glucose ketone bodies. early lactation increased milk yield negative energy balance

BOVINE KETOSIS

Glucose Ketone bodies

Early Lactation

Increased milk yield

Negative energy balance

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

KetosisType I

Type II

Type I: Gluconeogenic pathways are maximally

stimulated . Low fat accumulation in liver

gluconeogenesis

NEFA’S

Triglycerid

es

More Less

Type II: Gluconeogenic pathways are not maximally

stimulated. “Fatty Liver condition”

gluconeogenesis

NEFA’S

Triglycerides

MoreLess

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

Etiology:

NEGATIVE ENERGYBALANCE

TYPES:

•“Estate Acetonemia”

•In cows with high lactation yield and good quality ration but in negative energy balance

PRIMARYketosis

•Secondary to other disease with decreased feed intake

•Eg., Abomasal displacement, TRP etc.

Secondaryketosis

•Feeding of silage with high butyric acid

•Feeding spoiled silage

Alimentaryketosis

1.

3.

2.

•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

defeciencies

4.

5.

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.

Economic significance:

- Decreased milk yield

- Lower milk protein & Lactose

- Delayed estrus

- Increased risk of Mastitis, metritis, cystic ovarian disease

- Lowered first conception rate.

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.

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

Clinical signs

Wasting form

Nervous form

Wasting form:

Decreased appetite

Woody appearance

Decreased body weight

Depressed & hang dog appearance

T,P,R normal

Odour of ketones in breath

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

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.

Cystitis & Nephritis

TRP

Diabetes mellitus

Indigestion

Wasting form

Abomasal displacemen

t

DIFFERENTIAL DIAGNOSIS

Nervous form

Rabies Hypomagnesemia

Bovine spongiform

encephalopathy

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

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.