3.1.4: Anaemia in sheep Flashcards
Why should you be cautious about immediately performing a PM exam on a farm animal that died suddenly?
Anthrax
Source: James Russell - “All sudden death is anthrax until proven otherwise.”
What are some parasitic causes of sudden death in sheep?
- Haemonchus contortus
- Nematodirus battus
- Fasciola hepatica - especially if acute infestation
- Coccidiosis - common secondary finding in a sudden death
True/false: you should wait for a rise in faecal egg counts of Nematodirus battus before opting for treatment.
False
* Nematodirus battus cannot be adequately monitored using faecal eggg counts and we should not use these to time treatment.
* Use changes in temperature/environment to predict when to treat - when temp is above 10C, huge numbers of parasites will hatch out and animals will die quickly
Note to self: check details of this card
What is a sensible approach to a sudden death in practice?
- Consider that it could be anthrax
- Take history (and try to rule out anthrax because of this)
- Examine animal from distance (and try to rule out anthrax i.e. can you see marking in earth suggesting muscle contractions/seizure activity etc.)
- Undertake PM exam
What are the 3 mechanisms through which anaemia can arise?
- Loss of blood: overt (major trauma/post op) or covert (parasites)
- Haemolysis
- Lack of production
What is the life cycle and prepatent period of Haemonchus contortus ? What impact does this have?
- Life cycle takes 20 days
- Short prepatent period = 14-15 days
- Haemonchus contortus are prolific breeders and this can lead to an outbreak with rapid onset
True/false: Haemonchus contortus survives poorly at pasture.
False
Haemonchus contortus survives well at pasture, but does need warmer weather (i.e. >10C).
Due to climate change, the worm is no longer going into hypobiosis in winter, so is emerging as a year-round threat.
Identify this beastie
Haemonchus contortus
(“Barber’s pole worm”)
Which part of the sheep does Haemonchus contortus colonise?
Abomasum
True/false: diarrhoea is seen with chronic Haemonchus contortus infestation.
False
Diarrhoea is not seen as a result of Haemonchus contortus
Clinical signs of acute Haemonchus infection
Acute = many larvae ingested in a short period
* Weakness
* May collapse if driven
* Marked pallor of mucous membranes
* Hypernoea
* Tachypnoea
* Sudden death
* (May still be in good BCS with acute infection)
How much blood does Haemonchus contortus drink and what is the relevance of this?
- Each worm can ingest 0.05ml of blood per day
- A 45kg sheep has around 3L of blood
- 15,000 worms could drain this in 4 days
Clinical signs of subacute Haemonchus infection
- Submandibular oedema (bottle jaw) -> this is due to hypoproteinaemia
Clinical signs of chronic Haemonchus infection
- Ill thrift
- Poor BCS
- Bottle jaw
- Lethargy
- Weakness
- Microcytic anaemia: chronic nature depletes iron reserves
With what duration of Haemonchus infection might you expect to see nucleated RBCs on a blood smear? Why would this happen?
- Nucleated RBCs and reticulocytes seen in chronic Haemonchus infection
- Chronic blood loss -> regenerative anaemia
Treatment for Haemonchus infection
- Improve diet and correct losses of iron and copper
- Consider pasture (move them to a clean pasture/be mindful of shedding -> need to consider what will work best for the given situation)
- Levamisoles and ivermectins (yellow and clear drenches)
Which common toxins cause haemolysis in sheep?
- Sulphur toxins from onions and brassicas
- Nitrates
- Nitrites
- Copper
True/false: breeds like Texels and Suffolks are more resistant to copper toxicity than most other sheep. Goats, on the other hand, are much more vulnerable.
False
Texels and Suffolks are more likely to suffer chronic copper toxicity, goats are less likely.
Describe the pathogenesis of chronic copper toxicity and relate this to its presentation
- Chronic copper toxicity is seen after the animal’s liver capacity for copper storage is exceeded
- The liver keeps working until suddenly it doesn’t -> this means that these animals present acutely, but in fact there has been a chronic buildup
- Sudden release of copper into circulation results in liver damage, destruction of RBCs and jaundice
True/false: blood copper levels are a poor measure of copper levels in the animal.
Explain your answer and why this is true/false.
True
Copper is stored in the liver; blood copper levels are not representative of copper levels in the entire animal.
This is relevant especially for chronic copper toxicity; in acute copper toxicity, blood Cu will be high.
Clinical presentation of copper toxicity
- Anorexia
- Depression
- Diarrhoea
- Abdominal pain
- Weakness
- Found dead
What are normal blood copper levels? What kind of increase might you expect in the acute toxicity crisis?
- Normal blood Cu = 50-200µg/dL
- In the acute crisis = 10-20-fold increase
In acute copper toxicity (e.g. caused by inadvertant over-administration on a single, recent occasion) would you expect liver animals to be high, low, or normal?
- Liver enzymes would probably be normal
- The copper likely hasn’t had time to damage the liver yet
What is the most common presentation for acute copper toxicity (sheep)?
These sheep are usually found recumbent or dead.
Describe and explain the appearance of this kidney, and relate it to the findings you might see on biochemistry
- The kidneys of the animal with chronic copper toxicity have a gunmetal appearance
- This is because the copper has settled here
- Biochemistry will show an azotaemia
How might you diagnose chronic copper toxicity? What clinical exam/PM findings would be compatible with this diagnosis?
- Jaundice of the sclera and skin
- Urine that is black in colour (haemolysis occurring)
- Azotaemia + isosthenuria = indicates acute renal failure
- Increased liver enzymes due to damage
- Liver is bronze-coloured (due to copper settling here)
- Kidneys have gunmetal appearance (due to copper settling here)
How do you treat copper toxicity in the sheep? What is the prognosis?
- Treatment is usually futile and has a poor success rate
- Need to support the acute renal failure -> fluid therapy, blood transfusion if indicated
- No licensed direct treatments (trietine used in humans as it binds to copper, but has had variable effects in sheep)
- Prevention is better than cure
How much copper should sheep receive in their diet?
- Mb binds to copper
- The copper in the diet should be less than 1/7Mb in diet
What is another name for water toxicity?
Water deprivation sodium ion toxicosis
Describe the aetiology of water toxicity
4 possible causes:
1. Excess Na ingestion with adequate water intake
2. Normal Na ingestion with inadequate water intake
3. Consumption of high Na water (seawater, marshlands)
4. Administration of hypertonic oral electrolytes
Describe the pathophysiology of water toxicity
- Effective dehydration results in hypernatraemia
- Hypernatraemia results in net movement of water extracellularly
- Rapid re-introduction of water causes rapid movement back into intracellular compartments
- This causes cerebral oedema and vascular haemolysis
How can water toxicity be linked to anaemia?
- If we rapidly reintroduce water, it explodes cells including RBCs
Clinical signs of water toxicity
- Thirst
- Somnolence
- Hyperthermia
- Tachycardia
- Muscle fasciculation
- Rumen stasis
- Diarrhoea (this is excretory/mucoid diarrhoea because the animal is trying to excrete Na)
- Mucoid faeces
- Nasal discharge
- Convulsions (associated with cerebral oedema)
- Found dead
How do you diagnose water toxicity?
Compatible clinical signs and relevant history
Treatment of water toxicity
- Must be gentle: IV fluid therapy at a modest rate if indicated, or restricted water intake giving little and often
- Corticosteroids ro reduce CNS oedema -> dexamethasone 1-2mg/kg IV
- Furosemide (alongside fluid therapy) to help kidneys into action (animal may be completely anuric) -> this hopefully takes ions with the fluid into urine
Prevention of water toxicity
- Maintain fresh, clean waer intake
- If salt limited feeds are offered, animals may not get the usual thirst triggers even in warmer weather -> need to anticipate this
- Ensure appropriate oral electrolyte solutions are used when appropriate (avoid temptation to make up at home, there are good existing products)
True/false: the first sign of staggers (hypomagnesaemia) in sheep is typically sudden death.
True
Prevention of hypomagnesaemia
- Offer supplementary feed that is high in fibre -> this slows down digestion and gives more time for magnesium to be absorbed in the intestine
- Modify bagged fertiliser application so applications high in K take place later in the season
- Offer free access to minerals so there is always adequate Mg available in the diet.
