BOVINE KETOSIS
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
Triglycerides
More Less
Type II: Gluconeogenic pathways are not maximally
stimulated. “Fatty Liver condition”
gluconeogenesi
s
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 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.
•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.
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.