Anaemia in sheep Flashcards
3 causes of anaemia
- Blood loss
- Haemolysis
- Lack of production
Blood loss
- Normally parasites
- Sometimes major trauma or post-op complications
- Initially, blood count remains normal, before anaemia and hypoproteinaemia are seen
Most common cause of parasitic blood loss
- Haemonchus contortus
Haemonchus contortus
- Called barbers pole worm
- Colonise the abomasum (here they’re not really exposed to the immune system, hence no/little immune response)
- Each one can ingest 0.05ml of blood per day
- Prolific breeders so rapid onset of outbreak
- Widespread in the UK
- Short life cycle (20 days)
- Short pre-patent period (14-15 days)
- High daily egg output (5-15,000/day)
- Needs warmer weather (>10oC)
- Survives well at pasture
- Adapting to changing environment (now fewer inhibited L4 larvae on PME over winter, L3 can complete their life cycle in the host, giving year round challenge in some warmer climates (Australia)).
- Possibly no resistance acquired (unclear on resistance as may just be due to the suppressive nature of treatment regimes)
- No diarrhoea seen
Haemonchus contortus acute infection
- Many larvae ingested in short period
- Animals weak, may collapse if driven
- Marked pallor of mucus membranes
- Hyperpnoea
- Tachycardia
- Still in good body condition (when very acute)
- Sudden death
Haemonchus contortus sub-acute infection
- Bottle-jaw
= submandibular oedema
Haemonchus contortus chronic infection
- Ill thrift
- Poor Body Condition
- Bottle-jaw
- Lethargy
- Weakness
- Microcytic anaemia – because the chronic nature depletes iron reserves
Overt blood loss in sheep
Usually major trauma
- Usually injury
– Dog bites
– Running into things
- Can be iatrogenic
– Castration
– Dehorning in cattle
Clinpath of overt blood loss
- Complete blood count remains normal at first, even with massive blood loss
- Later see anaemia and hypoproteinaemia
- Regeneration seen after a couple of days
– Macrocytosis
– Reticulocytosis
– Nucleated RBCs
Babesia
Babesia Venatorum identified in sheep in the UK in 2019
- Does not seem to infect cattle
- Has been found in sheep
Babesia Divergens, more common
- Causes redwater fever
- Seen when ticks are active – May/June
- Urine goes from red to black (as haemoglobin being excreted in the urine)
Ticks in UK
- Ixodes Ricinus is found on sheep and deer
- Ixodes Ovis is made up
- Ixodes hexagonus is found on hedgehogs
- Haemaphysalis punctata found in some specific coastal areas of UK
- Dermacenter reticulatus is a cattle tick
- Ixodes arbaricola is found in tree hole nesting birds
Haemolysis - primary ddx
- a result of toxin ingestion
Haemolysis - secondary ddx
- Parasitism of RBCs
- IV injection of hyper or hypotonic solutions
- Contact with bacterial toxins
- Water intoxication
Ingested toxins causing haemolysis - common toxins
- Sulphur toxins from onions and brassicas
- Nitrates
- Nitrites
- Copper (far more sheep are seen post mortem with copper toxicity than copper deficiency)
Diagnosis of chronic copper toxicity
- Jaundice seen – of sclera and skin (breakdown products of blood settling in these places)
- Urine – black in colour (due to trying to excrete the copper and the breakdown of products of haemolysis - so get lots of haemoglobin in the urine)
- Liver – bronze coloured
- Kidneys – gun-metal appearance (where the copper has settled into the nephrons)
Chronic copper toxicity presentation
- anorexic
- depressed
- diarrhoea
- abdominal pain
- weakness
- found dead
Chronic copper toxicity clinpath
- anaemia
- haemaglobinaemia
- increased liver enzymes
- azotaemia
Chronic copper toxicity urinalysis
- haemoglobinuria
- isothenuria
What findings with chronic copper toxicity indicate ARF?
The combination of azotaemia and isothenuria indicates acute renal failure
Why does chronic copper toxicity cause jaundice?
- Chronic copper toxicity is seen after the sheep’s liver capacity for copper storage is exceeded.
- This is often exacerbated by stress
- The sudden release into the circulation results in liver damage, destruction of red blood cells and so jaundice
Breeds prone to chronic copper toxicity
- Texels and Suffolks are particularly prone, goats are less prone
Acute copper toxicity
- Acute copper toxicity is seen after inadvertent over-administration
- Usually found recumbent or dead
Acute copper toxicity diagnosis
- Definitive diagnosis of acute disease requires measurement of Cu
- Normal blood Cu = 50-200µg/dl, in an acute crisis see 10-20 fold increase
- In this acute phase, liver levels may be normal as they have released their excess into the bloodstream
Treatment of acute copper toxicity
- Usually futile
- Supportive of acute renal failure
– Fluid therapy
– Blood transfusion if indicated
– No licensed direct treatments
-> Trietine is used in humans but has had variable effects in sheep.
–> This drug binds to copper creating a complex which is excreted through the kidneys. It also reduces absorption from the GIT.
Copper toxicity prevention
- ensuring that available Cu is <7 X Molybdenum levels in diet
Chronic copper toxicity
- Much more common cause of death than copper deficiency in sheep
- Only ‘spills over’ to hypercupraemia when the storage capacity of the liver is exceeded
- Will then present as acute toxicity
Water toxicity
- ‘Water deprivation Sodium ion toxicosis’
4 possible causes of water poisoning
- Excess Na ingestion with adequate water intake
- Normal Na ingestion with inadequate water intake
- Consumption of high Na water
- Administration of hypertonic oral electrolytes
Water poisoning pathophysiology
- Dehydration results in hypernatraemia
- Hypernatraemia results in net movement of water extracellularly
- Rapid re-introduction of water causes rapid movement back into intracellular compartments (damages/explodes them)
- This causes
– cerebral oedema
– Intravascular haemolysis
Water poisoning clinical signs and diagnosis
- Thirst
- Somnolence (sleepy/drowsy)
- Hyperthermia (ion pumps working hard to correct sodium balance, burning lots of energy in the body)
- Tachycardia
- Muscle fasciculation (due to ion imbalances)
- Rumen stasis (the rumen doesn’t have enough energy/ions to cope with ruminal contractions)
- Diarrhoea
- Mucoid faeces
- Nasal discharge
- Convulsions
- Found dead
Water poisoning tx
- Restrict water intake, give little and often
- Corticosteroids to reduce CNS oedema – dexamethasone 1-2mg/kg i/v
- Frusemide – 1-2mg/kg I/v (to improve renal function)
- IV fluid therapy at modest rate if indicated
- If possible give all fluids orally
Water poisoning prevention
- Maintain fresh, clean water intake
- If salt-limited feeds are offered, then you must anticipate the changes in water intake associated with weather.
-Ensure that appropriate oral electrolyte solutions are used where appropriate
Lack of production
Usually nutritional i.e. deficiencies in anything that goes to make RBCs
- Fe deficiency – microcytic anaemia as not enough haemoglobin
- Cu deficiency – often seen with a neutropenia
- Se deficiency – sometimes see Heinz bodies
- Co deficiency - anaemia
- Vit B12 deficiency -> Cachexia, anaemia, anorexia
Bottle jaw ddx
- haemonchus contortus
- liver fluke
- Johnes
- CHF
- haemolysis
- hypoproteinaemia.
What is bottle jaw?
- bottle jaw = fluid leaking out of blood vessels due to the osmotic potential of the tissues relative to the blood
Nitrates and nitrites causing haemolysis
- tends to be more over-fertilised / over mucked land
Why are blood copper levels not a good indicator of chronic copper toxicity?
It will maintain normal blood levels for a long time, until cant anymore i.e. run out of storage.
