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BOVINE KETOSIS

Date post: 22-Mar-2016
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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: - PowerPoint PPT Presentation
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BOVINE KETOSIS
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Page 1: BOVINE KETOSIS

BOVINE KETOSIS

Page 2: BOVINE KETOSIS

Early Lactation

Increased milk yield

Negative energy balance

Page 3: 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

Ketogenesis & gluconeogenesis

liver

Page 4: BOVINE KETOSIS

KetosisType I

Type II

Page 5: BOVINE KETOSIS

Type I: Gluconeogenic pathways are maximally

stimulated . Low fat accumulation in liver

gluconeogenesis

NEFA’S

Triglycerides

More Less

Page 6: BOVINE KETOSIS

Type II: Gluconeogenic pathways are not maximally

stimulated. “Fatty Liver condition”

gluconeogenesi

s

NEFA’S Triglycerides

MoreLess

Page 7: BOVINE KETOSIS

In Case of early lactation there will be low Insulin:glucagon ratio & this will stimulate Lipolysis in adipose tissue & ketogenesis in liver.

Ketone bodies will be produced from butyrate in rumen and by mobilization of fat which will yield aceto acetate in absence of oxaloacetic acid

Page 8: BOVINE KETOSIS

Etiology:

NEGATIVE ENERGYBALANCE

Page 9: BOVINE KETOSIS

TYPES:

•“Estate Acetonemia”•In cows with high lactation yield and

good quality ration but in negative energy balancePRIMARY

ketosis

•Secondary to other disease with decreased feed intake

•Eg., Abomasal displacement, TRP etc.Secondaryketosis

•Feeding of silage with high butyric acid•Feeding spoiled silageAlimentar

yketosis

1.

3.

2.

Page 10: BOVINE KETOSIS

•Feeding with poor quality feed & animals with poor condition

•Can be corrected with proper feeding

Starvation ketosis

•Cobalt is needed for metabolizing propionic acid into TCA cycle

•Def. of phosphorus & Diet low in TDN.Ketosis due

to defeciencie

s

4.

5.

Page 11: BOVINE KETOSIS

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.

Page 12: BOVINE KETOSIS

Economic significance:

- Decreased milk yield

- Lower milk protein & Lactose

- Delayed estrus

- Increased risk of Mastitis, metritis, cystic ovarian disease

- Lowered first conception rate.

Page 13: BOVINE KETOSIS

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.

Page 14: BOVINE KETOSIS

Production of ISOPROPYL ALCOHOL a break down product of aceto acetic acid in rumen

Defeciency of glucose which is needed for normal function of nervous tissue

Nervous signs will be due to

Page 15: BOVINE KETOSIS

Clinical signs

Wasting form

Nervous form

Page 16: BOVINE KETOSIS

Wasting form:

Decreased appetite

Woody appearance

Decreased body weight

Depressed & hang dog appearance

T,P,R normal

Odour of ketones in breath

Page 17: BOVINE KETOSIS

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

Page 18: BOVINE KETOSIS

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.

Page 19: BOVINE KETOSIS

Cystitis & Nephritis TRP

Diabetes mellitus

Indigestion

Wasting form

Abomasal displacemen

t

DIFFERENTIAL DIAGNOSIS

Page 20: BOVINE KETOSIS

Nervous form

Rabies Hypomagnesemia

Bovine spongiform

encephalopathy

Page 21: BOVINE KETOSIS

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

Page 22: BOVINE KETOSIS

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.

Page 23: BOVINE KETOSIS

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