SYNONYM
ACETONEMIA
DEFINITION
Ketosis
is a metabolic disease of high yielding
animals, characterized by hypoglycemia,
ketonemia & ketonuria
OR
Ketosis
means accumulation of abnormal amount of
ketone-bodies in the tissues & tissue fluids
ETIOLOGY
☆ DIETARY FACTORS:
a) ➡️ Under nutrition/starvation or feeding of low carbohydrate diet
b) ➡️ Feeding of excess amount of protein rich diet
c) ➡️ Excess feeding of silage
d) ➡️ Deficiency of cobalt & phosphorus
☆ ANIMAL FACTORS-
a) ➡️ High milk yield
b) ➡️ Loss of exercise
c) ➡️ Hepatic insufficiency
☆ HORMONAL FACTORS-
a) ➡️ Adreno-cortical insufficiency
b) ➡️ Hypothyroidism
c) ➡️ Insulin insufficiency
☆ ENVIRONMENTAL FACTORS- expose
to cold climate
☆ DISEASES RESPONSIBLE FOR LOSS OF APPETITE-
a) ➡️ Systemic disease- metritis, mastitis, pneumonia, TRP, abomasal displacement
b) ➡️ Infectious disease- surra, theileriosis
Ketone formation:
Ketones arise from 2 major sources 1. butyrate in the rumen and 2.mobilization of fat
⇩.
A high proportion of
butyrate is produced by rumen fermentation and converted to BHB in the rumen
epithelium and absorbed as such form.
⇩
Free fatty acids are
produced by the mobilization of fat and transported to the liver and oxidized,
which produce acetyl-CoA and NADH.
⇩
Acetyl-CoA is oxidized via
the tricarboxylic acid (TCA) cycle and metabolized to acetoacetyl-CoA.
⇩
Complete oxidation of
acetyl-CoA through the TCA cycle which depends on supply of oxaloacetate and
from the precursor of propionate.
⇩
If propionate and oxaloacetate
are deficient so oxidation of acetyl-CoA through TCA cycle is limited and
acetyl-CoA is metabolized to acetoacetyl CoA and produce the acetoacetate and
BHB.
⇩
Here acetoacetate and BHB
both are utilize as an energy source and they are normally present in serum or
plasma in bovine.
⇩
Acetoacetate is convert to acetone
which is volatile and so it was exhaled in the breath.
⇩
Sometimes acetone cross
ruminal epithelium and ruminal flora metabolize acetone and convert into
isopropanol which absorbed in rumen and increase plasma concentration.
CLASSIFICATION
1. Primary
ketosis/production ketosis/estate acetonemia
➡️ Is occurs in high yielding animals, having
well to excellent body condition & fed good quality rations, but are in
negative energy balance
➡️ Heavy
body condition & high dietary protein may lead to excessive mobilization of
fat
2. Secondary
ketosis
➡️ Caused
by various systemic or infectious diseases, which results in decreased food
intake
➡️ Commonly due to abomasal displacement, traumatic
reticulitis, mastitis or other diseases common to the post-parturient period
➡️ In
this type, animal takes inadequate feed due to loss of appetite even though
sufficient feed is offered
3. Alimentary
ketosis
➡️ This
form due to excessive amount of butyrate
in silage
➡️ Also
due to decreased food intake resulting from poor palatability of high butyrate
silage
➡️ Silage
made from succulent material may be more highly ketogenic than other types of
ensilage
4. Starvation
➡️ It occurs in cattle that are in poor body
conditions & fed poor-quality feed stuffs
➡️ It
is due to deficiency of propionate in the diet & a limited capacity of gluconeogenesis
from body reserves
➡️ Ketosis due to specific nutritional deficiency-
Specific
dietary deficiency of cobalt & also phosphorus may lead to high incidence
of ketosis
EPIDEMIOLOGY
Species: cows & buffaloes
are affected
Breeds: buffaloes and crossbred
cows are more susceptible than indigenous cows
Sex: primary ketosis is
actually a disease of females
Age: common in 6-9 year
old animals
Number
of lactation: disease incidence is higher during the 3rd to 5th lactation
Physiological
status: is a disease of lactating cows
& buffaloes
Stage
of lactation: commonly occurs b/w 10 days to 2 months of calving
Milk
yield: high yielding animals are susceptible than low yielding animals
Season: incidence is higher
during calving season (winter, September-December)
Feeding
system: more common in housed or stall fed animals
Predisposing
factors: cold stress
Economic
importance: loss of milk production (25-100%), about 30-40% cases are complicated b
concurrent diseases like metritis, TRP, abomasal diseases, surra, theileria
& sometimes death of animal
CLINICAL
SIGNS
➡️ Ketosis
can be grouped as clinical & sub-clinical ketosis, based on presence or
absence of signs
Clinical ketosis: It mainly occurs in two forms
1. Digestive/wasting
form
2. Nervous
form
1. Digestive/wasting
form
➡️ Most common form ( about 90% cases )
➡️ Selective appetite: Refusal of
concentrate first, then ensilage but may continue to eat hay
➡️ Marked drop in milk yield (25-100%)
➡️ Emaciation/woody appearance, due to rapid loss of body weight
➡️ Moderate depression, hanghog appearance & disinclination to move
➡️ Loss of skin elasticity, due to disappearance of sub-cut fat
➡️ Dull skin & rough body coat
➡️ Faeces- firm, dry & covered with mucus
➡️ Ruminal motility- reduced & weak
➡️ Sweetish smell to breath,
milk & urine
➡️ Body temperature, pulse
& respiration- normal
➡️ If not treated, animal may die
➡️ Can spontaneously recover within a month but milk yield not re-gained
2. Nervous
form
➡️ Less common (about 10%)
➡️ Begins quiet suddenly
➡️ Walking in circles
➡️ Straddling or crossing of legs
➡️ Head pushing
➡️ Aimless wandering
➡️ Vigorous licking of skin & inanimate objects
➡️ Depraved appetite
➡️ Chewing movements with profuse salivation
➡️ Animal bellowing on pinching
➡️ Nervous signs like hyperaesthesia, tremor, convulsions may occurs in short episodes which last for 1 or 2 hours
at an interval of about 8-12 hours
SUB-CLINICAL/SPONTANEOUS
KETOSIS
➡️ It occurs in high yielding cattle, due to excessive production of
aceto-acetic acid in mammary glands
➡️ Many cows that are in negative energy balance in early pregnancy will
have ketonuria without showing clinical signs, but have decreased milk yield
& reduction in fertility
DIAGNOSIS
1. History
➡️ Recent calving
➡️ High milk yield ( 2-8 weeks post-partum)
➡️ Underfeeding of carbohydrates
➡️ Excess feeding of protein rich concentrates
➡️ Exposure to cold climate
2. CLINICAL PATHOLOGY
i. Biochemistry:
➡️ BLOOD GLUCOSE-
Decreased to 20-40mg/dl (normal: 50-60-mg/dl)
➡️ BLOOD KETONES-
increased to 20-100mg/dl (normal:
<10mg/dl)
➡️ KETONE BODIES IN URINE-
increased upto 80-130mg/dl (normal:
little or <10mg/dl)
➡️ MILK KETONE LEVEL-
increased upto 10-40mg/dl (normal: not
excreted, but may be upto 3mg/dl)
ii. Haematology:
➡️ DLC- indicate neutopenia (10%), lymphocytosis (60-80%) & eosinophlia (15-40%)
iii. Milk examination:
➡️ Milk
samples are positive for ketone bodies
iv. Urinanalysis:
➡️ Urine samples are positive for ketone bodies
Rothera's test
➡️ 5 ml of urine + Saturated ammonium sulfate + Add small crystal of sodium nitroprusside mixed well
➡️ Add amoonia slowly slowly at the one side of test tube.
Positive : Purpule ring at the junction of two fluid.
➡️ Selective appetite
Differential diagnosis
Wasting
form
✔️ Abomasal displacement
✔️ Traumatic reticulitis
✔️ Cystitis & pyelonephritis
✔️ Diabetes mellitus
Nervous
form
✔️ Rabies
✔️ Hypomagnesemia
✔️ Bovine spongiform encephalopathy
TREATMENT
Principle of the treatment of ketosis-
➡️ To relieve the need for glucose formation, from tissues & allow ketone body (KBs) utilization to
continue normally
1. REPLACEMENT
THERAPY-
Glucose
(dextrose):
➡️ Glucose 20% @ 0.5g/kg IV ,for 2-3 days (relieve need for glucose &
allow to utilize KBs)
or
➡️ Glucose 500gm orally as drench, following pre-medication with 30gm
sodium bicarbonate solution orally
➡️ Advantages- Simple and safe
treatment
➡️ Orally
glucose reaches directly to abomasums due to closure of reticular groove
slow & transient absorption of
glucose
stimulate insulin release through
gut-acting hormones
Glucose
precursors:
➡️ Sodium propionate @ 80g PO, for 3-6 days
or
➡️ Propylene glycol @ 225g PO, b.i.d. , for 2 days, followed by 110g daily
for 2 days
or
➡️ Propylene glycol @ 200-700g daily, or salts of propionic acid, can be
administered in feed
➡️ Advantages- absorbed directly
from rumen
Avoid
repeated injections
2. HORMONAL
THERAPY-
i. Gluco-corticoids-
Dexamethasone
@ 0.04mg/kg IV daily, for 2-3 days
Role
of corticosteroids:
➡️ Decreases
tissue uptake of glucose
➡️ Promotes
gluconeogenesis
➡️ Reduce
milk production for 3 days
ii. Role of insulin:
➡️ Suppresses mobilization of fat
➡️ promote glucose uptake by tissues
➡️ stimulate hepatic gluconeogenesis
iii. Anabolic steroids:
➡️ Durabolin/trenbolone acetate @ 60-120 mg
single dose
role of anabolic steroids;
➡️ stimulate appetite
➡️ Decrease ketone body & FFA concentration
➡️ Increases concentration of citrate in liver
which helps in uptake of acetyl CoA
3. MISCELLANEOUS THERAPY-
➡️ Niacin @ 8gm orally daily, for 5-6 days (niacin is antilipolytic)
➡️ Cobalt sulphate @ 100mg/kg or Vit. B12 @ 1-2mg/kg IM/IV (Vit. B12 converts
propionate to glucose
4. SUPPORTIVE THERAPY-
➡️ Injection Liver extract with B-complex @ 5-10
ml IM, on alternate days
➡️ Add mineral mixture comprising phosphorus and
cobalt
CONTROL
➡️ Avoid either starvation or overfeeding at calving, so animal should neither thin nor over fat
➡️ Provide balanced ration to dairy animals as per feeding standards
Give extra allowance of concentrate ration (protein 16%) @ 1.5kg/day during advance pregnancy
After calving give concentrate ration (1kg concentrate for every 2.5-3 kg of milk produce)
➡️ Provide ration which increases propionate production & decreases acetate production, eg. Finely ground roughage, cooked grain
➡️ Provide ration containing adequate amount of phosphorus, cobalt & iodine
➡️ Avoid sudden changes in type of feed so as to prevent indigestion
➡️ Give adequate exercise to lactating animals, t promote utilization of ketone bodies
➡️ Protect lactating animals from cold stress
➡️ Select cows/buffaloes having good feed capacity & appetite
➡️ Give glucose precursors (propylene glycol) @ 200-400 ml daily, from 5 days before to 10 days after calving
Post a Comment