The Periparturient Ewe Flashcards

1
Q
  1. Average ewe mortality.
  2. Ewe mortality in hill flocks.
    – % peri-parturient ewe deaths.
  3. Target ewe mortality?
A
  1. 4-6%.
  2. > 10%.
    – 75%.
  3. ~2%.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

General ewe debility.

A
  • Increased incidence of lamb rejection (sick ewe too ill to bother w/ lambs).
  • Reduced colostrum production.
  • Reduced milk production.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Mastitis and teat lesions.

A

Mammary/teat pain will reduce lambs ability to suck:
- Poor lamb growth.
- Increased lamb deaths.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Investigating ewe mortality.

A
  • Hx of incident.
  • Incidence of losses compared to previous seasons.
  • Timing of losses in relation to parturition.
  • If mortality before lambing, check for signs of impending abortion, scouring, evidence of recumbency.
  • If mortality at lambing, check whether lambing has commenced, skill of shepherd, evidence of trauma, neglected vaginal or cervical prolapse or prolapse of intestines.
  • If mortality after lambing, check for bruising, haemorrhage, severe swelling or discolouration (clostridial infection), metritis or acute mastitis.
  • BCS of affected ewes and rest of group.
  • Any clinical signs observed.
  • Any treatments given and their efficacy.
  • Vaccination history.
  • PM exam needed, Must answer following questions:
    – was death direct result of pregnancy or parturition?
    – was death due to other disease but triggered by stress of pregnancy or parturition?
    – was death unrelated to pregnancy or parturition?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

PM exam.

A
  • BCS, fat deposits.
  • Evidence of pregnancy toxaemia (fatty liver, ketones in urine, multiple pregnancy).
  • Death before parturition (cervix closed).
  • Dystocia, evidence of unskilled manual interference.
  • Signs of placental separation, impending abortion, foetal mummification.
  • Metabolic disease (Calcium, Magnesium levels in aqueous humour).
  • Clostridial disease (rapid decomposition).
  • Retained cleansing, metritis.
  • Other disease (e.g. Pasteurellosis).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pre-partum diseases.

A
  • Abortion.
  • Pregnancy toxaemia.
  • Hypocalcaemia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pregnancy toxaemia – Twin Lamb disease/Ovine Ketosis.

A
  • Extremely common.
  • Seen in ewes and goats.
  • Usually last 2 weeks of pregnancy.
  • Seen up to 6wks before lambing.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q
  1. Primary pregnancy toxaemia.
  2. Fat-ewe pregnancy toxaemia.
A
  1. Decline in plane of nutrition during late pregnancy or temporary period of fasting e.g. due to diet change, transport, adverse weather conditions.
  2. Seen in over-conditioned animals w/ BCS >3.5 on 5-point scale. Excessive intra-abdominal fat limits rumen capacity and thus feed intake.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  1. Starvation pregnancy toxaemia.
  2. Secondary pregnancy toxaemia.
A
  1. Seen in underconditioned animals that have undergone long period of undernutrition.
  2. Development secondary to concomitant disease in the ewe e.g. dental disease, fasciolosis, chronic wasting diseases.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pregnancy toxaemia clinical signs.

A

Early:
- Dull.
- Reduced appetite.
- Separate from the flock.
Progresses to:
- CNS signs (hepatic encephalopathy).
- Appear blind w/ negative menace response but pupillary light reflex ok. (central blindness).
- Wander aimlessly.
- Head pressing.
- Ataxia.
Progresses to:
- Trembling/twitching of ears.
- Champing jaws.
- Frothing at the mouth.
- Smell ketones.
Progresses to:
- Ewe become recumbent and dies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Feed requirements of ewe in last 2 months of pregnancy w/ twin foetuses.

A

1.75X maintenance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
  1. Betahydroxybutyrate levels in pregnancy toxaemia.
  2. Best sample to confirm hyperketonaemia.
A
  1. > 1.1 mmol/l consistent w/ ovine pregnancy toxaemia.
    Levels in clinically affected animals usually >3mml/l.
    Levels >2 mmol/l considered diagnostic.
    Levels >0.8 mmol/l considered supportive.
  2. Aqueous humour.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pregnancy toxaemia main common causes.

A
  • No scanning of ewes.
  • Inadequate concentrate feed.
  • Poor quality/unpalatable concentrates.
  • Competition for food, inadequate trough space.
  • Reduced food availability e.g. snow cover.
  • Failure to check BCS regularly.
  • Decreased voluntary food intake, esp. fat ewes w/ multiple foetuses.
  • Overfeeding of bulky feeds e.g. silage or turnips may limit overall DMI, reducing ME intake.
  • Intercurrent disease e.g. lameness, dental problems, liver disease.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Pregnancy toxaemia on PM exam.

A
  • Fatty infiltration of the liver.
  • Liver appears swollen and pale.
  • BHB in aqueous humour >2.5 mmol/l.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pregnancy toxaemia treatment.

A

Early detection.
Careful nursing.
Correct hypoglycaemia:
- 50=150ml warmed 40% dextrose IV.
- Glucose precursors orally for approx. 4d – Propylene Glycol (Forketos).
- Offer palatable feed (beet, corn).
Reduce glucose drain:
- Glucocorticoids, stim gluconeogenesis.
- If >140d pregnant, can induce lambing w/ 8-16mg dexamethasone.
- Dexamethasone protocols for inducing lung maturation of preterm lambs.
- Perform c section only if in early stages of disease.
Stimulate appetite:
- Anabolic steroids.
- Correct acidosis.
- Give sodium bicarbonate IV (1-2 mmol/kg).
- If base deficit known, give: bwt x base deficit (mmol/l) = HCO3- mmol.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Ewes w/ subclinical pregnancy toxaemia.

A

More likely to get pregnancy toxaemia.
Produce small, weak lambs.
Produce less colostrum.

17
Q

How to protect rest of flock from pregnancy toxaemia.

A
  • Increase feed available.
  • Increase trough space.
  • Separate over thin/fat ewes and feed appropriately.
  • Give high quality forage.
  • Scan ewes.
  • Avoid stress in late pregnancy.
18
Q
  1. When does hypocalcaemia occur?
  2. Hypocalcaemia aetiology.
  3. Hypocalcaemia clinical signs.
A
  1. Late pregnancy and first few days of lactation.
    Often follows stress e.g. change of feed/change of weather/transport.
  2. Inability of ewe to mobilise calcium from skeleton sufficiently rapidly at times of stress.
  3. Initially restless.
    Unsteady walking.
    Trembling.
    Rapidly become dull and recumbent.
    Fast and shallow resp.
    Sternal recumbency w/ head turned towards flank.
    Often bloated.
    May prolapse vagina.
19
Q

Hypocalcaemia treatment.

A

Calcium borogluconate (products licensed for sheep).
- 100ml 20% solution IV (or SC).
- OR 50ml of 40% solution SC.

20
Q

Control of hypocalcaemia.

A

Adequate calcium in diet.
Calcium : Phosphorus ratio 1:1 to 2:1.
Get problems w/ adequate diets if sudden change or exertion.

21
Q

Main post-partum disease.

A

Hypomagnesaemia.

22
Q
  1. What is hypomagnesaemia often associated with?
  2. Source of magnesium.
  3. Time hypomagnesaemia seen.
  4. What decreases Mg absorption into foliage?
A
  1. Sudden cold weather.
  2. Continued dietary intake, no body reserves.
  3. 4-6w after lambing.
  4. Potassium/ammonia fertilisers.
23
Q

Signs of hypomagnesaemia.

A

Often found dead.
Dull but become excitable if disturbed.
Muscle tremors, staggering and unsteady gait develop.
Collapse ad lateral recumbency.
Opisthotonus (muscle spasm of head, neck and spine causing backward arching).
Often nystagmus and frothing at the mouth.

24
Q

Hypomagnesaemia treatment.

A
  • 25ml magnesium sulphate SC.
    DO NOT GIVE IV! – WILL STOP HEART!
  • Can give 100ml Ca borogluconate 20% Mg 40mg/ml slow IV.
25
Q

Prevention of hypomagnesaemia.

A
  • Mg supplements in feed, water, mineral blocks, licks or powders.
  • Mg bolus (Rumbul; Agrimin) 15g bolus.
    (Magnesium/aluminium/copper alloy).
    – One per ewe lasts approx. 3wks.
    – Remember these contain copper so do not give copper supplements!
26
Q
  1. Estimated incidence of mastitis.
  2. How does ovine mastitis cost the farmer?
  3. Acute mastitis.
A
  1. 13-50%.
    • Death from peracute mastitis.
      - Replacement ewes.
      - Lamb starvation.
      - Vet treatments.
      - Reduced growth rates.
  2. Severe condition, often fatal.
    90% cases caused by Mannheimia haemolytica and staphylococcus aureus.
    Occurs soon after lambing or during peak lactation (4-8w).
27
Q

Predisposing factors for acute mastitis.

A

Leaking teats.
Damaged teats.
Orf infection.
Spread infection by dirty hands when shephers check for colostrum.

28
Q

Acute mastitis clinical signs.

A

Hungry lambs.
Apparent hind leg lameness.
Swollen, red, hot udder.
Pyrexia.
If ewe survives:
- Udder become purple/black and cold and clammy to the touch.
- Gangrene to sloughing.
- Lesions take weeks/months to heal so may be best to euthanise on welfare grounds.
- Less acute cases may have less swollen udder w/ variable secretions from watery to thick containing blood or pus.

29
Q

Acute mastitis treatment.

A

Aimed at saving ewe’s life:
- remove lambs.
- Parenteral ABX (e.g. oxytetracycline).
- NSAIDs.
- IV fluids for endotoxic shock.

30
Q
  1. Acute mastitis control.
  2. Pain relief?
A
  1. Vaccination.
    - VIMCO emulsion for injection for ewes and female goats.
    – prevents acute mastitis cases.
    – Reduces SCC in sub-clinical mastitis.
    If udder full of pus, can remove teat.
    - Should be done by vet using LA.
  2. Meloxicam has been shown to be highly effective in sheep.
31
Q
  1. What does sub-clinical mastitis cause?
  2. Subclinical mastitis prevalence?
  3. Age group affected?
A
  1. Reduced growth rates in lambs.
  2. 10-30% (remains constant throughout lactation).
  3. Older ewes.
32
Q
  1. Bacteria that cause subclinical mastitis and the percentages of subclinical mastitis cases they cause?
  2. How can subclinical mastitis be detected in the ewe?
A
  1. Streptococci sp. - 42%.
    Staphylococci (coagulase negative) - 33%.
    Mannheimia haemolytica - 17%.
    Staphylococcus aureus - 8%.
  2. CMT.
    Culture of bacteria.
    Udder may be a bit lumpy and distorted post-weaning.
33
Q

Subclinical mastitis control.

A

Only really sone in dairy sheep.
1/2 Streptopen Dry Cow IMM tube (licensed in sheep) into each gland.
MUST be done HYGIENICALLY (as for dairy cattle).
Mostly S. aureus.
Cull animals w/ persistently high CMT and udder lesions on palpation.
Post milking teat dipping and routine use of ABX tubes at drying off.
Vimco Staph mastitis vaccine by HIPRA is licensed for sheep and goats.

34
Q

Infectious agalactia.

A
  • Many ewes w/ insufficient colostrum despite good BCS.
  • Leptospira interrogans var hardjo causes “milk drop” in sheep.
  • Dx on culture.
  • Serology can be difficult to interpret due to prior exposure.