Volume 45 | Issue 1
Article 2
1983
Pregnancy Toxemia in the Ewe
Leanne M. Schulz
Iowa State University
Richard L. Riese
Iowa State University
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Recommended Citation
Schulz, Leanne M. and Riese, Richard L. (1983) "Pregnancy Toxemia in the Ewe," Iowa State University Veterinarian: Vol. 45: Iss. 1,
Article 2.
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Pregnancy Toxemia in the Ewe
Leanne M. Schulz·
Richard L. Riese, DVM **
INTRODUCTION
Pregnancy toxemia, also known as ovine
ketosis, lambing sickness, twin lamb disease,
or domzietke, is a widespread, usually fatal
disease of sheep. I. l.3.4. 5 The disease also occurs
occasionally in goats, and the clinical course is
very similar to that in sheep.6.7
Pregnancy toxemia occurs during late pregnancy, and although death losses in a given
flock are usually sporadic, they can exceed
13 % . I Among severely affected ewes, the
death rate often approaches 95 %. I These factors, combined with the prevalence of the
disease, make pregnancy toxemia of major
economic importance to the sheep industry.
Pregnancy toxemia is significantly different
from bovine ketosis, even though ketosis is a
major factor in both diseases and the clinical
signs are often similar. 7.8 The two major
differences are the time of onset and the response to treatment. 9 • IO Pregnancy toxemia
occurs prior to lambing, while bovine ketosis
occurs from a few days to several weeks postcalving. Pregnancy toxemia does not respond
readily to any treatment, unlike bovine
ketosis, which responds quickly to intravenous
glucose combined with the administration of
either propylene glycol orally or glucocorticoids intramuscularly.
INCIDENCE AND PREVALENCE
Although most common in ewes carrying at
least two fetuses, pregnancy toxemia can be
seen in ewes carrying a single large fetus. I.6.7
Published literature indicates that the disease
is seen during the second and subsequent pregnancies, but the authors believe that it may
• Ms. Schulz is a fourth-year student in the College of
Veterinary Medicine, Iowa State University.
•• Dr. Riese is an assistant professor in Veterinary
Clinical Sciences at Iowa State University.
Vol. 45, No. 1
also occur in ewe Iambs during their first
pregnancy. Elderly ewes often have a higher
incidence because poor teeth, parasites,
disease, and other age-related syndromes
affect their plane of nutrition and therefore
their body condition. 2
The disease occurs during late pregnancy
and is nearly always seen in ewes that are
either very thin or are overweight at this
time. 4.5.6.7.11 This indicates that a ewe in
moderate flesh during late gestation is the ideal
type not to have the disease. Also, the disease
is more common in pasture and farm flocks
than in range flocks, possibly because range
flocks receive more exercise. 4.7 Pregnancy toxemia occurs almost exclusively in the spring,
but only because nearly all ewes are bred to
lamb in the spring.4
Pregnancy toxemia occurs in all areas of the
world in which sheep are raised. 3 . 4.11 The incidence has been reported to be higher than
average in areas of New Zealand, Australia,
Britain, South Africa and the United States. 4
This may be due to differences in management
of flocks in these areas, but more likely it is
because these are the major sheep producing
areas of the world and thus the disease is more
likely to be recognized and reported in these
areas.
PATHOGENESIS
Most authors are in agreement that
pregnancy toxemia is caused primarily by a
reduced
food
intake
during
late
gestation.I.4.6.7.11 This reduced intake may occur in both thin and fat ewes that are being
malnourished. However, in fat ewes it may occur as a result of inadequate capacity of the
stomachs due to compression by body fat in
combination with a large, gravid uterus. 6 It
may also occur in both thin and fat ewes that
voluntarily reduce their food intake due to
some stress such as worming, shearing,
11
transportation, sorting or sickness. 4.6 • 12
Seventy percent of fetal growth occurs during the last six weeks of pregnancy, and this
growth causes a large demand for glucose by
fetal tissues. 13 If the ewe's energy intake is insufficient to supply the fetal demand plus her
own needs for glucose, the ewe's tissue stores of
glucose are drawn upon to meet these needs.
When these tissue stores are used up, hypoglycemia occurs, which in itself causes some central nervous system depression. Also, when
there is a hypoglycemic state present, fatty
acids begin to be mobilized from fat stores in
the body in order to meet the body's energy demands. These fatty acids are oxidized in the
liver, which produces acetyl-CoA as one of the
metabolites. Normally, acetyl-CoA is utilized
in the tricarboxylic acid cycle and forms nontoxic end-products. However, when there is a
deficiency of glucose in the body, this acetylCoA cannot be utilized in the tricarboxylic
acid cycle and is instead used in a biochemical
process that produces ketone bodies as its endproduct. The resulting ketosis leads to an
acidosis, and this ketoacidosis causes an increase in severity of clinical signs and eventually contributes to the death of the ewe. 6
CLINICAL DESCRIPTION
There are two major syndromes of the disease: the malnutrition syndrome and the stress
syndrome. 2.3 In the malnutrition syndrome,
the disease is produced because of an ongoing
lack of glucose precursors in the diet, which
results in the above events taking place. In the
stress syndrome, the ewes are maintaining a
normal glucose metabolism until some stress
such as sorting or shearing causes them to go
off feed, which reduces the availability of
glucose precursors from the diet and shifts the
ewe's metabolism to the production of ketone
bodies. 6 • 14
Clinical signs are subtle in the early stages
and may go unnoticed. Initially, affected ewes
merely seem sluggish and often lag behind the
flock when it moves. 6 • 11 Signs gradually progress over the next 2-10 days to include
anorexia, incoordination and weakness. In the
late stages, severe neurological signs such as
blindness, muscle tremors, convulsions and
coma progress and eventually cause the death
of the ewe.2.3.4.5.6.7.11
In the early stages of the disease, clinical
pathology shows a hypoglycemia, increased
plasma levels of fatty acids and glycerol, and
12
hyperketonemia. 6 There may also be
ketonuria, and plasma cortisol levels are
elevated in an attempt to increase blood
glucose levels. (One author has suggested that
this increase in plasma cortisol may be the
precipitating cause of pregnancy toxemia
rather than being a secondary change, but this
theory is not widely accepted. 15) In advanced
cases showing acidosis and concommitant
renal failure, plasma bicarbonate levels will be
low and blood urea nitrogen levels will be
elevated. 6 In terminal stages, there may be a
shift to a hyperglycemia in response to the
elevated plasma cortisol, but by this stage the
central nervous system has become unresponsive to glucose and death is usually inevitable. 6
NECROPSY
The following lesions, when found at necropsy, are strongly indicative of pregnancy
toxemia. The uterus almost always contains
two or more fetuses, although in rare cases a
single large fetus may be present. 1.2.6 These
fetuses may be found in various states of decomposition if fetal death occurred prior to
maternal death. The liver is pale, enlarged and
friable due to fatty infiltration which occurs as
the body mobilizes large quantities of fat
depots. 2.6 An analysis of fat content of the liver
may show a rise from the normal 3 % to a value
exceeding 30 % .4
Another lesion often seen, although not consistently, is adrenal gland enlargement. In
some instances, they may be greater than 65 %
larger than normal. 2.4 This enlargement of the
gland is a secondary hypertrophy that occurs
as the gland is stimulated to produce more cortisone in an attempt to raise blood glucose
levels. 4 •14 Grossi y, the adrenal cortex is dark in
color, while the medulla is lighter than
normal. 2 Other lesions that are inconsistantly
seen include pale, fatty kidneys and heart, and
distended mesenteric blood vessels. 2.6.11
None of the above lesions by itself is pathognomonic for pregnancy toxemia. However,
when seen in combinations of several or all of
the above, these findings are highly suggestive
of pregnancy toxemia, especially if the lesions
are seen in a carcass that is either emaciated or
obese.
DIAGNOSIS
Pregnancy toxemia is unique in that the
symptoms are primarily central nervous system
in origin, and that these symptoms develop onIowa State Veterinarian
ly during the last 3-6 weeks of gestation. Also,
these CNS signs are accompanied by fatty liver,
hypoglycemia and ketonuria. 4 •11 When confronted by these typical clinical signs and
laboratory findings as described above in combination with the typical post-mortem lesions,
a diagnosis of pregnancy toxemia is strongly
indicated.
The major differential diagnosis that must
be considered is hypocalcemia. 4 •6 Both diseases
show CNS signs; however, these signs are
usually more pronounced and varied with
pregnancy toxemia. In hypocalcemia, nervous
signs are usually limited to tremors and dullness
which progress to coma and death. 4 The course
of the disease is usually much shorter with hypocalcemia, death occurring within 24 hours
in untreated cases. In contrast, death may not
occur until 5-7 days after the first appearance
of clinical signs in cases of pregnancy toxemia. 6
Also, with hypocalcemia there is a rapid and
dramatic response to calcium salts administered
intravenously. This treatment is not beneficial
in cases of pregnancy toxemia. 4. 7
Other sporadically occurring diseases that
may produce nervous signs and occasionally be
confused with pregnancy toxemia include
listeriosis, rabies, cerebral abscesses, otitis
media, infestation with Coenurus cerebra/is larvae,
and louping ill. However, these diseases can
usually be differentiated by such factors as
duration and severity of clinical signs and morbidity rates in the flock. Also, many of these
diseases show characteristic gross and
histological post-mortem lesions and thus
should not normally be mistaken for pregnancy toxemia. 7.12
THERAPY
In general, treatment of pregnancy toxemia
is only moderately successful even if started in
the early stages of the disease. If treatment is
not initiated until the ewe is comatose, the mortality rate approaches 100% in spite of intensive therapy.4.6.7.16
One of the earliest treatments for pregnancy
toxemia consisted of either oral or intravenous
administration of glucose. I Although this
seems to be a very logical treatment when
faced with hypoglycemia, results were not
promising. In some trial studies, giving
intravenous glucose as the sole treatment raised the mortality rate above that for untreated
control animals. 8.17 The reasons for this are
not totally understood.
Vol. 45, No. 1
More recent treatments have included the
use of corticosteroids and/or ACTH to increase gluconeogenesis and thus increase the
blood glucose levels. I 6.l8 This treatment may
be successful in early cases, although it may
also induce parturition as a side-effect. In
severe cases, however, this treatment is often
unsuccessful. In fact, it may be of no benefit at
all since many advanced cases show elevated
endogenous steroid levels prior to treatment as
a natural physiological response that occurs in
an attempt to reverse hypoglycemia. 2
Another treatment, used with some success
in early cases of pregnancy toxemia, is oral
dosing with glycerol or propylene glycol, both
of which are glucogenic substances. A suggested dosage is 200 ml of 50% glycerol solution twice daily until the appetite returns to
normal. 6 This can be fairly effective if the
disease has been detected in the early stages
before it has progressed to total anorexia and
recumbancy. Because of this relative efficacy
in early cases and because of the relative ease
of administration by the layman, this is considered by many to be the treatment of
choice. 3 •6
Insulin has also been suggested as a treatment, either alone or in conjunction with
glucose therapy, to aid in the utilization of any
available glucose.6.7.8.17 Some early studies
seemed to show favorable results, especially
with the insulin-glucose combination, but this
treatment has since fallen into disfavor and is
rarely used at present. 17.10
In recent years, work has been done in the
use of anabolic steroids, in particular trenbolone acetate, as another treatment for
pregnancy toxemia. These products cause
marked appetite stimulation which may be
sufficient to reverse the disease in those cases
precipitated by a period of anorexia. There is
also some evidence which indicates that trenbolone acetate may be useful in causing reversal of signs even in moderately severe cases
that have progressed to the stage of
recumbancy.19 There is more work to be done
in this area, but these preliminary findings appear promising.
A final treatment that is used with some success is inducing parturition either chemically
or by surgical intervention. 20 This often produces good results in moderate cases, because
once the fetal drain on maternal glucose is
gone, the ewe easily returns to a normal state
of glucose metabolism and will recover com-
13
pletely, provided irreversible nervous system
lesions have not already occurred. 12 This treatment is restricted to use within 1 week of the
expected lambing date, unless the production
of a viable lamb is inconsequential. The
pregnancy may need to be terminated at any
time in the course of the disease in order to
save the dam. Chemical intervention is
simpler and easier than surgical intervention,
and parturition can usually be accomplished
by a single intramuscular dose of 10-15 mg of
dexamethasone or 15 mg of ECP.
A major reason that none of these
treatments is successful in severe, advanced
cases of pregnancy toxemia is that the changes
in the brain, although precipitated by
hypoglycemia, become unresponsive to
glucose and thus irreversible in the later
stages. 14 Consequently, treatments aimed at
restoring normal blood glucose levels may be
successful in doing this and still be unsuccessful in reversing the changes that have occurred within the nervous system.
PREVENTION
Since treatment of pregnancy toxemia is
often unrewarding, prevention of the disease is
v.ery important. If the majority of ewes are thin
in late gestation, the best and easiest way to
prevent pregnancy toxemia is to insure that
these ewes are on a rising plane of nutrition
during late pregnancy. 6 In those cases where
the ewe is overweight at breeding or in midgestation, she should be placed on a reducing
diet to get her into moderate condition by late
gestation, at which time she can be placed on
the same rising plane of nutrition as the thin
ewe. During the last 6 weeks of gestation, the
ewe should be fed hay supplemented with
grain as needed to insure good nutrition. Also,
avoid any sudden changes in feed which may
cause the ewe to become anorectic long enough
to precipitate the disease. 5 . 11
Since it is often difficult to assess a ewe's condition simply by looking at her, it is often
helpful to utilize condition scoring to determine her status. 13 Under this program, the
prominence of the lumbar spinous and
transverse processes and the amount of rib-eye
muscle and fat cover between the two lumbar
processes are determined, and the animal is
given a score from 0-5 based on these determinations. A score of 0 indicates severe
emaciation, while a score of 5 indicates obesity. In general, a ewe in late gestation should
14
have a condition score between 2 and 3.
Other factors that are important in preventing pregnancy toxemia are prevention of
stress in all ewes and insuring adequate exercise in well-fed ewes to prevent obesity, since
both stress and overweight may reduce voluntary feed consumption and thus precipitate the
disease. 3 •4 • 14 Also, concurrent disease states
should be eliminated, and old ewes with bad
teeth should be culled from the flock. 2 •6
CONCLUSION
Pregnancy toxemia is an important disease
in major sheep-producing areas. It contributes
to economic loss both through death of affected
ewes and their offspring and through substandard performance in ewes that survive the
disease. The condition is difficult to treat successfully in the early stages and becomes nearly impossible to treat in the late stages, which
makes prevention a very important consideration. The producer must be informed how to
properly manage his flock during gestation.
With proper management, the incidence of the
disease will approach zero and it will cease to
be an economically important entity in sheep.
REFERENCES
1. Bourne RF; The Physiology of Disease III. Pregnancy Disease in Ewes. N Am Vet 31:157-160, 1950.
2. Bruere AN; Pregnancy Toxemia, in Morrow DA
(ed); Current Therapy in Theriogenology. Philadelphia,
WB Saunders Co, 1980, pp. 903-907.
3. Pregnancy Toxemia, in Cole VG (ed); Diseases oj
Sheep. Sydney, Grazcos Cooperative Ltd, 1966, pp.
202-206.
4. Pregnancy Toxemia, in Jensen R, Swift BL (eds);
Diseases <if Sheep 2nd cd. Philadelphia, Lea and
Fcbiger, 1982, pp. 19-20.
5. Reid RL: The Physiopathology of Undernourishment in Pregnant Sheep, With Particular Reference
to Pregnancy Toxemia. Ado Vet Sci 12; 163-238, 1968.
6. Caple IW, McLean JG; Pregnancy Toxemia, in
Howard JL (ed); Current Veterinary Therapy, Food
Animal Practice. Philadelphia, WB Saunders Co, 1981,
pp. 348-352.
7. Blood DC, Henderson JA, Radostits OM (cds);
Ketosis of Ruminants (Acetonaemia of Cattle,
Pregnancy Toxaemia of Sheep), in Vetm'nary Medicine
5th cd. Philadelphia, Lea and Febiger, 1979, pp.
849-857.
8. Kronfeld DS; Ketosis in Pregnant Shecp and Lactating Cows. A Review. Aust Vet J 48:680-687, 1972.
9. Ketosis in Cattle, in The Merck Veterinary Manual, 5th
cd. Rahway NJ, Merck and Co Inc, 1979, pp.
508-511.
10. Pregnancy Toxemia in Ewes, in The Merck Veterinary
Manual, 5th ed. Rahway NJ, Merck and Co Inc,
1979, pp. 512-513.
11. Marsh H (ed); Pregnancy Disease, in Newsom's Sheep
Diseases, 3rd ed. Baltimore, Williams and Wilkins Co,
1965, pp. 294-297.
12. O'Ncill AR; Pregnancy Toxemia and Its Treatment.
Irish Vet J 19(2):21-25, 1965, abst in Smithcors JF,
Catcott EJ (cds); Progress in Cattle and Sheep Practice,
Iowa State Veterinarian
Ifl.
14.
15.
16.
vol. 2 (Part 2). Santa Barbara, American Veterinary
Publications Inc, 1974, pp. 3IB-319.
Russel AJF: The Nutrition of the Pregnant Ewe, in
The Management and Diseases of Sheep. London, The
British Council, 1979. pp. 221-240.
Reid RL: Pregnancy Toxaemia in Ewes. Ag Rev, London 4(2):20-25, 195B.
McDonald LE: Veterinary Endocrinology and Reproduction, 3rd cd. Philadelphia, Lea and Febigcr, 19BO, p.
192.
Holm LW: Studies on the Treatment of Ovine
Pregnancy Toxemia With Corticosteroids and
ACTH. Cornell Vet 4B:34B-357. 195B.
17. Thomson GG: Observations On Some Treatments of
Ovine Pregnancy Toxaemia. New Zealand Vet J
4:136-144, 1956.
18. Hazzard TC, Russell AM: Treatment of Pregnancy
Toxemia In Sheep. Vet Rec 80:359-360, 1968.
19. Heitzman RJ. Herriman ID, Austin AR: The
Response of Sheep With Pregnancy Toxemia to
Trenbolone Acetate. Vet Rec 100:317-3IB, 1977.
20. Hunt ER: Treatment of Pregnancy Toxaemia in
Ewes By Induction of Parturition. Aust Vet J
52:33B-339, 1976.
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