Flock Metabolic & Nutritional Conditions Flashcards
why is nutrition important in sheep
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
what is the BCS for tupping
2.5-3.5
what nutrition changes can be done at tupping
flushing? affects ovulation rate and preg rate (care with red clover)
inadequate cobalt (vit B12) reduces lamb viability at birth
what occurs during the first trimester in flock management
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
what is the BCS of ewes in second trimester
2-3
what effect does nutrition have in the second trimester
placental development
effect on fetal size and lamb’s birthweights
what BCS changes can occur in the second trimester
can drop 1/2 unit
what day does US scanning occur in second trimester
50-105 days
what should BCS be at lambing
2-3
what occurs during third trimester
75% of fetal growth
what is nutrition critical for in the third trimester
nutrition is critical for ewes and lambs (birthweights, colostrum)
when should concentrates be fed
concentrates possibly required during last 6-8 weeks
what are ewes grouped according to during lambing
group ewes according to energy need
how much does DMI drop in the last trimester
DM intake decreases to 1.8-2.0%
what should BCS be during weaning
2-2.5
how can you monitor the nutritional status of the ewe (4)
- BCS
- weighing
- metabolic profiles
- lamb birth weights
when would you do a pre lambing metabolic profile
2-4 weeks pre lambing
how many ewes per group woud you sample for pre lambing metabolic profile
5 ewes per group representative (not outliers)
10-15 if unscanned
what bood values would you test for a metabolic profile
albumin
globulin
urea
BHB
what can albumin indicate
Alb long term measurement of protein level in diet
what can globulin indicate
Globulin up in chronic disease, albumin will decrease in response to maintain osmotic pressure
what can urea indicate
Urea gives short term measure of rumen degradable protein
what can beta hydroxybutyrate indicate
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
how do you ensure the timing of metabolic profiles is appropriate
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)
what are the energy requirements of an ewe
Maintenance for ewe is 8-11MJ
Late pregnancy is 19MJ (twins 1.8x maintenance)
Peak lactation is 30MJ
what is the intake of an ewe
1kg DM to just under 3kg
what are periparturient diseases
Abortion
Pregnancy toxemia
Hypocalcemia
Hypomagnesemia
(Listeriosis)
(Septicemia)
(Johne’s, Ovine pulmonary adenocarcinoma (OPA; Jaagsiekte) and all the other usual suspectS)
what is the timing of clinical disease in sheep compared to dairy cows
Hypocalcemia typically post parturition in cattle
Hypomagnesemia is similar
Pregnancy toxemia is post parturient in cattle (increased milk yield demands)
what is pregnancy toxemia
metabolic disease
Caused by inadequate energy intake coupled with excessive energy drain
what is the cause of pregnancy toxemia
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
what is the clinical disease of pregnancy toxemia
hypoglycemia encephalopathy
what is pregnancy toxemia compounded later by (2)
- hyperketonemia
- ketoacidosis
what are the clinical signs of pregnancy toxemia
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)
what would be seen on biochem with pregnancy toxemia
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)
what is the treatment of pregnancy toxemia (9)
- Glucose (parentally)
- IV glucose will cause an infected thrombus
- Source of glucogenic precursors (propylene glycol 120ml BID in first 24hrs then 60ml BID)
- Fluids (oral)
- Calcium?
- Anything to encourage eating
- Grass?
- Social eaters?
- Treat concurrent disease
- Pyrexia, lameness, pneumonia etc
- Remove lambs (abort/caesarean)
- Steroids
- 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)
what ewe is at risk for pregnancy toxemia
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
how do we determine whether this is a flock or individual problem
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
what is the subcinical disease of pregnancy toxemia
Decrease birthweight
Decreased lamb viability
Decreased mothering ability
Decreased colostrum quality
how do you prevent pregnancy toxemia (6)
Group ewes according to feed requirements, feed appropriately and manage concurrent disease
- Provide good quality roughage (grass > silage > hay) that can be accessed by all ewes
- Appropriate concentrate feeding if necessary from 6 weeks before lambing
- Control concurrent disease
- Scan ewes and use paddle marks (with resultant, informed, management changes)
- Regular condition scoring
- Metabolic profiling
what is hypocalcemia
Demand exceeds supply:
- Increased demand: fetal bone (no relationship with fetal #)
- Decreased availability
when does hypocalcemia occur
peak 1-3 week pre partum
what are the causes of hypocalcemia
Decreased food intakes (+ oxalates)
Frequently associated with stress (ex. snow)
does hypocalcemia present as a individual or group problem
group problem
what can contribute to hypocalcemia
high estrogens/low magnesium
and anion/cation diets
what are the early clinical signs of hypocalcemia
Staggering gait
Weakness
Tremor (shoulder)
Sluggish pupillary light reflex
Tachycardia
what are the late clinical signs of hypocalcemia
Tachypnea
Recumbency
Death (<24h)
how is hypocalcemia treated
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
how is hypocalcemia prevented
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
what is the etiology of hypomagnesemia
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
what are risk factors of hypomagnesemia (2)
- decrease supply
- increased demand
what causes a decreased supply of magnesium
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
what causes increased demand of magnesium
lactacting ewes with twins
what are the clinical signs of hypomagnesemia
Mostly sudden death
Anxiety, hyperesthesia/tachycardia
Unsteady gait, staggering
Apparent blindness
Nystagmus
Recumbency (+ paddling)
Opisthotonus
Hypersalivation (frothing at mouth)
how is hypomagensemia diagnosed
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)
how is hypomagensemia treated
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
how is hypomagnesemia prevented
Mg supplementation:
how is mg supplemented
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
