KETOSIS

• Associated with negative energy

balance
• Generally occurs in dairy cows from
parturition to 6 weeks after parturition
• Incidence ranges from 5-16%
• Occasionally seen prior to parturition in
beef and dairy cows
• Economic impact
 The pathogenesis of bovineKETOSIS
The exact pathogenesis is not understood, but:
At early lactation There is:
• Milk synthesis creates a high glucose
demand
• Negative energy balance leads to adipose
mobilization

• High blood serum conc. Of NEFA

• Intense gluconeogenesis, during which a
large portion of serum NEFA is directed to
ketone body synthesis in the liver
 KETOSIS
- The serum ketone bodies are :
• Acetone, Acetoacetate, and β-hydroxybutyrate
(BHB).
- Cattle with hyperketonemia do not have
concurrent acidemia in contrary to other spp.
- Cases of ketosis in very early lactation are
usually associated with fatty liver.
- Cases occurring closer to peak milk prod.,
may be assoc. with underfed cattle
experiencing a metabolic shortage of
gluconeogenic precursors than with
excessive fat mobilization.
 Normal pathways of carb. Metabolism in ruminants
•
Acetic A Butyric A Propionic A
• Ketogenic acids Glucogenic Acds
• Reach liver for metabolism

• Active acetate Oxaloacetate

Ketones
Kreps cyc
Oxaloacetate Fat depots Glucose,
-- ve Oxal. Acet. for need lactose
++ve
 Incidence of Ketosis
• All high lact. dairy cows at first 6 wk of
lactation are at risk of ketosis with incidence
of 5-16%,
• Ketosis occurs in all parities & less common
in primiparous animals)
• It appear to have no genetic predisposition,
• Cows with excessive adipose stores (BCS
≥3.75 out of 5.0) at calving are at increased
risk of ketosis.
• Lactating cows with hyperketonemia
(subclinical ketosis—serum BHB
concentrations >12 mg/dL) are at increased
risk of developing clinical ketosis.
 :Clinical Findings
I- Digestive form:
• More common in highly fed cattle.
• In confinement cows, reduced feed intake
is usually the first sign of ketosis.
• Cows often refuse grain before forage.
• In group-fed herds, reduced milk
production, lethargy, and an “empty”
appearing abdomen are usually the signs
of ketosis noticed first.
• Cows are a febrile and may be slightly
dehydrated.
 :Clinical Findings
• Rumen motility is variable, being
hyperactive in some cases and
hypoactive in others.
II- Nervous signs
• CNS disturbances (abnormal licking and
chewing, with cows sometimes chewing
incessantly on pipes and other objects in
their surroundings.
• Incoordination and gait abnormalities
occasionally are seen, as are aggression
and bellowing.
• Nystagmus, spasm of muscle of neck,
back
• Convulsions
• Paddling of Legs, walking in circles.
 :Clinical Findings
III- Milk fever form:
• Loss of consciousness,
• tremors, pariesis.
• Not respond for Ca.
• Appearance of ketones on
urine and expired airs
Ketonemia
 Diagnosis
• Is based on presence of risk factors (early
lactation), clinical signs, and ketone bodies in
urine or milk.
• When a diagnosis of ketosis is made, a thorough
physical examination should be performed
because frequently ketosis occurs concurrently
with other peripartum diseases.
• Common concurrent diseases include displaced
abomasum, retained fetal membranes, and
metritis.
• Rabies and other CNS diseases are important
differential diagnoses.
 Diagnosis
• Cow-side tests for the presence of ketone
bodies in urine or milk .
• Due to the large surge in plasma NEFA at
calving, a positive test for ketones is very
common during this period.
• Urine ketone body conc. are always higher
than milk ketone body concentrations
• Mild ketones in urine, milk without signs
indicate suclinical ketosis.
 Diagnosis of ketosis
• Milk tests for acetone and acetoacetate are
more specific than urine tests.
• Positive milk tests for acetoacetate and/or
acetone usually indicate clinical ketosis
• A dipstick to detect BHB in milk, available in
Japan and Europe, is more sensitive than
milk tests for acetone and acetoacetate and
may be useful for monitoring incidence of
subclinical ketosis.
 Diff. Diagnosis of ketosis
The disease should be differentiated from:
• 1- Milk fever.
• 2- Ruminal acidosis
• 3- LDA, RDA
• 4- Hypomagnesemia
• 5- BSE (Mad cow sydm)
 Treatment
Treatment is aimed at:
I- Reestablishing normoglycemia
II- Reducing serum ketone body
concentrations.
This could be achieved via:
1- I.V. admin. of ½-1 L of 50% dextrose/ or
glucose which is very hyperosmotic and, if
admin. perivascularly, results in severe
tissue swelling and irritation, so care should
be taken to assure that it is given I.V.
 Treatment
2-Admin. of glucocorticoids (Dexamethasone or
isoflupredone acetate at 5-20 mg/dose, IM,.
3-Glucose and glucocorticoid therapy may be
repeated daily as necessary.
4-Propylene glycol (250-400 g/dose, PO, [~8-14
oz]) twice d. acts as a glucose precursor in
combination with other therapy avoiding
overdosing.
5- Cases occurring at first 1-2 wk after calving
are more refractory to therapy than those
occurring nearer to peak lactation.
 Treatment
• In these cases, a long-acting insulin preparation
given IM at 150-200 IU/day may be beneficial.
6- Insulin suppresses both adipose mobilization and
ketogenesis, but should be given in combination
with glucose or a glucocorticoid to prevent
hypoglycemia
7- I.V. Ca-gluconate 20 % (1/4 L for cows) for 5 days.
8- Vit B12 or cobalt.
9- 2 L Molass per os for cows
10-Chloral hydrate 10- 30 gm by st. tube once, half
dose up the next days for 5 days.
 :Prevention and Control
I-Nutritional management aiming to.
1- Maintaining and promoting feed intake
near calving
2- Reduction of BCS in the dry period
3- Avoiding excessive adipose mobilization
prepartum
N.B:When cows become too fat, the dry period
is generally too late to reduce BCS.
 :Prevention and Control
• It is likely that optimal energy and fiber
concentrations in rations for cows in the last
3 wk of gestation vary from farm to farm
• Feed intake should be monitored and rations
adjusted to maximize dry matter and energy
consumption in late gestation.
• After calving, diets should promote rapid and
sustained increases in feed and energy
consumption.
 :Prevention and Control
• Rations should be relatively high in nonfiber
carbohydrate concentration, but contain
enough fiber to maintain rumen health and
feed intake.
• Neutral-detergent fiber concentrations
should be in the range of 28-30% with
nonfiber carbohydrate concentrations in the
range of 38-41%.
• Dietary particle size will influence the optimal
proportions of carbohydrate fractions
 :Prevention and Control
• Some feed additives, including niacin,
calcium propionate, sodium
propionate, propylene glycol, and
rumen-protected choline, may be
beneficial in preventing and managing
ketosis.
• To be effective, these supplements
should be fed in the last 2-3 wk of
gestation, as well as during the period
of ketosis susceptibility
PREGNANCY TOXEMIA IN EWES
• Commonly affects ewes in late
pregnancy
• Commonly occurs in the last 2-4 weeks
of pregnancy due to increased demand
from rapidly growing fetus (es)
• Clinical cases generally follow a period
of negative energy balance
PREGNANCY TOXEMIA IN EWES
Stressors lead to decreased feed intake in the
last trimester:
• Exhaustion, Sudden transport, winds &n
storms, other diseases.
• Twins or more feti, Obesity near lambing.
• Decreased Progest., Prolact.,Insulin Hrms
and increased GH, All initiate excess
glucose demands.
• Feeding only roughgaes deteriorate ewes
health
 Pathogenesis
• Negative energy balance leed to:
• Encephalopathy due to Hypoglycemia in brain.
• Hypoglycemia & stimulated adrenal gland
resulting in lipomobilization resulting in excessive
FAs, fatty infeltration of liver.
• During this, an upsets in oxaloacetate metabolism
reulting in ketone formation and may metab.
Acidosis.
• There may be another factors such as liver,
kidney, endocrine disorders contributing to
occurrence of ketosis.
 Pathogenesis
• Decreased feed intake at late preg. In
time of excessive needs for energy for
the growing feti is critical in occurrence
of PT
• Increased energy demands of fetus
combines with decreased available
energy result in clinical disease
• Morbidity is low (1-2%); Mortality is high
(80%)
 Pathogenesis
In addition to the needs for
maintenance, Fetus gain 70- 80 % of
its weight in last trimester, requiring
70-80 gm glucose daily, while ewe
produce less than this amount
producing a condition of negative
energy balance
PREGNANCY TOXEMIA IN EWES
Clinical signs:
– Weak ewes in late pregnancy
-- Anorexia, inappetance, isolation
• Depression, Head pressing,
tremors, seizures in later stages,
aimless walking as blind, stuck
into walls, fens, incoordination
– Sluggish, fail to eat (but still come
up to the feed bunk)
 :Clinical signs
– Lie down and refuse to get up in
later stages
• Grunting sounds
• Loss of sensation, coma and
– Generally die within 3-10 days
(mortality up to 80%)
Pregnancy toxemia
 Diagnosis
History
• An obese ewe near lambing, carrying more
than one fetus
Signs
• Change behaviour, nervous signs
Lab:
• Hypoglycemia,
• hyperketonemia
• Metabolic acidosis.
• In\creased blood urea
• Ketonuria
 Treatment
– Remove source of glucose drain on the
ewe (abort the lambs)
– Correct energy, electrolyte imbalances,
dehydration (propylene glycol and IV
treatments)
– Call veterinarian for best chance at
survival
– Even with aggressive treatment,
survival is unlikely
 Prevention
– Work with nutritionist to tailor a
nutritional program specific for the
production requirements of the flock
(need specific nutritional program
throughout the pregnancy of ewes)
– Minimize all stress factors during the
last 2 months of gestation