Diseases of PP ewes, Pregnancy toxaemia, hypocalcaemia, hypomagnesia Flashcards

1
Q

What is Preg toxaemia

A
  • energy deficiency disease
  • hypoglycaemia therefore body starts metabolising fat therefore hyperketonaemia
  • this affects the brain
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2
Q

Common risk factors to pregnancy toxaemia

A

– Late Pregnancy (last 6 weeks)
– Thin ewes (<BCS 2.0)
– Fat ewes (>BCS 4.0)
– Stress
– Broken mouth (teeth)
– Concurrent disease (fluke, worms)
– Multiple foetuses
– Inadequate diet
– Change in diet which upsets rumen

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3
Q

What are clinical signs of pregnancy toxaemia

A

– Stem from toxaemia affecting the brain – V neurological pres
– Separate from group
– Inappetant
– Central blindness (Positive PLR negative menace)
– Tremors face and ears
– Hyperaesthesia
– jumpy
– Other neuro disturbances (head pressing, star gazing, persistent drinking)
– Progress to recumbency
– Death
– 0-10 days

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4
Q

Diagnosis of pregnancy toxaemia

A

– Clinical signs
– (beta hydroxy butamate) BOHB >1.1 mmol/l abnormal/subclinical
– BOHB >3 mmol/l  clinical signs
– Rapid diagnosis

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5
Q

What advice should you give with pregnancy toxaemia?

A
  • Separate, provide highly palatable feed
  • Fresh food and water
  • Tx = i.v glucose 50-100ml 40%dextrose
  • Propylene glycol (glucose precursor) 120ml BID (day 1) 60ml BID after this (or dose depending on proprietary product)
  • warm Calcium supplementation (i.v or s.c as per hypocalcaemia)
  • Non steroidal anti-inflammatory (meloxicam) to get sheep back on feet, feeling better and eating
  • Check for concurrent disease that may trigger
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6
Q

Ewe with pregnancy toxaemia, farmer has done your first advice but not working what are next steps

A

– Consider stage of pregnancy, viability of lambs welfare of ewe
– Abort ewe/Induce labour after 135 days pregnancy with 16mg dexamethasone corticosteroid to abort and push blood glucose up to help get rid of the pressure on the ewe
– Caesarean
– PTS

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7
Q

Flock treatment of pregnancy toxaemia/ TLD

A
  • Review nutrition urgently of flock
  • (not enough trough space, too much concentrate, terrible forages)
  • Separate out thin or older ewes (susceptible ewes supplementary feeding)
  • Ad lib treacle/molasses for extra energy
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8
Q

Prevention TLD

A
  • Ensure adequate feeding
    – Feed according to number of foetuses, body condition score
    – BCS 6-8 weeks before lambing
    – Avoid sudden changes/ stress last 6 weeks pregnancy
  • Metabolic profile  Monitor for ketone body levels in blood (Beta hydroxy butyrate) 2-3 weeks before lambing.
  • Don’t keep old broken mouth ewes
  • Manage concurrent disease (fluke, parasites , lameness etc….) that have held the ewe back
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9
Q

What is hypocalcaemia

A

*Ca deficiency in late preg due to inc demand foetus and colostrum production
*Drain on ewe immobilised ability of her to mobilise from bones and kideys **
** Same pathogenesis as milk fever hypocalcaemia in cattle
– Increased demand of foetus and colostrum production for calcium
– ability to absorb calcium for gut and kidneys,
– mobilise calcium from bones
– Mediated by Parathyriod Hormone and 1,25 hydroxy vitamin D

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10
Q

When do we see hypocalcaemia

A
  • Usually pre-lambing 6 weeks onwards (but not always, can be early lactation)
  • Often stress induced precipitates
    – Moving, handling, gathering for vaccinations etc
    – change in diet pasture, snow, water deprivation
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11
Q

Risk factors of hypocalcaemia

A

– Acidosis cereal diet
– Older ewes
– Rapid growing lush pasture

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12
Q

CS hypocalcaemia

A

– All to do with shortage of Ca
– Initial Weakness (smooth muscle skeletal and cardiac muscle require Ca for contraction) and excitement
– Progress to recumbent = collapses
– Dilated pupils, Smooth muscle not contracting so constipated, bloated, comatose, death

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13
Q

How do we diagnosis and treat hypocalcaemia

A

Diagnosis by pre-treatment blood sample for calcium, response to treatment
* Treatment – respond nicely
– Slow i.v 40- 80ml 20% (20-40ml of 40%) Calcium borogluconate
* Don’t give too fast, needs to be given slowly
– Rapid response as muscles now working so can get up straight away
– Sub cut 1ml/kg 20%CaBG (50-100ml) warmed Ca to act as reservoir to stop collapsing early on
– Slow response to this
* Monitor as may relapse
* Address risk for rest of flock

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14
Q

What is hypomagnesia aka

A

Staggers

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15
Q

What causes hypomagnesia in sheep, how common and when most often seen?

A
  1. insufficient mg
  2. uncommon in sheep but classically happens post lambing at pasture with wet lush grass that’s short of mg
  3. most often seen beef suckler in autumn
  4. often sheep sound dead so why more uncommon
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16
Q

Why does hypomagnesia have the effect on the body that it does?

A

magnesium depresses the nervous system so when the body is short of Mgs the nervous system is hyper excitable = CS
convulsions, tremors, dead = v diff to hypocalcaemia which is recumbent animal

17
Q

Clinical signs of hypomagnesia?

A

– Rapid onset, neurological symptoms
– Excitable, tremors, convulsions death
– Found Dead

18
Q

When do we see hypomagnesia?

A

– Post lambing, peak lactation
– Lush grass or bare pastures

19
Q

Diagnosis and tx of hypomagnesia

A

Diagnosis
– History and Clinical Signs
– Blood Sample Mg <0.2mmol/l
Treatment
– 40ml-80ml 20% calcium i.v warmed
– 20ml -40ml 25% Mg So4 s.c NEVER give Mg into vein as kills

20
Q

What should you never do with magnesium?

A

NEVER give iv, stops heart, always sub cut

21
Q

Ddx of recumbent ewe at lambing time

A
  • Hypocalcaemia
  • Pregnancy toxaemia
  • Hypomagnesaemia
  • Listeria
  • Mouldy silage
  • Mastitis
  • Metritis
  • Bloat
  • Pasturellosis
  • Bacterial pneumonia, v common
  • Poisoining – not v common
  • Acidosis
  • eating too much concentrates