Good Ppt about Ketosis in Bovinez

1. Karnataka Veterinary Animal & Fisheries
Sciences University, Bidar
Veterinary College Bidar
BOVINE KETOSIS

2. INTRODUCTION
● Also called Acetonemia, Ketonemia.
● It is a metabolic disease 🡪 lactating dairy cows.
● Weight loss, pica, inappetance, decreased milk production, and neurologic
abnormalities.
● Usually occur during the first 6 weeks of lactation.
● Highest during the third and fourth week of lactation in closely confined.

3. ETIOLOGY
▪ Result of a negative energy balance after parturition.
▪ The cow is unable to eat or assimilate enough nutrients to meet her energy
needs for maintenance and milk production.
▪ Blood glucose levels drop 🡪 Hypoglycemia
▪ Predisposing factors 🡪 retained fetal membranes, metritis, mastitis, displaced
abomasum, fatty livers, environmental stresses, faulty nutrition, and
mismanagement.

4. PATHOPHYSIOLOGY
Low CHO diet,
under nutrition,
starvation
Excess feeding of
silage or protein
rich diets
Heavy milk
production
↓ Propionate formation, ↑ butyrate production,
↑ glucose requirement
↓ Oxaloacetate
production
Hypoglycaemia
Hyglycaemic
encephalopathy
Nervous
signs
Mobilisation of fat
Fats 🡪 FFA + glycerol
Loss of body
weight
Propionate
Glucose
TCA cycle

5. Production of ketone
bodies
Fatty acids 🡪 acetyl COA
Acetoacetyl
COA
Ketone bodies viz;
Acetoacetate
Beta-hydroxy butyrate
Acetone
KETOSIS
Nervous signs;
Isopropyl alcohol
hypoglycaemia
Acidosis
Acetoacetate &
acetone are toxic

6. CLINICAL FINDINGS
▪ Initial signs - slight decrease in
feed intake, drop in milk
production, lethargy, and firm
mucus-covered stools.
▪ Pica is seen, refuse concentrates
🡪 feeds on coarse hay, straw🡪
Selective feeding.
▪ Depression deepen, humpbacked
posture 🡪 due to loss of
subcutaneous fat.

7. CLINICAL KETOSIS
TWO FORMS
DIGESTIVE/ WASTING FORM NERVOUS FORM
Common form Aimless wandering
Selective feeding Staggering gait
Emaciation Circling movement
Faeces are dry, firm & covered with mucus Licking of inanimate objects
Ruminal motility reduced Chewing movements,
Sweetish smell in breath, milk, urine Hyperaesthesia
Temp, Pulse & RR are normal Tremor, convulsions

8. SUB-CLINICAL KETOSIS
● Occurs in high yielding cattle.
● Excessive production of aceto-acetic acid in mammary glands.
● Mild drop in milk production.
● Reduced fertility 🡪
⬇️ Steroid hormones
Licking behaviour

9. CLINICAL PATHOLOGY
Parameters Abnormal (mg/dl) Normal range (mg/dl)
Blood glucose 20-40 40-60
Blood ketone 20-100 < 10
Milk ketone bodies 10-40 < 3
Serum calcium Slightly decreased 8-12
Serum mg Slightly decreased 2-3
Total lipids 227-400 < 200
Ketone bodies in urine 80-130 < 10

10. NECROPSY FINDINGS
● Non specific
● Yellowish friable enlarged liver
● Enlargement of adrenal cortex
● Fatty changes in kidney and heart.

11. DIAGNOSIS
▪ History 🡪 recent calving, not feeding CHO, feeding high protein diet, high milk production.
▪ Clinical signs 🡪 Acetone odour from breath, urine, or milk.
▪ Clinical pathology 🡪 hypoglycemia, ketonemia, ketouria etc.
▪ Rothera’s test for urine, milk
▪ Dipstick test for urine & milk.
▪ Cowside test 🡪 Beta Hydroxybutyrate
▪ Hematology 🡪 neutropenia(10%), lymphocytosis(60-80%), eosinophilia(15-40%)

13. DIFFERENTIAL DIAGNOSIS
DISEASES DIFFERENTIAL SIGN
TRP Recurrent bloat, pain, x-ray
Vagus Indigestion Papple shaped abdomen
Metritis Purulent vaginal discharge
Surra Org. in blood smear
Theileriosis Swollen lymph nodes, tick infestation
Diabetes mellitis Response to insulin
Tetanus Signs of tetany, no response to glucose
Rabies Dog bite, salivation, bellowing
Lead poisoning Blindness, no response to glucose
Encephalitis/ Meningitis Fever, no response to glucose

14. TREATMENT
The treatment should be initiated through:
▪ Replacement therapy
▪ Hormonal therapy
▪ Miscellaneous therapy

15. Replacement therapy:
▪ Glucose therapy 🡪 20% glucose @ 0.5 g/kg for 2-3 days.
▪ This will lead to:
✔Transient hyperglycaemia
✔Increase insulin secretion
✔Decrease Glucagon
✔Decreased NEFA
▪ Propylene glycol – slow but prolong action(225 g, b.i.d. for 2 days, followed by 100 g, daily
for 2 days) or
▪ Other glucose precursors like sodium propionate @ 80g P.O for 3-6 days – slow response.
▪ Oral glucose @ 500g after administering 30g of sod.bicarbonate solution.

17. Hormonal therapy:
▪ Glucocorticosteroids (Dexamethasone @ 0.04mg/kg i.v for 2-3 days.
▪ Insulin as protamine zinc @ 0.5 IU/kg, SC every 24-48 hrs.
▪ Anabolic steroids. (trenbolone acetate or durabolin @ 60-120mg single dose).
▪ Milk production may temporarily decrease after glucocorticoids administration but
increases rapidly after several days.

18. Miscellaneous treatments:
▪ Vitamin B12 (1-2mg/kg) converts propionate to glucose.
▪ Cobalt sulphate @ 100mg/day.
▪ Niacin @ 8g orally for 5-6d – antilipolytic.
▪ Chloral hydrate @ 30g p.o followed by 7g daily for 3-5d – converts
starch into glucose in rumen.
▪ Cysteamine (a biological precursor of coenzyme A) have been used to
treat cases - 750 mg IV for three doses at 1-3 day intervals.

19. PREVENTION
▪ Propylene glycol 🡪 drenched to cattle in early lactation @ 350 to 1000 mL daily for 10
days after calving or 1 L/day oral drench for 9 days prior to parturition has also been
shown efficacious.
▪ Sodium propionate @ 110g daily p.o for 6weeks after calving.
▪ Glycerol in large volume of water and be substituted for propylene glycol at equivalent
dose rates.
▪ Ionophores (Monensin as capsule 25g, 2-4 weeks before calving), alter bacterial flora of
the rumen, leading to ↓ Gram positive bacteria, protozoa, and fungi and ↑ Gram-negative
bacteria.
▪ The net effect 🡪 ↑ propionate production and ↓ acetate and butyrate production.

20. ▪ Feed additives 🡪 propylene glycol, sodium propionate, yeasts, niacin,
choline, etc. have been recommended.
▪ After calving 🡪 concentrate ration @ 1kg per 3kgs of milk.
▪ Cows should be properly conditioned during late lactation and the dry
period.
▪ 2 weeks before parturition, small amount of the concentrate ration then
gradually increased, @ parturition 🡪 1.5 kg/day.
▪ Highly fermentable feeds such as molasses helps to check ketosis.
▪ The ration should contain adequate amounts of essential vitamins and
minerals.
● Give adequate exercise to lactating animals.
● Perform Rothera’s test on urine & milk, regular glucose estimation.

21. ● Reference ;
● Veterinary Medicine by Peter D Constable
● Clinical Veterinary Medicine by Amalendu Chakrabarti
● https://www.msdvetmanual.com/metabolic-disorders/ketosis-in-cattle
THANK YOU!!!
Submitted By :
Ismail K M
VSK 1820
VETERINARY COLLEGE
SHIVAMOGGA
Submitted to :
Department of VCC
VETERINARY COLLEGE
BIDAR