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Lecture 2

POPM 4230 Lecture 2: Dairy Lecture 2 Summary Notes
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7 Pages
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Fall 2016

Department
Population Medicine
Course Code
POPM 4230
Professor
Terri O' Sullivan
Lecture
2

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Transition Cow Health Management
*** MAKE NOTES FOR SLIDE 3
FEED INTAKE AROUND CALVING
~ go from eating 2% of BW when growing and peak at 4% when grown
- 30% drop in intake (~at calving)
TRANSITION = moving from not milking to milking (8 wks centered around calving)
Time for Transitions When does a Lactation Begin?
- development of lactation in mammary gland ~ 3 weeks
- rumen microflora adaption ~ 10-14 days (due to diet change)
- altering metabolic set-point ~ 6 weeks
~ goes from 2-4% intake, change in nutrient flow going to liver, liver had to be ale to handle this
- social adjustment to new group ~1 week
Why does DMI drop?
Diet composition, BCS, parity, and time from calving together explain only 18% of cow-to-cow variation in prepartum DMI
- little evidence for lack of rumen/gut space (early on thought to be gut fill)
- burning NON-EFA in liver may inhibit DMI
~ burning fat, feedback through leptin which could limit DMI
- probable roles of insulin (esp. postpartum) and leptin in decrease DMI
~ ILs or other inflammatory mediators stimulated = cause acute phase proteins liberated & interfere w. intake &stimulate NEFA
- All these are Amplified by..
- crowding/lack of feed access
- heat stress
- excessive dietary changes
- social changes
PERIPARTURIENT DISEASES
Median Days from Calving to Diagnosis
~ common diseases and happen in 1st month after calving
MILK FEVER 0 (right at calving)
RP < 24 hrs post calving
METRITIS 3-7 days
LDA 8-12, 90% in the 1st 6 weeks
KETOSIS 7-12 days
SUBACUTE ACIDOSIS 2 groups 1-20 days (transition phase)
45-150 DIM (peak lactation)
Bottom Line = majority of metabolic problems occur in the 1st 4 weeks of lactation
TRANSITION COW DISEASE RATES
DISEASE TYPICAL LACTATIONAL INCIDENCE RATE
Milk fever 5-15% of >=3rd Lactation
RP 5-15%
Metritis 5-20%
Clinical Ketosis 2-3%
Subclinical Ketosis 15-40%
Displaced Abomasum 2-5%
Early Lactation Clinical Mastitis ~ 10%
Clinical Endometritis (PVD) 15-20%
~ can get many diseases, but usually only get 1 or 2 of these diseases
~ 40-50% of cows on a diary farm are getting clinical disease
ECONOMIC IMPACT OF DISEASE
- unrealized milk production
- tx costs (ex. displaced abomasum can be very expensive)
- discarded milk
- delayed or non-pregnancy (reproduction effect)
- culling
- death (high risk)
- direct costs of most transition diseases (milk fever, metritis, ketosis, DA) = $175 - $450/case
~ up to $750 for DA
Peripartum metabolic
changes and challenges
Fetal growth
Rumen and gut
adaptation to diet
change
Initiation of
lactation
“Opening” of teats
and reproductive
tract
Rapid, large calcium
demand
Hypocalcemia
Immunosuppression
¯ DMI
Negative
Energy balance
Fat mobilization
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MILK FEVER (Hypocalcemia (low Ca), Parturient Paresis)
- large, rapid net output of Ca into colostrum (~30g of Ca in 1 day)
- all cows have some degree of hypocalcemia in the 1-2 days after calving
~ cows continue to increase lactation production and the metabolic receptors become less effective to deal w. sudden Ca demand
- MF is a disease of cows in 3rd + lactation
- especially Jersey
- Ca is a key part of the mechanism of muscle contraction
~cow calves and then she can’t get up, Ca is needed for muscle contraction
- If blood Ca falls too low to support muscle function cows become weak and eventually unable to rise
CLINICAL SIGNS OF MILK FEVER
Stage 1
- Unsteady on their feet
- cool extremities skin, ears
- can be hyperexcitable
Stage II
- unable to rise sternal recumbency
- depressed, head on flank
Stage III
- Lateral recumbency
- Bloat Death
~ give her Ca or she will die
Mechanism of Ca Regulation
~ Ca is absorbed in the gut
~ immobilize Ca from the bone
Prevent = give diet that increases metabolic acidosis?
~ give them before demand for Ca starts
Metabolic acidosis, (-) DCAD
High dietary K+, Alkalosis, (+) DCAD
Hypocalcemia (Clinical or Subclinical)
~ affects both types of muscles
~ skeletal and smooth function decrease
MILK FEVER TREATMENT
- IV Ca injection ~ need Ca spike to allow her to get up
- required to treat Stage II or III
- short duration of effect (4h)
- Oral Ca gel, bolus, or drench
~takes too long to get absorbed, won’t get up for a bit
- SQ Ca injection
Milk Fever Treatment Outcomes:
FULL RECOVERY if they do stand up from injections
- production loss
- risk of other diseases
RELAPSE ~ in about 10% of cows treated
DOWNER COW SYNDROME
~ get necrosis of muscles for just being down, blood circulation cut off
- Ischemic Necrosis of the hind leg muscles
- Estimated that only 1/3 recover
- Bright/alert, eat/drink, but will NOT get up
~ deal w. through lifting, float tanks
- Can also be the result of Acute Toxic Mastitis OR Calving Paralysis
PREVENTION OF MILK FEVER
- cows have adequate whole-body Ca, most of which is stored in bond
- - the challenge is to be able to maintain blood Ca by fast enough mobilization of Ca from bone (via PTH)
- - extra dietary Ca is NOT absorbed as fast as loss in colostrum (although PTH via Vit D3 enhances absorption)
- traditional theory:
- restrict Ca intake prepartum <20g/d (~limit diet to less than 20 g/day)
- < 100g/day is difficult
- CURRENT Theory:
- balance dietary Cations (Na & K) and Anions (Cl & S) to create a Negative
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Description
Transition Cow Health Management Peripartum metabolic changes and challenges *** MAKE NOTES FOR SLIDE 3 •Fetal growth •¯ DMI •Rumen and gut adaptation to diet •Negative change Energy balance FEED INTAKE AROUND CALVING •Fat mobilization ~ go from eating 2% of BW when growing and peak at 4% when grown •Initiation of lactation - 30% drop in intake (~at calving) •“Opening” of teats TRANSITION = moving from not milking to milking (8 wks centered around calving) and reproductive tract •Hypocalcemia Time for Transitions – When does a Lactation Begin? •Immunosuppression •Rapid, large calcium - development of lactation in mammary gland ~ 3 weeks demand - rumen microflora adaption ~ 10-14 days (due to diet change) - altering metabolic set-point ~ 6 weeks ~ goes from 2-4% intake, change in nutrient flow going to liver, liver had to be ale to handle this - social adjustment to new group ~1 week Why does DMI drop? Diet composition, BCS, parity, and time from calving together explain only 18% of cow-to-cow variation in prepartum DMI - little evidence for lack of rumen/gut space (early on thought to be gut fill) - burning NON-EFA in liver may inhibit DMI ~ burning fat, feedback through leptin which could limit DMI - probable roles of insulin (esp. postpartum) and leptin in decrease DMI ~ ILs or other inflammatory mediators stimulated = cause acute phase proteins liberated & interfere w. intake &stimulate NEFA - All these are Amplified by.. - crowding/lack of feed access - heat stress - excessive dietary changes - social changes PERIPARTURIENT DISEASES Median Days from Calving to Diagnosis ~ common diseases and happen in 1 month after calving MILK FEVER 0 (right at calving) RP < 24 hrs post calving METRITIS 3-7 days LDA 8-12, 90% in the 1 6 weeks KETOSIS 7-12 days SUBACUTE ACIDOSIS 2 groups 1-20 days (transition phase) 45-150 DIM (peak lactation) Bottom Line = majority of metabolic problems occur in the 1 4 weeks of lactation TRANSITION COW DISEASE RATES DISEASE TYPICAL LACTATIONAL INCIDENCE RATE Milk fever 5-15% of >=3 Lactation RP 5-15% Metritis 5-20% Clinical Ketosis 2-3% Subclinical Ketosis 15-40% Displaced Abomasum 2-5% Early Lactation Clinical Mastitis ~ 10% Clinical Endometritis (PVD) 15-20% ~ can get many diseases, but usually only get 1 or 2 of these diseases ~ 40-50% of cows on a diary farm are getting clinical disease ECONOMIC IMPACT OF DISEASE - unrealized milk production - tx costs (ex. displaced abomasum can be very expensive) - discarded milk - delayed or non-pregnancy (reproduction effect) - culling - death (high risk) - direct costs of most transition diseases (milk fever, metritis, ketosis, DA) = $175 - $450/case ~ up to $750 for DA MILK FEVER (Hypocalcemia (low Ca), Parturient Paresis) - large, rapid net output of Ca into colostrum (~30g of Ca in 1 day) - all cows have some degree of hypocalcemia in the 1-2 days after calving ~ cows continue to increase lactation production and the metabolic receptors become less effective to deal w. sudden Ca demand - MF is a disease of cows in 3 + lactation - especially Jersey - Ca is a key part of the mechanism of muscle contraction ~cow calves and then she can’t get up, Ca is needed for muscle contraction - If blood Ca falls too low to support muscle function cows become weak and eventually unable to rise CLINICAL SIGNS OF MILK FEVER Stage 1 - Unsteady on their feet - cool extremities – skin, ears - can be hyperexcitable Stage II - unable to rise  sternal recumbency - depressed, head on flank Stage III - Lateral recumbency - Bloat  Death ~ give her Ca or she will die Mechanism of Ca Regulation ~ Ca is absorbed in the gut ~ immobilize Ca from the bone Prevent = give diet that increases metabolic acidosis? ~ give them before demand for Ca starts  Metabolic acidosis, (-) DCAD  High dietary K+, Alkalosis, (+) DCAD Hypocalcemia (Clinical or Subclinical) ~ affects both types of muscles ~ skeletal and smooth function decrease MILK FEVER TREATMENT - IV Ca injection ~ need Ca spike to allow her to get up - required to treat Stage II or III - short duration of effect (4h) - Oral Ca gel, bolus, or drench ~takes too long to get absorbed, won’t get up for a bit - SQ Ca injection Milk Fever Treatment Outcomes: FULL RECOVERY –if they do stand up from injections - production loss - risk of other diseases RELAPSE ~ in about 10% of cows treated DOWNER COW SYNDROME ~ get necrosis of muscles for just being down, blood circulation cut off - Ischemic Necrosis of the hind leg muscles - Estimated that only 1/3 recover - Bright/alert, eat/drink, but will NOT get up ~ deal w. through lifting, float tanks - Can also be the result of Acute Toxic Mastitis OR Calving Paralysis PREVENTION OF MILK FEVER - cows have adequate whole-body Ca, most of which is stored in bond - - the challenge is to be able to maintain blood Ca by fast enough mobilization of Ca from bone (via PTH) - - extra dietary Ca is NOT absorbed as fast as loss in colostrum (although PTH via Vit D3 enhances absorption) - traditional theory: - restrict Ca intake prepartum <20g/d (~limit diet to less than 20 g/day) - < 100g/day is difficult - CURRENT Theory: - balance dietary Cations (Na & K) and Anions (Cl & S) to create a Negative ~ add negative charge ions to the diet to try and reduce the risk of milk fever - Dietary Cation Anion Difference (DCAD) - ie. Acidic - point is to facilitate mobilization of Ca by producing slight metabolic acidosis (favors the function of Osteoclast cells) DCAD (mEq/kg) = (Na + K) – (Cl + S) - lowering the DCAD lowers the risk of milk fever - adjust dry cow ration by: - feeding low Potassium (K) forages - low Ca diet (<0.5%) - feeding adequate Magnesium (Mg) ~ Mg has to be high enough in diet to allow for adequate amount of Ca to be absorbed - feeding Anionic Salts - N.B. intake is Critical - - better to eat and not have anionic salts rather than feed anionic salts and suppress intake ~ have to monitor pH (6.5-7) of urine, need for Cl and K changes over time ~ if below 6 you stop the activities of some intake PREVALENCE OF SUBCLINICAL HYPOCALCEMIA – SW ONT Data - 429 cows sampled after calving w. no evidence of clinical hypocalcemia - subclinical hypocalcemia present in 32.3% of sampled cows (Ca<= 2.0mmol/L) ~ increasing risk w. increasing parody (amount of times cow has calved) Consequences of Subclinical Hypocalcemia - some other studies have shown subclinical hypocalcemia associated w.: - increased odds of DA - greater odds of culling - ~ 3kg/d lower milk yield in early lactation - reduced immune function (~impaired by reduce Ca intake and lactation) - a difference in early lactation fatty acid metabolism - a recent study supplemented cows w. oral Ca after calving found: - an increase in milk production in higher producing cows - decrease in health problems among lame cows Metabolic Fuel Sources (~Ketosis) - CHOs (glucose) are the primary metabolic fuel - cows’ diets are mostly CHO - BUT, d
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