GI Flashcards
(128 cards)
1
Q
causes of palatoschisis in lambs and piglets
A
Lamb:
• Dam ingests Veratrum californicum
• genetic
Piglet:
• Dam ingests poison hemlock at days 3-45 of gestation
• ingestion of Crotalaria
retusia by dam
• ingestion of tobacco by dam (experimental)
2
Q
causes of enamel hypoplasia/dysplasia?
A
- Canine distemper
- BVD
- high doses of tetracycline
- hypophosphatemia
- Chronic fluoride toxicosis (“fluorosis”)
3
Q
causes of abnormal pigmentation of teeth?
Which of these causes fluoresces under UV light?
A
Pigs, calves, cats:
• hereditary porphyria
Cows:
• fluorosis
Dogs and other species:
• ingestion of tetracycline during mineralization of teeth (permanent)
Fluorescence:
• tetracycline and porphyrins
4
Q
pathogenesis of ulceration mouth secondary to renal failure?
A
renal failure
- -> increased ammonia (and BUN) in saliva
- -> vascular necrosis and mucosal damage (ulceration)
NOTE: ulceration associated with vascular necrosis and ammonia secretion also occurs in the stomach
5
Q
pathogenesis of oral ulceration secondary to vitamin C deficiency (“scurvy”)?
A
Hypovitaminosis C
- -> decreased collagen hydroxyproline synthesis
- -> fragile oral mucosa (and blood vessels)
- -> erosions and ulceration (and hemorrhage)
NOTE: collagen is in bone thus with scurvy you can have bone malformations
6
Q
Gingivitis in dogs and cats
• What bacteria is implicated in K9 gingivitis
• What enzyme does it produce that contributes to bone loss and loss of gingival collagen?
A
• usually proliferative, but can be associated with loss of collagen due to increased MMPs and enzymes from bacteria
- Porphyromonas gingivalis
- Enzyme = gingipains
7
Q
In the cat, gingivitis is the first and most consistent sign of infection with which virus?
• Why?
A
FIV
• they virus reduce CD4+ lymphocytes (immunosuppression)
8
Q
2 causes of necrotizing and ulcerative gingivitis?
A
1 - F. necrophorum
(“calf diphtheria”)
2- Borrelia vincentii
(“trench mouth”- primates)
9
Q
F. necrophorum
A
- produces many toxins
* leukotoxins (kill WBCs)
* hemolysin (hemolysis of RBCs)
• etiology of necrotizing stomatitis/glossitis/gingivitis
10
Q
clinical signs would you expect to see in an animal with gingivitis
A
- Ptyalism
- ulcers
- halitosis
- weight loss
- difficulty chewing
11
Q
Ddx for a proliferative mass in the mouth of a dog
• how are they differentiated microscopically?
A
1 - Proliferative gingivitis (MC in brachycephalic breeds)
2- FEPLO
3- Acanthomatous Ameloblastoma (AA)
4- Various benign or malignant neoplasms
- if causing bony destruction and/or metastasizes it is NOT
benign
12
Q
Proliferative gingivitis
A
brachycephalic breeds - mixed inflammation - proliferation of granulation tissue - hyperplastic gingival mucosa \+/- bacteria \+/- ulcers and erosions \+/- necrosis
13
Q
FEPLO
A
- dense cellular fibrous connective tissue
+/- foci of bone - hyperplastic gingival mucosa
• 2° inflammation if the mass is ulcerated or eroded
14
Q
Acanthomatous Ameloblastoma (AA)
A
- dense cellular fibrous connective tissue
- w/ trabeculae, cords or sheets of neoplastic odontogenic epithelium
• arises from the gingival basal epithelium or epithelial cell rests of Malassez - hyperplastic gingival mucosa
• 2° inflammation if the mass is ulcerated or eroded
15
Q
How do FEPLO and AA differ biologically?
A
FEPLO
• proliferative & expansile
• may cause some tooth loss, but not usually, surgery is curative
AA
• locally invasive and destructive • recurrence is common and often worse than primary tumor
• may metastasize locally in some large breeds of dogs (very rare)
16
Q
eosinophilic stomatitis
• (suspected) etiology?
• common location?
• defining histological features?
A
Cats & dogs (esp, young Huskies)
• often also have a peripheral eosinophilia
Etiology:
Immune mediated/hypersensitivity reaction
Cats = lips Dogs = underside of tongue
Histo: • eosinophils • collagenolysis • granulation tissue • ulceration (lymphocytes, plasma cells, macrophages, MNGs, and mast cells may be seen too),
17
Q
viral causes in large animals of vesicular stomatitis
• what species is affected by each virus?
• which viruses are foreign?
A
FMD (picorna)
• Pigs / ruminants
Vesicular Exanthema (Calici) • Pigs
Swine Vesicular Dz
• Pigs
Vesicular stomatitis (Rhabdo)
• Pigs / Ruminants / Horse
• USA
All need reported to Fed Vets bc look the same clinically
18
Q
etiology of proliferative stomatitis in cattle, sheep/goats?
What is the disease name in these species?
A
Parapoxvirus (cattle, sheep, goats)
• Contagious ecthyma/orf:
- sheep and goats
- zoonotic
• Papular stomatitis:
- cattle
19
Q
Pathogenesis of Proliferative Stomatitis in ruminants
A
Pox viruses infect the epithelia of stratum spinosum → hydropic degeneration → exudation → pustules/crusts → erosions → ulcers
20
Q
histological lesions in Proliferative Stomatitis in ruminants
A
- epidermal hyperplasia
- ballooning degeneration
- vesicle
- neutrophils accumulating in the vesicle
- scabs and crusts can form late in the disease 2° to vesicle rupture
21
Q
clinical significance of Orf and Papular stomatitis?
A
Orf:
• high morbidity & economic losses
Papular stomatitis:
• usually insignificant
22
Q
etiology of thrush
• animals most likely affected?
A
Candida albicans
- Young animals
- immunosuppressed animals
- animals receiving broad spectrum antibiotics –>causes death of the normal flora –> for overgrowth of the commensal fungus
23
Q
lesions with thrush
• grossly and microscopically
A
Gross:
- gray-green pseudomembrane
• easily scraped off the intact underlying mucosal surface
Histo:
- hyphae of Candida albicans growing in the superficial keratin of the tongue
- better visualized with special stains like GMS and PAS
24
Q
most common oral neoplasms
• dog & cat
• IHC used to identify them?
A
(most common to least common) Dog:
- melanoma
- SCC
- Fibrosarcoma
Cat:
- SCC
- Fibrosarcoma
25
Biological behavior of oral melanoma
* (90-100%) malignant
| * local invasion with early metastasis to regional lymph nodes (LNs) and eventually, distant sites (e.g. lungs)
26
Biological behavior of oral SCC
* malignant
* local invasion with metastasis later in the course of disease to regional LNs
* distant metastasis less common
27
Biological behavior of oral Fibrosarcoma
* malignant
* local invasion
* low metatastic rate
28
Canine oral papilloma virus (“warts”)
• biological behavior
• gross/histo appearance
- Benign growths in young dogs
- regress spontaneously
- lifelong immunity
Gross:
• proliferative growths (“cauliflower-like”)
Histo:
• mucosal epithelial cells
- hyperplastic
- rest on a hyperplastic folded CT stroma
• stratum spinosum
- hyperplastic and ballooned
• Cytoplasmic inclusion bodies are sometimes present.
29
Canine oral papilloma virus (“warts”)
| • pathogenesis
Papillomavirus (oncogenic) enters epidermis through abrasion
→ infects squamous epithelial cells
→ induces proliferation
30
causes of granulomatous glossitis (general)?
• Foreign bodies (dogs, horses)
• higher bacteria
- A. lignieresii
(1° bovine but also equine and small ruminants)
31
pathogenesis of “wooden tongue”?
Trauma to the tongue
-->A. lignieresii normal inhabitant of the mouth gain access to the
submucosal tissue
--> pyogranulomatous inflammation and fibrosis
--> hard, swollen tongue
32
characteristic gross & histological features of “wooden tongue”?
Gross:
- proliferative lesion (may have ulcers and necrosis) with “sulphur granules” on cut section
- “sulphur granules” are the bacterial colonies
Histo:
- pyogranulomatous (neutrophils, macrophages, MNGs)
- mixed inflammation
- Splendore-Hoeppli rxn
• colony of bacteria w/ surrounding radiating “clubs” of
Ig
33
ranula vs sialocyst
• pathogenesis
• histopathology
Ranula:
- dilated sublingual or submaxillary duct in the floor of the mouth
- Lined by epithelium
Sialocyst:
- Distended cyst caused by ruptured duct
- Not lined by epithelium
34
What is a sialolith?
Sialolith
- rare, but most common in horse
- inflammation in salivary gland w/ sloughed cells
OR
- inflammatory exudate forming a nidus for mineral accretion
• may be the cause of the duct
obstruction in ranula
35
Acute vs Chronic sialoadenitis
• gross differences
• causes in dog
Acute:
- swollen, firm, congested
Chronic:
- Hard, fibrotic firm
```
Cause:
- Foreign bodies (trauma)
- Ascending bacterial infections
- Rabies (suspect with
ptylasim)
- Canine Distemper
```
36
Causes of acquired & congenital megaesophagus
Acquired:
1 - Idiopathic
2 - 2° to: Polymyositis (includes inflammation of esophageal muscles)
3 - Myasthenia gravis
4 -Tick paralysis (salivary neurotoxin produced by certain ticks [Ixodes])
5 - Hypothyroidism
→ muscle atrophy and denervation
6 - Lead & thallium poisoning
--> affects innervation by disrupting metabolic pathways in neurons
7 - Neuropathies
Congenital:
1 - hereditary
2 - persistent right aortic arch
3- myasthenia gravis
37
Clinical presentation of Megaesophagus
- Regurgitation (not vomiting)
- weight loss
- dehydration
- aspiration pneumonia
38
Differentiate the location of the dilation of the esophagus in acquired versus congenital (due to persistent right aortic arch).
PRAA:
- obstruction occurs cranial to the heart
Acquired (and other forms of congenital)
- obstruction occurs cranial to the
stomach/diaphragm
39
clinical sequelae to S. lupi infection in canids?
- dysphagia
- aortic aneurysms
- hemothorax
- esophageal FSA and OSA
- spondylosis deformans can develop in vertebral body adjacent to the aortic granuloma
40
differentials for ulcerative esophagitis (stomatitis/glossitis/enteritis etc) in herbivores?
* BVD
* Papular stomatitis (lesions may ulcerate)
* MCF
* Rinderpest
* viral vescular disease
41
toxic principle in Pteridium aquilinum?
| • what diseases are assoc'd w/ this toxin?
Ptaquiloside (causes DNA damage)
--> SCC or enzootic hematuria
42
saliva production related to bloat susceptibility
What types of diets affect saliva production?
Saliva inhibits stable foam formation & ↓ viscosity of the rumen contents
more susceptible animals have lower production of saliva
• Succulent and high carb feed
--> reduces saliva production
43
pathogenesis of Pasture bloat?
a type of 1° bloat
< 3 days after new diet w/ higher levels of certain legumes
• alfalfa, ladino clover
--> Proteins released from the plant
--> degraded by rumen microflora
--> ruminal fermentation ↓'s rumen pH to 5 - 6
= optimal for formation of bloat
---> proteins become denatured & insoluble and stabilize the foam
--> foam rises to surface
--> foam mixed w/ rumen contents physically blocks the cardia
--> preventing eructation
--> rumen distends w/ the gases of fermentation
44
pathogenesis of Feedlot bloat ?
Type of 1° bloat
rations high in concentrate & low in roughage
• reduce saliva production
• change the rumen microflora --> promote ↑ # of encapsulated polyssaccharide bacteria
--> ↑ polysaccharides
--> foam stabilization
--> foam rises & blocks cardia preventing eructation
• bacteria promote acidosis that causes ruminal atony
45
2 causes of Free gas bloat and the pathogenesis of each
Type of 2° bloat
1. Physical blockage of cardia
- -> prevents eructation
- -> rumen distends w/ gases of fermentation
2. Functional:
• Vagal nerve damage
(organophosphate toxicity, lymphosarcoma infiltrates, abomasal displacements, volvulus)
⇒ ruminal atony
```
• Bucket-fed calves
⇒ open esophageal groove due to lack of suckling
⇒ milk replacer enters rumen
⇒ putrefaction/fermentation
⇒ acidosis
⇒atony
```
```
3. Diet of poor quality grass roughage
⇒ ↓ digestible nutrients
⇒ ↓ cellulytic microflora
⇒ undigested roughage accumulates
⇒ dilates forestomachs
⇒ inhibition of reticular contraction and eructation
```
46
features are present in antemortem bloat that are not seen in postmortem bloat?
* “stable” foam in 1° bloat (disappears 10-12 hours after death)
* Esophageal bloat line
* Congestion and edema of tissues of neck
* Atelectasis (high intrathoracic pressure)
* Pale (tan) liver (loss of blood from sinusoids due to high intraabdominal pressure)
47
pathogenesis of acute ruminal acidosis?
Sudden availability of lg. quantities of a highly fermentable CHO substrate
- -> ↑production of volatile fatty acids by ruminal flora
- -> ↓pH
- -> death of Gram (-) bacteria & protozoa
- -> overgrowth of Gram (+) bacteria
- -> production of lactic acid
- -> further ↓in pH
- -> death
48
3 mechanisms of death secondary to acute ruminal acidosis?
1. Bloat:
• ruminal acidosis pH ≤ 5 and/or ↑ VFA
--> ↓rumen motility & rumen atony
--> bloat
```
2. Hypovolemic shock:
• ↑lactate
--> ↑osmotic pressure
--> fluid drawn into rumen &
intestine
--> hemoconcentration
--> hypovolemia, anuria, shock & diarrhea
```
3. Metabolic acidosis:
• absorption of D-lactate
--> metabolic acidosis
--> circulatory collapse
• in “real life” these mechanism can and often do occur concurrently
49
acute ruminal acidosis
| • gross & histological changes
Gross:
- Dehydration (sunken eyes, inelastic skin)
- rumen distended with grain
- an acidic smell in rumen
- Mucosa of forestomachs reddened ± adherent to submucosa
- blunting of ruminal papillae
Histo:
- hydropic degeneration of epithelia
- inflammation
- vesicles
- pustules
- ulcers
50
angioinvasive fungi that can proliferate under bouts of ruminal acidosis
• lesions gross/histo
• Zygomycetes
(Mucor, Rhizopus, Absidia, and Mortierella spp)
• Aspergillus
Gross:
- central necrotic foci rimmed by hypermic tissue (infarcts)
- ulcers
Histo:
- mycotic hyphae invade blood vessels (vasculitis)
→ hemorrhage & infarction
→ multifocal necrohemorrhagic rumenitis
• Fusobacterium necrophorum (necrobacillosis)
or Arcanobacterium
(Actinomyces) pyogenes
- can cause bacterial rumenitis under these conditions
w/ 2° systemic inflammation (hepatic abscesses)
51
pathogenesis of hardware disease
| • gross lesions?
Metal foreign body is ingested
→ perforation of reticulum
± diaphragm ± pericardial sac (↑ late pregnancy)
→ leakage of ruminal contents/flora
→ localized or extensive fibrinosuppurative inflammation
```
Gross:
- Fibrinosuppurative peritonitis
- pleuritis
- pericarditis
• later in the disease
- peritoneal, pleural or pericardial fibrous adhesions (scars)
```
52
When is abomasal displacement most commonly seen in dairy cattle?
To what side is it most common?
6 weeks post calving
• 85% left side (15% upper right side, can result in torsion or volvulus)
53
pathogenesis of the metabolic alkalosis that can be seen with abomasal displacement
6 wks Post-calving
→ hypocalcemia, lactic acidosis (heavy grain)
→ atony
→ displacement
→ obstruct abomasal outflow
→ metabolic alkalosis (hypochloremia & hypokalemia
54
pathogenesis of GDV in dogs?
stomach is distended w/ food and gas
→ It rotates on the mesenteric axis clockwise
(180, 270, or 360 degrees on a ventrodorsal axis when the abdomen is viewed from the ventral surface)
→ gastric volvulus w/ obstructed esophagus
→ prevention of eructation
→ further contributes to gastric dilation
spleen
= attached to the stomach by the gastrosplenic ligament
- rotates w/ the stomach
→ folded back upon itself
→ located in the right cranial abdomen against the diaphragm
→ compression of splenic vein → congested spleen
55
D. megastoma
| • Life cycle
Horses
- infected by ingesting flies that contain infective larvae
OR
- by free larvae that emerge from flies as they feed around the lips
→ larvae migrate to the stomach
→ live in a brood pouch near the margo plicatus in the glandular stomach
→ Eggs produced in the cysts are extruded through a pore in the brood pouch to the gastric lumen
→ eggs pass out w/ the feces
→ consumed by fly
56
G. intestinalis
| • Life Cycle
Horse
• fly lays its eggs on the distal limbs of the horse
→ moistened and warmed by licking
→ larvae hatch
→ swallowed
→ live in the nonglandular (stratified squamous) portion of the equine stomach
57
G. nasalisI
| • Life Cycle
Horse
• fly lays its eggs around the nose of the horse
→ moistened and warmed by licking
→ larvae hatch
→ swallowed
→ live in the glandular stomach and duodenum
58
pathogenesis of “bottle jaw” in ruminants?
```
Soil infested with H. contortus
→ consumed during grazing
→migrate to stomach
→ Blood feeders
→ severe anemia & hypoproteinemia
→ edema (“bottle jaw”)
```
59
What parasite causes the abomasum of cows and small ruminants to have a “Moroccan leather”appearance?
What other clinical signs can be seen?
cattle
• O. ostertagia
small ruminants
• O. circumcincta
- “unthrifty”
- Hypoproteinemia
- ventral edema
60
ulcerative gastritis
| • Pathogenesis in pigs
located in the pars esophagea region of the stomach
Ulcers in this location characteristically have a multifactorial cause,
• ingestion of finely ground grain or pelleted feed (possibly deficient in vitamin E)
• fermentation of sugars in the feed
• stress of confinement rearing
- frequently bleed
- can cause exsanguination
61
NSAID toxicity in horses
| • pathogenesis
Causes Ulcerative Gastritis
NSAIDS work by inhibiting two enzymes
• COX-1 and COX-2.
→ produce prostaglandins
→ promote pain, inflammation, and fever.
COX-1
- protects the stomach lining from stomach acid
- helps control bleeding
By inhibiting COX-1, NSAIDs ↑ the risk of a peptic ulcer developing and bleeding.
62
Mast cell tumors in dogs
| • pathogenesis for ulcerative gastritis
mast cell tumors
→ release histamine into the bloodstream
→ ↑ production of stomach acid,
→ sometimes results in ulcers
63
Cause of Ulcerative gastritis in dogs
1 - Mast cell tumor
2-Uremia
3- Gastrin secreting pancreatic islet tumor
( → hypersecretion of gastric acid)
64
potential sequelae to ulcerative gastritis (in general)?
```
• Bleeding:
• melena
• anemia
• exsanguination
• Perforation
→ peritonitis
• 2° infection by bacteria or fungi
• Healing → scar
```
65
etiology of lymphoma in cattle
• 4 common sites of tumor development?
BLV (retrovirus)
* Abomasum
* Heart (right atrium)
* Uterus
* Lymph nodes/lymphoid system
Approx 30% of cattle infected w/ BLV develop non-neoplastic persistent lymphocytosis
• Of these, < 5% develop lymphoma
66
What strain of γ-herpesvirus is carried in each reservoir (show no clinical symptoms) species?
What species are susceptible?
Carrier/reservoir:
• African wildebeests and other African ruminants (Alcelaphine herpesvirus-1 (AHV-1)
• Sheep OHV-2
• Goats: Caprine herpes virus 2 (CpHV-2)
Susceptible species:
• cattle, deer, bison, water buffalo, & pigs
67
pathogenesis of Herpes in susceptible species?
What 3 strains cause disease in the US?
Susceptible species
- contact secretions (primarily nasal) of infected carrier species & contract infection
- NOT contagious btwn susceptible animals they are dead-end hosts for these viruses
- YOUNG lambs shed > amts of virus than older sheep
* OHV-2 and AHV-1 cause disease in:
* cattle, deer, bison, and water buffalo
• MCFv-WTD causes disease in WTD (carrier species for this strain has not been identified)
68
What cells does the γ-herpesvirus virus replicate in?
- lymphoid cells (also macrophages)
- causes death of vascular endothelial cells
→ necrotiaing vasculitis & thrombosis
69
γ-herpesvirus
• Clinical signs
• Gross & Histo lesions
- quite variable presentations
- exudation of the oral & upper respiratory MM
- sudden death
- high fever
- diarrhea (sometimes bloody)
- seizures
- depression
- weakness
- off feed
```
Gross:
• bilateral corneal opacity
• inflammation
• ulceration,
• exudation of the oral &
upper respiratory MM
• crusting around the muzzle
• lymphadenomegaly
```
Histo:
• lymphoplasmacytic necrotizing arteritis & phlebitis
• primarily the small muscular arteries affected, but also veins and lacteals
• lymphadenomegaly
- lymphoid atrophy
- followed by massive lymphoid prolif
• ulcerative stomatitis, glossitis, esophagitis, abomasitis
• enterotyphlocolitis assoc'd w/ vasculitis.
70
What age animal is affected by Rota/Coranvirus?
??
TGE: pigs <2 weeks
Calves: 0-7 days
• Coronavirus days the disease is most significant
```
Rota:
pigs
• 1-7 weeks of age
beef and dairy calves
• 0-7 days
```
71
pathogenesis of diarrhea seen with Rota/Coronavirus?
Corona/Rota:
Virus infects
--> cytolysis of the enterocytes of the upper 2/3 of the villi
--> Malabsorptive diarrhea
```
Rota:
• production of enterotoxin
1. ↑ chloride secretion
2. ↓ absorption of glucose/sodium
→ solutes in lumen
→ Secretory diarrhea
(nonstructural protein4; NSP4)
```
```
Death usually assoc'd w/ concurrent infections that affect villous enterocytes
• coronavirus
• C. parvum
• E. coli
• coccida
```
72
prominent histological lesion in Rota/Coronavirus infection?
Villous blunting / fusion
Coronavirus also affects colon
73
disease presentation of coccidiosis in:
• Sheep/goat
• Dog /cat / cattle / bird
• Pig
sheep and goats:
• proliferative
dogs, cats, cattle, birds:
• hemorrhagic (and necrotizing)
Pigs:
• fibrinonecrotic pseudomembrane, w/o blood
74
cell types are affected by coccidian & where the protozoa proliferate?
* villous or crypt epithelial cells
* Obligate, intracelluar pathogens
- protozoa can be seen free in the lamina propria once they are released from cells
- reproduction occurs w/in the enterocytes
75
* most common type of enterolith?
* Predisposing diets?
* breed of horse most susceptible?
* Where do they most commonly lodge?
Struvite
Diets high in:
• Phos (i.e. bran) OR
• magnesium (i.e. alfalfa)
Arabians
at pelvic flexure
76
Torsion VS volvulus
• Differentiate
• where does each most commonly occur?
Torsion:
• Rotation of a tubular organ parallel to its long axis
• large intestine of horse
Volvulus:
• Rotation of a tubular organ perpendicular to the long axis around the mesentery
• small intestine
77
postmortem VS antemortem intussusception
False intussusception:
• Easily reduced
• no circulatory disturbances
```
True intussusception:
• difficult to reduced
• hyperemic
• hemorrhagic
• inflamed
• necrotic
```
78
some causes of postmortem and antemortem intussusception
False intussusception:
• postmortem peristalsis
```
True intussusception:
• generally unknown
• assoc'd w/ intestinal irritability and hypermotility.
- 2° to enteritis
- 2° to parasites
- foreign bodies
- neoplasms
- general debility
```
79
What age animal most commonly develops diarrhea due to ETEC (enterotoxigenic E. coli) infection?
Neonatal calves
(lambs, foals, puppies, kittens, least commonly piglets)
Post weaning pigs
• 1-2 weeks post weaning
= 3-5 weeks old
80
pathogenesis of diarrhea due to ETEC?
Bacteria attaches to apical villus enterocytes
--> secretes up to 3 enterotoxins/shigatoxins
(STa, STb, LT)
--> upregulation of cAMP & cGMP
--> enterocytes secrete water & e-lytes
--> secretory, watery diarrhea
81
gross & histological lesions seen with ETEC infection?
Gross:
• Voluminous, yellow to white, watery to pasty diarrhea
• Fluid distended small intestine
• chyle in lacteals
```
Histo:
• epithelial cell morphology is normal w/in 1st 24 hours
• bacteria adhered to brush border
• mild blunting & fusion of villi
• minimal to mild enteritis
```
82
What characteristics of the hemolytic E. coli of Edema Disease in pigs are responsible for its pathogenic effects
• how do these features elicit their effects?
F18ab (fimbrial protein):
• allows attachment to enterocyte (doesn’t wash out with peristalsis)
```
Shiga toxin 2e:
• causes generalized vascular endothelial injury
- arterioles and arteries
• synonyms:
- verotoxin
- exotoxin
- angiotoxin
- enterotoxin
- edema disease principle
```
83
pathogenesis of Edema Disease
| • how is it related to the age pig that can be affected?
hemolytic E. coli attaches to enterocytes via F18ab & secretes S2e
→ toxin is absorbed & distributed systemically
(via Neuts that are recruited when IL-8 is secreted)
→ toxin causes angiopathy
→ widespread edema & arteritis
• generally a post-weaning disease of pigs
- 6 to 14 weeks of age
• usually assoc'd w/:
- dietary changes@weaning,
- loss of maternal Abs
- ↑ expression of receptors for toxins, which occurs w/ age
84
most common clinical presentation of Edema Dz in pigs?
• Sudden death
- due to a toxic shock-like syndrome
• Neurological signs
• animals don’t usually present for intestinal disease
85
In Edema Dz of pigs, what are the characteristic sites of edema?
* gastric submucosa
* eyelids
* forehead
* gallbladder
* mesentery of spiral colon
86
What cell types does Salmonella proliferate in
what is the most common route of entry of infection?
Phagocytic cells
→ granulomatous inflammation
Fecal-oral
87
What type of diarrhea can be seen with Salmonella?
```
Secretory:
• enterotoxins similar to shigatoxins
→ hypersecretion of Cl

Malabsorptive:
• cytotoxin kills enterocytes
```
88
Gross / Histo lesions in Pigs Chronically infected w/ S. typhimurium?
Gross:
• Button ulcers in cecum & colon
• rectal strictures
• fibrinonecrotic enterotyphylocolitis
```
Histo:
• ulcers
• fibrosis at stricture sites
• fibrinoid necrosis in Lg & Sm intestine
• vasculitis w/ vascular thrombosis
```
•Salmonellosis can occur in pigs, horses, and cattle
- calves pathognomonic lesion = fibrinous cholecystitis
Salmonella is potentially zoonotic
89
etiology of enterotoxic hemorrhagic enteritis of neonatal lambs, foals, calves and piglets?
C. perfringens type C
• produce α and β toxins
• adult horses can be affected • animals are usually hrs to days old when affected
90
C. perfringens type C
• Clinical signs
• Gross/histo lesions
* sudden death
* bloody diarrhea
* when piglets are affected, the whole litter dies.
Gross/histo:
• hemorrhagic or necrotizing enteritis of the small intestines
• sometimes w/ gas in lumen & w/in Intestinal walls
91
Etiology of colitis X in horses?
C. difficile
92
etiologies of BVD & Rinderpest?
```
BVD: Pestivirus
• 2 genotypes
(BVD1 and BVD2)
• 2 biotypes
(NCP and CP)
• both genotypes can have both biotypes
• CP biotype used most often in vaccines
```
Rinderpest: Morbillivirus
93
Age of cattle most commonly affected by BVD dz (diarrhea)?
8mo-2y (younger animals)
- but all ages of animal can be affected
94
pathogenesis of persistent infection with BVD?
Dam is infected w/ virulent noncytopathic (NCP) or becomes infected with virulent NCP BVD
- -> fetus is exposed btw days 40-120 of gestation
- -> fetal immune system is not developed
- -> virus is not recognized as foreign
- -> virus replicates in the fetus/calf for the rest of its life
- -> animal sheds virus
• PI calves usually are born from unvaccinated dams
• has to cross the placenta and infect the fetus, IF this happens, the fetus will MOST LIKELY be PI
- sometimes the fetus does not become infected, sometimes it can be aborted, but USUALLY under these circumstances a PI calf will be born
95
Clinical Signs can be seen in PI calves infected with BVD?
None, born small/stunted growth, reduced productivity or reproductivity
• PI calves = major reservoir for BVD virus
- shed lifelong in urine, feces, milk
96
most common method of diagnosis of PI in calves (BVD)?
IHC of skin biopsies
| - bc calves shed large amts of virus thru the skin
97
most likely outcome when the fetus is infected with NCP BVD prior to day 40 of
gestation?
After day 120 of gestation?
Prior to day 40:
• abortion
• embryonic death/resorption
After day 120:
• stillborn
• congenital defects
• calf born w/ BVD virus Ab's
98
BVD pathogenesis of mucosal disease
• clinical signs?
• lesions?
PI animal subsequently infected w/ CP or its NCP virus mutates to CP
--> virus attacks lymphoid cells --> mucosal disease
* Low morbidity/high mortality
* BLOODY DIARRHEA
* anorexia
* depression
* PROFUSE H2O-Y DIARRHEA w/ staining of the perineum & tail
* agalactia
* pyrexia
* rumen atony
* ptyalism,
* acrimation,
* mucopurulent nasal discharge
Lesions:
• ulceration of GI mucosa (any site is possible, mouth-anus);
• LYMPHOID NECROSIS at GALT sites
99
pathogenesis of acute BVD
• clinical signs?
• lesions?
???? whats the diff
1° infection w/ virulent strain of BVD
(usually BVD2, but can be a virulent strain of BVD1)
→ virus attacks lymphoid cells & platelets
→ thrombocytopenic syndrome
• mucosal hemorrhage
• bleeding
• bloody diarrhea
```
Clinical signs
• Low morbidity/high mortality
• bloody diarrhea
• anorexia
• depression
• profuse watery diarrhea w/ staining of the perineum & tail
• agalactia
• pyrexia
• rumen atony
• ptyalism
• lacrimation
• mucopurulent nasal discharge
```
Lesions:
ulceration of GI mucosa (any site is possible, mouth-anus); lymphoid necrosis at GALT sites
100
Lesions assoc'd w/ R. equi infections
```
• lung pyogranulomas,
• pyogranulomatous
• lymphadenitis
- GALT & LN
• pyogranulomatous ulcerative enterotyphylocolitis
```
101
Johne’s disease
| • in cattle vs pygmy goats?
Older cattle (>19 months)
• chronic, intractable diarrhea
• emaciation
• hypoprotienemia
Pygmy goats
• explosive diarrhea
• die quickly
102
etiologic agent of Johne’s disease
• Gross & Histo lesions
• special stain is used to visualize the organisms
Mycobacterium avium ssp. Paratuberculosis (MAP)
```
Gross:
• Granulomatous enteritis
• thickening of the mucosa,
- smooth and shiny (intact)
- not ulcerated
```
```
Histo:
• lamina propria markedly expanded by granulomatous inflammatory cells
- compress the crypts
→ eventually loss (atrophy)
• lymphangiectasia
```
Special Stain:
• Acid Fast
(aka: Ziehl-Neelsen stain)
103
etiology & clinical presentation of TGE in pigs?
Etiology: Coronavirus
= cytolytic, → death of enterocytes
Neonatal piglets <10 days old
• Virtually 100% on the farm are sick & dying during the winter (virus inactivated by sunlight)
• (malabsorptive) diarrhea
- odoriferous undigested milk
• dehydration
• vomiting
• animals that survive are poor doers but have lifelong immunity
Sows
• morbidity = 100%,
• clinical signs are mild & transient (fever, vomiting, inappetence, and agalactia),
• Immunity is solid
104
gross & microscopic lesions seen w/ TGE infection?
```
Gross:
• Dilated small intestine
• thin walled
- due to loss of enterocytes
• contains yellow fluid & gas
• malabsorption
→ Mesenteric lymph vessels devoid of chyle
```
Virus Target
= epithelial cells of the tips & upper sides of intestinal villi
Histo:
• necrosis of enterocytes & atrophy of the villi
• Acute:
- cells are sloughed & replaced by flattened epithelial cells
migrating up the basement membrane from progenitor cells in the crypts
- Inflammation is minimal
• Chronic:
- severe blunting (marked villus atrophy) of intestinal villi w/ fusion of their basement membranes.
- Chronic inflammation is prominent in the lamina propria & submucosa
105
etiology of swine dysentery
• Transmission
• Clinical presentation
Etiology: Brachyspira hyodysenteriae
Fecal-oral
Clinical presentation:
• ~90% of post-weaning piglets (8-14 wks)
- bloody, mucoid diarrhea w/ fibrin & undigested feed
• only ~30% of affected animals die
106
gross & histological lesions assoc'd w/ swine dysentery?
* Mucohemorrhagic
* Fibrinonecrotic inflammation
• generally confined to the Lg intestine
(spiral colon, colon, cecum, and rectum)
107
virulent factor of Brachyspira hyodysenteriae?
cytotoxic hemolysin
| • responsible for the bloody diarrhea
108
etiology & clinical presentation of proliferative ileitis?
???
Etiology = Lawsonia ????
```
Postweaning (>4wks) pigs
• mucoid or watery, w/ or w/o blood
- 5 - 15 days’ duration.
• partial anorexia
• vomiting
• slight fever
```
109
Lawsonia
| • Gross & histo lesions
Gross:
1 - Hemorrhagic Bowel Form
• folds of HYPERPLASTIC MUCOSA
• concurrent hemorrhage
2- Necroproliferative form
• prominent necrosis of the ileal mucosa
• diphtheritic membrane (cast)
- formed by cellular debris & inflammatory exudate
• hyperplastic mucosa.
```
Histo:
• notable hyperplasia of enterocytes
→ distortion of normal architecture
+/- hemorrhage & necrosis
• silver stain reveals bacteria in APICAL CYTOPLASM OF ENTEROCYTES
```
110
Lawsonia Pathogenesis
Bacteria stimulate proliferating of crypt epithelium
→ preventing their maturation to absorbent villous enterocytes
(→ malabsorptive diarrhea)
→ overcrowding, outgrow blood supply
→ necrosis (+/- hemorrhage)
• infection → immunosuppression w/ ↓ in CD8+ T & B lymphocytes
111
C. parvum
• transmission
• what conditions are clinical signs of diarrhea seen?
Fecal-oral transmission
```
Disease (secretory diarrhea) seen in immunodeficient animals
• Calves
- Failure of Passive Transfer
- co-infected
• Arabian foals
- CID
• Monkeys
- SIV
• Zoonotic
```
112
cellular habitat of C. parvum
Protoza lives in a PARASITOPHOROUS VACUOLE
- contains membrane components from both the host and C. parvum
• INTRACELLULAR
...but EXTRA-CYTOPLASMIC
113
3 syndromes of Canine Parvovirus 2 infections in puppies?
```
<2 weeks:
• generalized Dz
• focal necrosis in organs w/ rapidly dividing cells
- liver
- kidney
- bone marrow
- lung
- intestine
- ♥
• uncommon due to maternal Ab protection
```
In utero-8 wk:
• myocarditis (rare)
• uncommon due to maternal Ab protection
6wk-6mo:
• acute enteritis
• Death from dehydration & shock w/in 24 hrs
114
What cell types does Canine Parvovirus2 replicate in?
Rapidly dividing cells:
- crypt cells
- bone marrow cells
- lymphoid tissue
115
Gross & Histo lesions seen w/ CPV2 infection in 6wk puppies?
```
Gross:
• HEMORRHAGIC ENTERITIS
• dilated, fluid-filled, flaccid, and hemorrhagic small
intestine
• serositis
• diffusely reddened mucosa
• contents of the small intestine
- brown to red-brown
- fluid w/ a fibrinous exudate, with or without hemorrhage
• lymphadenomegaly
• BM DEPLETION
```
```
Histo:
• loss of crypts → Villous Atrophy
• crypt necrosis (“collapse of mucosa)
• lymphocyte necrosis
• crypt abscess
• hemorrhage
• necrosis
• denuded and blunted villi
• eventually regeneration
+/- Villous fusion
```
(maybe basophilic intranuclear inclusion bodies early infection)
116
Histiocytic Ulcerative Colitis
• suspected etiology
• clinical presentation
Etiology:
• unknown; possibly E. coli
Presentation:
• large bowel diarrhea
- frequent bloody mucoid stools
• progressing to chronic debilitation, weight loss, anemia, & hypoalbuminemia
117
prototheca
• Transmission
• most common sites of infection in the dog?
Transmitted:
• contaminated, stagnant water
intestine & eye
118
H. capsulatum
• transmission
• What is the intestinal lesion seen?
Aerosol
granulomatous & ulcerative enteritis/colitis
119
clinical presentation of inflammatory bowel disease in dogs?
MALABSORPTIVE diarrhea & protein losing enteropathy
120
IBD in dogs
| • gross & histological lesions
No characteristic gross lesions
Histo:
• Lymphoplasmacytic enteritis
121
How does IBD differ in cats compared to dogs?
Cats:
1. Lymphoplasmacytic enteritis may be prelude to lymphosarcoma
2. disease may be regulated by controlling diet
122
Most common cause of Protein-losing enteropathy
in the dog
• clinical presentation
• gross/histological lesion
Lymphangiectasia
Clinical presentation:
• Pot belly
- due to hypoproteinemia
• Malabsorptive diarrhea
Gross:
• Pot belly
• thick mucosa w/ dilated lacteals & lymphatics
Histo:
• thick mucosa w/ dilated lacteals & lymphatics
• inflammation
123
causes of lymphangiectasia?
1 - Congenital developmental disorder of lymphatics
2- Acquired 2° to lymphatic obstruction
- Granulomatous or other inflammatory dz
- Neoplasia
3. Idiopathic (most cases)
124
horses with strangulating lipomas
• most common clinical presentation
• gross findings
Presentation:
• colic & death
• muscle tremors
• fever other general signs of pain or septicemia if the bowel has died
Gross:
pedunculated lipoma wrapped around the mesentery & strangling the bowel --> infarction
125
species is most susceptible to cantharadin toxicity
| • what is the intestinal lesions?
Horses
| • Sloughing of epithelium of the stomach & enterocytes of prox small intestine
126
What insect secretes cantharadin
| • how are animals exposed (usually)?
Striped blister beetle
| • beetles are Incorporated into crimped hay
127
What anal tumor is assoc'd w/ persistant hypercalcemia?
| • pathogenesis
Apocrine Gland Adenocarcinoma
- malignant
tumor secretes PTH-like hormone
--> persistent hypercalcemia
these tumors are more common in female dogs
128
causes of rectal prolapse in various species?
1- Tenesmus
```
2- Hyperestrogenism
--> relaxation of vaginal/rectal muscles
• Sheep:
- phytoestrogens
• Swine:
- Zearalenone
(estrogenic Fusarium sp. mycotoxin)
```
3- Advanced pregnancy
4. Piling for warmth in extreme cold (swine)
5. Severe coughing
