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Milk Fever
Milk fever
• Milk fever
– Parturient paresis,
– Within 48 hrs of parturition
– Lactation tetany in horses
– Occurs in ewes also in group
– Rarely occurs in sows
• The Ca homeostatic mechanisms, which normally
maintain blood Ca between 9 and 10 mg/dl, fail
and the lactational drain of Ca causes blood Ca to
fall <5mg/dl.
Milk fever
• Colostrum Ca: 2.3 g/L
– 10 L of colostrum: 23 g Ca drain in single milking
– Nine times as much as present in plasma pool
• All cows experience hypocalcemia
• Hypocalcemia occurs despite normal functioning of
parathyroid and Vit. D endocrine system
• Milk fever is easy to treat but cows with MF are more
prone to mastitis, DA, RP and Ketosis
• Sub-clinical hypocalcemia contributes to inappetance
in the fresh cow and predispose to other disease
Etiology and pathogenesis
• Severe hypocalcemia
• Hypophosphatemia and hypomagnesemia can
be a complicating factors
Etiology and pathogenesis
Increase in PTH
Reduce urinary Ca loss
Stimulate bone Ca
resorption
Increase 1,25-dihydroxy
Vitamin D synthesis
Adaptation after onset of lactation
Etiology and pathogenesis
• Important determinant is acid-base status of
cow at parturition
• Metabolic alkalosis impairs the physiologic
activity of PTH so that bone resorption and
production of 1,25-dihydroxyvitamin D are
impaired reducing the ability to successfully
adjust to the calcium demands of lactation
Etiology and pathogenesis
Metabolic
alkalosis
• Induce conformational changes in the PTH
receptor, which prevents tight binding of PTH
to its receptor
Etiology and pathogenesis
• Cows fed diets that are relatively high in K+ or
Na+ are in a relative state of metabolic
alkalosis, which increases the likelihood that
they will not successfully adapt to the Ca
demands of lactation and will develop milk
fever.
PTH recognize onset of
hypocalcemia
Secrets PTH
Poor response of tissue to PTH
Inadequate osteoclastic bone
resorption
Inadequate 1, 25-dihydroxyvitamin
D production
Etiology and pathogenesis
Milk Fever Risk Factors
• Age
– Heifers almost never develop milk fever
• Low colostrum production
• Still growing, growing bones have more osteoclasts
– Aged cows have fewer intestinal vitamin D
receptors
• Breed
– Jersey>Holstein
• High Ca in colostrum in Jersey and fewer intestinal
vitamin D receptors
Nutritional Considerations
• DCAD (Dietary Cation Anion Difference)
– Metabolic alkalosis
• High blood pH due to cation especially K+
• Cation-Minerals with positive charge K+, Na+, Ca++, Mg++
• Dietary absorption reduce blood pH
– Nearly all of the K and Na in the diet is absorbed by
cows, making these two elements very powerful
alkalinizing cations.
– Ca and Mg are poorly absorbed from the diet of the
dry cow so these cations are not strong alkalinizing
agents.
– Dry cow ration high in K and Na increases susceptibility of
cow for MF
– Prepartal diet with high K and Na increases incidences of
MF
• Hypomagnesemia
– Second common cause of MF
– Low Mg in blood can reduce PTH secretion from the
parathyroid glands; and can alter the responsiveness of
tissues to PTH by inducing conformational changes in the
PTH receptor and G-stimulatory protein complex
– Blood Mg <2.0mg/dl within 24h after calving suggest
inadequate dietary magnesium absorption
Prevention of MF
• Adjustment of DC
– (Na++K+)-(Cl-+S--)
– Na++K+-Cl-
– Na++K++Ca+++Mg++
• Reduce Dietary Sodium and Potassium
• Add Anions to Induce Mild(Compensated) Metabolic
Acidosis
– Ammonium, calcium and magnesium salts of chloride or
sulphate (Acidifying anions)
– Chloride salts are more acidogenic than sulphate salts
– HCL (Monitoring urine pH, addition of anions, pH 6.2-6.8)
Prevention of MF
• Magnesium
– 0.3 to 0.45 in the peri-partal ration prevent decline
– Passive and active absorption mechanism in rumen (K
inhibits the active process)
– There is no labile body store and hence higher levels are
necessary to accommodate decline in DMI
• Phosphorus
– P requirements are met by feeding 40 to 50g P/cow/d
– Less than 25 g-hypo-phosphatemia
– More than 80 g may induces milk fever
• Very Low Calcium Diets to Prevent Milk Fever
• Less than 15g Ca/cow/d at least 10d before calving
Prevention of MF
• Very Low Calcium Diets to Prevent Milk Fever
• Less than 15g Ca/cow/d at least 10d before calving
– Negative Ca balance
– Stimulating PTH secretion prior to calving.
– This activates bone osteoclasts stimulating bone calcium
resorption and activates renal tubules to resorb urinary
calcium and begin producing 1,25-dihydroxyvitamin D
prior to calving.
• Thus at the onset of lactation these homeostatic
mechanisms for calcium are active, preventing a severe
decline in the concentration of calcium in the plasma
of cows.

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Milk fever.pptx

  • 2. Milk fever • Milk fever – Parturient paresis, – Within 48 hrs of parturition – Lactation tetany in horses – Occurs in ewes also in group – Rarely occurs in sows • The Ca homeostatic mechanisms, which normally maintain blood Ca between 9 and 10 mg/dl, fail and the lactational drain of Ca causes blood Ca to fall <5mg/dl.
  • 3. Milk fever • Colostrum Ca: 2.3 g/L – 10 L of colostrum: 23 g Ca drain in single milking – Nine times as much as present in plasma pool • All cows experience hypocalcemia • Hypocalcemia occurs despite normal functioning of parathyroid and Vit. D endocrine system • Milk fever is easy to treat but cows with MF are more prone to mastitis, DA, RP and Ketosis • Sub-clinical hypocalcemia contributes to inappetance in the fresh cow and predispose to other disease
  • 4. Etiology and pathogenesis • Severe hypocalcemia • Hypophosphatemia and hypomagnesemia can be a complicating factors
  • 5. Etiology and pathogenesis Increase in PTH Reduce urinary Ca loss Stimulate bone Ca resorption Increase 1,25-dihydroxy Vitamin D synthesis Adaptation after onset of lactation
  • 6. Etiology and pathogenesis • Important determinant is acid-base status of cow at parturition • Metabolic alkalosis impairs the physiologic activity of PTH so that bone resorption and production of 1,25-dihydroxyvitamin D are impaired reducing the ability to successfully adjust to the calcium demands of lactation
  • 7. Etiology and pathogenesis Metabolic alkalosis • Induce conformational changes in the PTH receptor, which prevents tight binding of PTH to its receptor
  • 8. Etiology and pathogenesis • Cows fed diets that are relatively high in K+ or Na+ are in a relative state of metabolic alkalosis, which increases the likelihood that they will not successfully adapt to the Ca demands of lactation and will develop milk fever.
  • 9. PTH recognize onset of hypocalcemia Secrets PTH Poor response of tissue to PTH Inadequate osteoclastic bone resorption Inadequate 1, 25-dihydroxyvitamin D production Etiology and pathogenesis
  • 10. Milk Fever Risk Factors • Age – Heifers almost never develop milk fever • Low colostrum production • Still growing, growing bones have more osteoclasts – Aged cows have fewer intestinal vitamin D receptors • Breed – Jersey>Holstein • High Ca in colostrum in Jersey and fewer intestinal vitamin D receptors
  • 11. Nutritional Considerations • DCAD (Dietary Cation Anion Difference) – Metabolic alkalosis • High blood pH due to cation especially K+ • Cation-Minerals with positive charge K+, Na+, Ca++, Mg++ • Dietary absorption reduce blood pH – Nearly all of the K and Na in the diet is absorbed by cows, making these two elements very powerful alkalinizing cations. – Ca and Mg are poorly absorbed from the diet of the dry cow so these cations are not strong alkalinizing agents.
  • 12. – Dry cow ration high in K and Na increases susceptibility of cow for MF – Prepartal diet with high K and Na increases incidences of MF • Hypomagnesemia – Second common cause of MF – Low Mg in blood can reduce PTH secretion from the parathyroid glands; and can alter the responsiveness of tissues to PTH by inducing conformational changes in the PTH receptor and G-stimulatory protein complex – Blood Mg <2.0mg/dl within 24h after calving suggest inadequate dietary magnesium absorption
  • 13. Prevention of MF • Adjustment of DC – (Na++K+)-(Cl-+S--) – Na++K+-Cl- – Na++K++Ca+++Mg++ • Reduce Dietary Sodium and Potassium • Add Anions to Induce Mild(Compensated) Metabolic Acidosis – Ammonium, calcium and magnesium salts of chloride or sulphate (Acidifying anions) – Chloride salts are more acidogenic than sulphate salts – HCL (Monitoring urine pH, addition of anions, pH 6.2-6.8)
  • 14. Prevention of MF • Magnesium – 0.3 to 0.45 in the peri-partal ration prevent decline – Passive and active absorption mechanism in rumen (K inhibits the active process) – There is no labile body store and hence higher levels are necessary to accommodate decline in DMI • Phosphorus – P requirements are met by feeding 40 to 50g P/cow/d – Less than 25 g-hypo-phosphatemia – More than 80 g may induces milk fever • Very Low Calcium Diets to Prevent Milk Fever • Less than 15g Ca/cow/d at least 10d before calving
  • 15. Prevention of MF • Very Low Calcium Diets to Prevent Milk Fever • Less than 15g Ca/cow/d at least 10d before calving – Negative Ca balance – Stimulating PTH secretion prior to calving. – This activates bone osteoclasts stimulating bone calcium resorption and activates renal tubules to resorb urinary calcium and begin producing 1,25-dihydroxyvitamin D prior to calving. • Thus at the onset of lactation these homeostatic mechanisms for calcium are active, preventing a severe decline in the concentration of calcium in the plasma of cows.