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  Hunger centers in the brain  Higher senses to locate food  Lips – especially in herbivores  Tongue  Teeth  Esophagus

Digestion

 Mouth   Grinding Salivary enzymes – starches  Stomach  Mixing vat  Acidification (monogastrics)  Fermentation (ruminates)

Digestion

 Small intestine  Pancreas • • Enzymes Buffer  Bile • Emulsifies lipids

Digestion

 Carbohydrates  Polysaccharides  Enzymatically broken down to monosaccharides • Hydrolysis

Digestion

 Proteins  Polypeptides  Enzymatically broken down to amino acids • Hydrolysis

Digestion

 Fats  Triglycerides – 3 fatty acids on a glyceride backbone  Enzymatically broken down to monoglycerides and fatty acids • Hydrolysis

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

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

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

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

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

Defense mechanisms

 Enzyme control  Secreted in an inactive form • • • Protein cleavage pH Cofactors  Fuse or pin

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

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”

Defense mechanisms

 Innate immunity  Paneth cells • • • • Antimicrobial peptides Defensins Cathelicidins Toll-like receptors  Neutrophils  Macrophages

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

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

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

Oral Cavity

 Developmental  Traumatic  Toxic  Inflammatory  Infectious • Viral, bacterial, fungal  Autoimmune  Neoplastic

Developmental

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

Developmental

 Cleft lip/hare lip  Brachygnathia  Superior – shortened maxillae  Inferior – shortened mandibles  Prognathism

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

 Fractures  Dislocations  Foreign bodies   Bones –dogs Linear – cats

Traumatic

Inflammatory

 Stomatitis – general term  Glossitis, gingivitis, pulpitis  Infectious diseases of the oral cavity  Viral  Bacterial  Fungal

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

Oral Cavity – Vesicular Stomatitides

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

Foot & Mouth, bovine

Vesicular Stomatitides - VS

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

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

BVD Mucosal Disease

 Bovine viral diarrhea virus (BVDV)  Highly contageous  Rarely fatal  Fever, diarrhea, mucosal ulcerations, leukopenia  Multiple serotypes • • Cytopathic Non-cytopathic

BVD Mucosal Disease

 “Normal” disease course  Immunocompetent animal  Subclinical or mild disease  Mucosal disease course  Infection during 4 th • month of gestation Abortion, fetal mummification, develpmental anomalies (cerebellar hypoplasia) • Surviving animals   Persistent infection Immunotolerant to virus

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

BVD Mucosal Disease

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

Malignant Catarrhal Fever (MCF)

 Gross lesion is ulceration of mucosal surfaces, edema, mucopurulent nasal discharge, lymphadenopathy  Microscopic lesions  Lymphoid proliferation  Fibrinoid vascular necrosis

Malignant Catarrhal Fever (MCF)

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

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”

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

Bovine Papular Stomatitis

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

Contagious Ecthyma (Orf)

Papillomatosis

 Papovavirus  Bovine papilloma virus  Canine papilloma virus  Papillomas (warts) on mucosa of mouth, esophagus, rumen (cattle)  Usually self-limiting lesions

Papillomatosis

Papillomatosis

Papillomatosis

Bacterial Stomatitides

 Associated with trauma  Feeding, iatragenic, foreign body  Opportunistic normal bacterial inhabitant  Actinobacillus, actinomyces, fusobacterium

Necrotizing stomatitides

 Oral necrobacillosis    Calf diphtheria Necrotic membrane Foul breath, anorexia, fever

Wooden tongue

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

Wooden tongue

 Pyogranulomas  Club-shaped bacterial colonies   “Splendora-Hepli” “sulfur granules”

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

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

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

Inflammatory, non-infectious

 Inappropriate immune/inflammatory response   “Self” antigen – autoimmune Unknown antigen – immune mediated  Generally a problem of small animals (Dogs and Cats)

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

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

Immune Mediated

 Feline plasma cell gingivitis  Raised, erythematous, proliferative lesion   Glossopalatine arch Periodontal gingiva

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

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

Immune Mediated

 Eosinophilic ulcer  Histologic appearance • • Ulcerated surface Moderate to large numbers of eosinophils with macrophages, lymphocytes, and plasma cells • Collagenolysis

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

Uremic glossitis

 Histologic appearance  Necrosis of mucosal epithelium with ulceration  Vascular necrosis of small arterioles of tongue  Ischemic vascular lesion  Pathogenesis poorly understood  Poor correlation between blood ammonia levels and lesion development

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

Gingival hyperplasia

 Histologic appearance  Mature fibrous connective tissue   Hypocellular May have focal areas of ulceration and inflammation

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

Epuloides

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

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

Epuloides

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

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

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

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

Squamous cell carcimona

  2 nd most common oral neoplasm in dogs       Usually involves tonsil Small granular plaque  of the tonsil 2-3x size 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

Melanoma

       Most common oral tumor in dogs  Rare in cats and large animals Almost always malignant  Most have metastasized by the time of dx More common in males than females More common in pigmented animals No correlation between degree of pigmentation and biologic behaviour Met to lymph nodes, distant organs, especially lungs Median survival time ~ 65 days in untreated animals

Melanoma

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

Melanoma

Melanoma

 Microscopic appearance  Variable   Heavily pigmented to amelanotic Cytologically appear as round cells

Melanoma

Fibrosarcoma

 Can occur in all animals, but usually seen in dogs  3 rd 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

Fibrosarcoma

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

Fibrosarcoma

 Histologic appearance   Moderately cellular • Streams of fibroblastic cells High mitotic rate  Collagenous extra cellular matrix

Osteosarcoma

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

Round cell tumors

 Mast cell tumors  Discreet mass  Lymphosarcoma  Tonsillar  Epitheliotrophic  Plasma cell tumors  Discreet mass  Pleomorphic plasma cells

Salivary Glands

    

Sialoadenitis

medicine   = inflammation of salivary gland – uncommon in vet 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

Salivary Ranula

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

Salivary gland

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

Esophagus

 Tube    Smooth and striated muscle Glands Mucosal epithelium

Esophagus: developmental anomalies

 Developmental anomalies of the esophagus are rare  Segmental aplasia  Esophago-respiratory fistula  Esophageal diverticulae  Hyperkeratosis/squamous metaplasia

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

Esophagus

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

Esophagus

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

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

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

Megaesophagus

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

Megaesophagus

Dilated esophagus anterior to stomach

Megaesophagus

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

Spirocerca lupi

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.

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 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.

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.

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

Ruminant Forestomach

Normal Anatomy Rumen papillae Reticulum epithelial folds Omasum epithelial folds

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

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

Ruminant Forestomach – Foreign Bodies



Trichobezoars

hairballs =  Hair forms nidus 

Phytobezoars

plant balls =

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

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)

Grain Overload

Reticulitis/Rumenitis

Rumenitis

Mycotic Rumenitis

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

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

Stomach and Abomasum

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

Abomasal Disorders

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

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

Right Displaced Abomasum with Rotation

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Abomasal Ulcers

Seen in adult cattle and calves Many etiologic possibilities such as viral disease (BVD, rinderpest, MCF) Nonviral feeding?) – in dairy cows 6 weeks after parturition (stress, heavy grain 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

Perforating Abomasal Ulcer

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

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

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 gut lesions) – paired serum samples with 4 fold rise in titer, PCR, virus isolation (submit lymph node, spleen,

Abomasal Parasites

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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)

Haemonchus

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

Abomasal Parasites

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Ostertagiosis

 Sheep and goats =

O. circumcincta

    Cattle =

O. ostertagia Live as larval stages in gastric glands giving mucosa a rough and thick appearance Chronic inflammation, mucous cell hyperplasia and lymphoid nodules Poor weight gain, diarrhea, and hypoproteinemia

Abomasal Lymphosarcoma

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

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

Stomach Colic Conditions

 Gastric dilatation  Gastric rupture  Gastric impaction  Gastric Ulcer Syndrome (adults/foals)  Gastric parasites  Gastric neoplasia

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

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

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

Equine Gastric Ulcer Syndrome

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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)

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 contents at bottom – has higher pH than more liquid Bottom contents adjacent to HCL-producing parietal cells

Normal Gastric Acid Secretion

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

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

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

Primary Glandular Ulcer Disease

 Multiple sites of glandular mucosal ulceration (yellow arrows) induced by NSAID toxicity  Squamous mucosa (upper right) is free of lesions

Secondary Squamous Ulceration

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

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 mucosal erosion lesions can scar and result in stricture that – yellow arrow indicates – such reduces gastric emptying

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

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

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

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

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

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

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

Horse Bots

Large numbers of larvae attached to gastric mucosa Adult bot fly

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

Habronema

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

Stomach Conditions of Pigs

 Gastric ulcers  Edema disease  Parasites

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

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

Edema disease

Periocular edema Submucosal edema in glandular region Edema in stomach wall

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

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