular/bullous disease of humans, dogs, cats Flaccid bullae & erosions of muco-cutaneous junctions, oral mucosa, skin to lesser extent Clinical signs Salivation, halitosis, mucosal erosion/ulceration Severity varies greatly Histology Basal cells remain attached to basement membrane “tomb stone” appearance Destruction of acanthocytes (acantholysis) Lichenoid infiltration of lymphocytes and plasma cells Scattered neutrophils and eosinophils

58 Auto-immune Bullous pemphigoid
Grossly impossible to tell from pemphigus vulgaris Histology Subepidermal blister formation No acantholysis Reported in humans, dogs, horses, possible cases in cats

59 Immune Mediated Feline plasma cell gingivitis
Raised, erythematous, proliferative lesion Glossopalatine arch Periodontal gingiva

60 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

61 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

62 Immune Mediated Eosinophilic ulcer Histologic appearance
Ulcerated surface Moderate to large numbers of eosinophils with macrophages, lymphocytes, and plasma cells Collagenolysis

63

64 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

65 Uremic glossitis Histologic appearance Ischemic vascular lesion
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

66 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

67 Gingival hyperplasia Histologic appearance
Mature fibrous connective tissue Hypocellular May have focal areas of ulceration and inflammation

68 Epuloides Fibromatous epulis
Fibrous mass arising from the periodontal ligament Firm, hard, gray to pink Similar in appearance to focal gingival hyperplasia Between teeth or on hard palate near teeth Carnasal teeth in brachycephalic breeds May mechanically displace the teeth Attached to the periosteum Do not invade bone

69 Epuloides Fibromatous epulis Histologic appearance
Interwoven bundles of fibroblastic tissue More cellular than gingival hyperplasia May have areas of bone production “Ossifying epulis”

70 Epuloides Acanthomatous epulis (acanthomatous ameloblastoma)
Odontogenic epithelial origin Rough, cauliflower-like lesion Dental arcade of dogs Locally invasive Invades and destroys bone Do NOT metastasize

71 Epuloides Acanthomatous epulis Histologic appearance Highly cellular
Interconnecting odontogenic epithelial sheets bordered by columnary to cuboidal cells Contain numerous, usually empty, blood vessels

72 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

73 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

74 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

75 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

76 Melanoma Most common oral tumor in dogs Almost always malignant
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

77 Melanoma Gross appearance Nodular, variably pigmented masses
Anywhere in the oral mucosa Invasive and destructive May or may not be ulcerated

78 Melanoma

79 Melanoma Microscopic appearance Variable
Heavily pigmented to amelanotic Cytologically appear as round cells

80 Melanoma

81 Fibrosarcoma 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

82 Fibrosarcoma Gross appearance Local invasion
Nodular to multi-nodulare +/- ulceration Firm Local invasion ~ 35% metastasize to lymph nodes Early pulmonary metastasis

83 Fibrosarcoma Histologic appearance Moderately cellular
Streams of fibroblastic cells High mitotic rate Collagenous extra-cellular matrix

84 Osteosarcoma Bones of the skull or jaw
Similar in appearance to fibrosarcoma Bone lysis and proliferation on radiographs

85 Round cell tumors Mast cell tumors Lymphosarcoma Plasma cell tumors
Discreet mass Lymphosarcoma Tonsillar Epitheliotrophic Plasma cell tumors Pleomorphic plasma cells

86 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

87 Salivary Ranula

88 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

89 Salivary gland Chronic inflammation of mandibular salivary gland secondary to sialocoele in dog Sialocoele wall composed of granulation tissue

90 Esophagus Tube Smooth and striated muscle Glands Mucosal epithelium

91 Esophagus: developmental anomalies
Developmental anomalies of the esophagus are rare Segmental aplasia Esophago-respiratory fistula Esophageal diverticulae Hyperkeratosis/squamous metaplasia

92 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

93 Esophagus Complications of choke
Esophageal rupture  cellulitis, death Esophageal dilation – mega-esophagus Ulceration with subsequent stricture Common in cattle Hedge apples Aspiration pneumonia

94 Esophagus

95 Esophagitis 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

96 Megaesophagus 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

97 Megaesophagus 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

98 Megaesophagus

99 Megaesophagus Diagnosis Survey and contrast radiography Esophagoscopy
T3 and T4 before and after TSH stimulation (R/O hypothyroidism) Cortisol concentrations with dexamethazone suppression (R/O hypoadrenalcorticism) Plasma cholinesterase levels (R/O OP tox) Antiacetylcholine receptor antibody assay (R/O MG) Toxoplasma titer

100 Megaesophagus Dilated esophagus anterior to stomach

101 Megaesophagus

102 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

103 Spirocerca lupi

104 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.

105 Epidemiology 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 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.

106 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.

107 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

108 Ruminant Forestomach Normal Anatomy Rumen papillae
Reticulum epithelial folds Omasum epithelial folds

109 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

110 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

111 Ruminant Forestomach – Foreign Bodies
Trichobezoars = hairballs Hair forms nidus Phytobezoars = plant balls

112 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

113 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)

114 Grain Overload

115 Reticulitis/Rumenitis

116 Rumenitis

117 Mycotic Rumenitis

118 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

119 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

120 Stomach and Abomasum Similar function and response to injury among ruminant abomasum and simple-stomached animals Normal horse stomach Histologic appearance

121 Abomasal Disorders Abomasal displacement (LDA, RDA) Abomasal volvulus
Abomasal ulcers Abomasal Impaction Abomasal inflammation (abomasitis) Bovine viral diarrhea and mucosal disease Abomasal parasites Lymphosarcoma

122 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

123 Right Displaced Abomasum with Rotation

124 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

125 Perforating Abomasal Ulcer

126 Dietary Abomasal Impaction
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

127 Abomasal Inflammation
Braxy in sheep and cattle Caused by Clostridium septicum Hemorrhagic abomasitis with submucosal emphysema Bacteria produces exotoxin that leads to toxemia and shock

128 BVD-MD 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)

129 Abomasal Parasites 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)

130 Haemonchus Residual damage in abomasal mucosa caused by third stage larvae There is focal destruction of deep glands and lymphocytic inflammation

131 Abomasal Parasites Ostertagiosis Sheep and goats = O. circumcincta
Cattle = O. ostertagia Live as larval stages in gastric glands giving mucosa a rough and thick appearance Chronic inflammation, mucous cell hyperplasia and lymphoid nodules Poor weight gain, diarrhea, and hypoproteinemia

132 Abomasal Lymphosarcoma
Lymphosarcoma can be primary, metastatic or multicentric in origin In cattle, often caused by bovine leukemia virus

133 Horse Stomach 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

134 Stomach Colic Conditions
Gastric dilatation Gastric rupture Gastric impaction Gastric Ulcer Syndrome (adults/foals) Gastric parasites Gastric neoplasia

135 Gastric Dilatation 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

136 Gastric Rupture 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

137 Gastric Impaction 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

138 Equine Gastric Ulcer Syndrome
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)

139 Normal Equine Stomach Fill
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

140 Normal Gastric Acid Secretion

141 Equine Gastric Ulcer Syndrome
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

142 EGUS (proposed pathogenesis)*
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

143 Primary Glandular Ulcer Disease
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

144 Primary Glandular Ulcer Disease
Multiple sites of glandular mucosal ulceration (yellow arrows) induced by NSAID toxicity Squamous mucosa (upper right) is free of lesions

145 Secondary Squamous Ulceration
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)

146 Secondary Squamous Ulceration
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

147 Gastric Ulcer 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

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

149 Advanced GDUD in foals 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

150 Advanced 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

151 Primary Erosion/Ulceration of Squamous Mucosa in Foals
May cause unthriftiness and/or mild colic Etiology and pathogenesis are unknown Must always rule out partial obstruction of gastric outflow as after a previously unrecognized GDUD

152 Stress-Related Gastric Ulcers in Foals
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

153 Gastric parasites 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

154 Horse Bots Large numbers of larvae attached to gastric mucosa
Adult bot fly

155 Gastric Parasites 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

156 Habronema Posterior end of adult Habronema spp worm showing spicule
Cutaneous habronemiasis Nodule in stomach caused by D. megastoma

157 Stomach Conditions of Pigs
Gastric ulcers Edema disease Parasites

158 Pig Gastric Ulcers 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

159 Edema Disease 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

160 Edema disease Periocular edema Submucosal edema in glandular region
Edema in stomach wall

161 Stomach Parasites of Pigs
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

162 Stomach Neoplasia 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