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FARM ANIMAL > 3.1.4: Anaemia in sheep > Flashcards

3.1.4: Anaemia in sheep Flashcards

1
Q

Why should you be cautious about immediately performing a PM exam on a farm animal that died suddenly?

A

Anthrax

Source: James Russell - “All sudden death is anthrax until proven otherwise.”

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2
Q

What are some parasitic causes of sudden death in sheep?

A
  • Haemonchus contortus
  • Nematodirus battus
  • Fasciola hepatica - especially if acute infestation
  • Coccidiosis - common secondary finding in a sudden death
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3
Q

True/false: you should wait for a rise in faecal egg counts of Nematodirus battus before opting for treatment.

A

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

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4
Q

What is a sensible approach to a sudden death in practice?

A
  • 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
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5
Q

What are the 3 mechanisms through which anaemia can arise?

A
  • Loss of blood: overt (major trauma/post op) or covert (parasites)
  • Haemolysis
  • Lack of production
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6
Q

What is the life cycle and prepatent period of Haemonchus contortus ? What impact does this have?

A
  • 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
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7
Q

True/false: Haemonchus contortus survives poorly at pasture.

A

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.

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8
Q

Identify this beastie

A

Haemonchus contortus
(“Barber’s pole worm”)

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9
Q

Which part of the sheep does Haemonchus contortus colonise?

A

Abomasum

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10
Q

True/false: diarrhoea is seen with chronic Haemonchus contortus infestation.

A

False

Diarrhoea is not seen as a result of Haemonchus contortus

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11
Q

Clinical signs of acute Haemonchus infection

A

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)

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12
Q

How much blood does Haemonchus contortus drink and what is the relevance of this?

A
  • 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
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13
Q

Clinical signs of subacute Haemonchus infection

A
  • Submandibular oedema (bottle jaw) -> this is due to hypoproteinaemia
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14
Q

Clinical signs of chronic Haemonchus infection

A
  • Ill thrift
  • Poor BCS
  • Bottle jaw
  • Lethargy
  • Weakness
  • Microcytic anaemia: chronic nature depletes iron reserves
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15
Q

With what duration of Haemonchus infection might you expect to see nucleated RBCs on a blood smear? Why would this happen?

A
  • Nucleated RBCs and reticulocytes seen in chronic Haemonchus infection
  • Chronic blood loss -> regenerative anaemia
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16
Q

Treatment for Haemonchus infection

A
  • 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)
17
Q

Which common toxins cause haemolysis in sheep?

A
  • Sulphur toxins from onions and brassicas
  • Nitrates
  • Nitrites
  • Copper
18
Q

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.

A

False
Texels and Suffolks are more likely to suffer chronic copper toxicity, goats are less likely.

19
Q

Describe the pathogenesis of chronic copper toxicity and relate this to its presentation

A
  • 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
20
Q

True/false: blood copper levels are a poor measure of copper levels in the animal.

Explain your answer and why this is true/false.

A

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.

21
Q

Clinical presentation of copper toxicity

A
  • Anorexia
  • Depression
  • Diarrhoea
  • Abdominal pain
  • Weakness
  • Found dead
22
Q

What are normal blood copper levels? What kind of increase might you expect in the acute toxicity crisis?

A
  • Normal blood Cu = 50-200µg/dL
  • In the acute crisis = 10-20-fold increase
23
Q

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?

A
  • Liver enzymes would probably be normal
  • The copper likely hasn’t had time to damage the liver yet
24
Q

What is the most common presentation for acute copper toxicity (sheep)?

A

These sheep are usually found recumbent or dead.

25
Q

Describe and explain the appearance of this kidney, and relate it to the findings you might see on biochemistry

A
  • 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
26
Q

How might you diagnose chronic copper toxicity? What clinical exam/PM findings would be compatible with this diagnosis?

A
  • 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)
27
Q

How do you treat copper toxicity in the sheep? What is the prognosis?

A
  • 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
28
Q

How much copper should sheep receive in their diet?

A
  • Mb binds to copper
  • The copper in the diet should be less than 1/7Mb in diet
29
Q

What is another name for water toxicity?

A

Water deprivation sodium ion toxicosis

30
Q

Describe the aetiology of water toxicity

A

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

31
Q

Describe the pathophysiology of water toxicity

A
  • 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
32
Q

How can water toxicity be linked to anaemia?

A
  • If we rapidly reintroduce water, it explodes cells including RBCs
33
Q

Clinical signs of water toxicity

A
  • 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
34
Q

How do you diagnose water toxicity?

A

Compatible clinical signs and relevant history

35
Q

Treatment of water toxicity

A
  • 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
36
Q

Prevention of water toxicity

A
  • 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)
37
Q

True/false: the first sign of staggers (hypomagnesaemia) in sheep is typically sudden death.

A

True

38
Q

Prevention of hypomagnesaemia

A
  • 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.

FARM ANIMAL (56 decks)

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