Title: Pathology of the GI tract
1Pathology of the GI tract
2Alimentary Canal
- Continuous tube
- Tube within a tube
- Mouth (oral end)
- Anus (aboral end)
- Function
- Acquire nutrients
- Digest nutrients
- Absorb nutrients
- Expel non-digestible portion
3Prehension
- Fairly complex series of events
- Hunger centers in the brain
- Higher senses to locate food
- Lips especially in herbivores
- Tongue
- Teeth
- Esophagus
4Digestion
- Mouth
- Grinding
- Salivary enzymes starches
- Stomach
- Mixing vat
- Acidification (monogastrics)
- Fermentation (ruminates)
5Digestion
- Small intestine
- Pancreas
- Enzymes
- Buffer
- Bile
- Emulsifies lipids
6Digestion
- Carbohydrates
- Polysaccharides
- Enzymatically broken down to monosaccharides
- Hydrolysis
7Digestion
- Proteins
- Polypeptides
- Enzymatically broken down to amino acids
- Hydrolysis
8Digestion
- Fats
- Triglycerides 3 fatty acids on a glyceride
backbone - Enzymatically broken down to monoglycerides and
fatty acids - Hydrolysis
9Absorption
- 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
10Absorption
- 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
11Absorption
- 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
12Dilemma
- 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
13Defense 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
14Defense mechanisms
- Enzyme control
- Secreted in an inactive form
- Protein cleavage
- pH
- Cofactors
- Fuse or pin
15Defense 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
16Defense 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
17Defense mechanisms
- Innate immunity
- Paneth cells
- Antimicrobial peptides
- Defensins
- Cathelicidins
- Toll-like receptors
- Neutrophils
- Macrophages
18Defense 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
19Summary
- 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
20Clinical 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
21Oral Cavity
- Developmental
- Traumatic
- Toxic
- Inflammatory
- Infectious
- Viral, bacterial, fungal
- Autoimmune
- Neoplastic
22Developmental
- Cleft palate (palatoschesis)
- Failure of maxillary bones to fuse
- Variably sized defect in hard palate
- May interfere with nursing, feeding, chronic
nasal infections
23Developmental
- Cleft lip/hare lip
- Brachygnathia
- Superior shortened maxillae
- Inferior shortened mandibles
- Prognathism
24Developmental
- 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
25Traumatic
- Fractures
- Dislocations
- Foreign bodies
- Bones dogs
- Linear cats
26Inflammatory
- Stomatitis general term
- Glossitis, gingivitis, pulpitis
- Infectious diseases of the oral cavity
- Viral
- Bacterial
- Fungal
27Viral Stomatitis vesicular stomatitides
- Vesicle small circumscribed elevation of the
epidermis/MM containing a serous liquid - Vesicular stomatitides cannot be differentiated
grossly call state or federal vet immediately - Foot and mouth disease (Picornavirus)
ruminants, pigs not in US - Vesicular stomatitis (Rhabdovirus) ruminants,
pigs, horses in US - Vesicular exanthema (Calicivirus) pigs not in
US - Swine vesicular disease (Enterovirus) pigs
not in US
28 Oral Cavity Vesicular Stomatitides
Ruptured vesicle, sheep, FMD
Ruptured vesicles, snout, pig, FMD
29Foot Mouth, bovine
30 Vesicular Stomatitides - VS
Ruptured vesicles, coronary band,
horse, VS
Vesicle on teat of cow, VS
31Viral Stomatitis Erosive Ulcerative
Stomatitides
- Erosion loss of superficial layers of epidermis
or mucosal membrane - Ulceration loss of all layers of epidermis or
mucosal membrane - Penetrates the basement membrane
- Viral erosive ulcerative stomatitides
- BVD-MD
- Malignant Catarrhal Fever
- Rinderpest
- Bluetongue
- Equine Viral Rhinotracheitis
- Felince Calicivirus
32 BVD Mucosal Disease
- Bovine viral diarrhea virus (BVDV)
- Highly contageous
- Rarely fatal
- Fever, diarrhea, mucosal ulcerations, leukopenia
- Multiple serotypes
- Cytopathic
- Non-cytopathic
33BVD Mucosal Disease
- Normal disease course
- Immunocompetent animal
- Subclinical or mild disease
- Mucosal disease course
- Infection during 4th month of gestation
- Abortion, fetal mummification, develpmental
anomalies (cerebellar hypoplasia) - Surviving animals
- Persistent infection
- Immunotolerant to virus
34BVD 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
35BVD Mucosal Disease
36Malignant 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
37Malignant Catarrhal Fever (MCF)
- Gross lesion is ulceration of mucosal surfaces,
edema, mucopurulent nasal discharge,
lymphadenopathy - Microscopic lesions
- Lymphoid proliferation
- Fibrinoid vascular necrosis
38Malignant Catarrhal Fever (MCF)
39Feline 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
40Viral 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
41Bovine 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
42Bovine Papular Stomatitis
43Contagious Ecthyma (Orf)
- Sheep and lambs, goats, rarely man
- Parapox virus
- Epidermal proliferation
- Lips, mouth, teats
- Weight loss/poor growth due to pain
- Self limiting
44Contagious Ecthyma (Orf)
45Papillomatosis
- Papovavirus
- Bovine papilloma virus
- Canine papilloma virus
- Papillomas (warts) on mucosa of mouth, esophagus,
rumen (cattle) - Usually self-limiting lesions
46Papillomatosis
47Papillomatosis
48Papillomatosis
49Bacterial Stomatitides
- Associated with trauma
- Feeding, iatragenic, foreign body
- Opportunistic normal bacterial inhabitant
- Actinobacillus, actinomyces, fusobacterium
50Necrotizing stomatitides
- Oral necrobacillosis
- Calf diphtheria
- Necrotic membrane
- Foul breath, anorexia, fever
51Wooden tongue
- Actinobacillus lignieresii
- Often associated w/lingual groove
- Chronic infection
- Severe fibrosis
- Wooden tongue
52Wooden tongue
- Pyogranulomas
- Club-shaped bacterial colonies
- Splendora-Hepli
- sulfur granules
53Periodontal Disease
- Periodontal tissues
- Gingiva, cementum, periodontal ligament, alveolar
supporting bone - gt85 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
54Periodontal 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
55Stages of Periodontal Disease
Stage I gingivitis, gingival edema
Stage III stroma loss, deep pockets
Stage II gingivitis, pockets
Stage IV bone loss, loose teeth
56Inflammatory, non-infectious
- Inappropriate immune/inflammatory response
- Self antigen autoimmune
- Unknown antigen immune mediated
- Generally a problem of small animals (Dogs and
Cats)
57Auto-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
58Auto-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
59Immune Mediated
- Feline plasma cell gingivitis
- Raised, erythematous, proliferative lesion
- Glossopalatine arch
- Periodontal gingiva
60Immune 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
61Immune 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
62Immune Mediated
- Eosinophilic ulcer
- Histologic appearance
- Ulcerated surface
- Moderate to large numbers of eosinophils with
macrophages, lymphocytes, and plasma cells - Collagenolysis
63(No Transcript)
64Uremic 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
65Uremic 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
66Proliferative 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
67Gingival hyperplasia
- Histologic appearance
- Mature fibrous connective tissue
- Hypocellular
- May have focal areas of ulceration and
inflammation
68Epuloides
- 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
69Epuloides
- Fibromatous epulis
- Histologic appearance
- Interwoven bundles of fibroblastic tissue
- More cellular than gingival hyperplasia
- May have areas of bone production
- Ossifying epulis
70Epuloides
- Acanthomatous epulis (acanthomatous
ameloblastoma) - Odontogenic epithelial origin
- Rough, cauliflower-like lesion
- Dental arcade of dogs
- Locally invasive
- Invades and destroys bone
- Do NOT metastasize
71Epuloides
- Acanthomatous epulis
- Histologic appearance
- Highly cellular
- Interconnecting odontogenic epithelial sheets
bordered by columnary to cuboidal cells - Contain numerous, usually empty, blood vessels
72Other 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
73Other 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
74Oral 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
75Squamous 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
76Melanoma
- 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
77Melanoma
- Gross appearance
- Nodular, variably pigmented masses
- Anywhere in the oral mucosa
- Invasive and destructive
- May or may not be ulcerated
78Melanoma
79Melanoma
- Microscopic appearance
- Variable
- Heavily pigmented to amelanotic
- Cytologically appear as round cells
80Melanoma
81Fibrosarcoma
- Can occur in all animals, but usually seen in
dogs - 3rd most common oral tumor of dogs
- 25 occur in dogs lt 5 yrs of age
- Occur in gums around upper molars and in the
cranial ½ of the mandible
82Fibrosarcoma
- Gross appearance
- Nodular to multi-nodulare
- /- ulceration
- Firm
- Local invasion
- 35 metastasize to lymph nodes
- Early pulmonary metastasis
83Fibrosarcoma
- Histologic appearance
- Moderately cellular
- Streams of fibroblastic cells
- High mitotic rate
- Collagenous extra-cellular matrix
84Osteosarcoma
- Bones of the skull or jaw
- Similar in appearance to fibrosarcoma
- Bone lysis and proliferation on radiographs
85Round cell tumors
- Mast cell tumors
- Discreet mass
- Lymphosarcoma
- Tonsillar
- Epitheliotrophic
- Plasma cell tumors
- Discreet mass
- Pleomorphic plasma cells
86Salivary Glands
- Sialoadenitis inflammation of salivary gland
uncommon in vet medicine - Sialodacryoadenitis (SDA) coronavirus of lab rats
- Rabies and canine distemper
- Ranula cystic distention of duct of sublingual
or mandibular glands - Occurs on floor of mouth alongside the tongue
- Cause is unknown
- Salivary mucocoele (sialocoele) pseudocyst
filled with saliva that causes inflammation with
formation of granulation tissue - Possible causes include trauma, foreign body or
sialolith - Sialolith stone in gland or duct
- Formed from sloughed gland epithelium that
becomes surrounded by mineral - Tumors usually derived from glandular/duct
epithelium (adenoma, adenocarcinoma) - May also see mesenchymal or mixed tumors
including osteosarcoma
87Salivary Ranula
88Diagnosis 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
89Salivary gland
Chronic inflammation of mandibular salivary gland
secondary to sialocoele in dog
Sialocoele wall composed of granulation tissue
90Esophagus
- Tube
- Smooth and striated muscle
- Glands
- Mucosal epithelium
91Esophagus developmental anomalies
- Developmental anomalies of the esophagus are rare
- Segmental aplasia
- Esophago-respiratory fistula
- Esophageal diverticulae
- Hyperkeratosis/squamous metaplasia
92Esophagus traumatic lesions
- Obstruction
- choke
- Occurs at areas of esophageal narrowing
- Larynx
- Thoracic inlet
- Base of heart
- Diaphragmatic hiatus
- Clinical signs
- Salivation, wretching, regurgitation, dehydration
93Esophagus
- Complications of choke
- Esophageal rupture ? cellulitis, death
- Esophageal dilation mega-esophagus
- Ulceration with subsequent stricture
- Common in cattle
- Hedge apples
- Aspiration pneumonia
94Esophagus
95Esophagitis
- 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
96Megaesophagus
- 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, OPs
- Parasites such as Toxoplasma gondii and
Trypanosoma cruzi - Idiopathic
97Megaesophagus
- 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
98Megaesophagus
99Megaesophagus
- 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
100Megaesophagus
Dilated esophagus anterior to stomach
101Megaesophagus
102Esophageal 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
103Spirocerca lupi
104Aortic 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.
105Epidemiology
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.
106Egg 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.
107Esophagus 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
108Ruminant Forestomach
Normal Anatomy
Rumen papillae
Reticulum epithelial folds
Omasum epithelial folds
109Ruminant 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
110Ruminant 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
111Ruminant Forestomach Foreign Bodies
- Trichobezoars hairballs
- Hair forms nidus
- Phytobezoars plant balls
112Ruminant 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
113Rumenitis (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)
114Grain Overload
115Reticulitis/Rumenitis
116Rumenitis
117Mycotic Rumenitis
118Miscellaneous 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
119Miscellaneous 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
120Stomach and Abomasum
- Similar function and response to injury among
ruminant abomasum and simple-stomached animals
Normal horse stomach
Histologic appearance
121Abomasal Disorders
- Abomasal displacement (LDA, RDA)
- Abomasal volvulus
- Abomasal ulcers
- Abomasal Impaction
- Abomasal inflammation (abomasitis)
- Bovine viral diarrhea and mucosal disease
- Abomasal parasites
- Lymphosarcoma
122Abomasal 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
123Right Displaced Abomasum with Rotation
124Abomasal 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
125Perforating Abomasal Ulcer
126Dietary 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
127Abomasal Inflammation
- Braxy in sheep and cattle
- Caused by Clostridium septicum
- Hemorrhagic abomasitis with submucosal emphysema
- Bacteria produces exotoxin that leads to toxemia
and shock
128BVD-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 Peyers 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)
129Abomasal 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)
130Haemonchus
- Residual damage in abomasal mucosa caused by
third stage larvae - There is focal destruction of deep glands and
lymphocytic inflammation
131Abomasal 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
132Abomasal Lymphosarcoma
- Lymphosarcoma can be primary, metastatic or
multicentric in origin - In cattle, often caused by bovine leukemia virus
133Horse 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
134Stomach Colic Conditions
- Gastric dilatation
- Gastric rupture
- Gastric impaction
- Gastric Ulcer Syndrome (adults/foals)
- Gastric parasites
- Gastric neoplasia
135Gastric 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
136Gastric 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
137Gastric 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
138Equine Gastric Ulcer Syndrome
- Currently recognized EGUS in adults gt1 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 lt1 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)
139Normal 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
140Normal Gastric Acid Secretion
141Equine 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
142EGUS (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
143Primary 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
144Primary Glandular Ulcer Disease
- Multiple sites of glandular mucosal ulceration
(yellow arrows) induced by NSAID toxicity - Squamous mucosa (upper right) is free of lesions
145Secondary Squamous Ulceration
- Primary lesion commonly occurs in duodenum (GDUD)
of foals never seen in horses gt1 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)
146Secondary Squamous Ulceration
- Endoscopic view of normal pyloric sphincter
region (yellow arrow, upper right) in its
commonly open state- this allows for reflux of
duodenal contents - Endoscopic view of severe inflammation around
pyloric canal yellow arrow indicates mucosal
erosion such lesions can scar and result in
stricture that reduces gastric emptying
147Gastric 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
148Current Syndromes in Foals (lt 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
149Advanced 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
150Advanced 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
151Primary 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
152Stress-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
153Gastric 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
154Horse Bots
Large numbers of larvae attached to gastric mucosa
Adult bot fly
155Gastric 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
156Habronema
Posterior end of adult Habronema spp worm showing
spicule
Cutaneous habronemiasis
Nodule in stomach caused by D. megastoma
157Stomach Conditions of Pigs
- Gastric ulcers
- Edema disease
- Parasites
158Pig 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
159Edema 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
160Edema disease
Periocular edema
Submucosal edema in glandular region
Edema in stomach wall
161Stomach 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
162Stomach 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