Pregnancy Toxemia

PREGNANCY TOXAEMIA IN SHEEP/GOA
Syn
Pregnancy ketosis
Twin lamb disease
Lambing or kidding sickness
Paralysis or ketosis
Introduction
It is highly fatal disease occurring in late pregnancy characterized

by
Hypoglycaemia, ketoneaemia and low liver glycogen
content.
Negative energy balance
Multiple foetuses predispose the disease.
ETIOLOGY
Decline in the plane of nutrition during the last 4 to 6 weeks of
pregnancy.
This is the period when foetal growth is rapid and the demands for
energy markedly increased, particularly in ewes that are carrying
twins or triplets.
Classification <cause basis> :
Primary pregnancy toxaemia
Fat ewe pregnancy toxaemia
Starvation pregnancy toxaemia
Secondary pregnancy toxaemia
Stress-induced pregnancy toxaemia.
Primary pregnancy toxaemia
Fall in the plane of nutrition

Fat ewe pregnancy toxaemia
•This occurs without a stress induction.
Fat ewes will experience a voluntary fall in food intake in late
pregnancy,
This is due to the reduction of the rumen volume by the pressure of
intra-abdominal fat and the developing foetus.
Starvation pregnancy toxaemia

•This occurs in ewes that are excessively thin. It is relatively
uncommon
Secondary pregnancy toxaemia
•This usually occurs as a sporadic disease as the result of the effect

of inter current disease such as foot rot or foot abscess, which
affects food intake.
Heavy worm infestation, e.g. with Haemonchus contortus, would
add a similar drain on glucose metabolism and increase the chances
of development of the disease.
Stress-induced pregnancy toxaemia

•This is the least common cause of the disease, one where stress is
the initiator.
•Examples are close shepherding , the transport of late pregnant
sheep
PATHOGENESIS
• It is initiated by a period of negative energy balance (NEB)
where ketone bodies (KB) accumulate to a pathologic level
• Factors involved in the NEB dynamic include

• Decreased feed intake
• Increased energy demands from carrying multiple late-
term foetuses, hormonal dysregulation of fat and
carbohydrate metabolism
• Altered glucose utilization by the tissues,
• Or a combination of the above
PATHOGENESIS
Ewes that are predisposed to the disease
• Have an ineffective gluconeogenic response to the continued,
preferential demands for glucose by the growing foetuses
• Result in hypoglycemia, lipid mobilization and the accumulation of

ketone bodies and cortisol
• The subsequent disease and metabolic changes are associated with

excessive lipid mobilization.
PATHOGENESIS
• Elevated concentrations of B hydroxybutyrate further
• Suppress endogenous glucose production
• Exaggerates the development of ketosis
• Negative feedback of hyperketonemia on glucose production
•The disease manifests with an encephalopathy,

Hypoglycemic encephalopathy resulting from
Hypoglycemia in the early stages of the disease.
•There is an abnormally high level of cortisol in plasma

Clinical Signs
Weakness, dull attitude, and poor appetite.
Separation from the flock or herd.
Inability to rise.
Apparent blindness, staring off into space.
Constipation is usual, the faeces are dry and scanty.
There is grinding of the teeth.

Clinical Signs
In later stages, marked drowsiness develops and episodes of more severe nervous signs
occur.
In these episodes, tremors of the muscles of the head cause twitching of the lips,
champing of the jaws and salivation.
The muscle tremor usually spreads to involve the whole body and the ewe falls with
tonic-clonic convulsions.
Abnormal postures including unusual positions of the limbs and elevation of the chin - the
'stargazing‘ posture and incoordination and falling when attempting to walk.
Recumbent in 3-4 days and remain in a state of profound depression or coma for a further
3-4 days.
Clinical Signs
The respirations are rapid
There may be an expiratory grunt
Foetal death occurs commonly and is followed by transient recovery of

the ewe
But the toxaemia caused by the decomposing foetus soon causes a

relapse.
Rumen contractions are weak or absent .

Diagnosis
• History of pregnancy
• Clinical signs
• Confirmation of pregnancy status as well as the number of live fetuses

present via transabdominal ultrasound (3.5 MHz curvilinear probe)
• Ketone bodies high in blood and in urine

• (Acetoacetate 0.24-0.36mg/dl Acetone 0-10mg/dl β-Hydroxybutyrate
>5mmol/L)
• Blood glucose below 25mg/dl. (50 -80mg/dl)

DIFFERENTIAL DIAGNOSIS
• Listeriosis
• Cerebral abscess
• Acidosis
• Uterine torsion or impending abortion
• Rabies.
• Hypocalcemia, hypomagnesemia
• Polioencephalomalacia
• Bacterial or viral encephalitis
• Meningeal worm (P. tenuis)
• Severe haemonchosis.
TREATMENT
• Treatment of pregnancy toxemia requires that any predisposing
illness, such as pneumonia or foot rot
• Sheep treated very early in the course of the disease generally
respond favourably, but response to therapy is poor once sheep
have become recumbent .
Parentral therapy
• Electrolytes and glucose (5% dextrose) given over a prolonged
period of time
• Corticosteroids Isoflupredone/ ISOFLUD {2mg/ml} dose;2-
5mg)
• Trenbolone acetate 30mg i/m daily. > Triamcinolone
TREATMENT
Oral therapy
• propylene glycol or glycerine (110 g/day) given orally is
used to support parenteral glucose therapy.
Caesarean section
• Lambs are close to term
• Alternate to replacement therapy.
• The demand for glucose by the lambs is immediately
removed
• Both the ewe and the lambs have a high chance of survival
IF
• Caesarean section is conducted before there is irreversible
brain damage in the ewe and is not in the recumbent stage
Treatment goals
Include
• Correction of ketosis
• Negative Energy Balance (NEB)
• Hypoglycemia
• Hypoinsulinemia
• Hydration status
• Electrolyte imbalances
• Metabolic acidosis
• Stimulation of appetite and feed intake
• Removal of source of energy demand (fetuses) if necessary
Prevention
• Feed ewes and does appropriately to avoid excessively fat or thin body
condition during pregnancy
• Ultrasound exams at 40-60 days post-breeding can be used to identify

ewes and does with twins or triplets-feed more energy
• Sudden changes in type of feed should be avoided and extra feed provided
during bad weather
• Feed high-quality grass hay and/or alfalfa;
• Provide plenty of clean, fresh water at all times
• Parasitic burden should be ruled out

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PREGNANCY TOXAEMIA IN SHEEP/GOA

It is highly fatal disease occurring in late pregnancy characterized

Fall in the plane of nutrition

Starvation pregnancy toxaemia

•This usually occurs as a sporadic disease as the result of the effect

Stress-induced pregnancy toxaemia

• Factors involved in the NEB dynamic include

• Result in hypoglycemia, lipid mobilization and the accumulation of

• The subsequent disease and metabolic changes are associated with

•The disease manifests with an encephalopathy,

•There is an abnormally high level of cortisol in plasma

Weakness, dull attitude, and poor appetite.

Separation from the flock or herd.

Apparent blindness, staring off into space.

Constipation is usual, the faeces are dry and scanty.

There is grinding of the teeth.

There may be an expiratory grunt

Foetal death occurs commonly and is followed by transient recovery of

But the toxaemia caused by the decomposing foetus soon causes a

Rumen contractions are weak or absent .

• Confirmation of pregnancy status as well as the number of live fetuses

• Ketone bodies high in blood and in urine

• Blood glucose below 25mg/dl. (50 -80mg/dl)

• Ultrasound exams at 40-60 days post-breeding can be used to identify

• Feed high-quality grass hay and/or alfalfa;

• Provide plenty of clean, fresh water at all times

• Parasitic burden should be ruled out

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