3.1.3: Anaemia and haemolytic conditions Flashcards
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Differentials for epistaxis in adult cattle
- 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
What is this?
Schistosoma nasale (blood fluke)
* Trematode that lives in blood and invades nasal mucosa
* Prevalent in India, not currently present in the UK
Describe how subacute ruminal acidosis can lead to caudal vena cava syndrome
- 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
True/false: cows with caudal vena cava syndrome develop nephritis, but not endocarditis.
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
True/false: subacute ruminal acidosis is always the underlying cause of caudal vena cava syndrome.
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)
Explain how caudal vena cava syndrome can lead to epistaxis
- 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
Diagnosis of caudal vena cava syndrome
- 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
Treatment and prognosis of caudal vena cava syndrome
- Prognosis is poor; if they don’t die suddenly, these animals often develop co-morbidities e.g. pneumonia
- Euthanasia is recommended
Differentials for disorders of primary haemostasis in cattle
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)
How does bracken fern toxicity develop and what syndromes does it cause?
Ingestion of bracken (Pteridium species) over weeks-months can cause acute haemorrhagic syndrome, or over months-years, can cause enzootic bovine haematuria.
What is the cause of enzootic bovine haematuria and what are the clinical signs?
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
What are the clinical signs of acute haemorrhagic syndrome associated with bracken fern toxicity?
- 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
Treatment and prognosis of acute bracken fern toxicity
- 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.
Differentials for disorders of secondary haemostasis
- 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)
What is trichothecene mycotoxicosis and how does it cause disease?
- 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
Signalment for bovine neonatal pancytopaenia
Calves <4 weeks old
Cause and pathogenesis of bovine neonatal pancytopaenia
- 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
Clinical signs of bovine neonatal pancytopaenia
- 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
Treatment and control of bovine neonatal pancytopaenia
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
Treatment of acute haemorrhage in cattle
- 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
Conditions that result in anaemia due to blood loss
- 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
Clinical signs of caudal vena cava syndrome
- Epistaxis, coughing up blood, melena
- Increased respiratory rate and effort, previous history of respiratory disease
- Weight loss
- Intermittent pyrexia
- Sudden death
Clinical signs of Fasciola hepatica infection
- 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
True/false: spreading slurry from cattle infected with Fasciola hepatica can contaminate the pasture and lead to more cattle being infected.
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.
Treatment of Fasciola hepatica
- 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
Diagnosis of Fasciola hepatica
- 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
How does the fluke coproantigen ELISA work?
- 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/
