3.1.3: Anaemia and haemolytic conditions

Question 1

1 and 2

Answer 1

Question 2

3

Answer 2

Question 3

Differentials for epistaxis in adult cattle

Answer 3

• Trauma (unilateral epistaxis more common than bilateral)
• Caudal vena cava syndrome (and associated pulmonary haemorrhage)
• Foreign body (unilateral epistaxis most common)
• Aspergillosis (rarer in cattle compared to dogs)
• Bovine neonatal pancytopenia
• Bovine Petechial Fever (not in UK)
• Coagulation disorder/ anticoagulant rodenticidies
• Congestive heart failure
• Drug reaction e.g. penicillin
• Schistosoma nasale
• Snake bite
• Tooth root abscess
• Vascular malformation

Malignant catarrhal fever does not cause true expistaxis.

Bold = common differentials

Question 4

What is this?

Answer 4

Schistosoma nasale (blood fluke)
* Trematode that lives in blood and invades nasal mucosa
* Prevalent in India, not currently present in the UK

Question 5

Describe how subacute ruminal acidosis can lead to caudal vena cava syndrome

Answer 5

• Subacute ruminal acidosis -> leads to rumenitis, erosion and ulceration of the ruminal epithelium
• Bacteria invade and reach the liver, creating liver abscesses
• Septic emboli are released into circulation
• Cattle may die as a result of embolism of large thrombus, or rupture of massive amount of purulent material into vena cava

Question 6

True/false: cows with caudal vena cava syndrome develop nephritis, but not endocarditis.

Answer 6

False.
* 10% of cows with caudal vena cava syndrome develop endocarditis
* They can also develop suppurative nephritis if septic thrombi travel to the kidneys
* The lungs are the most common site for septic thrombi to end up

Question 7

True/false: subacute ruminal acidosis is always the underlying cause of caudal vena cava syndrome.

Answer 7

False.
* Subacute ruminal acidosis may cause caudal vena cava syndrome when liver abscesses form due to this condition
* However emboli from inflammatory processes elsewhere in the body can also cause this syndrome (e.g. from udder, uterus, or claws)

Question 8

Explain how caudal vena cava syndrome can lead to epistaxis

Answer 8

• Septic emboli break off (usually from liver abscesses) and travel via the caudal vena cava to the lungs
• In the lungs, bacteria cause bronchopneumonia
• Bronchopneumonia can lead to intrapulmonary or intrabronchial haemorrhage, because the pulmonary vessels are eroded by bacteria
• Blood coming from the lungs is shown as epistaxis

Question 9

Diagnosis of caudal vena cava syndrome

Answer 9

• Ultrasonography of the caudal vena cava (identify thrombus) - image from 11th and 12th intercostal spaces on the right side
• Further diagnostics (radiography, endoscopy) could in theory be performed to rule out other respiratory disease

Question 10

Treatment and prognosis of caudal vena cava syndrome

Answer 10

• Prognosis is poor; if they don’t die suddenly, these animals often develop co-morbidities e.g. pneumonia
• Euthanasia is recommended

Question 11

Differentials for disorders of primary haemostasis in cattle

Answer 11

Primary haemostasis can fail due to thrombocytopaenia or platelet malfunction.

Thrombocytopaenia:
* Acute bracken fern toxicity
* Bovine neonatal pancytopaenia
* Certain strains of BVD can cause a haemorrhagic syndrome
* Ingestion of bone marrow suppressive substances
* Trichothecene mycotoxicosis

Platelet malfunction
* Inherited bovine thrombopathia (Simmental cattle)

Question 12

How does bracken fern toxicity develop and what syndromes does it cause?

Answer 12

Ingestion of bracken (Pteridium species) over weeks-months can cause acute haemorrhagic syndrome, or over months-years, can cause enzootic bovine haematuria.

Question 13

What is the cause of enzootic bovine haematuria and what are the clinical signs?

Answer 13

Cause: chronic low-level ingestion of bracken over months-years.

Clinical signs
* Intermittent and can occur weeks after cessation of exposure
* Episodes can be precipitated by stress (transport, parturition)
* Intermittent haematuria
* Coagulum in urine
* Progressive weight loss
* Ruminal atony, bloat, diarrhoea
* Dysphagia, regurgitation, salivation
* Cough, dyspnoea

Question 14

What are the clinical signs of acute haemorrhagic syndrome associated with bracken fern toxicity?

Answer 14

• Haemorrhages vary in severity; include epistaxis/ bloody nasal discharge, blood in milk, vaginal bleeding, large blood clots in faeces, excessive bleeding from minor cuts/ insect bites
• Death due to internal haemorrhage/ secondary infection
• Lethargy
• Inappetance
• Loss of condition
• Pronounced pyrexia
• Pallor
• Rumen stasis
• Submandibular oedema with laboured breathing especially in young cattle

Question 15

Treatment and prognosis of acute bracken fern toxicity

Answer 15

• Remove cattle from exposure to bracken fern
• No specific treatment - all supportive
• Blood or platelet transfusion; large volumes may be required
• Antibiotics if secondary infection
• Treatment is often ineffective. Euthanasia is necessary in advanced disease.

Question 16

Differentials for disorders of secondary haemostasis

Answer 16

• Inherited deficiency of coagulation factors (Factor XI deficiency, seen in Holstein-Friesians)
• Acquired deficiency of coagulation factors (anticoagulant rodenticide toxicity, mouldy sweet clover poisoning)
• Disseminated intravascular coagulation (DIC)

Question 17

What is trichothecene mycotoxicosis and how does it cause disease?

Answer 17

• Type of toxin produced by many species of fungi
• Ingestion of mouldy feed can result in haemorrhage as fungal toxin interferes with platelets
• Mycotoxin binders may not prevent this toxin being ingested

Question 18

Signalment for bovine neonatal pancytopaenia

Answer 18

Calves <4 weeks old

Question 19

Cause and pathogenesis of bovine neonatal pancytopaenia

Answer 19

• Ingestion of colostrum containing alloantibodies from dams vaccinated with a killed BVD virus vaccine (e.g. Pregsure BVD - withdrawn from market) which contained a novel adjuvant
• Alloreactive antibodies target MHC 1 complex on bovine cells, binding to WBCs and platelets, as well as haematopoietic precursors in bone marrow
• Circulating RBCs are not damaged
• There is normochromic, normocytic, non-regenerative anaemia

Question 20

Clinical signs of bovine neonatal pancytopaenia

Answer 20

• Prolonged bleeding from ear tag or injection sites
• Unexplained bleeding from nose, skin, rectum
• Petechial haemorrhages in mouth and on ears
• Pyrexia and concurrent infection
• Lethargy, dyspnoea
• Sudden death

Question 21

Treatment and control of bovine neonatal pancytopaenia

Answer 21

Treatment
* Whole blood transfusion NOT from the dam; improvement usually only lasts 24-48hrs. Catheterisation for transfusion risks massive haemorrhage
* Antibiotic cover may be justified as immunocompromised
* Prognosis is poor and treatment likely to expensive; euthanasia may be in calf’s best interests

Control
* Vaccine associated with initial outbreak has been withdrawn, however other vaccines have since been implicated, so must remain aware of this syndrome

Question 22

Treatment of acute haemorrhage in cattle

Answer 22

• Pressure/ clamp bleed
• Stabilisation with IV hypertonic crystalloids then oral isotonic fluids (restores circulating volume in cases of haemorrhagic shock where there is 30-40% volume lost)
• Blood transfusion may be indicated

Question 23

Conditions that result in anaemia due to blood loss

Answer 23

• Abomasal ulceration
• Caudal vena cava syndrome
• Fasciola hepatica infection - anaemia rare in cattle, more common in sheep
• Haemonchus contortus infection (sheep); heavy Ostertagia infection (cattle)
• Heavy infections of sucking lice
• Trauma

Question 24

Clinical signs of caudal vena cava syndrome

Answer 24

• Epistaxis, coughing up blood, melena
• Increased respiratory rate and effort, previous history of respiratory disease
• Weight loss
• Intermittent pyrexia
• Sudden death

Question 25

Clinical signs of Fasciola hepatica infection

Answer 25

• Pallor, anaemia (more common in sheep)
• Weakness
• weight loss, ill-thrift
• Ventral oedema (brisket and submandibular)
• Sudden death (sheep); cattle are less susceptible compared to sheep

Question 26

True/false: spreading slurry from cattle infected with Fasciola hepatica can contaminate the pasture and lead to more cattle being infected.

Answer 26

True.
* Provided there is a suitable intermediate host, infection can be established.
* Metacercariae can survive for short periods on preserved forage and thus infect cattle.

Question 27

Treatment of Fasciola hepatica

Answer 27

• Some benzimidazoles (Group 1, white) e.g. albendazole are active but only against adult fluke; Groups 2 and 3 are NOT effective against fluke
• Triclabendazole is effective against all stages; resistance may occur
• Combination products may be effective against adults ± immature fluke; for example Combinex Cattle (Levamisole + triclabenazole) is effective against all stages

Question 28

Diagnosis of Fasciola hepatica

Answer 28

• FEC (fluke egg sedimentation test) is only indicative of adult fluke (immature ones do not lay eggs), and eggs are shed sporadically in faeces
• Fluke coproantigen ELISA can detect the presence of fluke from 3-9 weeks post-infection
• At PM , can see a pale liver with haemorrhagic tracts and hyperplastic bile ducts

Question 29

How does the fluke coproantigen ELISA work?

Answer 29

• Detects digestive enzymes produced in the gut of F. hepatica which are associated with fluke migration and feeding
• Can detect infection from 3-4 weeks post-infection, but more commonly 6-9 weeks
• Positive results indicate infection with late immature or adult fluke
• After fluke death (e.g. treatment with effective wormer), the ELISA returns negative results within 1-2 weeks -> can be used to assess if wormer/ flukicide resistance is present

Useful link: https://www.sruc.ac.uk/business-services/veterinary-laboratory-services/veterinary-diagnostics/test-and-price-lists/farm-animal-diagnostic-tests/liver-fluke-coproantigen-elisa-individual-sample/