GIT

Fill out the following table

Term	Definition
	Gum inflammation
	Mouth inflammation
Rumenitis/reticulitis/omasitis/abomasitis/gastritis	Forestomach/stomach inflammation
	Caecum inflammation
	Colon inflammation
Diarrhoea	Small bowel diarrhoea = Large bowel diarrhoea =
Melaena vs. Haematochezia
Dysphagia
Vomiting vs. Regurgitation vs. Dysentery
Ill-thrift

Term	Definition
Gingivitis	Gum inflammation
Stomatitis	Mouth inflammation
Rumenitis/reticulitis/omasitis/abomasitis/gastritis	Forestomach/stomach inflammation
Typhlitis	Caecum inflammation
Colitis	Colon inflammation
Diarrhoea	Excess water in faeces Small bowel diarrhoea = Infrequent passage of large amounts of fluid faeces Large bowel diarrhoea = Frequent passage of small amounts of fluid faeces
Melaena vs. Haematochezia vs. Dysentery	Digested blood in faeces from stomach/proximal GIT = Black and tarry Undigested blood in faeces from lower GIT = Bright red Severe haemorrhagic diarrhoea with flecks of mucosa (term derived from human dysentery)
Dysphagia	Difficulty swallowing
Vomiting vs. Regurgitation	Forceful expulsion of gastric contents through oesophagus and mouth Passive retrograde movement of food and fluid from oesophagus
Ill-thrift	Weight loss/poor BCS in production animal

7 Diagnostic tests for GI diseases

1. Imaging (best for structural diseases eg. GDV)

2. Haematology and serum biochemistry

3. Serology

4. PCR

5. Faecal samples

   1. Bacterial culture (culture ≠ disease)

   2. Faecal egg counts

   3. PCR

6. GIT samples fixed in formalin (biopsy or histology)

7. FNA (cytology)

When/what should PM samples of the GIT be taken and analysed? Why?

ASAP! Collect histology samples from recently dead animals OR euthanising multiple (eg. calf diarrhoea) that are unlikely to recover due to rapid autolysis of the GIT which interferes with diagnostic tests

Which image shows TRUE enteritis?

BOTH

1. L: Dark red discolouration = Congestion

2. R: Fibrin strands = Difficult to pull apart

4 Tips for PM examination of the GIT

1. Open multiple parts/organs of the GIT (NOT just in the abdomen (split mandible and move pluck)

2. Pay close attention to mucosal surfaces

3. Take multiple histology samples even with no gross lesions present

4. Handle carefully and do NOT scrape mucosa and place into formalin for histology (removed top layer of mucosa)

Sample to collect from a ruminant GIT when parasitism is a DDx

ENTIRE abomasal contents + first 10m of small intestine for worm count

Describe the bon-bon technique

Used to collect fresh/uncontaminated intestinal samples for culture or PCR

Method: Tie either end of short intestinal segment and cut → Place in STERILE pottle with NO FORMALIN to avoid contamination of contents

Which image shows TRUE AM intusussception?

LEFT: True intussusception (dark areas = true haemorrhage) and difficult to pull apart

RIGHT: PM intussusception (Hb imbibition OR hyperaemia due to inflammation?) and easy to pull apart

Small Animal Diseases of the Oral Cavity

• Congenital DDx

• 5 Tooth DDx

• 3 Inflammatory DDx

• 7 Neoplastic DDx

Congenital DDx: Cleft palate (palatoschisis) and cleft/hare lip (cheiloschisis) (3)

Tooth DDx:

1. Dentigerous cysts (3)

2. Enamel hypoplasia (3)

3. Pigmentation of teeth (3)

4. Dental attrition (4)

5. Dental plaque/calculus and periodontal disease (5)

Inflammatory DDx:

1. Feline indolent/eosinophilic ulcer (4)

2. Feline ulcerative stomatitis/glossitis (3)

3. Other causes of oral ulcers in dogs and cats (5)

Neoplastic DDx:

1. Gingival hyperplasia (3)

2. Epulis = Reactive, hyperplastic and benign lesions (3)

3. Canine oral papilloma (4)

4. Oral squamous cell carcinoma (SCC) (5)

5. Sarcomas (3)

6. Oral melanoma (4)

7. Oral lymphoma (3)

What is this?

• Definition (+ 2 types)

• 3 Aetiologies

• Pathogenesis

• Sequelae

• 2 Other skeletal abnormalities

Cleft Palate (Palatoschisis) and Cleft/Hare Lip (Cheiloschisis) (3)

Definition:

• Cleft Lip = Congenital cleft of the upper lip which may be superficial or extend into the nostrils

• Cleft Palate = Congenital cleft of the hard and/or soft palate

Aetiologies: Sporadic/unknown

1. Teratogenic plants (hemlock, lupines)

2. Teratogenic drugs (griseofulvin)

3. Genetics (Charolais calves, some dog breeds)

Pathogenesis: During embryonic development, two halves of the face do not completely come together → Gap formation

Sequelae: Death due to aspiration pneumonia

Other Abnormalities: Crooked calf = Lupine ingestion in early gestation

1. Arthrogryposis = Contracted joints

2. Scoliosis/Kyphosis = Curved spine

What is this? (2)

Brachygnathia Superior/Inferior (2)

• LEFT = Brachygnathia superior

  • Definition: Shortening of the upper jaw (pugs, pekinese, boxers, Jersey and Angus cattle)

• RIGHT = Brachygnathia inferior

  • Definition: Shortening of the lower jaw (ruminants and horses = parrot mouth)

Aetiology: Inherited

Sequelae: Severe → Difficulty prehending and chewing food → Malocclusion → Attrition and periodontal disease

What is this?

• Structure and appearance

• 3 Signalments

• Behaviour

Dentigerous Cyst/Odontogenic Cyst (3)

Appearance: Swelling in the jaw/gums which contains part/all of tooth protruding into liquid-filled lumen lined by epithelium

Signalment:

1. Common in NZ sheep (mandibular incisors)

2. Brachycephalic dogs = Bilateral cysts

3. Vestigial wolf teeth (horses)

Behaviour: Benign, but can destroy adjacent tissue as they enlarge

What is this?

• Appearance

• Pathogenesis

• 3 Causes

Enamel Hypoplasia (3)

Appearance: Pitted areas/irregular indentations in enamel with discolouration (vs. tartar)

Pathogenesis:

1. Inflammatory/metabolic disease in utero or in young animals

2. Systemic disturbance affects ameloblast function to make white/shiny enamel

3. Enamel fails to form in young animals (deciduous and permanent respectively)

Causes:

1. Canine distemper in dogs (permanent teeth)

2. BVDV in calves (in utero)

3. Fluorine poisoning in cattle (brown discolouration of teeth)

Pigmentation of Teeth (3)

4 Causes

1. Fluorosis = Brown due to enamel hypoplasia

2. Tetracycline in young/pregnant dam = Yellow ± enamel hypoplasia

   

3. Congenital erythropoietic porphyria in calves, cats and pigs = Pink teeth/bones (fluoresce under UV) due to inherited defect in enzymes involved in heme synthesis → Porphyrin accumulation in teeth and bones

   

4. Mineral salts in ruminant cheek teeth become impregnated with chlorophyll = Black teeth (incidental finding)

   

Dental Attrition (4)

• Sequelae

• 5 Causes of accelerated dental attrition

Sequelae: Ill-thrift

Causes:

1. Malocclusion

2. Abnormally soft teeth (eg. odontodystrophies)

3. Abnormal chewing movement (eg. due to pain)

4. Loss of opposing tooth

5. Abrasive diet

   • NZ sheep grazing low and chewing abrasive soil = #1 reason for culling

   • Horses crib biting

Dental Plaque/Calculus and Periodontal Disease (5)

• Structure of plaque vs. calculus

• 6 Sequelae

Plaque: Non-mineralised composite mass of

1. Bacteria

2. Food particles

3. Tissue cells

Calculus: Mineralised plaque mainly formed mainly from calcium carbonate precipitated from saliva

Sequelae:

1. Gingivitis and periodontitis (carnivores)

2. Tooth loss

3. Osteomyelitis and pulpitis

   • → Euthanasia due to poor penetration of AB into bone

4. Retrobulbar abscess

5. Oronasal fistula (tracking infection through sinuses, nasal cavity and face)

6. Caries (infundibular necrosis) = Cavities/erosive lesions of the teeth

   • Signalment: Horses and sheep

   • Pathogenesis: Organic acids produced by bacteria in plaque → Decalcification of enamel

   • Location: Occlusal surface of maxillary 1st molar

What is this? (cat lip)

• 3 Locations

• Signalment

• Appearance

• Cytology

• 2 Aetiologies

• Treatment

• Prognosis

• 2 DDx

Feline Indolent/Eosinophilic Ulcer (4)

Location: Chronic ulcerative lesion of the mucocutaneous junctions of the

1. Lips (esp. upper lip either side of midline)

2. Oral mucosa (tongue, palate or gums)

3. Skin

Signalment: Cats of ALL ages/sex/breed

Appearance: Well-demarcated, reddish-brown shallow ulcers which may progress rapidly

• Indolent/rodent ulcers = Upper lip

Cytology: Eosinophils and neutrophils (also plasma cells and mast cells)

Aetiologies:

1. Immune-mediated allergic disease

   • Part of the eosinophilic granuloma complex

2. Primary dysfunction of eosinophils

Treatment: DIFFICULT (steroids, cryosurgery, cyclosporine, antibiotics???)

Prognosis: Recurrence common unless 1˚ allergen identified

DDx: Differentiate with impression smear/skin scraping for cytology

1. Oral mast cell tumours

2. Oral SCC

What is this?

• Signalment

• Pathogenesis

• 4 Clinical signs

• 4 Predisposing factors

• 3 Locations

Feline Ulcerative Stomatitis/Glossitis (3)

Signalment: Older cats

Aetiology: Multifactorial → Imbalance in oral microflora (spirochetes and G- anaerobes #1)

Clinical Signs: Chronic disease often in conjunction with periodontal disease

1. Dysphagia

2. Hypersalivation

3. Halitosis (necrotic tissue)

4. ± Weight loss

Risks: Viral infection

1. Calicivirus

2. Feline herpesvirus-1

3. Feline leukaemia virus

4. Feline immunodeficiency virus

Location:

1. Fauces #1 = Junction of mouth and pharynx

2. Gingiva

3. Tongue

DDx:

1. Feline plasma cell gingivitis/pharyngitis

2. Catarral stomatitis

4 Other causes of oral ulcers in dogs and cats

1. Renal failure and uraemia

   1. Excess urea in blood → saliva

   2. Urea broken down by urease-producing bacteria normally present in mouth

   3. Ammonia production which is caustic to the oral mucosa resulting in oral ulcers

2. Ingestion of caustic chemicals

3. Biting electrical cords

4. Feline calicivirus (more virulent strains form vesicles → ulcers esp. tongue)

What is this?

• Signalment

• Location

• Pathogenesis

• Sequelae

• Treatment

• Prognosis

• DDx

Gingival Hyperplasia (4)

Signalment: Cats and brachycephalic dogs (esp. Boxers)

Location: Upper canines most obvious

Pathogenesis: Chronic inflammation (eg. periodontal disease) → Locally extensive and proliferative reaction → Increased cell number

• Potentially caused by cyclosporine, Ca channel blockers and anticonvulsants?

Sequelae: Extra tissue creates pockets which accumulate food and plaque

Treatment: Surgical removal

Prognosis: Recurrence

DDx: Peripheral odontogenic fibroma (solitary lesion NOT proliferative as with gingival hyperplasia)

What is this?

• Definition

• Diagnosis

• 4 Types

Epulis

Definition: Group of reactive, hyperplastic and benign lesions within the oral cavity

Diagnosis: Histology with curative biopsy

Types:

1. Peripheral odontogenic fibroma (fibromatous epulis) = POFs

2. Pyogenic granuloma

3. Peripheral giant cell granuloma

4. Other odontogenic tumours which originate from the dental germinal cells (eg. ameloblastoma, odontoma, cementoma)

What is this?

• Appearance

• Location

• Agent

• Prognosis

Canine Oral Papilloma (4)

Appearance: Benign epithelial proliferations (warts) which appears as smooth and pale nodules → White-grey, cauliflower-like

Location: Lips, hard palate, gums, tonsil and buccal mucosa

Agent: Canine papillomavirus 1 infection (highly infectious often involving several puppies in a kennel)

Prognosis: GOOD

• Regression and recovery in 2 - 3 months due to strong immune response (dogs at puberty)

• Older dogs = Immunosuppression due to underlying disease process/immunosuppressive therapy

What is this? (cat)

• Location

• Appearance

• Behaviour

• DDx

FELINE Oral Squamous Cell Carcinoma (SCC) (5)

Location: Ventral tongue

Appearance: Red-grey friable mass with ulcerated centre that bleeds easily

Behaviour: Highly malignant with extensive local invasion into soft tissue and bone

• Metastasis to lymph nodes late in disease process (early resection → Good prognosis)

• Rarely lung metastasis

• Neoplastic epithelial cells with neutrophils due to ulceration and inflammation

DDx: Early gingival SCC similar to gingivitis

What is this? (dog tongue and liver)

• Location

• 3 Aetiologies

• Behaviour

Canine Oral Squamous Cell Carcinoma (SCC) (5)

Location: Tonsil and occasionally gums (usually unilateral)

Aetiology: Multifactorial??? More common in older animals:

1. Gingivitis

2. Carcinogens in smoke

3. Canine papillomavirus

Behaviour: Tonsillar SCC = Fast to metastasis to regional lymph nodes (retropharyngeal), thyroids, lungs and bones vs. gingival = Similar behaviour as cats

What is this?

• Behaviour

• Signalment

• Appearance

• Prognosis

Oral Fibrosarcoma (3)

Behaviour: Highly malignant tumours with local invasion into bone and rapid metastasis (rapid growth)

Signalment: Younger dogs (25% in dogs < 5yr)

• Large breeds (esp. Golden Retriever)

Appearance: Large, nodular fleshy masses arising from the gums and attached to underlying bone

Prognosis: Local recurrence common after surgical removal

• Metastasis to regional lymph nodes and lungs likely present at time of diagnosis

What is this?

• Signalment

• Location

• Diagnosis

Oral Lymphoma (3)

Signalment: Reported in dogs, cats and horses (less common oral tumour)

Location: Tonsils, tongue, gums, mucocutaneous junctions or pharynx ± other widespread organ involvement (multicentric lymphoma)

Diagnosis: FNA and biopsy (differentiate from inflammation)

What is this?

• Signalment

• Location

• Appearance

• Behaviour

• Prognosis

Oral Melanoma (4)

Signalment: #1 oral malignant tumour of dogs (rare in cats)

Location: Gums and lips

Appearance: Grey to black (sometimes no pigment = Amelanotic melanoma)

Behaviour: Rapid grow with ulceration, bone invasion and metastasis

Prognosis: ~2 - 3m survival (even with treatment)

• Metastasis to regional lymph nodes and lungs likely present at time of diagnosis (also spinal cord and brain)

2 Most common malignant oral tumours in CATS vs. DOGS

CATS:

1. Oral SCC

2. Oral fibrosarcoma

DOGS:

1. Oral melanoma

2. Oral SCC

3. Oral fibrosarcoma

Large Animal Oral Cavity Diseases

• 4 Viral vesicular DDx

• 6 Erosive and ulcerative DDx

• 3 Papular DDx

• 4 Bacterial/fungal DDx

Viral Vesicular DDx:

1. Foot-and-mouth disease (FMD) (5)

2. Vesicular stomatitis (VS) (3)

3. Swine vesicular disease (SVD) (3)

4. Senecavirus A (SVA) (3)

Erosive and Ulcerative DDx:

1. Bovine viral diarrhoea (mucosal disease) (5)

2. Malignant catarrhal fever (MCF) (4)

3. Calf ulcerative stomatitis (3)

4. Acorn poisoning (3)

5. Glossitis in photosensitisation (3)

6. Bluetongue (3)

Papular DDx:

1. Bovine papular stomatitis (3)

2. Contagious ecthyma (“scabby mouth”, contagious pustular dermatitis) (5)

Bacterial/Fungal DDx:

1. Oral necrobacillosis (necrotic stomatitis/laryngitis, calf diphtheria) (3)

2. Actinobacillosis (”woody tongue”) (4)

3. Actinomycosis (”lumpy jaw”) (3)

4. Thrush (4)

Vesicular vs. ulcerative viral diseases

Vesicular diseases usually present as ulcers → Vesicular and ulcerative viral diseases should be on the SAME DDx list for oral ulcers

• Cannot differentiate between viral vesicular diseases → Assess which species are infected

Describe the ONLY endemic VESICULAR disease similar in appearance for FMD in NZ

• Species and aetiology

• Pathogenesis

• Appearance of lesions

Species/Aetiology: Pigs grazing furanocoumarin-containing plants (eg. celery/parsnips)

Pathogenesis: Furanocoumarin compounds react with UV light to form vesicles

Appearance: ≤5cm vesicles/bullae on the lips, snout and legs

Foot-and-Mouth Disease (FMD) (5)

• Agent

• Signalment

• Pathogenesis

• Clinical signs

  • Cattle (6)

  • Pigs (3)

  • Sheep/goat (3)

• Prognosis

• Prevention

Agent: Family = Picornaviridae

• Aphthovirus (aphtho- = ulcer)

• 7 serotypes with numerous subtypes (vaccination against SPECIFIC serotype in the area)

Signalment: Highly contagious disease of cloven-footed animals

• Cattle = Indicator host (severe lesions → Easy detection)

• Sheep, goats, deer = Maintenance host (mild lesions, primarily lameness)

• Pigs = Amplifier hosts (shed lots of virus with milder lesions that predominate on hooves)

• Camelids = Reasonably resistant (no transmission or carrier status) Horse NOT affected by FMD

Pathogenesis:

1. Viraemia

2. Degeneration of middle layers in stratified squamous epithelium

3. Potential space created fills with serous fluid → Vesicles

4. Vesicles coalesce → Bullae

5. Bullae rupture within 24hr → Erosions/ulcers

Clinical Signs:

• Cattle

  1. Generalised: Fever (>40˚C), anorexia and depression

  2. Reduced milk production

  3. Drooling and thick saliva (vesicles in mouth = painful)

  4. Lameness (vesicles in interdigital skin and coronet)

  5. Vesicles on teats, vulva and rumen

  6. Neonates = Death from myocarditis (Tiger heart = streaks of inflammation)

• Pigs

  1. Small vesicles on snout ± mouth

  2. Lameness (hoof lesions)

  3. Mortality in piglets due to GI, pancreas and heart lesions

• Sheep/Goats = Mild

  1. ± 2˚ bacterial infection (eg. footrot)

  2. Abortion/foetal mummification

  3. Sudden death in young lambs (lesions in heart/muscle)

Prognosis: Low mortality (1 - 5%)

• High morbidity (massive outbreaks of highly contagious disease) → Consider lameness and loss of production

Prevention: Prohibited to feed pigs uncooked food waste from ships or aircrafts

• Pigs have highest risk for virus entering NZ (spread via direct contact/wind)

Vesicular Stomatitis (VS) (3)

• Agent

• Species affected

• Appearance

• Geographical distribution

• Transmission

• Importance

Agent: Rhabdoviridae family (genus = vesiculovirus)

Species: Cattle, pigs and HORSES/equids (ONLY vesicular disease of horses)

• Sheep and goats relatively resistant

Appearance: As for FMD

Geographic Distribution: Endemic in some USA states, Central and South America

Transmission: Direct contact and insects

Importance: Production loss in cattle + resembles FMD

Swine Vesicular Disease (SVD) (3)

• Agent

• Species affected

• Geographical distribution

• Location of lesions

• Prognosis

• Prevention

• Importance

Agent: Picornaviridae family (enterovirus)

Species: Pigs ONLY

Geographical Distribution: Europe and Far East

Location: Feet (between heel and coronary band) ± oral lesions (10%)

Prognosis: Often mild/subclinical (more significant loss in piglets)

Prevention: Do NOT feed pigs food waste from ships/aircrafts

Importance: Clinical indistinguishable from all other vesicular diseases

Senecavirus A (SVA) Infection of Pigs (3)

• Agent

• Species affected

• Geographical distribution

Agent: Picornaviridae family (emerging enterovirus)

Species: Pigs ONLY

Geographical Distribution: USA, Canada, Brazil and China Location and appearance as for other swine vesicular diseases

Bovine Viral Diarrhoea Virus (BVDV) (5)

• Agent

• Signalment

• 8 Clinical signs (+ stage of gestation)

Agent: Family = Flaviviridae → Genus = Pestivirus 2 genotypes = BVD-1 and BVD-2 2 biotypes = Non-cytopathic and cytopathic

Signalment: Cattle, deer and camelids

Clinical Signs:

1. Embryonal death (0 - 40 days)

2. Abortion (40 - 120 days)

3. Premature birth

4. Stillbirth (120 - 280 days)

5. Foetal mummification

6. Dummy calves = Weak and non-viable (120 - 280 days)

7. Teratogenesis (75 - 150 days)

   1. Cerebellar hypoplasia

   2. Hydranencephaly

   3. Hypomyelinogenesis

   4. Alopecia

   5. Retinal pathology

   6. Cataracts

   7. Microphthalmia

   8. Brachygnathism

   9. Enamel hypoplasia

8. Subclinical immunosuppression (post-natal infection)

   • Pregnant cows may give birth to clinically normal/small/weak calves that are Ab+ and Ag-

Acute BVDV

• Agent

• Transmission

• 4 Clinical signs

• Signalment

• Prognosis

• 4 Methods of diagnosis

Agent: Non-cytopathic strain of BVDV (BVDV-2 may cause more severe lesions resembling MD)

Transmission: Direct/indirect contact with bodily fluids

Clinical Signs: Subclinical or mild

1. Lethargy

2. Mild occulonasal discharge

3. Occasional mild oral erosions

4. Occasional diarrhoea

Signalment: Acute BVD = 3 - 6m calves (waning maternal immunity)

• MD = 6 - 24m cattle

Prognosis: High morbidity and low mortality (clears within 2 - 3w)

Diagnosis:

1. Ag ELISA

2. Ab ELISA = Pooled milk/serum

3. PCR = Pooled milk/serum

4. SNAP test on serum/ear-notch

Mucosal Disease (5)

• Signalment

• Pathogenesis

• 5 Clinical signs

• Prognosis

• 5 PM findings

Signalment: 6 - 24m cattle

Pathogenesis:

1. PI calf = Infection of dam at 40 - 120 days gestation with non-cytopathic strain of BVDV in utero

   • Foetus becomes infected → Immunological tolerance

   • Ab- and Ag+

2. Superinfection OR mutation of non-cytopathic BVDV in PI animals

3. Cytopathic BVDV infection

4. Lack of immune response in PI calves

5. Death

Clinical Signs:

1. Lethargy and anorexia

2. Dehydration

3. Diarrhoea

4. Nasal discharge

5. Rough coat

PM:

1. Erosions and ulcers around muzzle, in mouth, oesophagus (linear and irregular ulcers), reticulorumen and omasal leaves

2. Small, punctate ulcers and areas of haemorrhage in abomasal mucosa

3. Blood and fibrin overlying Peyer's patches (BVD attacks rapidly dividing cells eg. crypts of intestine and lymphoid cells in germinal centres)

4. ± Congestion, necrosis, ulceration and fibrinous inflammation of large bowel

5. ± Exudative skin lesions around perineum, base of horns, interdigital skin and heels of feet

How to differentiate between Mucosal Disease and MCF? (2)

1. Necrotic/haemorrhagic in Peyer’s patches is a feature of MD and NOT MCF (lymphoid hyperplasia)

2. Brain, kidney and adrenal glands = Vasculitis with MCF ONLY

What is this? (calf)

• Signalment

• 3 Clinical signs

• Appearance

• Location

• Histology

• 4 DDx

• Aetiology

• Prognosis

Calf Ulcerative Stomatitis (CUS) (3)

Signalment: 3 - 6m dairy calves (call MPI)

Clinical Signs:

1. Ill-thrift

2. Oral ulceration (± oesophagus and forestomach)

3. Diarrhoea

Appearance: Mild/solitary to multifocal/severe ulcers

Location: Mouth → oesophagus and forestomach

Histology: Inflammation of intestinal crypts and enteritis

DDx:

1. BVDV (rule out with BVDV test)

2. MCF

3. Uraemia

4. Caustic ingestion

Aetiology: Multifactorial? Similar to summer scour in Australia and UK

Prognosis: Variable morbidity and mortality

• Recovery in 4 - 6 weeks

• Outbreak may last 3 - 8 weeks on farm

What is this? (cow oesophagus and kidney)

• Pathogenesis

• 2 PM findings

• Diagnosis

Acorn Poisoning (3)

Pathogenesis:

1. Cattle ingests acorns/oaks leaves

2. Tannins are toxic to the kidneys → AKI

3. Uraemia

4. Uraemic toxins cause oral ulceration and haemorrhage

PM:

1. Shallow oral ulceration and haemorrhage (also oesophagus, rumen, intestines)

2. Swollen and pale kidneys surrounded by haemorrhage and oedema

Diagnosis: Serum biochemistry with urinalysis = Renal azotaemia and isosthenuria

• Cannot use faecal sampling for tannins (already passed out by the time of diagnosis)

What is this?

• Agent

• Transmission

• Geographical distribution

• Signalment

• Pathogenesis

• 3 Clinical signs

• 2 Sequelae

Bluetongue (3)

Agent: Family = Reoviridae → Genus = Orbivirus

• 25 serotypes with variable pathogenicity (10 serotypes in Australia)

Transmission: Culicoides spp. (midges/gnats)

Distribution: Africa, Middle East, parts of Asia, Australia, USA, parts of Europe

• Exotic to NZ

Signalment: Sheep = Clinical disease

• Goats and cattle = Subclinical/mild disease

Pathogenesis:

1. Endothelial damage

2. Microthrombi formation

3. Ischaemic necrosis

4. Ulceration of oral cavity

5. Oedema and haemorrhages

PM:

1. Cyanosis of tissues → Blue tongue and mouth (rare)

2. Petechiae of coronets and bulbs of sheep claws

3. Ecchymoses in pulmonary artery wall

Sequelae:

1. Torticollis (wry neck) in recovering sheep due to scarring after muscle necrosis of neck

2. Foetal malformations (eg. hydranencephaly) after infection during pregnancy

What is this?

• Species affected

• Location and appearance

• Pathogenesis

Glossitis in Photosensitisation (3)

Species: Cattle with photosensitisation of ANY cause (eg. FE)

Location/Appearance: Erosions of ventral midline of tongue

Pathogenesis: Light of certain wavelengths excite photodynamic compounds in the tongue when animal licks its nares and muzzle

What is this?

• Agent

• Signalment

• 4 Causes

• Appearance

• Location

• Diagnosis

Oral Necrobacillosis (Necrotic Stomatitis/Laryngitis, Calf Diphtheria) (3)

Agent: Fusobacterium necrophorum (anaerobic G+ bacteria that likes necrotic tissue)

Signalment: Cattle

Aetiology: 2˚ to previous mucosal damage in caudal pharynx

1. Trauma (eg. drenching, bolus)

2. Infectious bovine rhinotracheitis (herpesvirus)

3. BVD

4. Papular stomatitis infection

Appearance: Large, well-demarcated, yellow-grey, dry areas of coagulative necrosis surrounded by a hyperaemic zone

Location:

• Adults = Oral cavity ONLY

• Young animals = Spread to trachea (→ aspiration pneumonia), oesophagus or systemically

Diagnosis: Gross lesions ± organism in smears

• Difficult to culture as strict anaerobes

What is this?

• Agent

• Signalment

• Aetiology

• Inflammatory response

Actinobacillosis (“Woody Tongue”) (4)

Agent: Actinobacillus lignieresi (G- coccobacilli part of NORMAL oral flora)

Signalment: Cattle

Aetiology: Trauma allows bacteria to invade

Inflammatory Response: Pyogranulomatous inflammation and fibrosis centred on club colonies

• Club colonies = Immune complexes surrounding the bacteria often seen grossly as sulphur granules

• Associated lymphangitis and regional lymphadenitis common

What is this?

• Agent

• Aetiology

• Inflammatory response

• Location

• Appearance

Actinomycosis (“Lumpy Jaw”) (3)

Agent: Actinomyces bovis (G+ filamentous bacteria that is normal flora in the GIT)

Aetiology: Trauma (eg. tooth eruption or rough feed) → Invasion of oral submucosa and mandible/maxilla

Inflammatory Response: Pyogranulomatous osteomyelitis

Location: Mandible and maxilla ± soft tissue and lymph node involvement

Appearance: Similar lesions to actinobacillosis (including sulphur granules)

Prognosis: Lesions develop slowly over months with bone involvement = Difficult to treat

What is this?

• Agent

• Inflammatory response

• Location

• Risk factor

• Signalment

• Appearance

Thrush (4)

Agent: Candida albicans (yeast)

• NOT likely primary pathogen

Inflammatory Response: Superficial inflammation of stratified squamous epithelium

Location: Mouth, oesophagus, stomach or rumen) → Accumulation of excess epithelial debris on surface

Risk: Concurrent mild debilitating disease or antibiotic therapy resulting in altered microbial flora

Signalment: Young animals (worse in piglets)

Appearance: White layer of excessive, partly keratinised epithelium and exudate ± hyphae

Oesophagus and Stomach Diseases

• 5 Oesophageal DDx

• 6 Rumen DDx

• 4 Displacement DDx

• 3 Circulatory DDx

Oesophageal DDx:

1. Oesophageal stenosis (3)

2. Oesophageal obstruction (3)

3. Megaoesophagus (3)

4. Oesophagitis (3)

5. Parasitic diseases (3)

Rumen DDx:

1. Primary (frothy) bloat (4)

2. Secondary (free gas) bloat (4)

3. Rumen acidosis (5)

4. Milk rumenitis (4)

5. Mycotic rumenitis/reticulitis/omasitis (zygomycosis) (5)

6. Traumatic reticuloperitonitis (5)

Displacement DDx:

1. Diaphragmatic hernia (4)

2. Gastric dilation/volvulus (GDV) in dogs (5)

3. Abomasal displacement and/or volvulus in cattle (4)

4. Dilation of the stomach/abomasum in other species (4)

Circulatory DDx:

1. Gastrorrhagia and hyperaemia (3)

2. Oedema of the stomach/abomasal wall (3)

3. Infarction of the stomach in pigs (3)

Overview of the Oesophagus

• Structure

• 3 OTHER types of oesophageal diseases

Structure: Lined by stratified squamous epithelium with mucus glands

• Inner circular + outer longitudinal layer of skeletal muscle

Other DDx:

1. Viral diseases causing oral ulceration → Erosion/ulceration of mucosa (eg. BVD and MCF)

2. Skeletal muscle diseases (eg. nutritional myopathy)

3. Neuromuscular junction diseases (eg. myasthenia gravis)

What is this? (horse and dog oesophagus)

• 4 Causes (+ DDx)

• Appearance

• 2 Clinical signs

Oesophageal Stenosis (3)

Causes:

1. Cicatrisation (scar tissue formation) due to previous injury/reflux

2. External pressure (eg. tumour, lymph node as for TB, thyroids)

3. Developmental defect (eg. persistent right aortic arch in puppies)

4. Spirocerca lupi round worm granuloma

Appearance: Often mucosal necrosis at stenosis with dilation of proximal oesophagus

Clinical Signs:

1. Difficulty swallowing

2. Regurgitation of food

What is this? (horse oesophagus and dog thorax)

• 3 Causes

• 4 Sequelae

Oesophageal Obstruction (3)

Causes:

1. 2˚ to stenosis

2. Foreign bodies (eg. turnips, apples, bones)

   • Choke = Oesophageal obstruction in horses (or ruminants) caused by impaction of inadequately chewed feed → Stretched oesophagus

     • Associated with dental disease

3. Gastro-oesophageal intussusception in dogs (stomach telescopes into oesophagus)

Sequelae:

1. Pressure necrosis and ulcerated mucosa

2. → Oesophageal rupture/perforation → Pleuritis (esp. grass awns)

3. Ruminant oesophageal obstruction → Free gas bloat

4. Healing of large ulcers → Scarring and stenosis

6 Causes of oesophagitis (+ DDx)

1. Viral disease

   1. Papular stomatitis → Circular mucosal erosions more common at the proximal end

   2. BVD → Superficial longitudinal erosions more common at the distal end

   3. Mucosal disease → Deeper + more haemorrhagic erosions BVD

   4. MCF → Deeper + more haemorrhagic erosions than BVD

2. Necrobacillosis

3. Thrush

4. Traumatic injury (eg. doxycycline pill in small animals)

5. Chemical injury (eg. acids/alkalis, batteries, oak)

6. Reflux oesophagitis = Gastric acid and bile salts reflux into distal oesophagus → Erosion and ulceration due to:

   1. Dysfunction of the lower oesophageal sphincter due to anaesthesia (eg. not fasting for Caesarean section)

   2. Increased abdominal pressure

   3. Airway occlusion

   4. Hiatal abnormalities

What is this?

• Pathogenesis

• 3 Sequelae

• 2 Aetiologies (+ DDx)

Megaoesophagus (3)

Pathogenesis:

1. Motor dysfunction causes the entire oesophagus to become flaccid and dilated

2. Failure of normal peristaltic waves to develop and pass food down (achalasia)

3. Ingesta accumulates in dilated lumen (may become larger than stomach)

4. Undigested food is regurgitated

Sequelae:

1. Oesophagitis

2. Malnutrition

3. 2˚ aspiration pneumonia

Aetiologies:

1. Congenital megaoesophagus = Defect in afferent autonomic part of reflex

   • Signalment: Great dane, GSD, Irish setter

2. Secondary to diseases affecting NMJ

   1. Myasthenia gravis

   2. Hypoadrenocorticism (Addison's disease)

   3. Neuropathies/myopathies

   4. Lead poisoning

   5. Canine distemper

What is this?

• Appearance

• Host

• Importance

Sarcocystis gigantea

Appearance: Giant protozoal cysts = White nodules ≤1cm long resembling rice grains beneath the oesophageal serosa

Host: IH = Sheep

• DH: Cat

Importance: Incidental finding

3 Parasitic diseases of the oesophagus (+ which are exotic to NZ + species affected)

1. Gasterophilus in horses (occasional)

2. Sarcocystis gigantea in sheep

3. Spirocerca lupi in dogs (EXOTIC)

5 Features to examine in rumen contents at PM (+ most likely DDx)

1. Dry = Dehydration

2. Ammonia smell = Urea toxicity

3. Low rumen pH = Acidosis

4. Flakes of lead paint = Toxicity

5. Toxic plants (eg. oleander, yew, tutu, weeds, sump oil)

   • Yellow pollen from pine tress = Incidental finding

What is this?

Gastric Foreign Bodies (1)

• Trichobezoars = Hair balls

• Phytobezoars = Plant fibre balls

Predisposing factors:

1. Very young animals deprived of dietary fibre

2. Lice infestation and excessive licking

Importance: Incidental finding

What is this?

• 2 Causes

• 6 PM findings

Ruminal Tympany (Bloat) (4)

Causes:

1. Primary (frothy) bloat

2. Secondary (free gas) bloat

PM:

1. Distended rumen with foamy contents

2. Dark blood which does not clot due to anoxia from impaired respiration (deoxygenated blood and congestion)

3. Bloat-line in the oesophagus = Congested/dark cervical (cranial) oesophagus with pale/blanched thoracic (caudal) mucosa → Distinguish from PM bloat

4. Pale lungs compressed into cranial thorax by bulging diaphragm

5. ± Haemorrhage, congestion and oedema of cervical muscles

6. ± SC oedema of inguinal and perineal regions (decreased venous return)

Primary (Frothy) Bloat

• Cause

• Pathogenesis

Cause: Cattle grazing pastures with high legume content

Pathogenesis:

1. Cattle graze lots of legumes which contain cytoplasmic proteins

2. Proteins stabilises gas bubbles produced by rumen fermentation

3. Layer of foam created (vs. bubbles normally popping)

4. Prevents formation of free gas cap in the dorsal sac of rumen which is required to stimulate eructation

5. Accumulated foam blocks cardia

6. Rumen pressure increases → Increased intra-abdominal pressure on diaphragm, abdominal organs and vena cava

7. Impaired respiration + Reduced venous return + Rumen mobility ceases → Sudden death

Secondary (Free Gas) Bloat

• 3 Causes

Less common

Cause: Physical/functional defects in eructation of gas

1. Foreign body obstruction (eg. turnip, potato, plastic bag)

2. Oesophageal stenosis

3. Vagal nerve damage

Normal rumen pH (+ 4 regulators of rumen pH)

Normal pH: > 5.5 and regulated by

1. Saliva (bicarbonate)

2. Epithelial absorption of VFAs

3. Microbial metabolism of VFAs

4. Movement of fluid into distal GIT

What is this?

• Aetiology (+ 3 example causes)

• 3 Clinical signs

• 2 Types (+ characteristics)

Rumen Acidosis (5)

Aetiology: Ingestion of lots of readily fermentable carbohydrates which animal has not been accustomed

• Grey and watery rumen contents with rumenitis

Examples:

1. Grain introduction (eg. barley, maize and wheat)

2. Accidental breakout → Access to grain, apples, kiwifruit, turnips, swedes, potatoes, kumara, fodder beet

3. Break-feeding/drought-feeding → Hungry/dominant animals get more feed

4. Recently calved cows transitioned to lactation rotation too quickly (high CHO and insufficient fibre for saliva production) → SARA

Clinical Signs: 3Ds

1. Diarrhoea

2. Dehydration

3. Decreased milk production

Types:

Subacute Rumen Acidosis (SARA)

1. Rumen pH = 5 - 5.5

2. Increased concentration of VFAs in rumen

3. Relatively low concentrations lactic acid (< 10 mmol/L)

4. Dominance of G- flora

Acute Clinical Rumen Acidosis (ACRA)

1. Rumen pH < 5

2. Dramatic increase in lactic acid concentrations (mainly D-lactate)

3. Defaunation = Absent rumen protozoa

4. Dominance of G+ flora (Streptococcus bovis and Lactobacillus spp.)

Rumen Acidosis (5)

• Pathogenesis

• 5 Methods of diagnosis

• 6 Sequelae

Pathogenesis: Increased fatty acids in both SARA and ACRA (which buffering capacity cannot keep up with) leads to:

1. Absorption of fatty acids and acidosis (profound uncompensated metabolic acidosis → Collapse and death in ARCA)

2. Ruminal atony (fatty acids act on receptor that inhibit reticulorumen motility)

3. Increased intraruminal osmotic pressure → Fluid moves from blood into rumen → Dehydration + haemoconcentration + diarrhoea

4. ± 2˚ infection (diagnosis depends on amount of fermentable grain relative to amount expected)

   • Fusobacterium necrophorum

   • Trueperella pyogenes

   • Fungal

Diagnosis:

1. History and diet

2. Clinical signs (ACRA → Dehydration, colic, rumen stasis, increased HR, ± CNS signs when severe)

3. CBC/biochemistry (metabolic acidosis with reduced BE but similar to other metabolic disorders: hypocalcaemia, toxic mastitis, metritis)

4. Measure rumen pH with electronic pH meter/narrow range indicator paper (immediately after sample collection)

5. Microscopy: No motile protozoa

6. Histology: Epithelial necrosis and inflammation (red)

Sequelae:

1. Frothy bloat

2. Zygomycosis of forestomach wall

3. Ruminal/abomasal necrobacillosis → Superficial foci of mucosal coagulative necrosis → Liver abscesses → Caudal vena cava thrombosis → Pulmonary embolic aneurysm (PEA) = Rupture of pulmonary vasculature → Fatal bilateral epistaxis

4. Abomasal/duodenal ulcers

5. Polioencephalomalacia (reduced thiamine-producing bacteria)

6. Laminitis (release of histamine and endotoxin → Peripheral vasoconstriction)

What is this? (calf rumen)

• Signalment

• Pathogenesis

• 2 Clinical signs

• Sequelae

Milk Rumenitis (4)

Signalment: Calves < 4 - 6w

Pathogenesis:

1. Calves fed milk from bucket/stomach tube (no suckling reflex)

2. Failure of oesophageal groove reflex

3. Milk spills into immature rumen and reticulum

4. Milk putrefaction → Rumen distension and rumenitis (milder than grain overload)

5. Damaged rumen mucosa

Clinical Signs:

1. Diarrhoea

2. Bruxism

Sequelae: Mycotic rumenitis

What is this?

• Agents

• Pathogenesis

• 3 PM findings

Mycotic Rumenitis (Zygomycosis) (5)

Agent: Zygomycete fungi of the genera: Mucor, Rhizopus and Absidia = Saprophytic fungi found in environment

Pathogenesis:

1. Damage to mucosa of the rumen/reticulum/omasum

2. Fungi invade venules in submucosa

3. → Thrombosis and infarction of the forestomach wall

4. Lesions spread through ALL layers of the forestomach wall

5. Fungi may spread through blood to liver

PM:

1. Large, circular, red-black areas of thrombosis and necrosis which extend throughout the forestomach wall

2. ± Localised fibrinous peritonitis

3. ± Spleen and liver affected

Importance of paramphistomes (Calicophoron calicophorum) (2)

Incidental finding when adult stages in reticulum

What it this?

TWO aetiologies

Diaphragmatic Hernia (4)

Stomach displaced into pleural cavity through:

1. Traumatic diaphragmatic hernia (eg. HBC) = Left image

2. Congenital diaphragmatic hernia

   • Incomplete development of lungs due to presence of intestines in chest = Right image

What is this?

• Signalment

• Pathogenesis

• 3 PM findings

• 5 Clinical features

Gastric Dilation Volvulus (GDV) (5)

Signalment: Deep-chested dogs after large meal

Pathogenesis:

1. Food, fluid and gas accumulate in stomach

2. Impaired eructation and pyloric outflow

3. Stomach rotates around oesophagus

4. Spleen move into a right ventral position and oesophagus becomes occluded →

5. Obstruction of gastric and splenic veins →

6. Infarction of gastric mucosa and congestion/infarction of spleen

PM:

1. Stomach contents is blood-stained

2. Congested stomach wall

3. ± Ruptured stomach due to ischaemic necrosis

Clinical Features: Requires emergency treatment to prevent death

1. Circulatory shock (decreased venous return and CO)

2. Electrolyte imbalance

3. Acid-base imbalance

4. ± Cardiac arrhythmia

5. ± DIC

Abomasal Displacement (4)

• Timing

• 2 Types

• Diagnosis

Timing: Common around calving (underlying metabolic disease, ketosis, metritis → Atony) and seldom fatal unless complicated by volvulus

Types:

1. LDA

2. RDA → Volvulus

Diagnosis: Ping heard on percussion of abdomen somewhere between olecranon and tuber coxae ± blood work

6 Clinical pathology findings of displaced abomasum

1. PCV, Hb, RBC

2. WBC

3. Creatinine and urea

4. Electrolytes

5. Muscle enzymes

6. BOH

1. Haemoconcentration due to dehydration

2. ± Inflammatory/stress leukogram (neutrophilia with left shift)

3. Pre-renal azotaemia due to dehydration (increase urea and creatinine with concentrated urine)

4. Mild hyponatraemia and hypokalaemia with marked hypochloraemia due to loss of HCl and electrolytes into lumen of abomasum

5. Elevated CK and AST if cow was down

6. Increased BOH = Common in any ruminant off-feed and indicate ketosis

What is this> (horse stomach)

• Cause

• Pathogenesis

• Sequelae

Stomach Dilation in Horses (4)

Cause: Consumption of excess carbohydrates or excessive feeding

Pathogenesis:

1. Bacteria fermentation of carbohydrates

2. Production of gas and acid → Increased osmotic pressure

3. Water moves into stomach down osmotic gradient → ± Gastric rupture along greater curvature, and death due to shock and peritonitis

Sequelae: Survival → Laminitis

What is this?

• Pathogenesis

• Diagnosis

Vagal Indigestion

Pathogenesis:

1. Sequel to traumatic damage and scarring of the vagus nerve (eg. traumatic reticuloperitonitis) which assists with digestion

2. Abomasum and rumen become greatly distended with lots of dry ingesta

3. → Visible distension of abdominal wall (papple-shape: LEFT = Apple, RIGHT = Pear)

Diagnosis: Clinical appearance of papple + exclusion of other DDx

What is this?

TWO causes (+ pathogenesis)

Lamb/Calf Abomasal Distension (4)

Causes:

1. 2˚ to pyloric outflow obstruction (eg. straw impaction)

2. Abomasal bloat associated with Sarcina or Clostridia bacteria

   1. Bottle-fed animals given large volumes of milk in a single feed

   2. → Bacteria ferment lactose → ∆abomasal pH

   3. → Lots of gas production (Sarcina and Clostridia) → ± Abomasal rupture

2 Causes of active gastric hyperaemia

1. Physiological after ingestion of food

2. Pathological due to acute gastritis

4 Causes of gastrorrhagia (gastric haemorrhage)

1. Uraemia in dogs (damaged submucosal arteries ± mineralisation of gastric wall)

2. Gastric ulceration

3. Haemonchosis in sheep (attachment of worms)

4. Trauma and coagulopathies

What is this? (pig stomach)

• Agent

• 6 Causes in ruminants

Oedema of Stomach Wall (3)

Agent: Oedema disease caused by E. coli infection

Ruminants: oedema of abomasal folds due to

1. Chronic wasting diseases (cachexia)

2. Haemonchus

3. Ostertagia/Teladorsagia infections

4. Arsenic poisoning

5. MCF

What is this? (pig stomach)

• Pathogenesis

• 5 Aetiologies

• Location

• Appearance

Infarction of the Stomach in Pigs (3)

Pathogenesis:

1. Severe acute infectious disease causes endotoxaemia/septicaemia

2. → DIC resulting in widespread coagulation

3. Venous infarction of fundic mucosa of the stomach

Aetiologies:

1. Salmonellosis

2. Coliform enteritis

3. Erysipelas

4. Swine fever

5. Swine dysentery

Location: Mucosal surface of greater curvature

Appearance: Large, dark red-black areas of infarction ± fibrin/excessive mucus

Describe 6 causes of gastritis/abomasitis

1. Acute enteric infection

   • eg. Abomasitis in sheep = Salmonella Typhimurium OR Hindmarsh

2. Irritant/caustic poison

   • eg. Arsenic and fluoride in superphosphate fertiliser → Fluid intestinal contents and nephrosis

3. Fusobacterium necrophorum

   • 2˚ to ulcerative disease (eg. BVDV)

4. Mycotic haemorrhagic abomasitis

   • 2˚ to ulcerative disease (eg. BVDV)

5. Nematodes

6. Braxy = Sporadic abomasitis in lambs and calves caused by Clostridium septicum

   • Pathogenesis:

     1. Associated with ingestion of frozen food in cold weather

     2. Creates local tissue damage which allows bacterial invasion

     3. Exotoxin produced by Cl. septicum causes rapid death

Ulceration of the Stomach/Abomasum (5)

• 2 Normal mucosal protective mechanisms of the abomasum

• 2 Mechanisms causing stomach ulceration

Normal Mucosal Protection:

1. Bicarbonate (secreted by saliva) covers the mucosa of the cardia, fundus and pylorus

2. Prostaglandins stimulate bicarbonate and mucus secretion AND enhance gastric mucosal blood flow

Stomach Ulceration:

1. Compromised mucosal protective mechanisms #1 (eg. loss of mucus, prostaglandins or bicarbonate)

2. Hypersecretion of acid

What is this?

• Appearance

• 4 Clinical signs

• 2 Sequelae

Ulceration of the Stomach/Abomasum (5)

Appearance:

• Small ulcers = Red/haemorrhagic OR black due to blood digested by acid → Heal by granulation

• Large ulcers = Haemorrhage ± death (esp. pigs)

Clinical Signs:

1. Melaena = Dark and tarry faeces due to digestion of blood

2. Haematemesis = Coffee ground appearance due to digested blood

3. Anaemia

4. Sudden death due to haemorrhage

Sequelae:

1. 2˚ fungal infection (Aspergillus or Mucor) in ruminants

2. Peritonitis due to perforation into peritoneal cavity

5 Causes of gastric ulceration in cattle (+ pathogenesis)

1. Acute stress → Hyperacidity → Small punctate (1 - 2mm)/linear areas of haemorrhage and ulceration in abomasum

2. Undeveloped rumen → Roughage enter abomasum → Irritation → Ulcerated abomasum of young calves

3. Traumatic reticuloperitonitis/displaced abomasum → Abomasal atony in adults

4. Malignant lymphoma → Grossly thickened folds susceptible to ulceration and haemorrhage

5. Viral infection: BVD, MCF, FMD

What is this? (pig stomach)

• Pathogenesis

• Other location

Ulceration of the Pars Oesophagea

Pathogenesis: Young growing pigs

1. Finely ground rations (also associated with high dietary copper, whey, starchy diets low in protein, high dietary unsaturated fatty acids)

2. Increased water in stomach and loss gastric content partitioning

3. Pars oesophagus = Square area of tissue at the entry of the stomach = Squamous epithelium with no buffering capacity becomes susceptible to attack by gastric acid

4. → Fissures in hyperplastic parakeratotic epithelium ± Candida albicans hyphae

5. Progression to erosion and ulceration

Other Location: Ulceration of fundus in older pigs due to chronic infection with Hyostrongylus rubidus

• ± Fatal haemorrhage

What is this? (horse stomach)

• Location

• 4 Causes

Ulceration of the Margo Plicatus

Location: Margo plicatus

Causes: May perforate and bleed (esp. foals)

1. Bots

2. Phenylbutazone (also small intestine and right dorsal colon #1)

3. Stress (eg. horse in training)

4. Surgery

3 Causes of gastric ulceration in dogs

Uncommon

1. Uraemia

2. NSAIDs

3. Foreign bodies

Main cause of gastric ulceration in cats

Aspirin poisoning

Forestomach Parasites

• 2 Horse parasites

• 3 Ruminant parasites

Horse:

1. Bots = Larval stage of Gasterophilus flies

2. Draschia (Habronema) megastoma

Ruminant:

1. Haemonchus contortus

2. Ostertagia/Teladorsagia

3. Trichostrongylus axei

What is this?

• Lifecycle

• 2 Sites

• Clinical signs

• Appearance

Horse Bots (3)

Lifecycle:

1. Gasterophilus flies deposit eggs on face and legs

2. Horses ingest eggs through licking

3. L1 penetrates oral mucosa and moults to L2

4. L2 migrate down the GIT

5. Larvae pass into faeces to pupate

Sites in GIT:

1. G. interstinalis = Attached to gastric mucosa of pars oesophagea in clumps

2. G. nasalis = Pylorus and proximal duodenum

Clinical Signs: Incidental

PM: ± Small areas of ulceration and granulomatous inflammation

What is this?

• Length of parasite

• Location in host

• Appearance of lesions

• Clinical signs

Draschia (Habronema) megastoma (3)

Length: 20mm nematode

Location: Burrows into stomach wall of horses

Appearance: Granulomatous inflammation 20 - 40mm diameter ± suppuration with 2˚ infection by pyogenic bacteria

Clinical signs: NONE!

What is this?

• Signalment

• Pathogenesis

• Diagnosis

• 3 Clinical signs

• 5 PM findings

• Haematology

Haemonchus contortus (Barber’s Pole Worm)

Signalment: Sheep and goats of ALL ages (lambs more susceptible to clinical disease = 2000 - 3000 significant burden)

• Insignificant in cattle

Pathogenesis: L4 and adult suck blood in abomasum

Diagnosis: High FEC (may be low due to acute death before PPP of 15 days or recent drench)

Clinical Signs:

1. Sudden death

2. Exercise intolerance

3. Submandibular oedema (panhypoproteinaemia) No diarrhoea

PM:

1. Pale carcass (MM)

2. ± Ventral SC oedema, hydrothorax and ascites due to hypoproteinaemia

3. Grossly visible worms in abomasum

4. Brown fluid in abomasum (formation of acid haematin from Hb)

5. Foam up trachea due to pulmonary oedema

Haematology: Iron-deficiency anaemia = Regenerative → Non-regenerative (keratocytes, schistocytes, hypochromasia and microcytosis)

Trichostrongylus axei

• Importance

• Appearance of lesions

Unimportant in ruminants of ALL ages in NZ

Appearance: Catarrhal gastroenteritis with small ulcers after mucosal emergence

What is this?

• Signalment

• Pathogenesis

• Appearance

• 2 Types

• 2 Clinical pathology findings

• # Larvae needed to produce disease

Ostertagia/Teladorsagia

Signalment:

• Type I = Sheep and cattle < 1yr (± adults)

• Type II Ostertagiosis = Cattle 1 - 2yr

Pathogenesis:

1. Larvae burrow into abomasal mucus glands

2. Gland hyperplasia and metaplasia of epithelium (unspecialised cuboidal cells replace chief and parietal cells)

3. Loss of chief cells → Reduced HCl production → Neutral abomasal pH

4. → Pepsinogen cannot be activated to pepsin → Reduced protein digestion → Diarrhoea

5. Bacteria are NOT killed

6. Pepsinogen absorbed into bloodstream

7. Hypoalbuminaemia → Ventral SC oedema (abomasal oedema when severe in lambs/calves)

Appearance: Small, pale, umbilicated nodules 1 - 2mm grossly on mucosal surface within a few days of infection → Morocco leather appearance with heavy infection → Superficial necrosis and inflammation with emergence of immature adults

Types:

• Type I = Lambs and calves ingest lots of larvae over short period

• Type II infection = Larvae retard development in mucosa to have mass emergence months later in winter/spring

Laboratory:

1. Hypoalbuminaemia (protein-losing gastroenteropathy)

2. Increased serum/plasma pepsinogen which increases from ingestion, then again with emergence (no pepsinogen increase when worms encysted)

Disease: 10,000+ larvae needed to produce clinical disease

What is this?

• Signalment

• 2 Aetiologies

• Pathogenesis

Atresia (4) = No patency in normal lumen

• eg. atresia jejuni, ilei, coli, ani

• Signalment: Holstein calves and foals → Spiral colon empty and flaccid

• Aetiologies:

  1. Recessive inherited trait (carrier bulls removed from AI serve in NZ)

  2. Potential association with early amniotic vesicle palpation for pregnancy diagnosis???

Atresia ani = Heritable trait occurring in most species (may be associated with spinal/genitourinary malformations

Progression: Normal at birth → Faecal accumulation → Abdominal distension → Death within few days

List 3 types of intestinal obstructions (+ definitions)

1. Intraluminal/Intrinsic obstructions = Obstructed LUMEN of intestine

2. Extrinsic obstructions = External factor compressing intestinal lumen

3. Functional obstructions = No physical occlusion, but food cannot pass through intestine due to lack of peristalsis

What is this?

Type of intestinal obstruction

• 7 Examples

Intraluminal/Intrinsic Intestinal Obstruction

1. Foreign body (eg. corn cob, strip of cloth, plastic bags, string, fruit sone, ball)

2. Bezoar

3. Ascarids in pigs and foals

4. Chronic constipation and colon impacted with faecal matter

5. Enterolith = Spherical mineral concretations occasionally found in horse colons (usually do NOT cause obstruction)

6. Congenital atresia

7. Scarring/stenosis

What is this?

Type of intestinal obstruction

• 5 Examples

Extraluminal/Extrinsic Intestinal Obstruction

1. Tumour (eg. sheep adenocarcinoma or horse lipoma)

2. Strangulation (eg. herniation or lipoma)

3. Fibrous adhesion

4. Fat necrosis in cattle (lipomatous proliferation of fat surrounding intestine)

5. Abscess

What is this?

Type of intestinal obstruction

• 2 Examples

  • Definition

  • Causes

Functional Obstruction

1. Grass sickness (equine dysautonomia) = Subacute partial paralysis of intestines in HORSES

   • Cause: Unidentified neurotoxin → Necrotic degeneration of autonomic ganglia in abdominal cavity

   • Diagnosis: Histology intestinal nerves

2. Paralytic ileus = Diffuse absence of normal intestinal tone and peristalsis → Flaccid intestines distended by fluid caused by:

   1. Post-abdominal surgery involving intestines, peritonitis

   2. Spina bifida

   3. Spinal injury

What 2 things does severity/consequences of intestinal obstruction depend on?

1. Location of intestine obstructed (upper vs. lower GIT): Obstructed intestines interfere with propagation of peristaltic contractions distally

2. Simple or strangulated

UPPER Small Intestinal Obstruction

• Pathogenesis

• Clinical pathology findings

  • RBC and TP

  • WBC

  • Urea, creatinine and USG

  • Electrolytes

  • Acid-base balance

  • Phosphorus

Pathogenesis: ACUTE AND MORE SEVERE

1. Lots of fluid normally produced by the upper GIT accumulates proximal to blockage

2. → Loss of water and electrolytes into lumen

3. Increased local peristalsis initially proximal AND distal to obstruction → Pain

4. Reverse peristalsis above point of obstruction → Intense vomiting

5. More fluid and gas accumulates → Intestinal ileus

Clinical Pathology:

1. Relative erythrocytosis and hyperproteinaemia (dehydration)

2. Inflammatory leukogram = Neutrophilia with left shift (damaged intestine)

3. Pre-renal azotaemia (dehydration) and optimally concentrated urine

4. Reduced serum Na, Cl and K (loss of electrolytes into gut/vomiting)

5. Metabolic alkalosis (loss of gastric acid) ± Hypercapnoea (compensatory respiratory acidosis)

6. ± Increased serum phosphorus (pre-renal azotaemia and reduced excretion of P in saliva of ruminants)

Pathogenesis of lower intestinal obstruction

LESS ACUTE AND OFTEN MORE CHRONIC AETIOLOGY

1. Lots of fluid normally produced by the proximal GIT accumulates proximal to blockage

2. Less significant loss of fluid and electrolytes into lumen (larger absorptive surface area)

3. Gas and fluid pressure build → Altered mucosal permeability

4. → Readily absorbed bacterial toxins

5. → Toxaemia

Prognosis of colon/rectum obstruction

Fluids sufficiently absorbed in the proximal GIT → Animal lives a considerable time → Large accumulation of inspissated faeces Common in working dogs