Assistant.Prof.Dr.M.A.

S
FAT COW SYNDROME, HEPATIC LIPIDOSIS, PREGNANCY
TOXEMIA IN CATTLE.
It is a major metabolic disease of dairy cows in early lactation and
is associated with decreased health status and reproductive
performance.
Etiology
Mobilization of excessive body fat to liver during periods of negative
energy balance at time of parturition or in early lactation of dairy
cows and late pregnancy of beef cows.
Epidemiology
High-producing dairy cows overfed during dry period may develop
fatty liver syndrome just before or after calving precipitated by any
factor or disease which interferes with feed intake. Occurs in well-
conditioned beef cattle in late pregnancy when energy intake
suddenly decreased. Moderate and subclinical degrees of fatty
infiltration may adversely affect reproductive performance of dairy
cows.
Pathogenesis
Fatty acids are a normal finding in all postpartum dairy cows as milk
production outstrips digestive capacity. Usually, these FAs are
esterified to triglycerides in the liver. Under normal circumstances,
triglyceridesare packaged into lipoproteins and transmrted to
tissues for a source of energy or to the mammary gland for - milk fat
synthesis. Ruminant fat cow syndrome seems to occur when serum
Fas are increased and triglycerides accumulate in the liver, while
hepatic lipoprotein production does not increase or is reduced. It is
suggested that fat begins to accumulate in the liver in late gestation,
is dynamic, and precedes the development of postpartum disease
Accumulation of fat in the liver disturbs hepatic architecture and
function, resulting in hypoglycemia and ketosis. There is also
concurrent leukopenia, which may be related to the increased
incidence of postpartum diseases seen with the condition
Clinical signs
1-fat cow syndrome occurs usually within the first few days
following parturition any condition which interferes with the
animal's appetite such as:
1- Parturient hypocalcaemia(milk fever)
Assistant.Prof.Dr.M.A.S
2-Left-side displacement of
the abomasum
3-Indigestion
4- Retained of fetal
membranes
5- Dystocia
2-Affected cows are usually excessively fat with body condition
scores of 5/5 or higher excessive quantities of SC fat are palpable
over the flanks, the shoulder areas and around the tail head.
3-The temperature, heart rate, and respiration are within normal
ranges but rumen contractions are weak or absent and the feces
are usually scant.
4-Periods of prolonged recumbency are common and affected cows
may have difficulty in standing.
5-Affected cows will not eat and gradually become weaker, totally
recumbent and die in 7-10 days.
6-Some cattle exhibit nervous signs consisting of staring gaze,
holding the head high and muscular tremors of the head and neck.
7-Terminally there is coma and tachycardia and the affected cows
will not eat and gradually become weaker, totally recumbent and die
in 7-10 days. Clinical pathology
1- Increase in serum hepatic enzyme levels(gama-glutamyl
transferase (GG1), aspartate aminotransferase (AS1), and sorbitol
dehydrogenase (SDH) activities and bile concentrations.
2-increase in ketone bodies.
3- Increased fat in liver biopsy
Necropsy finding
In severe fatal cases, the liver is grossly enlarged, pale yellow,
friable, and greasy. Mild and moderate cases are usually not fatal
unless accompanied by another fatal disease such as per acute
mastitis.
The histological changes include the occurrence of fatty cysts or
lipogranulomas, enlarged hepatocytes, compression of hepatic
Assistant.Prof.Dr.M.A.S
sinusoids, a decreased volume of rough endoplasmic reticulum and
evidence of mitochondrial damage.
Differential diagnosis
• Left-sided displacement of abomasum
• Right-sided displacement of abomasum
• Milk fever
• Parturition syndrome
• Abomasal impaction
• Vagus indigestion • Peritonitis.
Treatment
1-Fluid and electrolyte therapy. Intensive therapy directed at
correcting the effects of the ketosis and the fatty liver is required. A-
I.V. infusion of 5% glucose and multiple electrolyte solutions

B-intraruminal administration of rumen juice (5-10 L) in an attempt

to stimulate the appetite of affected cows. Water and multiple
electrolytes (10-30 L) can be administered intraruminally.
2-Glucagon. The subcutaneous injection of 15 mg/d of glucagon for
14 days beginning at day 8 postpartum.
3-Glucocorticoids. Prednisolone at 200 mg 1M daily for days
decreased liver triglyceride concentrations.
4-Propylene glycol given oraly at 1 L/day is used for the treatment
of ketosis.
5-Insulin as zinc protamine at 200-300 SC twice daily.
Control
Avoid overfeeding during late lactation and dry period. Avoid
situations which reduce feed intake at time of parturition.