GIT Pathology Equine

Question 1

1. What is the difference between the horse liver and that of other species?
2. What type of teeth do horses have?

Answer 1

1. Horses do not have a gall bladder.
2. Hypsodont.
   - enamel extends below gumline.
   - erupting continuously.

Question 2

Common signs of stomatitis?

Answer 2

Excessive drooling - sialorrhea.
Reluctance to eat - anorexia.
Difficulty swallowing - dysphagia.
Resistance to exam of the mouth.

Question 3

How can stomatitis be classified?

Answer 3

Based on features of the primary/main lesion:
- vesicular.
- papular.
- erosive/ulcerative.
- necrotising.
- lymphoplasmacytic.
- granulomatous.

Question 4

1. What is calculus?
2. What may be the consequence of a rotated tooth?

Answer 4

1. Mineralised plaque - mineral component mainly calcium carbonate.
2. Gapping between teeth, becomes packed with food material, increasing plaque depositions.

Question 5

1. What is caries?
2. Most common form of varies in horses.
3. As severity of disease increases, what is the main change seen?

Answer 5

1. Characterised by demineralisation of the inorganic part and enzymatic degradation of the organic matrix.
2. Infundibular necrosis.
3. Colour change from normal creamy white to blackish.

Question 6

1. What is fistulisation?
2. Foreign body stomatitis.

Answer 6

1. The process of forming a canal between 2 areas.
2. Caused by plant material or metallic objects e.g. wire.
   Acute cases may produce ulcers.
   Chronic cases characterised by exuberant granulomas.
   Sharp FBs can predispose to necrotic deep stomatitis.
   Body produces a granulomatous reaction to try and close the FB in.

Question 7

Infectious aetiologies of stomatitis in the horse.

Answer 7

Oral candidiasis in foals - superficial layers of oral epithelium are involved.
- grossly — patchy pale-grey pseudomembranous material of the oral cavity and tongue that can extend to the oesophagus and stomach.
— lesions are peel-able.
- may indicate immunosuppression.

Vesicular stomatitis - viral, affecting mainly donkeys, horses, cattle and pigs.
- Notifiable.
- Vesicular lesions and secondary ulceration are the main lesions.
- circular, multifocal, hyperaemic border, ulcerated in the centre.

Question 8

Gastritis in horses.

Answer 8

Uncommon except for those associated with gastric ulceration and parasites.

Question 9

1. Contributing aetiological factors to gastric ulceration in horses.
2. Where in the stomach do lesions generally occur?
3. Main factors of gastric ulceration in horses?

Answer 9

1. Stress, feeding type/frequency, enteric disease, colonic impaction, NSAID therapy, exercise, POSSIBLY infectious agents e.g. Helicobacter spp.
2. In both non-glandular and glandular regions.
3. Mucus secretion, increased acid production, blood flow, epithelium regeneration, gastric motility.

Question 10

1. Main factor causing ulceration in the non-glandular region?
2. Factor associated with ulceration of the glandular region?
3. What may occur with deep gastric ulceration?

Answer 10

1. Exercise and feeding patterns - reflux if acidic content into the non-glandular region.
2. Admin of NSAIDs.
3. May lead to tearing of the stomach wall and rupture, but usually gastric ulcers are considered incidental PM findings.

Question 11

Grading of squamous mucosa.

Answer 11

Grade 0 = no appearance of hyperkeratosis or hyperaemia and the epithelial walk is intact.
Grade 1 = areas of hyperkeratosis (yellow) and hyperaemia are visualised, but the mucosa wall is still intact.
Grade 2 = minor, single lesions visualised.
Grade 3 = large, single lesions visualised or extensive superficial lesions.
Grade 4 = extensive lesions visualised deep to the mucosa.

Question 12

2 main parasites involved in parasitic gastritis?

Answer 12

Gasterophilus spp. larvae (botflies).
Draschia megastoma and Habronema spp.

Question 13

Botfly pathogenesis.

Answer 13

Botflies lay eggs around horse’s mouth.
Horse licks eggs from around mouth and swallows them.
Botflies develop into larvae in the stomach.
Severity of signs and lesions related level of infestation.
Can cause ulceration of the stomach which can progress to rupture.

Question 14

Draschia megastoma and Habronema spo.

Answer 14

Nematodes.
Use flies to infect.
Come off the flies on the horse.
Horse licks them and then swallows them.
They complete their life cycle in the stomach.
Draschia megastoma produces modular lesions within stomach mucosa.
Habronema produces less invasive lesions in the stomach and in the cutis.
Severity of symptoms and lesions vary.

Question 15

Principle mechanisms of diarrhoea?

Answer 15

Malabsorption (osmotic).
Increased permeability/effusion.
Altered motility.
Hyper-secretion.

Question 16

Main cause type of intestinal issues in horses?

Answer 16

Infectious.

Question 17

Common bacteria affecting the intestines of horses.

Answer 17

Clostridium perfringens type C.
Clostridium difficile.
Clostridium piliforme.
Salmonella spp.
Rhodococcus equi.
Lawsonja intracellularis.

Question 18

1. Age of horses affected by C. perfringens - why?
2. Start of C. perfringens disease.
3. Effects on endothelial cells.
4. Main pathological finding of a C. perfringens infection in a horse.

Answer 18

1. Very young horses - the beta toxin produced by the bacteria is trypsin-labile.
2. Colonisation and proliferation in the intestine, and production and secretion of the beta toxin.
   Toxin causes entericyfe necrosis and haemorrhage.
3. Toxin crosses epithelial barrier and diffuses into the lamina propria, inducing damage to endothelial cells (studies suggest).
   This would increase vascular permeability, leading to extravasation of fluid, proteins, and erythrocytes, contributing to necrotic effect on enterocytes. This has not been explored in horses.
4. Necrotising enterotyphlocolitis.

Question 19

1. What gram is C. Difficile?
2. Age affected by C. Difficile?
3. Where in the environment does C. Difficile live.
4. Clinical signs.
5. Toxins produced by C. Difficile.
   - actions of these.
6. Main pathological finding of C. Difficile infection.

Answer 19

1. Gram positive - is a bacillus.
2. All ages.
   - more SI effect in young animals.
   - more LI effect in older animals.
3. Soil.
4. Diarrhoea
5. TcdA and TcdB.
   - damage mucosal epithelial cells.
6. Necrtoising enterotyphlocolitis plus submucosal gelatinous oedema in the colon and caecum.

Question 20

1. What gram is Rhodococcus equi?
2. Age affected?
3. Where is it found when in the environment?
4. In what cells can it survive and replicate?
5. Most common manifestation of infection?
6. The main pathological finding of infection of the intestines with Rhodococcus equi.

Answer 20

1. Gram positive - coccobacillus.
2. Foals around 5 months old.
3. In the soil.
4. Macrophages.
5. Respiratory disease.
6. Pyogranulomatous and ulcerative typhlocolitis.

Question 21

1. Rhodococcus equi gram…?
2. Age affected?
3. Where in the environment can this bacteria be found?
4. In what cells can this bacteria survive and replicate?
5. Most common manifestation of infection with this bacteria?
6. Main pathological finding (GI)?

Answer 21

1. Gram-positive coccobacillus.
2. Foals around 5 months old.
3. Soil.
4. Macrophages.
5. Respiratory disease.
6. Pyogranulomatous and ulcerative typhlocolitis.

Question 22

1. Species affected by Lawsonia intracellularis?
2. Route of infection?
3. Hallmark of this disease?
4. Main pathological finding?

Answer 22

1. Pigs, hamsters, rabbits, ferrets, canids, rats, sheep, deer, emus, ostriches, nonhuman primates, Guinea pigs.
2. Faecal-oral.
3. Intestinal mucosal hyperplasia due to rapid and unchecked division of crypt epithelial cells.
4. Proliferative enteropathy affecting mainly distal SI which causes malabsorption and is considered to be a PLE.

Question 23

Common viruses affecting the GIT in horses?

Answer 23

Rotavirus and coronavirus.

Question 24

1. Age affected by rotavirus?
2. Effect of rotavirus on GIT?
3. Age affected by coronavirus?
4. Coronavirus effect on GIT?

Answer 24

1. Foals around 3-4m.
2. Atrophy of villi due to increase in rate of loss of epithelium from the surface of villi and impairing sodium and/or glucose transport. Malabsorption is an important consequence.
   Dehydration and death without supportive care.
3. Adults.
4. Gross and microscopic changes.
   Necrotising enteritis.

Question 25

Parasites that affect git in horses.

Answer 25

Cryptosporidium spp., strongylidae, Cyathostominae.

Question 26

1. Age affected by cryptosporidium spp?
2. Cryptosporidium infection characterised by?
3. Strongyloides spp. affecting horses?
   - classic lesion produced by these larvae.
   — signs of this in foals?
4. Age affected by cyathostomes?
   - disease a result of what?

Answer 26

1. Up to 5-6 weeks.
2. Diarrhoea, mainly caused by villus atrophy and malabsorption.
3. Strongylus vulgaris.
   - endoarteritis, in particular the cranial mesentery artery and it’s main branches, which may lead to arterial infarction of the colon.
   — Acute syndrome characterised by weight loss, duarrhoea or constipation, colic and infarction of the intestine w/ large larva numbers for first time.
4. Young animals.
   - emergence of large numbers of third-stage larvae.

Question 27

Other causes of intestinal disturbances in horses?
Pathogenesis is of this syndrome?
Main aspects?

Answer 27

NSAIDs.
Associated with ulcerative colitis (esp. right dorsal) and typhlitis.
Pathogenesis = ischaemia caused by reduced perfusion due to inhibition of prostaglandin synthesis by inhibition of the cyclooxygenase enzyme.
Main aspects = colic, diarrhoea, ulceration of upper and lower alimentary system.

Question 28

1. Common neoplasia of the intestines in horses?
2. Possible it is secondary?
3. Features?

Answer 28

1. Lymphoma.
   Lipoma (mesentery).
   Adenocarcinoma.
   Leiomyoma/leiomyosarcoma.
   Gastrointestinal stromal tumour.
2. Rarely spread from elsewhere.
3. Focal or diffuse thickening of the wall.
   Malignant tumours invade all layers of wall.
   Mesenteric LNs/peritoneum (seeding).
   May stimulate a fibrous tissue reaction causing stenosis with proximal dilation.