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)


Proteins (amino acids)


Active transport
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


Nutrients kept in
Toxic compounds kept out
 Most

absorption
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

Paneth cells
•
•
•
•


immunity
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
Traumatic

Fractures
 Dislocations
 Foreign bodies


Bones –dogs
Linear – cats
Inflammatory
 Stomatitis

Glossitis, gingivitis, pulpitis
 Infectious



– general term
Viral
Bacterial
Fungal
diseases of the oral cavity
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”


Immunocompetent animal
Subclinical or mild disease
 Mucosal

disease course
disease course
Infection during 4th 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



Persistent infections



High rates of mutation
Variable virulence
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 II – gingivitis, pockets
Stage III – stroma loss, deep 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

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
Melanoma

Most common oral tumor in dogs


Almost always malignant


Rare in cats and large animals
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



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
Fibrosarcoma

Gross appearance




Nodular to multinodulare
+/- 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 extracellular 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


Lymphosarcoma



Discreet mass
Tonsillar
Epitheliotrophic
Plasma cell tumors


Discreet mass
Pleomorphic plasma
cells
Salivary Glands

Sialoadenitis = inflammation of salivary gland – uncommon in vet
medicine



Ranula = cystic distention of duct of sublingual or mandibular glands



Possible causes include trauma, foreign body or sialolith
Sialolith = stone in gland or duct


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


Sialodacryoadenitis (SDA) coronavirus of lab rats
Rabies and canine distemper
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


Esophagitis



Seen in horses, no clinical
significance
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


Foreign bodies




Esophageal foreign body, vagal nerve dysfunction, lymphosarcoma, etc.
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
parakeratosis – seen in cattle and
sheep fed diets with less than 10%
roughage
 Ruminal



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
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
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 – paired
serum samples with 4 fold rise in titer, PCR,
virus isolation (submit lymph node, spleen,
gut lesions)
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)
Haemonchus

Residual damage in
abomasal mucosa
caused by third stage
larvae
 There is focal
destruction of deep
glands and
lymphocytic
inflammation
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
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

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 – has
higher pH than more liquid
contents at bottom
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 intraabdominal 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 – 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)
Secondary Squamous Ulceration


Endoscopic view of
normal pyloric sphincter
region (yellow arrow,
upper right) in its
commonly open statethis 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
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 downregulation 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