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Pregnancy Toxemia in Sheep

Pregnancy toxemia in sheep (small ruminant) also known as twin lamb disease.

Pregnancy toxemia in sheep is multi factorial disorder of energy metabolism. Hypoglycemia and hyperketonemia are the primary metabolic disturbances in pregnancy toxemia.

The disease also occurs in goats during late pregnancy with the same initiating causes.

Etiology

The most important etiological factor in pregnancy toxemia is a decline in the plane of nutrition during the last 4 to 6 weeks of pregnancy. This is the period when fetal growth is rapid and the demands for energy markedly increased, particularly in ewes that are carrying twins or triplets.

Classification

Primary pregnancy toxemia: Fall in the plane of nutrition during the latter half of pregnancy often coupled with a short period of food deprivation
Fat ewe pregnancy toxemia : Over fat conditioned ewes in late pregnancy. Fat ewes will experience a voluntary fall in food intake in late pregnancy, due to the reduction of the rumen volume by the pressure of intra- abdominal fat and the developing fetus
Starvation pregnancy toxemia : prolonged drought and no alternative feed supply predisposes the pregnancy toxemia.
Secondary pregnancy toxemia: Result of the effect of intercurrent disease such as foot rot or foot abscess, Heavy worm infestation, e.g. with Haemonchus contortus, which affects food intake.
Stress-induced pregnancy toxemia: Transport of late pregnant sheep and outbreaks that occur following a period of flock attack by dogs.

Epidemiology

Pregnancy: The disease occurs only in ewes in the last 6 weeks of pregnancy usually during the last month, with the peak incidence in the last 2 weeks of pregnancy.
It occurs primarily in ewes carrying triplet or twin lambs, although ewes bearing a single, large lamb may also be affected.
Parity : The disease is uncommon in maiden ewes because of their low fecundity and increases in prevalence up to parity three.
Breed: The disease is more common in British lowland breeds and their crosses than the Merino. British hill-breeds are traditionally believed more resistant to the development of pregnancy toxemia.

Pathogenesis

Inadequate energy intake in late pregnancy in ewes with more than one fetus. Approximately 60% of fetal growth takes place in the last 6 weeks of pregnancy.
Ewes that are predisposed to the disease have an ineffective gluconeogenic response to the continued, preferential demands for glucose by the growing fetuses resulting in hypoglycemia, lipid mobilization and the accumulation of ketone bodies and cortisol.
Elevated concentrations of beta hydroxybutyrate further suppress endogenous glucose production and exaggerates the development of ketosis and the negative feedback of hyperketonemia on glucose production can result in a vicious circle.
The disease manifests with an encephalopathy believed to be a hypglycemic encephalopathy resulting from hypoglycemia in the early stages of the disease.
The increase of plasma concentrations of non-esterified fatty acids results in a depression of cellular and humoral immune responses.
Renal dysfunction is also apparent in the terminal stages of ovine ketosis, and contributes to the development of clinical signs and the fatal outcome.

Clinical Findings

Separation from the group
Failure to come up for feeding in pastoral animals or standing near the trough with the group of sheep but not eating,
Altered mental state and apparent blindness
Disinclination to move.
No attempt to escape.
Presses against wall with its head.
Constipation is usual, the feces are dry and scanty and there is grinding of the teeth
In later stages, marked drowsiness develops and episodes of more severe nervous signs occur.
Episodes, tremors of the muscles of the head cause twitching of the lips, champing of the jaws and salivation, accompanied by a cog-wheel type of clonic contraction of the cervical muscles causing dorsiflexin or lateral devition of the head, followed by circling.
In the periods between convulsions there is marked drowsiness which may be accompanied by head pressing, ‘stargazing’ posture
A smell of ketones may be detectable on the breath of the ewe.
Terminally there may be a fetid diarrhea. Fetal death occurs commonly and is followed by transient recovery of the ewe, but the toxemia caused by the decomposing fetus soon causes a relapse.
Affected ewes commonly have difficulty in lambing.

Diagnosis

Based in the history and clinical signs:

Pregnancy toxemia is usually suspected in late-pregnant ewes that show nervous signs and die within 2 to 7 days. There may be a history of exertion, stress, or sudden deprivation of food. Hypocalcemia can occur under similar circumstances, but the following help in differentiation:

The onset is within 12 hours of the stress.
A considerable proportion of the flock will be affected at the same time.
There is obvious myasthenia.
It has a much shorter course, 12 to 24 hours.
Affected animals respond well to treatment with solutions of calcium salts.

Based on Clinical pathology:

Hypoglycemia, ketonemia, and ketonuria are characteristic of the disease. The initial changes are similar to ketosis in cattle but the sequel is not.

Differential Diagnosis

Listeriosis
Cerebral abscess
Acidosis
Uterine torsion or impending abortion
Rabies

Treatment

Oral electrolyte and glucose (calf scours) concentrate solution (160 mL qid) OR Oral propylene glycol (60 mL bid or 100 mL/d for 3 days).
For more intensive treatment, include: oral calcium (calcium lactate 12.5 g/d for 3 days); oral potassium (7.5 g KCl/d for 3 days); insulin 0.4 [IU/kg]/d SC for 3 days.
If hypoglycemia: Dextrose (60 to 100 mL IV)

To abort fetus in affected animal:

Ewe: Dexamethasone (20 mg IV or IM)
Doe: Dexamethasone plus prostaglandin F2 α (10 mg IM) or synthetic analog (cloprostenol; 75 g/45 kg IM)
Cesarean section if late-term fetus and valuable ewe/doe

Control

Correct the contributing factors (e.g., insufficient feed or inadequate trough space, intercurrent disease such as foot rot or foot abscess).