morganpath1 lq patologia g.i

7/27/2019 MorganPath1 Lq PATOLOGIA G.I

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Alimentary Canal

Continuous tube

Tube within a tube

Mouth (oral end)

Anus (aboral end)

Function

Acquire nutrients

Digest nutrients Absorb nutrients

Expel non-digestible portion


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Prehension

Fairly complex series of events

Hunger centers in the brain

Higher senses to locate food Lips especially in herbivores

Tongue

Teeth Esophagus


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Digestion

Mouth

Grinding

Salivary enzymes starches

Stomach

Mixing vat

Acidification (monogastrics)

Fermentation (ruminates)


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Digestion

Small intestine

Pancreas

Enzymes

Buffer

Bile

Emulsifies lipids


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Digestion

Carbohydrates

Polysaccharides

Enzymatically broken down to

monosaccharides

Hydrolysis


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Digestion

Proteins

Polypeptides

Enzymatically broken down to amino acids

Hydrolysis


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Digestion

Fats

Triglycerides 3 fatty acids on a glyceride

backbone

Enzymatically broken down to

monoglycerides and fatty acids

Hydrolysis


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Absorption

Ingested fluid

1.5 liters

Secreted fluid

~7 liters

Total fluid

8-9 liters

Not having to pass 9 liters of fecal fluid aday

Priceless


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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


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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


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Dilemma

Nutrients are composed of same materialsas the GI tract

Enzymes/mechanisms that breakdown

nutrients can also affect GI tract Selective absorption

Nutrients kept in

Toxic compounds kept outMost contaminated environment

Up to 10 12 organisms per gram


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Defense mechanisms

Washing

Saliva, mucous, fluid secretion

Flushes bacteria etc. away before they get a

chance to adhere

Keeps cells moist and happy

Prevents buildup of harmful materials

Buffers


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Defense mechanisms

Enzyme control

Secreted in an inactive form

Protein cleavage

pH

Cofactors

Fuse or pin


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Defense mechanisms

Cell turnover

Stratified squamous epithelial cells in upper GI

Mucosal epithelial cells in lower GI

Cells shed from villous tips Crypts form proliferative pool

Cells become more mature as they move up the villi

Average turnover time ~ 3 days

Damage rapidly repaired by sliding of mucosalepithelial cells


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Defense mechanisms

Nutrient sequestration

Fe sequestration

Fe required for bacterial growth

Fe binding proteins

Bacterial response: hemolytic toxins

Competition

Large numbers of normal intestinal flora/fauna Limits niches available for invading organisms

Initial colonization very difficult to unseat


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Defense mechanisms

Acquired immunity Separate (sort of) immune system

GALT

Secretory IgA

Resistant to degradation Blocks uptake of toxic compounds

Very tight control Always bacteria present

Pathogenicity may depend on number or organisms or other

specific circumstances/conditions Always protein antigens present

Under-responsive infection

Over-responsive chronic inflammation IBD, Crohns, ulcerative colitis, PLE, amyloidosis


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Summary

Contradictory function Absorb nutrients/exclude toxins

Digest nutrients, dont digest self

React to pathogens, dont react too much

Effective defense mechanims Constant washing

Rapid turnover

Competition Environmental monitoring

Environmental control


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Clinical Signs

Ptyalism (drooling)

Regurgitation undigested food

Vomiting partially digested food

Diarrhea

Tenesmus

Dehydration not specific for GI disease

Abdominal pain (colic)

Electrolyte abnormalities

Melena digested blood

Hematochezia bloody feces

Cholemesis/hematemesis


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Developmental

Cleft palate

(palatoschesis)

Failure of maxillary

bones to fuse Variably sized defect

in hard palate

May interfere with

nursing, feeding,chronic nasal

infections


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Developmental

Cleft lip/hare lip

Brachygnathia

Superior shortened

maxillae Inferior shortened

mandibles

Prognathism


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Developmental

Dentition

Heterotopic polydontia

Common in horses

Anomalous dentition

Missing or retaineddeciduous teeth

Odontodystrophy

Enamal hypoplasia

Secondary to distemper

virus infection in dogs

Fluorine toxicity,

malnutrition, vitamin A

deficiency


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Traumatic

Fractures

Dislocations

Foreign bodies

Bonesdogs

Linear cats


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Viral Stomatitis: vesicular

stomatitides

Vesicle = small circumscribed elevation of theepidermis/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 inUS


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Oral Cavity Vesicular

Stomatitides

Ruptured vesicle, sheep, FMD

Ruptured vesicles, snout, pig, FMD


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Foot & Mouth, bovine


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Viral Stomatitis: Erosive &

Ulcerative Stomatitides Erosion loss of superficial layers of epidermis

or mucosal membrane

Ulceration loss of all layers of epidermis ormucosal membrane Penetrates the basement membrane

Viral erosive & ulcerative stomatitides BVD-MD

Malignant Catarrhal Fever

Rinderpest Bluetongue

Equine Viral Rhinotracheitis

Felince Calicivirus


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BVD Mucosal Disease

Bovine viral diarrhea virus (BVDV)

Highly contageous

Rarely fatal Fever, diarrhea, mucosal ulcerations,

leukopenia

Multiple serotypes Cytopathic

Non-cytopathic


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BVD Mucosal Disease

Normal disease course

Immunocompetent animal

Subclinical or mild disease

Mucosal disease course Infection during 4th month of gestation

Abortion, fetal mummification, develpmentalanomalies (cerebellar hypoplasia)

Surviving animals Persistent infection

Immunotolerant to virus


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BVD Mucosal Disease

Persistently infected, immunotolerant

animal

Super-infected with a cytopathic strain

Unable to mount effective immune response

Severe ongoing infection

Near 100% fatality rate

Anorexia, bloody diarrhea, fever, mucoid nasaldischarge, ulcerative lesions throughout GI tract


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BVD Mucosal Disease


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Malignant Catarrhal Fever (MCF)

Caused by several different gamma

herpes viruses

Cattle, deer, most other ungulates

Ovine herpes virus 2

North America

Alcelaphine herpes virus 1

Endemic in African wildebeest

Causes disease in zoo ruminants and cattle in

Africa


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Malignant Catarrhal Fever (MCF)

Gross lesion is ulceration of mucosal

surfaces, edema, mucopurulent nasal

discharge, lymphadenopathy

Microscopic lesions

Lymphoid proliferation

Fibrinoid vascular necrosis


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Feline Calicivirus

RNA virus High rates of mutation

Variable virulence

Persistent infections

Minimal clinical signs Virus shed in saliva, nasal

secretions, feces

Clinical signs Ulcers on tongue and foot

pads Conjunctival edema,

edema of face & limbs

Pneumonia in kittens


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Viral Stomatitis: Papular

Stomatitides

Papule small, circumscribed, superficial, solid

elevation of skin or mucous membrane

Pustule visible collection of pus within or

beneath the epidermis or mucous membrane Macule discolored circular area on skin or

mucous membrane that is not elevated above

the surface. Smoking remains of a papule or

pustule


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Bovine Papular Stomatitis

Young cattle 1 month to 2 years old

Parapox virus

Epidermal proliferation

Papules, nodules, macules

Tongue, gingiva, palate, esophagus, rumen,

omasum

Eosinophilic intracytoplasmic inclusions


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Bovine Papular Stomatitis


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Contagious Ecthyma (Orf)

Sheep and lambs, goats, rarely man

Parapox virus

Epidermal proliferation Lips, mouth, teats

Weight loss/poor growth due to pain

Self limiting


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Contagious Ecthyma (Orf)


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Papillomatosis


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Papillomatosis


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Papillomatosis


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Bacterial Stomatitides

Associated with trauma

Feeding, iatragenic, foreign body

Opportunistic normal bacterial inhabitant

Actinobacillus, actinomyces, fusobacterium


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Necrotizing stomatitides

Oral necrobacillosis

Calf diphtheria

Necrotic membrane

Foul breath, anorexia,fever


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Wooden tongue

Actinobacillus

lignieresii

Often associated

w/lingual groove Chronic infection

Severe fibrosis

Wooden tongue


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Wooden tongue

Pyogranulomas

Club-shaped bacterial

colonies

Splendora-Hepli sulfur granules


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Periodontal Disease

Periodontal tissues Gingiva, cementum,

periodontal ligament, alveolarsupporting bone

>85% of dogs and cats 4 yearsand older are affected

Pathogenesis Placque formation

Mucin, slouphed epithelialcells, aerobic gram + bacteria

Mineral salts deposite onplaque

Tartar/calculus

Tartar gingival irritation pH change

Pathogenic gram aerobic& anaerobic bacteriaproliferate beneath gingiva


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Periodontal Disease

Destructive inflammation

forms gingival crevice

Sub-gingival bacteria

continue to proliferate

Deeper pockets ofdestruction

Gingival stroma

Periodontal ligament

Alveolar bone

Tooth loss, bacteremia,

osteomyelitis, bacterial

endocarditis

St f P i d t l Di


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Stages of Periodontal Disease

Stage I gingivitis, gingival edema

Stage II gingivitis, pockets

Stage III stroma loss, deep pockets

Stage IV bone loss, loose teeth


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Inflammatory, non-infectious

Inappropriate immune/inflammatory

response

Self antigen autoimmune

Unknown antigen immune mediated

Generally a problem of small animals

(Dogs and Cats)


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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


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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


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Immune Mediated

Feline plasma cell

gingivitis

Raised, erythematous,

proliferative lesion

Glossopalatine arch

Periodontal gingiva


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Immune Mediated

Feline plasma cellgingivitis Histologic appearance

Gingival hyperplasia

Gingival ulceration Large numbers of

plasma cells

Russell bodies

Secondary suppurative

inflammation over areasof ulceration

Increased serumgamma globulin


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Immune Mediated

Eosinophilic ulcer

(Rodent ulcer,

Eosinophilic granuloma

complex)

Chronic superficialulcerative disease of

mucosa and

mucocutaneous junction

Frequently affects upper

lip of cats Siberian huskies

Affected area is thickened,

red, ulcerated


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Immune Mediated

Eosinophilic ulcer

Histologic appearance

Ulcerated surface

Moderate to large

numbers of eosinophilswith macrophages,

lymphocytes, and

plasma cells

Collagenolysis


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Uremic glossitis

Relatively common lesionassociated with renal

failure in dogs and less

commonly in cats

Clinical signs Cyanotic buccal mucosa

Fetid ulceration of tongue

Margins of ulcer swollen


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Uremic glossitis


Necrosis of mucosal

epithelium with ulceration

Vascular necrosis of small

arterioles of tongue Ischemic vascular lesion

Pathogenesis poorly

understood

Poor correlation betweenblood ammonia levels

and lesion development

Proliferative and neoplastic oral


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Proliferative and neoplastic oral

lesions


Non-neoplastic

proliferation of gingival

tissue

Caused by chronic

inflammation

May be associated with

periodontal disease

Generalized orlocalized

Brachycephalic breeds


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Histologic

appearance

Mature fibrous

connective tissue

Hypocellular

May have focal areas

of ulceration and

inflammation


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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 inbrachycephalic breeds

May mechanicallydisplace the teeth

Attached to the periosteum

Do not invade bone


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Epuloides

Fibromatous epulis


Interwoven bundles of

fibroblastic tissue

More cellular thangingival hyperplasia

May have areas of

bone production

Ossifying epulis


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Other tumors of dental origin

Less common than epuli

Ameloblastoma

Dental lamina

Outer enamel epithelium

Odontogenic epithelium

May produce dentin or

enamel matrix

Rare in all species, but less

rare in cattle

Young cattle


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Other tumors of dental origin

Complex odontoma

Fully differentiated dental components

Disorganized, no tooth like structures

Young horses Compound odontoma

Mass containing numerous tooth-like structures

denticles

Young dogs, cattle, and horses Mandibular or maxillary arch


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Oral tumors of non-dental origin

Squamous cell carcinoma Most common oral

neoplasm is cats

Ventral surface of the

tongue, along the

frenulum

Nodular, red-grey mass

Friable

Often ulcerated

Locally invasive

Metastasize to regionallymph nodes

Rarely metastasize to lung


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Squamous cell carcimona

2nd most common oral neoplasmin dogs Usually involves tonsil

Small granular plaque 2-3x sizeof the tonsil

Nodular, firm, white, frequentlyulcerated

Locally invasive Metastasize to regional lymph

nodes

Frequently met to distant sites,especially lung

SCC arising from the gingiva isless likely to met than tonsillarSCC in dogs

Horses & cattle Rare, slow growing, very

destructive, met to regional lymphnodes


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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 andbiologic behaviour

Met to lymph nodes, distant organs, especially lungs Median survival time ~ 65 days in untreated animals


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Melanoma

Gross appearance

Nodular, variably

pigmented masses

Anywhere in the oral

mucosa

Invasive and

destructive

May or may not be

ulcerated


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Melanoma

M l


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Melanoma

Microscopicappearance

Variable

Heavily pigmented toamelanotic

Cytologically appear

as round cells

M l


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Melanoma

Fib


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Fibrosarcoma

Can occur in all animals, but usually seenin 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 of the mandible

Fib


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Fibrosarcoma

Gross appearance Nodular to multi-

nodulare

+/- ulceration

Firm

Local invasion

~ 35% metastasize tolymph nodes

Early pulmonarymetastasis

Fib


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Fibrosarcoma

Histologicappearance

Moderately cellular

Streams of fibroblastic

cells

High mitotic rate

Collagenous extra-

cellular matrix

O t


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Osteosarcoma

Bones of the skull orjaw

Similar in appearance

to fibrosarcoma Bone lysis and

proliferation on

radiographs

R d ll t


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Round cell tumors

Mast cell tumors Discreet mass

Lymphosarcoma

Tonsillar Epitheliotrophic

Plasma cell tumors

Discreet mass

Pleomorphic plasma

cells

S li Gl d


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Salivary Glands

Sialoadenitis = inflammation of salivary gland uncommon in vetmedicine 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

S li R l


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Salivary Ranula

Diagnosis of Sialocoele


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Diagnosis of Sialocoele

Aspirate mass with largebore 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 affectedsalivary gland


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E h


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Esophagus

Tube Smooth and striated

muscle

Glands

Mucosal epithelium

Esophagus: developmental


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p g p

anomalies

Developmental anomalies of theesophagus are rare

Segmental aplasia

Esophago-respiratory fistula

Esophageal diverticulae

Hyperkeratosis/squamous metaplasia

Esophagus: traumatic lesions


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Esophagus: traumatic lesions

Obstruction choke

Occurs at areas ofesophageal narrowing

Larynx Thoracic inlet

Base of heart

Diaphragmatic hiatus

Clinical signs Salivation, wretching,

regurgitation,dehydration

Esophagus


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Esophagus

Complications ofchoke

Esophageal rupture

cellulitis, death

Esophageal dilation

mega-esophagus

Ulceration with

subsequent stricture

Common in cattle

Hedge apples

Aspiration pneumonia


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Esophagitis


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p g

Esophageal biopsy fromhorse with 2 month

history of regurgitation

Mucosal ulceration

Marked submucosalinflammation

Disruption of submucosal

glands

Outcome could bestricture or aspiration

pneumonia

Megaesophagus


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Megaesophagus

Dilation of esophagus due to insufficient or uncoordinated peristalsis in themid 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, OPs

Parasites such as Toxoplasma gondii and Trypanosoma cruzi

Idiopathic

Megaesophagus


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Persistent right aortic

arch Upper right normal

development of aortic arch

(inset shows normal

embryonic development of

great vessels)

Lower right when embryonicright fourth aortic arch

becomes adult aorta,

esophageal constriction

occurs (inset shows vascular

malformation

Constricting ring formed by rightaortic arch, pulmonary artery, and

ductus arteriosus

Dilation of esophagus occurscranial to heart

Megaesophagus


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Megaesophagus

Megaesophagus


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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


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Megaesophagus


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Esophageal Parasitic Disease


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Esophageal Parasitic Disease

Spirocerca Lupiof 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


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Spirocerca lupi

Aortic Nodules and Aneurysms


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During the time that parasites are normally in the aorta, or if

parasites are arrested in the aorta during migration, they maycause the formation of small nodules or larger, more diffuse

granulomas and aneurysms which can rupture leading to fatal

extravasation into the abdominal cavity.

y

Epidemiology


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The slide illustrates the general distribution of reported Spirocerca sarcoma in

the Southeast. Incidence of simple Spirocerca infection would follow a similar

distribution. Bailey at Auburn recorded an 8% infection rate in Alabama in a

survey between 1951 and 1963, but only 2% from 1963-1970. Georgia surveysshow 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 ofSpirocerca 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 ofSpirocerca lupi


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Note the small size, thick wall and larvae. A whipworm egg is

also present. Recovery of eggs is dependent on a patent openingto 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


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Conditions

Idiopathic muscularhypertrophy of distalesophagus

Seen in horses, no clinicalsignificance

Esophagitis

Often result of trauma

Secondary bacterial infection

Esophageal erosions/ulcers

Reflux, trauma, viral disease

BVD MD in cattle

Papillomas

Ruminant Forestomach


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Rumen papillae Reticulum

epithelial folds

Omasum epithelial

folds

Normal Anatomy

Ruminant Forestomach


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Bloat (ruminal tympany)- Overdistention of rumen and reticulum by gasesproduced during fermentation Primary tympany (legume bloat, frothy bloat)

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


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Ruminant Forestomach - Bloat

Post mortemdiagnosis often based

on observing bloat

line which is a line of

demarcation between

the bloodless distal

esophagus and the

congested proximalesophagus at thoracic

inlet

Ruminant Forestomach Foreign


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Bodies

Trichobezoars =hairballs

Hair forms nidus

Phytobezoars =plant balls

Ruminant Forestomach Foreign


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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)


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Rumenitis (Lactic Acidosis)

Common disease of cattle that consume excessive readily digestiblecarbohydrates, especially grain (grain overload)

Within 2-6 hours, microbial population of rumen changes to grampositive bacteria (Strep bovis) which results in production of lacticacid

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 acidosisresulting in cardiovascular collapse (shock), renal failure and death

If survive, may develop bacterial or mycotic rumenitis in severaldays, 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


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Grain Overload

Reticulitis/Rumenitis


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Reticulitis/Rumenitis


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Mycotic Rumenitis


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Miscellaneous Rumen Conditions


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Ruminal parakeratosis seen in cattle andsheep fed diets with less than 10%roughage

Papillae are enlarged, adhered together andfirm

Affected papillae contain excessive layers ofkeratinized epithelial cells, bacteria and foodmaterial

May alter nutrient absorption, decrease feedefficiency



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Vagus Indigestion (chronic indigestion) Seen in cattle and sheep

Gradual development of rumenoreticular and abdominaldistention

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 omasalcanal, 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 coarseroughage with restricted access to water, especially in winter

Type IV poorly characterized partial forestomach obstruction thatusually occurs during gestation, may be due to enlarging uterusshifting abomasum to more cranial position

Dx definitive may require exploratory left paralumbar fossalaparotomy and rumenotomy


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Abomasal Disorders


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Abomasal Disorders

Abomasal displacement (LDA, RDA)Abomasal volvulus

Abomasal ulcers

Abomasal ImpactionAbomasal inflammation (abomasitis)

Bovine viral diarrhea and mucosal disease

Abomasal parasites Lymphosarcoma

Abomasal Displacements


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Abomasal Displacements

Usually to left side in high producing dairy cattle withinone month of parturition Result of abomasal atony with gas distention and displacement

upward along left abdominal wall

Fundus and greater curvature displaced creating partialobstruction

No interference with blood supply but passage of ingesta slowedleading to chronic partial anorexia

Also see metabolic alkalosis related to sequestration ofchloride in abomasum (HCL production continues)

RDA occurs infrequently but atony, gas production anddisplacement occur as in LDA

Then have rotation (volvulus) of abomasum on its mesenteryresulting in ischemia

Rotation is usually in counterclockwise when viewed from rear

Leads to complete anorexia, necrosis of abomasal wall, shock


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Abomasal Ulcers Seen in adult cattle and calves


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Many etiologic possibilities such asviral disease (BVD, rinderpest, MCF)

Nonviral in dairy cows 6 weeks after

parturition (stress, heavy grainfeeding?)

Nonviral feedlot cattle on high grainrations

Nonviral hand fed dairy calves onmilk replacer that start to eat roughage

Nonviral suckling beef calves ongood summer pasture

Fungal secondary to rumen acidosis.Caused by infarcts due to fungalinvasion and destruction of smallarterioles

Ulcers most common along greatercurvature Type 1 = erosion/ulcer, no hem

Type II = hemorrhagic Type III = perforation/local peritonitis

Type IV = perforation with acute diffuseperitonitis

Perforating Abomasal Ulcer


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e o at g bo asa U ce

Dietary Abomasal Impaction


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Seen in cattle and sheep

fed poor quality,indigestible roughageduring cold weather, canalso be sand if on poorquality pasture with sandy

soil See abomasal atony andchronic dilation

Dehydration, anorexia,alkalosis, and progressive

starvation Abomasal emptyingdefect is an idiopathiccondition in Suffolk sheep

Abomasal Inflammation


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Braxy in sheep and cattle Caused by Clostridium septicum

Hemorrhagic abomasitis with submucosal

emphysema Bacteria produces exotoxin that leads to

toxemia and shock


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Abomasal Parasites


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Haemonchus contor tus common parasite ofsheep and otherruminants

Third stage larvae eaten

on grass enter gastricglands onto surface asadults

Feed on blood serious

anemia andhypoproteinemia (seen assubmandibular andmesenteric edema)

Haemonchus


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Residual damage inabomasal mucosa

caused by third stage

larvae

There is focal

destruction of deep

glands and

lymphocyticinflammation

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


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Horse Stomach


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Stomach capacity is onlyabout 2.5 gallons

Located on left side ofabdomen beneath ribcage

Junction of distalesophagus and cardia isone-way valve (in but notout) therefore, horses cannot

vomit gastric contents

Celiac artery suppliesblood to stomach

Stomach Colic Conditions


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Gastric dilatationGastric rupture

Gastric impaction

Gastric Ulcer Syndrome (adults/foals)

Gastric parasites

Gastric neoplasia

Gastric Dilatation


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

which inhibit gastric emptying

Obstruction usually in small intestine and fluidaccumulates in stomach

Right dorsal displacement of colon aroundcecum obstructs duodenal outflow

Proximal enteritis-jejunitis leads to gastric fluidbuildup

Gastric Rupture


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p

Stomach rupture is fatal outcome ofuncorrected gastric dilatation

Tear usually occurs along greater

curvatureMost (approximately 2/3) occur secondary

to mechanical obstruction, ileus or trauma

Remaining due to overload or idiopathiccauses

Gastric Impaction


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p

Uncommon cause of colicMay 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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y

Currently recognized EGUS in adults >1 yearof 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


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Gastric fill and contentscomposition in horse allowedfree access to forage

Fill line is not much abovelower esophageal sphincter

Coarser contents layer at topand fine particulates filter tobottom

Upper, coarser mat is furthestaway from acid secretingmucosa and more accessibleto swallowed saliva hashigher pH than more liquid

contents at bottom Bottom contents adjacent to

HCL-producing parietal cells

Normal Gastric Acid Secretion


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Equine Gastric Ulcer Syndrome


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Erosion and/or ulcerationof nonglandular

(squamous) mucosa

Seen as a primary or

secondary condition Seen in adult horses

under intensive training,

any breed

Pathogenesis is poorlyunderstood

EGUS (proposed pathogenesis)*


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Exercise in horsescauses pH change inproximal part of stomach

The more liquid, highlyacidic contents in thelower glandular stomachare squeezed up aroundthe more solid contentsby increased intra-abdominal pressure (redarrows) due to tensing of

abdominal muscles aspart of the movement atfaster gaits

*Merritt, AAEP, 2003

Primary Glandular Ulcer Disease


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Ulceration of glandularmucosa, especially inpyloric region

Causes include NSAIDtoxicity (leads to down

regulation of PGE2production withinglandular mucosa)

Changes in mucosalblood flow andHelicobacter infectionhave not beendemonstrated

Primary Glandular Ulcer Disease


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Multiple sites ofglandular mucosal

ulceration (yellow

arrows) induced by

NSAID toxicity

Squamous mucosa

(upper right) is free of

lesions

Secondary Squamous Ulceration


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Primary lesion commonlyoccurs in duodenum(GDUD) of foals neverseen in horses >1 yearold

In adults may see gastricoutflow obstructioncaused by duodenalstricture reflux?

In adults may also seesecondary to any

condition causingglandular ulcerativegastritis (NSAID)

Secondary Squamous Ulceration


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Endoscopic view ofnormal pyloric sphincterregion (yellow arrow,upper right) in itscommonly open state-this allows for reflux of

duodenal contents Endoscopic view of

severe inflammationaround pyloric canalyellow arrow indicates

mucosal erosion suchlesions can scar andresult in stricture thatreduces gastric emptying

Gastric Ulcer


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Stomach from adultthoroughbred mare

that was unthrifty and

partially anorectic

There are

erosions/ulcers in

both the glandular

and nonglandularportions of the

mucosa

Current Syndromes in Foals (< 1 yr

of age)


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of age)

Gastroduodenal ulcer disease(GDUD) - sucklings and earlyweanlings

Cause is unknown

In early stage of GDUD seeroughened duodenal mucosa

covered with fibrinous plaquecauses some disruption ofgastric emptying with somesecondary squamous erosionand ulceration

May recover after supportiveRx or develop advanceddisease

Advanced GDUD in foals


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Clinical signs include drooling,teeth grinding, periodic boutsof colic especially aftersuckling, and weight loss

If signs persist for a week, mayindicate stricture of duodenum

by inflammation andmechanical obstruction togastric emptying

Barium meal will be retainedlonger than 1 hour

Endoscopy will showerosion/ulceration ofsquamous mucosa of stomachand lower esophagus

Advanced GDUD in Foals


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Endoscopic views of reflux esophagitis

and squamous gastritis that are

commonly seen in foals with chronicGDUD. 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 distinctstrictures of duodenum (arrows) which

is a serious consequence of GDUD

Primary Erosion/Ulceration of

Squamous Mucosa in Foals


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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 previouslyunrecognized GDUD

Stress-Related Gastric Ulcers in

Foals


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Foals

Primarily seen in foalssuffering from a severeillness or trauma

May involve down-regulation of PGE2 due to

reduced mucosal bloodflow

Lesions usually confinedto glandular mucosa justadjacent to margoplicatus may be severeenough to perforate

Gastric parasites


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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 onhairs 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 oralhooks, cause mild gastritis, pass out in feces in 8-10

months


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Gastric Parasites


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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 inmanure

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

Larvae deposited on lips, nostrils and wounds of horses as flies feed iflicked and swallowed, larvae mature in stomach

If larvae in wounds not licked and swallowed, they stay in or aroundwound causing cutaneous habronemiasis

Infected flies can also be eaten by horse

In stomach, H. muscae and H. microstoma are on mucosal surfaceunder 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


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Posterior end of

adult Habronema

spp worm

showing spicule

Cutaneous habronemiasis

Nodule in stomach caused by D.

megastoma

Stomach Conditions of Pigs


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Gastric ulcers

Edema disease

Parasites

Pig Gastric Ulcers


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Seen in pigs of all ages butmost common in confinedgrowing pigs (45-90 kg)

Cause unknown but finelyground feed and stress are riskfactors

Lesions occur at parsesophagea and begin as areasof hyperkeratosis, this erodesand later have ulcer.

Pigs can bleed out andproduce tarry stool, or bechronically unthrifty

Edema Disease


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

Toxin affects capillaries and small arteriesleading to edema and ischemia in many organs

Usually occurs in young pigs 1-2 weeks afterweaning and affects healthiest animals in a

group We will talk more about this disease later

Edema disease


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Submucosal edema in glandular region

Periocular edema

Edema in stomach wall

Stomach Parasites of Pigs


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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


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Cattle lymphosarcoma anywhere inforestomach Usually associated with

BLV

Squamous cell carcinomaof rumen also seen rarely

Horse squamous cellcarcinoma ofnonglandular region of

stomach Pig tumors of stomach

morganpath1 lq patologia g.i

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