Ketosis- Metabolic disease

1. KETOSIS
SURYAADHIKARI

2. INTRODUCTION
• Synonym: Acetonaemia, Hypoglycemia , Ketonuria ,
Pregnancy Toxaemia in Sheep
• Ketosis is a metabolic disease that occurs when the cow
is in severe negative energy balance and cannot
efficiently use mobilized body fat for energy.
• Characterized by partial anorexia and depression with
ketonaemia,ketonuria,ketolactia,hypoglycaemia with
poor liver glycogen content.
• The condition is worldwide in distribution but is most
common where dairy cows are bred and managed for
high production.

3. ETIOLOGY
• It is caused by hypoglycemia occurring in the
first month of lactation in cattle and late
pregnancy in ewes.

4. SUSCEPTIBILITY
• Ketonaemia affects cows of all ages.
• It occurs in both stable and pastured animals.
• It is more pronounced in high milk cow commonly
secondary to parturition and it may occur at any
deliver.
• It may arise in the different parts of the pregnant
lactating cows.
• This disease affect sheep specially the ewes that are
pregnant in twines and in such cases it is called
pregnancy toxemia of sheep.

5. PATHOGENESIS
Biochemical theory of ketosis

6. • The combination of intense adipose mobilization and a high
glucose demand.
• Both of these conditions are present in early lactation, at which
time negative energy balance leads to adipose mobilization, and
milk synthesis creates a high glucose demand.
• Adipose mobilization is accompanied by high blood serum
concentrations of nonesterified fatty acids (NEFAs).
• During periods of intense gluconeogenesis, a large portion of
serum NEFAs is directed to ketone body synthesis in the liver.
• Thus, the clinicopathologic characterization of ketosis includes
high serum concentrations of NEFAs and ketone bodies and low
concentrations of glucose.
• The serum ketone bodies are acetone, acetoacetate, and β-
hydroxybutyrate (BHB).

9. CLINICAL FINDINGS IN KETOSIS
Bovine ketosis- There are four major forms the disease
a. Sub clinical Form
b. Nervous form
c. Alimentary or wasting form
d. Milk fever type form

10. WASTING FORM
• It is the most common form. It is manifested
• Gradual but moderate decrease in appetite and milk
production over a period of 2-4 days.
• Body weight is lost rapidly, from the decrease in appetite.
• Cows become woody (Woody cow) due to the apparent
wasting and loss of cutaneous elasticity.
• The feces are firm and dry due to ruminal atony.

11. • The cow is moderately depressed and disinclined to
move or eat may be due to abdominal pain.
• Temperature, pulse and respiration are normal.
• Ketone smell in breath, milk, sweat, urine and stable.
• Severely affected animal die.
• Spontaneous recovery in about a month, but milk
yield never return to normal level; sharp drop in SNF
content of milk in wasting form.

12. Cow with Ketosis, 6 weeks post calving. Note
the poor body condition.
Ketosis affected Cows

13. NERVOUS FORM
• Suddenly appear walking in circles, head pushing or leaning
onto stanchion, apparent blindness, aimless movements,
wandering, vigorous licking of the skin and inanimate objects
• Depraved appetite
• Chewing movements with salivation
• Hyperaesthetic- bellowing on pinching or stroking
• Moderate tremor and tetany
• Gait is usually staggering.
• Nervous sign usually occur in short episodes which last for 1
or 2 hrs and may recur at intervals of about 8 to 12 hrs
• Affected cows may injure themselves during the nervous
episodes

14. Subclinical ketosis:
Where the urine and blood contain ketone bodies in
excess amounts but there is no obvious sign of ketosis.
Milk fever like form:
Milk fever type where hypocalcaemia accompanies
hypoglycemia . It resembles milk fever disease but the
muscular twitching and hypersensation are constant
symptoms. This form responds to treatment with
calcium and glucose therapy due to presence of
hypoglycemia and hypocalcaemia.

15. NECROPSY FINDINGS
• Non specific
• Yellowish friable enlarged liver.
• Enlargement and hyperemia o f adrenal cortex.
• Fatty changes in kidney and heart.
• Pneumonic lungs due to hypostatic congestion.

16. CLINICAL PATHOLOGY
• Hypoglycemia, ketonemia, ketonuria, or elevated
ketones
• in milk.Blood suger level: Normal(N) =40mg/dl,
ketosis(K)= reduced
• Blood ketone body
– Acetoacetic acid N=0.1 mg/dl, K=>7mg/dl
– B-hydroxybutyric acid:N=8mg/dl, K=>30mg/dl
– FFA:N9mg/dl, K>28mg/dl
• Ketone body in milk: N=0, K= upto 40mg/dl
• Ketone body in urine:N=0, K= upto500-1000mg/dl

17. DIAGNOSIS OF KETOSIS
• History of calving or late pregnancy and winter season.
duration of pregnancy in ewes, feeding program
• Clinical symptoms of ketone odor, wasting and or
nervous form.
• Biochemical examination reveals hypoglycemia,
ketonemia and ketonuria.
• In cases of sub clinical ketosis: Ketonemia with absence
of clinical signs
• Ovine ketosis: die within 6-7 days

18. DIFFERENTIAL DIAGNOSIS
Wasting form:
• Traumatic reticulitis (no relation to calving and
normal serum glucose).
• Vagus indigestion (marked stasis of alimentary tract
with bloat).
• Abomasal displacement (marked abomasal sounds
and absence of ruminal sounds)

19. Nervous form:
• Rabies (mania and ascending paralysis)
Hypomagnesaemia.
• Hypocalcaemia
• Bovine spongiform encephalopathy.
• Lead poisoning are closely resemble nervous form in
addition to blindness, convulsion history.

20. TREATMENT
REPLACEMENT THERAPY- Oral Hyperglycaemic agent
Propylene glycol or glycerine
Adult cattle @ 100 mg bid for 2 or 3 days
Small cattle @ 50 mg bid for 2 or 3 days
Sodium propionate (glucogenic effect) @ 110 -225 mg/ day
for 3 days to cattle, but shows very slow response.
Lactates: Ca or sodium lactate 1 kg initially, later ½ kg / day
for 7 days
Sodium acetate 110-500 g/day.

21. • Dextrose 50% solution @ 500-800 ml should
be administered intravenously.
• Dexamethasone, Predinisolone @ 10 ml I/M
• Insulin @ 200 IU can be administered. It has
antiketogenic effect.

22. MISCELLANEOUS TREATMENTS
• Chloral hydrate- Initially, 30 g orally as capsule, later 7 g
bid for several days as drench in molasses or water. It
breaks the starch in the rumen and stimulates production
and absorption of glucose. Vitamin B12 and cobalt - for the
activation of coenzyme A.
• Cysteamine (precursor of co-enzyme A)- 750 mg i/v for 3
doses at 1-3 days interval.
• Sodium fumerate (precursor of co-enzyme A) 3 doses at 1-3
days interval.
• Monensin sodium enhances the propionate production in the
rumen. Dose 25mg/day in grain feed mix.

23. CONTROL MEASURES FOR KETOSIS
• Should not be starved or over fat at calving.
• Adequate calorie intake at early lactation.
• Feeding in preparation for the next lactation should not
begin until about 4 weeks to calving.
• 4 weeks prior to calving: silage or hay or pasture
maintenance + 1 Kg concentrate/ day; gradually increase
to 5 kg concentrate/day at calving.
• After calving, increase concentrate as production
increases i.e. 3 kg hay/ 100 kg b.wt. or 9 kg ensilage/
100kg b.wt. as maintenance + 1 kg concentrate /3 kg
milk produced.

24. • Protein should not exceed 16-18 %.
• Exercise is must in intensive rearing.
• Ration should contain Co, P and I2.
• Avoid wet ensilage or mouldy hay or dusty hay ( as
they have increased levels of butyrate).
• Prophylactic feeding of sodium propionate @ 110g
daily for 6 weeks.
• Sodium propionate 110 g/ day for 6 weeks
• Propylene glycol @ 350 ml / day for 10 days after
serving or 6% of concentrate ration for 2 months.
• Blood glucose and milk ketone estimation during 6th
week of lactation.

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