2018 SCIENCELINE  
Journal of Life Science and Biomedicine  
J Life Sci Biomed, 8 (4): 69-76, 2018  
ISSN 2251-9939  
Causes, Control and Prevention Methods of  
Pregnancy Toxemia in Ewe: A Review  
Ashenafi Kelay and Aschalew Assefa  
University of Gondar; College of Veterinary Medicine and Animal Sciences; Department of Animal Production and Extension, Gondar, Ethiopia P. O. Box 196  
Corresponding author’s Email: ashu.eth2006@gmail.com  
ABSTRACT  
Original Article  
PII: S225199391800011-8  
Pregnancy toxemia, also known as ovine ketosis, twin-lamb disease or gestational toxemia is a  
metabolic disease affecting pregnant ewes. The objective of this review is to highlight possible  
causes and predisposing conditions of pregnancy toxemia in ewe and to indicate successful  
control and prevention methods of the disease. English articles published from 1983 to date  
Rec. 04 May 2018  
Acc. 24 June 2018  
was searched with Google using toxemia, pregnancy, ewe, treatment, prevention, ketosis and  
diagnosis as key terms. The increased requirement for energy during pregnancy,  
accompanied by inadequate nutrition to meet metabolic requirement is the underlying cause  
of the disease. This negative energy balance initiates the onset of excessive lipid metabolism  
and ketosis, and eventually causes hepatic lipidosis. An excess of ketone bodies can occur in  
both poor and good conditioned sheep and in fact, excessively fat ewes can be more prone to  
pregnancy toxemia. Moreover, conditions that interrupt feed intake, such as storms, hauling  
or other diseases can also induce this metabolic disease. Affected sheep exhibit weakness and  
depression, usually within the last six weeks of pregnancy. It has seen more often in older  
ewes and those carrying multiple fetuses. Pregnancy toxemia is almost never observed in  
replacement ewe-lambs or yearlings lambing for the first time. If untreated, the disease  
progresses, causing neurological signs and eventually death. Therefore, Understanding the  
causes, pathogenesis, prevention and treatment of this disease is important in preventing  
production loss in sheep farming operations.  
Pub. 25 July 2018  
Keywords  
Beta-hydroxybutyrate,  
Ewe,  
Ketosis,  
Pregnancy Toxemia  
INTRODUCTION  
Among domestic farm animals metabolic diseases achieve the greatest importance in dairy cows, pregnant does  
and ewes. In other species these disease occur only sporadically. If the continued nutritional demand of  
pregnancy is exacerbated by an inadequate diet in the dry period, the incidence of metabolic disease increases.  
The effect of pregnancy is particularly important in ewes, especially those caring more than one lamb [1].  
Pregnancy toxemia, also known as ketosis, is the most commonly occurring metabolic disease of sheep and  
goats that occurs in late pregnancy. It commonly occurs in the last 6 weeks of gestation which causes  
significant economic losses and high mortality rate in pregnant ewes. It is most prevalent in ewes carrying two  
or more lambs or in very fat ewes. Ketosis is caused by a disturbance in carbohydrate usage in the animal [2]. As  
ewe’s pregnancy progresses, the energy demands of her body increase. At the same time, the capacity of her  
rumen shrinks since her growing lambs in the uterus take up more and more space inside leaving less space for  
the rumen [2, 3]. This combination can result in the ewe not receiving sufficient energy, through her diet. As a  
result she will have to resort to breaking down her own body tissues, usually fat, in order to provide energy for  
her growing lambs, thus releasing ketones (a toxic byproduct of fat breakdown) into her bloodstream. When  
this occurs too rapidly, the ewe’s body cannot detoxify the ketones fast enough and ketosis or pregnancy  
toxemia results. Ketosis can also occur when the ewe is too fat since fat also takes up room inside of the sheep  
resulting in less space for the rumen to hold feed. Additionally, conditions that interrupt feed intake, such as  
storms, hauling or other diseases, can also induce this metabolic disease [4].  
Kelay A and Assef A. 2017. Causes, Control and Prevention Methods of Pregnancy Toxemia in Ewe: A Review. J. Life Sci. Biomed. 8(4): 69-76;  
www.jlsb.science-line.com  
Ewes with ketosis are lethargic and have a poor appetite for the last 1 to 2 weeks of pregnancy. They also  
tend to have poor muscle control and balance. A classic symptom is sweet-smelling (ketotic) breath. Sheep may  
also grind their teeth. As the disease progresses, the neurological systems become compromised due to lack of  
glucose. Hence, encephalopathy results from depressed glucose metabolism in the brain [5]. Blindness,  
stargazing, tremors, aimless walking and ataxia are seen and eventually the ewes become comatose and are  
unable to rise. Death usually follows within a few days [6].  
The determination of blood glucose and beta hydroxyl butyric acid (BHBA) concentrations is very  
important for early diagnosis [7]. If pregnancy toxemia is diagnosed in the early stages, medical treatment can  
be successful [5, 6]. But the treatment of advanced pregnancy toxemia is usually unsuccessful [8]. In general  
Pregnancy toxemia, once develop result in stop eating, nervous sign, blindness, and eventually death so  
reviewing Pregnancy Toxemia in ewe important to know and avoid the predisposing condition, to prevent and  
control the disease occurrence besides to prevent production losses. The objective of this review is therefore to  
highlight possible causes, predisposing conditions of pregnancy toxemia successful control and prevention  
methods of pregnancy toxemia in ewe.  
METHODS  
A systematic review of English articles published from 1983 to date was conducted using Google. All  
articles related to the topic was also included without any preference to types of journals and publishers.  
Search terms included were toxemia, pregnancy, Sheep, ewe, treatment, prevention, ketosis and diagnosis.  
RESULTS AND DISCUSSION  
Etiology  
The cause of pregnancy toxemia is a metabolic disturbance of Carbohydrate or sugar and fats during the  
final stage of pregnancy [9]. This disturbance is caused by low glucose concentration in the blood and excessive  
breakdown of body fat to compensate glucose deficiency. Ketones are the toxic by-products produced during  
this rapid breakdown of fat and it is possible to test for their presence in the ewe's urine. Inadequate nutrition  
during the last 6 weeks of pregnancy is the primary cause of low blood sugar as ewes cannot consume enough  
feed or energy to meet the demands of their growing fetuses. This is because approximately 70% of fetal growth  
occurs during the last 6 weeks of pregnancy [10].  
Over-conditioned (BCS 4 or more) ewes are also susceptible to pregnancy toxemia because of fat in their  
abdominal region. In such fat ewes there isn't enough room in the gut for the ewes to eat sufficiently and there  
is an excessive fat resource for breakdown resulting in ketosis. Under-conditioned (BCS 2 or less) ewes are also  
susceptible because they cannot eat enough to meet their own nutritional needs, let alone the added burden of  
developing fetuses [4].  
Epidemiology  
Occurrence. It occurs in all parts of the world. With the drive to increase lambing percentages and  
margins dependent on feed costs, particularly in intensively farmed lowland flocks, the problem has become  
widespread. The disease is rarely seen under extensive production systems [5]. In part, this is because the  
breeds of sheep used in intensive farming are more likely to bear twins or triplets. Since the disease most often  
affects ewes/does pregnant with twins or triplets, it is characterized by low blood sugar. In contrast, sheep  
breeds in extensive grazing systems commonly bear single lambs and significant outbreaks of pregnancy  
toxemia are uncommon except where there is drought or poor pasture management. In general, the incidence  
of pregnancy toxemia is greater in ewes with more than one fetus during the last 6 weeks of gestation [1].  
Many farmers will be faced with a few cases annually, but in certain years up to 40% of ewes in a flock may  
be affected [5]. Death occurs in 2-10 days in about 80% of the cases. The incidence in a flock varies with the  
nature and severity of the nutritional deprivation and the proportion of the flock at risk. It can be very high in  
starvation Pregnancy toxemia, whereas fat ewe pregnancy toxemia is generally of sporadic occurrence. In  
outbreaks that follow management procedures or other stressors, clinical disease is not manifested until 48  
hours and afterwards new cases will develop over several days. The natural incidence in intensively farmed  
sheep is approximately 2% of pregnant ewes but where there are sever managemental deficiencies of the  
Kelay A and Assef A. 2017. Causes, Control and Prevention Methods of Pregnancy Toxemia in Ewe: A Review. J. Life Sci. Biomed. 8(4): 69-76;  
www.jlsb.science-line.com  
disease, it may affect the majority of late pregnant ewes. The case fatality is high unless treatment is initiated  
early in the clinical course. It causes 100% ewe mortality and High neonatal mortality in untreated case. Even  
with early treatment case fatality can be high [1].  
Risk factors  
Pregnancy. The primary predisposing cause of pregnancy toxemia is inadequate nutrition during late  
gestation, usually due to insufficient energy density of the ration and decreased rumen capacity as a result of  
fetal growth. 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. This is because in the last 6 weeks of gestation the  
requirement of metabolizable energy rises dramatically. It occurs primarily in ewes carrying twin lambs  
because twin pregnancy increases susceptibility of ewes to hypoglycemic stress and Pregnancy toxemia. For  
example, ewes carrying twins require 1.9 times more energy than ewes with singles and ewes with triple fetuses  
require 2.3 times more energy than ewes with singles [11]. Pregnancy toxemia may also affect ewes bearing a  
single large lamb [12].  
Body condition. Poor body condition, old age, obesity and low body weight are other predisposing factors  
for the onset of the disease. During late gestation, in the presence of obesity, the abdominal space is filled with  
accumulated fat and an expanding uterus. Because of lack of rumen space, these females have difficulty in  
consuming enough feedstuff to satisfy their energy requirements [13]. Ewes with poor body condition also  
cannot eat enough to meet their own nutritional needs and the energy requirement of their fetuses [4]. This is  
because susceptible thin ewes are chronically offered with inadequate ration, and in the face of increasingly  
insufficient energy to meet increasing fetal demands, the ewe mobilizes more body fat with resultant ketone  
body production and hepatic lipidosis [11].  
Diseases. Presence of other diseases like; foot rot, foot abscess and parasites can also influence the onset of  
pregnancy toxemia. Because such conditions acutely curtail feed intake [14] so that the animal becomes in  
negative energy balance.  
Environmental stress. Environmental stressors such as cold weather and rain increase the energy  
demand of the pregnant ewe so that induces stress (acute) syndrome [15]. Transportation, shearing, crutching  
or drenching also cause stress and may contribute to the onset of the disease.  
Parity. Clinical cases are typically limited to older goats and ewes during their second or subsequent  
pregnancies. The disease is uncommon in maiden ewes because of their low fecundity and increases in  
prevalence up to parity three [10].  
Breed. In sheep and goats, pregnancy toxemia is much more common in highly prolific selected breeds [16].  
Breed differences largely reflect differences in fecundity and differences in management systems. For instance,  
the disease is more common in British lowland breeds and their crosses than the Merino. On the other hand,  
British hill breeds are traditionally believed to be more resistant to the development of pregnancy toxemia in  
the face of nutritional deprivation of the ewe but resistance is achieved at the expense of lamb birth weight and  
has the penalty of higher neonatal mortality. There are however, differences in the susceptibility of individual  
sheep that appears to be related to differences in rates of hepatic gluconeogenesis [1].  
Pathology  
Pathogenesis. In late gestation, the liver increases gluconeogenesis to facilitate glucose availability to the  
fetuses. Each fetus requires 30–40 g of glucose/day in late gestation, which represents a significant percentage  
of the ewe's glucose production and which is preferentially directed to supporting the fetuses rather than the  
ewe. This is because approximately 70% of fetal growth takes place in the last 6 weeks of pregnancy.  
Mobilization of fat stores is increased in late gestation as a method of assuring adequate energy in the face of  
increased demands of the developing fetuses and impending lactation. However, in a negative energy balance,  
this increased mobilization may overwhelm the liver's capacity and result in hepatic lipidosis with subsequent  
impairment of function [11]. Ewes with hepatic lipidosis have an ineffective gluconeogenic response to the  
continued, preferential demands for glucose by the growing fetuses resulting in hypoglycemia, more lipid  
mobilization and accumulation of ketone bodies and cortisol. 80% of ewes have a high plasma cortisol  
concentration. This could be the consequence of increased adrenal output or reduced excretion by the liver [17].  
The reason for this predisposition is not known. Twin bearing ewes appear to have more difficulty in producing  
glucose and clearing ketone bodies, thus increasing their susceptibility to pregnancy toxemia. The subsequent  
disease and metabolic changes are associated with excessive lipid mobilization [8, 10].  
Kelay A and Assef A. 2017. Causes, Control and Prevention Methods of Pregnancy Toxemia in Ewe: A Review. J. Life Sci. Biomed. 8(4): 69-76;  
www.jlsb.science-line.com  
In late gestation, the liver increases gluconeogenesis to facilitate glucose availability to the fetuses. Each fetus  
requires 30–40 g of glucose/day in late gestation, which represents a significant percentage of the ewe's  
glucose production and which is preferentially directed to supporting the fetuses rather than the ewe. This is  
because approximately 70% of fetal growth takes place in the last 6 weeks of pregnancy. Mobilization of fat  
stores is increased in late gestation as a method of assuring adequate energy in the face of increased demands  
of the developing fetuses and impending lactation. However, in a negative energy balance, this increased  
mobilization may overwhelm the liver's capacity and result in hepatic lipidosis with subsequent impairment of  
function [11]. Ewes with hepatic lipidosis have an ineffective gluconeogenic response to the continued,  
preferential demands for glucose by the growing fetuses resulting in hypoglycemia, more lipid mobilization and  
accumulation of ketone bodies and cortisol. 80% of ewes have a high plasma cortisol concentration. This could  
be the consequence of increased adrenal output or reduced excretion by the liver [17]. The reason for this  
predisposition is not known. Twin bearing ewes appear to have more difficulty in producing glucose and  
clearing ketone bodies, thus increasing their susceptibility to pregnancy toxemia. The subsequent disease and  
metabolic changes are associated with excessive lipid mobilization [8, 10].  
According to Sargison [6], Ketone bodies (BHBA and acetoacetate) are strong acids and their accumulation  
in the blood leads to metabolic acidosis. Schlumbohm and Harmeyer [18] revealed that high BHBA impairs  
glucose metabolism. This further suppresses endogenous glucose production and exaggerates the development  
of ketosis. Since hyperketonemia exerts several adverse effects, e.g. on energy balance and glucose metabolism  
it appears that the impairment of ketone bodies disposal in late pregnancy facilitates development of Pregnancy  
toxemia, especially in ewes carrying twins [19].  
The disease manifests with an encephalopathy, believed to be a hypoglycemic encephalopathy resulting  
from hypoglycemia in the early stages of the disease. The encephalopathy and the disease are frequently not  
reversible unless treated in the early stages. The onset of clinical signs is always preceded by hypoglycemia and  
hyperketonemia, although the onset of signs is not related to minimum blood glucose or maximum ketone  
levels [20].  
Lesions  
Pale, swollen and friable fatty liver and enlarged adrenal glands are common findings. In addition, the  
uterus of the affected ewe usually has more than one fetus [21]. If fetuses are in a state of decomposition it  
indicates premortem death. Very thin ewes may appear starved with serous atrophy of the kidney and heart fat  
[11].  
Clinical findings  
The earliest signs of pregnancy toxemia are 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 in housed animals, altered  
mental state and apparent blindness, which is manifested by an alert bearing but a disinclination to move. They  
also lie down, become sluggish and show a loss of appetite. Affected ewes walk unsteadily, appear dull and they  
show little fear of humans or dogs. Blindness often results and eventually there can be convulsions, grinding of  
the teeth and labored respiration. If it is forced to move, it blunders into objects and when an obstacle is  
encountered, presses against it with its head. Many affected ewes stand in water troughs all day and lap the  
water [1].  
In later stages, marked drowsiness develops and episodes of more severe nervous signs occur but they may  
be infrequent and are easily missed. In these episodes, tremors of the muscles of the head cause twitching of the  
lips, champing of the jaws and salivation. These are accompanied by a cog-wheel type of clonic contraction of  
the cervical muscles causing dorsoflexion or lateral deviation of the head, followed by circling. The muscle  
tremor usually spreads to involve the whole body and the ewe falls with convulsions. The ewe lies quietly after  
each convulsion and rises normally afterwards but is still blind. In the periods between convulsions there is  
marked drowsiness which may be accompanied by head pressing, the assumption of abnormal postures  
including unusual positions of the limbs and elevation of the chin - the 'stargazing' posture - and in  
coordination and falling when attempting to walk. A smell of ketones may be detectable on the breath of the  
ewe. Affected ewes usually become recumbent in 3-4 days and remain in a state of profound depression or coma  
for a further 3-4 days. Most cases develop 1-3 weeks before lambing. Onset earlier than day 140 of gestation is  
associated with more severe disease and increased risk of mortality [11].  
Kelay A and Assef A. 2017. Causes, Control and Prevention Methods of Pregnancy Toxemia in Ewe: A Review. J. Life Sci. Biomed. 8(4): 69-76;  
www.jlsb.science-line.com  
Diagnosis  
The diagnosis of pregnancy toxemia is based on history and clinical findings but confirmatory diagnosis  
requires blood analysis [22]. Laboratory findings in individual ewes may include hypoglycemia, elevated urine  
ketone levels, elevated BHBA levels and frequently hypocalcaemia and hyperkalemia due to severe ketoacidosis.  
Low blood glucose level indicates pregnancy toxemia as well as CSF glucose level [20]. However, hypoglycemia  
is not a consistent finding. With up to 40% of cases having normal glucose levels while up to 20% having  
hyperglycemia. These gave rise to the idea that hypoglycemia might indicate that the fetuses are alive and  
hyperglycemia that the fetuses are dead. Wastney et al. [22] suggested that the hyperglycemia occurs because  
fetal death removes the suppressing effect of the fetus on hepatic gluconeogenesis [16], referred to the existence  
of a marked hyperglycemia in terminal cases. If the diagnosis needs further confirmation, BHBA is a more  
reliable indicator of disease severity than blood glucose levels. Non esterified fatty acids can also be elevated,  
indicating likely hepatic lipidosis resulting in impaired hepatic function [2, 8].  
For an accurate diagnosis, a differential diagnosis is important to determine pregnancy toxemia from  
other disorders with similar signs such as hypocalcaemia or hypomagnesaemia. These can be differentiated  
based on clinical and laboratory findings. Typical signs and indications that differentiate pregnancy toxemia  
from hypocalcaemia includes: in pregnancy toxemia there is slow progression of the disease with death after 5-  
7 days where as in hypocalcaemia there is rapid progression of the disease with death after 6-24 hours.  
Elevation of the chin ('star-gazing') with slow progression to recumbence over 2-3 days after onset of initial  
signs is seen in pregnancy toxemia but during hypocalcaemia rapid progression to recumbence over 3-4 hours  
and sternal recumbence with the head stretched out and chin on the ground with legs folded beneath or  
stretched out behind the ewe is usual. In post-mortem examination liver is yellowish with a fine mottled  
appearance characteristic of pregnancy toxemia but there are usually no significant and characteristic  
observable post mortem findings in hypocalcaemia. In response to treatment in pregnancy toxemia, there is no  
response to dose rates of hypocalcaemia treatment with commercial calcium solutions. Usually poor and slow  
response to doses of glucose or energy with best responses seen if treated whilst ewes are still alert.  
Treatment  
Successful treatment of pregnancy toxemia requires early detection and steps to quickly meet the energy  
(glucose) needs of the affected ewe. Therapy requires the correction of fluid, electrolytes and acid-base  
disturbances in addition to replacement therapy with glucose. Oral propylene glycol or corn syrup are quick  
sources of energy and should be given at the rate of 200 ml four times daily along with 3-4 liters of  
concentrated oral rehydration fluid [23]. Ewe treated very early in the course of the disease generally responds  
favorably, but response to therapy is poor once ewe has become recumbent. So if the ewe is already comatose,  
treatment should focus on the rest of the flock [11].  
Parenteral therapy  
Therapy with glucose should be accompanied by the IV injection of isotonic sodium bicarbonate or lactated  
Ringer's solution and the administration of further fluids by a stomach tube. Treatment with recombinant  
bovine somatotrophin (0.15 mg/kg body weight) in conjunction with dextrose and electrolytes may result in a  
shorter duration of treatment, improves ewe survival and results in a greater viability of lambs born but  
reported results are not impressive [24].  
Oral therapy  
Propylene glycol or glycerin (110 gram per day) given by mouth is used to support parenteral glucose  
therapy. Success is reported with the oral drenching, every 4-8 hours, of 160 ml of a solution containing 45 g  
glucose, 8.5 g sodium chloride, 6.17 g glycine and electrolytes, which is available commercially as a concentrated  
oral rehydration solution. Reported recovery rates are 90% in early cases and 55% in advanced cases [23].  
Treatment with insulin in addition to treatment with oral glucose precursors and electrolytes shows a  
significantly higher survival rate (87%) compared with treatment with oral glucose precursors and electrolytes  
alone [25].  
Caesarean section  
In advanced cases, a Caesarean section (C-section) may need to be performed to remove fetuses and save  
the ewe's life. Once animals become recumbent and refuse to get up, medical treatment is usually unrewarding  
Kelay A and Assef A. 2017. Causes, Control and Prevention Methods of Pregnancy Toxemia in Ewe: A Review. J. Life Sci. Biomed. 8(4): 69-76;  
www.jlsb.science-line.com  
and a C-section is recommended to immediately remove the negative energy drain of fetuses from the mother  
[26]. It can be used as an alternative to replacement therapy. If ewes are in the early stages of the disease,  
removal of the lambs by C-section has the greatest success rate where the demand for glucose by the lambs is  
immediately removed and both the ewe and the lambs have a high chance of survival provided the C-section is  
conducted before there is irreversible brain damage in the ewe and the lambs are close to term. If the ewe is in  
the recumbent stage, then her chance of survival is low. C-section can still offer the chance of survival for lambs  
but also less viable at this stage and may be dead. Induction of parturition with prostaglandin F2is a further  
option but should only be used if the ewe is in the early stage of the disease as lambs will be delivered no earlier  
than 36 hours after therapy and often later. If the ewe is judged unlikely to survive this period, C-section is a  
better option [1].  
Control and prevention  
Control. When clinical cases occur, the rest of the flock should be examined daily for any evidence of  
ketosis and affected ewes should be treated immediately with propylene glycol or glycerol or oral  
glucose/glycine/ electrolyte solutions. Supplementary feeding of the flock should be commenced immediately  
with particular attention given to an increase in carbohydrate intake. Cereal grain starting at 0.5 Ib/head per  
day and increasing to 2 lb/head per day (0.25-1kg/head per day) for large frame breeds is recommended [27].  
Prevention. Prevention of pregnancy toxemia involves three managemental goals. Adequate nutrition  
should be provided during the final weeks of pregnancy, there should be ample room for exercise and control of  
other conditions that might result in reduced feed intake or increase energy demand such as foot rot or  
parasitism [28]. Prevention can be readily achieved by nutritional means and is far more rewarding than  
therapy. Ewes must be fed in relation to their changing energy needs throughout the reproductive cycle [8].  
Thus, ewes should not enter the last 6 weeks of gestation with a BCS less than 2.5. This can be prevented by  
good feeding management and ration formulation [11]. One major factor in the nutrition of the pregnant ewe is  
that of the unborn lamb. The gestation period in sheep is short as compared to many other animals and the fetal  
demand for nutrients and glucose is at its greatest during the last 2 months of pregnancy. In fact, about 70 % of  
the growth of the fetus occurs during the last 6 weeks of pregnancy; if twins are present, the increase in total  
weight is considerable. The total metabolic rate increases by at least 50 percent during late pregnancy. It has  
been shown that late pregnant ewes require about 50 % more feed if bearing a single lamb and about 75 % more  
feed if carrying twins. The increased amount of feed, however, sometimes exceeds the sheep’s digestive capacity  
unless grain is substituted for part of the hay. Multiple fetuses will tend to crowd the animals digestive system  
and hence limiting intake, this is where concentrates can help. During the last 6 wk of gestation, grain is  
required as a source of carbohydrates in the ration to maintain the health of multiple-bearing ewes. Amount  
varies depending on forage quality, adult body weight, condition score and number of fetuses [11].  
Maiden ewes should feed as a separate group in order to provide the requirement for growth in addition to  
the requirement for pregnancy. Attention should also be given to broken-mouthed ewes to ensure that they are  
maintaining an adequate body condition. Sudden changes in type of feed should be avoided and extra feed  
should be provided during bad weather. Shelter sheds should be available and in purely pastoral areas, lambing  
should not be planned before the pasture is well grown. A high incidence is often encountered in small, well-fed  
flocks where the ewes get insufficient exercise. In such circumstances the ewes should be walked 30 minutes  
daily and, if pasture is available, only concentrate should be fed so that they will be encouraged to forage for  
themselves [1].  
CONCLUSION AND RECOMENDATION  
The principal cause of pregnancy toxemia is low blood sugar (glucose) in relation with high energy demand  
of the fetus especially occurs in pregnant ewes carrying twins. Onset of the disease is often triggered by one of  
several types of stress including nutritional or inclement weather. The disease is most prevalent in ewes  
carrying two or more lambs. The disease also affects ewes that are extremely fat or excessively thin. Diagnosis  
of the disease is based on clinical sign, history, and clinical tests of low glucose, high ketones, and necropsy  
findings. Successful treatment of pregnancy toxemia requires early detection and quick replacement therapy  
with glucose. Therefore; it can be recommended to feed high energy concentrates and grains during the last  
month of pregnancy and follow proper management to minimize and avoid farm losses.  
Kelay A and Assef A. 2017. Causes, Control and Prevention Methods of Pregnancy Toxemia in Ewe: A Review. J. Life Sci. Biomed. 8(4): 69-76;  
www.jlsb.science-line.com  
DECLARATIONS  
Acknowledgements  
This work was supported by the University of Gondar, college of veterinary medicine and animal sciences.  
Authors’ Contributions  
A. Kelay participated in the planning, collecting the required articles for review and execution of the  
review as a leader. A. Assefa participated in the critically revision of the manuscript for important intellectual  
contents and all authors of this review paper have read and approved the final version submitted.  
Competing interests  
The authors declare that they have no competing interests.  
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