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Module 18: Ruminant Production > Flock Metabolic & Nutritional Conditions > Flashcards

Flock Metabolic & Nutritional Conditions Flashcards

1
Q

why is nutrition important in sheep

A

If nutrition is inadequate we see disease in sheep

This most evident when there is high metabolic load-late pregnancy/lamb growth

Failure to correctly manage the nutrition of sheep almost guarantees disease

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2
Q

what is the BCS for tupping

A

2.5-3.5

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3
Q

what nutrition changes can be done at tupping

A

flushing? affects ovulation rate and preg rate (care with red clover)

inadequate cobalt (vit B12) reduces lamb viability at birth

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4
Q

what occurs during the first trimester in flock management

A

stress in the first 21 days post fertilization may cause early embryonic loss

in effect this is 6 weeks post start of tupping for the flock

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5
Q

what is the BCS of ewes in second trimester

A

2-3

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6
Q

what effect does nutrition have in the second trimester

A

placental development

effect on fetal size and lamb’s birthweights

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7
Q

what BCS changes can occur in the second trimester

A

can drop 1/2 unit

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8
Q

what day does US scanning occur in second trimester

A

50-105 days

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9
Q

what should BCS be at lambing

A

2-3

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10
Q

what occurs during third trimester

A

75% of fetal growth

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11
Q

what is nutrition critical for in the third trimester

A

nutrition is critical for ewes and lambs (birthweights, colostrum)

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12
Q

when should concentrates be fed

A

concentrates possibly required during last 6-8 weeks

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13
Q

what are ewes grouped according to during lambing

A

group ewes according to energy need

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14
Q

how much does DMI drop in the last trimester

A

DM intake decreases to 1.8-2.0%

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15
Q

what should BCS be during weaning

A

2-2.5

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16
Q

how can you monitor the nutritional status of the ewe (4)

A
  1. BCS
  2. weighing
  3. metabolic profiles
  4. lamb birth weights
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17
Q

when would you do a pre lambing metabolic profile

A

2-4 weeks pre lambing

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18
Q

how many ewes per group woud you sample for pre lambing metabolic profile

A

5 ewes per group representative (not outliers)

10-15 if unscanned

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19
Q

what bood values would you test for a metabolic profile

A

albumin

globulin

urea

BHB

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20
Q

what can albumin indicate

A

Alb long term measurement of protein level in diet

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21
Q

what can globulin indicate

A

Globulin up in chronic disease, albumin will decrease in response to maintain osmotic pressure

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22
Q

what can urea indicate

A

Urea gives short term measure of rumen degradable protein

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23
Q

what can beta hydroxybutyrate indicate

A

ketone

both NEFAs and volatile fatty acids produced from rumen metabolism can be used to form ketones.

ketones are excreted into the circulation, taken up by other tissues (e.g. skeletal muscle, mammary gland), where they are oxidized to yield energy or, in the case of the mammary gland, incorporated into milk fat.

increase in ketones in the blood =4 ketosis

Increased BHB concentrations in blood indicates stimulation of lipolysis (all species) or excess absorption of butyrate (ruminants) from feeding spoiled silage (also called alimentary ketosis

24
Q

how do you ensure the timing of metabolic profiles is appropriate

A

Earlier gives more time for intervention to work but later is more likely to find issues as the ewes are more under stress

But remember most flocks lamb over a 6 week period (majority of sheep lamb in the first 21 days)

25
Q

what are the energy requirements of an ewe

A

Maintenance for ewe is 8-11MJ

Late pregnancy is 19MJ (twins 1.8x maintenance)

Peak lactation is 30MJ

26
Q

what is the intake of an ewe

A

1kg DM to just under 3kg

27
Q

what are periparturient diseases

A

Abortion

Pregnancy toxemia

Hypocalcemia

Hypomagnesemia

(Listeriosis)

(Septicemia)

(Johne’s, Ovine pulmonary adenocarcinoma (OPA; Jaagsiekte) and all the other usual suspectS)

28
Q

what is the timing of clinical disease in sheep compared to dairy cows

A

Hypocalcemia typically post parturition in cattle

Hypomagnesemia is similar

Pregnancy toxemia is post parturient in cattle (increased milk yield demands)

29
Q

what is pregnancy toxemia

A

metabolic disease

Caused by inadequate energy intake coupled with excessive energy drain

30
Q

what is the cause of pregnancy toxemia

A

Rumen size is restricted due to increasing uterine size, this reduces feed intake

Energy derange is increased due to increasing fetal size

Altered insulin levels and sensitivity along with a reduced ability to metabolize ketones during late pregnancy

31
Q

what is the clinical disease of pregnancy toxemia

A

hypoglycemia encephalopathy

32
Q

what is pregnancy toxemia compounded later by (2)

A
  1. hyperketonemia
  2. ketoacidosis
33
Q

what are the clinical signs of pregnancy toxemia

A

Inappetent (separation at feeding time)

Dull, weak and lethargic

Neurological signs:

  • Blindness, incoordination, head tilt, head pressing (star gazing)
  • Tremor, convulsions
  • Depression
  • Recumbence

Diarrhea

Death

Progression relatively slow (2-16 days)

34
Q

what would be seen on biochem with pregnancy toxemia

A

Low glucose (<3.0 mmol/L)

High ketones (BHB >3mmol/L)

Frequently high urea (dehydration)

Frequently low calcium

Liver enzymes elevated

Low insulin

High growth hormone (interacting with prolactin, placental lactogen, estrogens and progesterones)

35
Q

what is the treatment of pregnancy toxemia (9)

A
  1. Glucose (parentally)
  • IV glucose will cause an infected thrombus
  • Source of glucogenic precursors (propylene glycol 120ml BID in first 24hrs then 60ml BID)
  1. Fluids (oral)
  2. Calcium?
  3. Anything to encourage eating
  • Grass?
  • Social eaters?
  1. Treat concurrent disease
  2. Pyrexia, lameness, pneumonia etc
  3. Remove lambs (abort/caesarean)
  4. Steroids
  5. Insulin? (illegal to use in food producing animals in UK and EU)
    * Bovine somatotropin (BST)? (illegal to use in food producing animals in UK and EU)
36
Q

what ewe is at risk for pregnancy toxemia

A

Any ewe with an energy intake/requirement mismatch:

Late pregnancy

Twins/triplets

Older ewes

Fat ewes/thin ewes

Often a group problem (iceberg disease)

Concurrent disease

Fluke, Johnes etc

37
Q

how do we determine whether this is a flock or individual problem

A

We need to understand whether this is an individual animal issue or a flock issue

  • Frequently a poor response to treatment
  • Treat early and aggressively to improve chances of success
  • Intervene to solve the flock issue — MOST IMPORTANT
38
Q

what is the subcinical disease of pregnancy toxemia

A

Decrease birthweight

Decreased lamb viability

Decreased mothering ability

Decreased colostrum quality

39
Q

how do you prevent pregnancy toxemia (6)

A

Group ewes according to feed requirements, feed appropriately and manage concurrent disease

  1. Provide good quality roughage (grass > silage > hay) that can be accessed by all ewes
  2. Appropriate concentrate feeding if necessary from 6 weeks before lambing
  3. Control concurrent disease
  4. Scan ewes and use paddle marks (with resultant, informed, management changes)
  5. Regular condition scoring
  6. Metabolic profiling
40
Q

what is hypocalcemia

A

Demand exceeds supply:

  • Increased demand: fetal bone (no relationship with fetal #)
  • Decreased availability
41
Q

when does hypocalcemia occur

A

peak 1-3 week pre partum

42
Q

what are the causes of hypocalcemia

A

Decreased food intakes (+ oxalates)

Frequently associated with stress (ex. snow)

43
Q

does hypocalcemia present as a individual or group problem

A

group problem

44
Q

what can contribute to hypocalcemia

A

high estrogens/low magnesium

and anion/cation diets

45
Q

what are the early clinical signs of hypocalcemia

A

Staggering gait

Weakness

Tremor (shoulder)

Sluggish pupillary light reflex

Tachycardia

46
Q

what are the late clinical signs of hypocalcemia

A

Tachypnea

Recumbency

Death (<24h)

47
Q

how is hypocalcemia treated

A

50ml 40% calcium borogluconate IV

There may be benefits in giving magnesium at the same time as the ewe may also have low magnesium and there may also be benefits to giving phosphate (stimulates PTH)

Response is not as good/dramatic as that seen in cows

Supportive treatment, including pregnancy toxemia prevention

48
Q

how is hypocalcemia prevented

A

Avoid stress in late gestation:

  • Transport
  • Dogs
  • Change of feed
  • Change of weather

Adequate calcium dietary intake — acidotic diet

Difficult to achieve while meeting the energy requirements of ewes

Supplement if feeding root crops and cereals

49
Q

what is the etiology of hypomagnesemia

A

Lack of available magnesium

  • +/- hypocalcemia

Absence of readily mobilized Mg store

Ineffective homeostatic mechanism

Diet must have Mg > 0.2% of DM

Remember most of the mobile magnesium is intra-cellular not extra-cellular

50
Q

what are risk factors of hypomagnesemia (2)

A
  1. decrease supply
  2. increased demand
51
Q

what causes a decreased supply of magnesium

A

High levels of potassium in grass (and low sodium)

Rapidly growing gas (decrease gut transit time)

Cold/wet stressful weather

  • Grass disproportionally absorbs K+ and Mg2+
  • Ewes don’t eat as much
52
Q

what causes increased demand of magnesium

A

lactacting ewes with twins

53
Q

what are the clinical signs of hypomagnesemia

A

Mostly sudden death

Anxiety, hyperesthesia/tachycardia

Unsteady gait, staggering

Apparent blindness

Nystagmus

Recumbency (+ paddling)

Opisthotonus

Hypersalivation (frothing at mouth)

54
Q

how is hypomagensemia diagnosed

A

Clinical signs and history

  • Otherwise the ewe will die

Pre-treatment blood to confirm diagnosis if there is a treatment failure

Anterior or posterior chamber Mg2+ level as part of a PM (this is easy)

55
Q

how is hypomagensemia treated

A

50ml 25% MgSO4 SC multiple sites (skin necrosis, not IV)

  • Better absorption

Also calcium borogluconate IV or SC

Often poor response to treatment observed

Treatment response may be slower as it is probably the intra-cellular CSF levels that have to return to normal for c/s to resolve

Into the cerebral tissues before resolution of clinical signs

Takes an hour usually to return to any form of normality

56
Q

how is hypomagnesemia prevented

A

Mg supplementation:

57
Q

how is mg supplemented

A

Rumen bolus

  • Not commonly used

In concentrates

  • Works well
  • 50% variation in the flock of intakes

Mg licks/buckets (variable intake)

  • More common, less effective

Top dressing pastures with calcined magnesite

Drinking water

Do not use potash fertilizers in spring

Magnesium is usually bitter when supplemented

Module 18: Ruminant Production (25 decks)

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