ketosis in animals

1. DR ANITA SEWAG
MVSc MEDICINE

2. Etiology
 Etiology A multifactorial disorder of energy
metabolism.
 Negative energy balance results in hypoglycemia,
ketonemia (the accumulation in blood of acetoacetate,
β-hydroxybutyrate [BHB] and their decarboxylation
products acetone and isopropanol), and ketonuria.

3. Hepatic Insufficiency in Ketosis
 In type I, or “spontaneous” ketosis, the gluconeogenic
pathways are maximally stimulated, and ketosis occurs
when the demand for glucose outstrips the capacity of
the liver for gluconeogenesis because of an insufficient
supply of glucose precursors.

4.  type II ketosis, manifest with fatty liver, gluconeogenic
pathways are not maximally stimulated, and
consequently mitochondrial uptake of NEFAs is not as
active, and NEFAs become esterified in the cytosol,
forming triglyceride.
 The capacity of cattle to transport triglyceride from the
liver is low, resulting in accumulation and fatty liver.
The occurrence of a fatty liver can further suppress
hepatic gluconeogenic capacity.

5.  In type III ketosis, cattle are fed a diet (typically a high-
maize ration) that results in a higher ruminal
production of butyrate, which is directly metabolized
by ruminal epithelial cells to butyrate.

6. Types of Bovine Ketosis
• Primary ketosis (production ketosis)
• Secondary ketosis
• Alimentary ketosis
• Starvation ketosis
• Ketosis resulting from a specific nutritional deficiency

7. Primary Ketosis (Production Ketosis)
 Primary ketosis occurs in cows in good to excessive
body condition that have high lactation potential and
are being fed good-quality rations but that are in a
negative energy balance.

8. Secondary Ketosis
 Secondary Ketosis Secondary ketosis occurs where the
presence of other disease results in a decreased food
intake.

9. Alimentary Ketosis
 Alimentary ketosis (also called type III in some
classification systems) is a result of excessive amounts
of butyrate in silage and possibly also a result of
decreased food intake resulting from the poor
palatability of high-butyrate silage.
 Silage made from succulent material may be more
highly ketogenic than other types of ensilage because
of its higher content of preformed butyric acid.

10. Starvation Ketosis
 Starvation Ketosis Starvation ketosis occurs in cattle
that are in poor body condition and that are fed
poorquality feedstuffs. There is a deficiency of
propionate and protein from the diet and a limited
capacity of gluconeogenesis from body reserves.
Affected cattle recover with correct feeding.

11. Nutritional Deficiency
 Ketosis Resulting From Specific Nutritional Deficiency
Specific dietary deficiencies of cobalt and possibly
phosphorus may also lead to a high incidence of
ketosis.

12. PATHOGENESIS
 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.

13.  Ketone Formation Ketones arise from two major
sources: butyrate in the rumen and mobilization of fat.

14.  In response to a negative energy balance and low
serum concentrations of glucose (and consequently
low serum concentrations of insulin), cows will
mobilize adipose tissue, with consequent increases in
serum concentrations of nonesterified fatty acids
(NEFA) and subsequent increases in serum
concentrations of β-hydroxybutyrate (BHB),
acetoacetate, and acetone.

17. CLINICAL FINDINGS
 Two major clinical forms of bovine ketosis are
described—wasting and nervous present in varying
degrees of prominence.

18. Wasting form
 The wasting form is the most common of the two and
is manifest with a gradual but moderate decrease in
appetite and milk yield over 2 to 4 days.
 In component-fed herds, the pattern of appetite loss is
often very specific in that the cow first refuses to eat
grain, then ensilage, but may continue to eat hay. The
appetite may also be depraved.
 “Woody” appearance because of the apparent wasting
and loss of cutaneous elasticity presumably resulting
from disappearance of subcutaneous fat.

19.  The temperature and the pulse and respiratory rates
are normal, and although the ruminal movements may
be decreased in amplitude and number, they are
within the normal range unless the course is of long
duration,
 The characteristic sweet odor of ketones is detectable
on the breath and often in the milk,

20. Nervous form (nervous ketosis)
 Walking in circles
 Straddling or crossing of the legs
 Head pushing or leaning into the stanchion
 Apparent blindness
 Aimless movements and wandering
 Vigorous licking of the skin and inanimate objects
 Depraved appetite
 Chewing movements with salivation Hyperesthesia
may be evident.

21.  The nervous signs that occur in some cases of bovine
ketosis are thought to be caused by the production of
isopropanol, a breakdown product of acetone in the
rumen,1 although the requirement of nervous tissue
for glucose to maintain normal function may also be a
factor in these cases.

22. Subclinical Ketosis (Hyperketonemia)
 Subclinical ketosis is defined as an increase in
blood/plasma/serum BHB above the normal reference
range or ketonuria in a cow without detectable clinical
signs of disease.
 Potential milk production in cows with subclinical
ketosis is reduced by 1% to 9%.

23. CLINICAL PATHOLOGY
 Hypoglycemia, ketonemia, and ketonuria are
characteristic of the disease.
 Glucose Plasma glucose concentrations are reduced
from the normal of approximately 50 to 65 mg/dL to
20 to 40 mg/dL
 BHB is the quantitatively highest circulating ketone
body in cattle.

24.  Normal cows have plasma BHB concentrations less
 than 1.0 mmol/L;
 cows with subclinical ketosis have blood or
plasma/serum concentrations greater than 1.0, 1.2, or
1.4 mmol/L
 Cows with clinical ketosis usually have serum/plasma
BHB concentrations in excess of 2.5 mmol/L, with
values rarely reaching 10.0 mmol/L.

25. Diagnosis
 In a given animal, urine ketone body concentrations
are always higher than milk ketone body
concentrations.
 Biochemical examination reveals hypoglycemia,
ketonemia and ketonuria.
 ROTHERA'S TEST Test For Ketone Bodies.
 Acetoacetic acid reacts with Sodium nitroprusside to
give a violet color.

26. NECROPSY FINDINGS
 The disease is not usually fatal in cattle, but fatty
degeneration of the liver and secondary changes in the
anterior pituitary gland and adrenal cortex may be
present.

27. DIFFERENTIAL DIAGNOSIS
 Wasting form:
•Abomasaldisplacement
• Traumatic reticulitis
• Primary indigestion
• Cystitis and
pyelonephritis
 Nervous form:
•Rabies
•Hypomagnesemia
•Bovine spongiform
encephalopathy

28. Treatment
 Treatment of ketosis is aimed at reestablishing
normoglycemia and reducing serum ketone body
concentrations.
 Dextrose 50% solution @ 500-800 ml should be
administered intravenously.
 Dexamethasone, Predinisolone @ 10 ml I/M
 Insulin @ 200 IU can be administered.
 Propylene glycol administered orally (250–400 g/dose [8–14
oz]) once per day acts as a glucose precursor and is effective
as ketosis therapy.
 Cyanocobalamin (vitamin B12, 1 to 4 mg daily IV)

29. Prevention and Control:
 Prevention of ketosis is via nutritional management.
Body condition should be managed in late lactation,
when cows frequently become too fat. Modifying diets
of late lactation cows to increase the energy supply
from digestible fiber and reduce the energy supply
from starch may aid in partitioning dietary energy
toward milk and away from body fattening.
 monensin sodium is approved for use in preventing
subclinical ketosis and its associated diseases. Where
approved, it is recommended at the rate of 200–300
mg/head/day.

30. Why Ionophores (monensin) is useful ?
 Ionophores alter bacterial flora of the rumen, leading
to decreases in gram-positive bacteria, protozoa, and
fungi and increases in gram-negative bacteria.
 The net effect of these changes in bacterial flora is
increased propionate production and a decrease in
acetate and butyrate production providing increased
gluconeogenic precursors.

31. Economic Significance
 Economic Significance Clinical and subclinical ketosis are
major causes of loss to the dairy farmer. In rare instances
the disease is irreversible and the affected animal dies, but
the main economic loss results from the loss of production
while the disease is present, the possible failure to return
to full production after recovery, and the increased
occurrence of periparturient disease.
 Decreased milk yields; lower milk protein and milk lactose;
increased risk for delayed estrus and lower first-service
conception rates; lower pregnancy rates; increased
intercalving intervals; increased risk of cystic ovarian
disease, metritis, and mastitis; and increased involuntary
culling

32. THANK YOU