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BOVINE KETOSIS

BOVINE KETOSIS. Peak yield at 4-6 wks but high dry matter intake at 8-10 wks so there will be negative energy balance. Low levels of glucose . Mobilisation of adipose tissue. Increase in NEFA & BHBA. liver. Ketogenesis & gluconeogenesis. Type I:

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BOVINE KETOSIS

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  1. BOVINE KETOSIS

  2. Peak yield at 4-6 wks but high dry matter intake at 8-10 wks so there will be negative energy balance. • Low levels of glucose Mobilisation of adipose tissue Increase in NEFA & BHBA liver Ketogenesis & gluconeogenesis

  3. Type I: Gluconeogenic pathways are maximally stimulated . Low fat accumulation in liver Less More

  4. Type II: Gluconeogenic pathways are not maximally stimulated. “Fatty Liver condition” Less More

  5. NEGATIVE ENERGYBALANCE

  6. 1. TYPES: 2. 3.

  7. 4. 5.

  8. Epidemiology: - Common in stall fed animal - Most common in first month - peak prevalance in first 2 wks post calving - Low prevalance in first lactation & high at 4th lactation.

  9. Economic significance: - Decreased milk yield - Lower milk protein & Lactose - Delayed estrus - Increased risk of Mastitis, metritis, cystic ovarian disease - Lowered first conception rate.

  10. Pathogenesis: Severity of clinical syndrome is proportional to degree of hypoglycemia. Acetoacetic acid may lead to coma Changes in ruminal flora occurs leading to indigestion Respiratory burst mechanism of neutrophils fail to occur leading to immunosupression.

  11. Nervous signs will be due to

  12. Wasting form: Decreased appetite Woody appearance Decreased body weight Depressed & hang dog appearance T,P,R normal Odour of ketones in breath

  13. Nervous form: Symptoms appear suddenly More of delirum rather than frenzy Characteristic signs are: walking in circles Crossing of legs Head pushing Aimless movements Licking of skin & inanimate objects Hyperesthesia

  14. Clinical pathology: Hypoglycemia: decreased to 20 -40 mg/dl ketonemia : BHBA estimation Ketonuria : Rothera’s test • Elevated NEFA’s & Cholesterol levels • Elevated Volatile fatty acids in rumen. • Declined hepatic glycogen levels.

  15. DIFFERENTIAL DIAGNOSIS

  16. Treatment: 1.Replacemnt therapy: Glucose/Dextrose 50% soln @ 500 ml Fructose , Glucose + fructose , Xylitol can be used to prolong the reponse. Propylene glycol as a drench @ 225 g twice daily for 2 days followed by 110 g daily for 2 days

  17. Glucose precursors : Sodium propionate @110-225 g daily. Ammonium lactate @ 200 g for 5 days. Hormonal therapy: Glucocorticoids: Produce hyperglycemia Insulin: facilitates cellular uptake of glucose , Suppress fatty acid metabolism , Stimulate hepatic glconeogenesis. Anabolic steroids: Trenbolone acetate Glucagon: Gluconeogenic & glycogenolytic.

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