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Pregnancy Care & Concerns

Gestational Toxemia in Sheep
By Pastor, J.; Loste, A.; Sáez, T.
Jul 3, 2003, 9:28pm

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Gestational toxemia in sheep


 

Pastor, J.; Loste, A.; Sáez, T.

Departamento de Patología Animal (Patología General, Médica y de la Nutrición). Facultad de Veterinaria. Universidad de Zaragoza

Study published in Pequeños Rumiantes, December 2001, Vol. 2, No. 3, pp.: 18-24.

Photo 1. Pregnant and overweight sheep. Photograph facilitated by Luis Miguel Ferrer.

 

INTRODUCTION

Gestational toxemia is a metabolic disorder characterized by hypoglycemia and hyperketonemia as a result of the incapacity of the animal to maintain an adequate energy balance. The clinical picture comprises neurological manifestations and weakness. In general, the problem develops in the last third of pregnancy, with a greater incidence in animals presenting two or more fetuses — though it can also be observed in poorly nourished sheep with only a single fetus (Hay and Baird, 1991; Prieto, 1994). Specifically, toxemia appears in the last six weeks of pregnancy when the fetuses have reached 2/3 or _ of their prenatal development.

PATHOGENESIS

The determining cause of toxemia is an alteration in energy metabolism, as a consequence of an imbalance between glucose offer and demand — thereby giving rise to a negative energy balance. This imbalance is caused by a reduction in energy supply due to poor or inadequate nutrition, deficient food absorption, or an incorrect metabolic use of the food ingested. To this must be added the increasing requirements of the fetus in its last prepartal growth phase and the pressure of the gravid uterus upon the digestive organs within the abdominal cavity (rumen, liver, etc.)(Hay and Baird, 1991; Van Saun, 2000).

The consumption of low energy levels, or poor utilization of the available energy supply gives rise to a gradual reduction in blood glucose levels, with depletion of the liver glycogen reserves and mobilization of the fatty deposits for use as an energy source — with the resulting formation of ketone bodies (Radostits et al., 1994).

Figure 3: Mass of hemorrhagic appearance seen on exposing the neck.

The following predisposing conditions may be mentioned:

1.- Quantitative nutritional factors (a scarcity or absence of food at the end of the gestational period) and qualitative nutritional aspects (imbalanced fodder rations, poorly preserved foodstuff, a lack of cyanocobalamin, biotin, etc.)(Prieto, 1994; González and Rejas, 1995).

In this context, it has been seen that an increase in fermentable fiber in the diet improves development of the animals, since it reduces the ruminal acidosis produced by excess starch fermentation. However, such fermentation is necessary for producing propionate. Consequently, in order to prevent the development of gestational toxemia in sheep, it is advisable for the diet supplied at the end of pregnancy to contain sufficient grain cereal. The use of subproducts which reduce the cost of fodder, generate an increase in fermentable neutrodetergent fiber (NDF) and a reduction in non-structural carbohydrates (NSC). The bacteria in turn ferment the NSC, giving rise to acetate and butyrate, which are used by the sheep as an energy source — though no net contribution to glucose production is made as a result (Van Saun, 2000).

Thus, it is essential to control the diet administered to the sheep, particularly in the later phases of pregnancy, with special emphasis on the provision of glucose precursors, fiber and energy availability (Van Saun, 2000).

Likewise, mention can be made in this section of animal handling practices. In this sense, the overfeeding of sheep in the first months of gestation leads to an excess accumulation of fat, which in the later stages of pregnancy will cause the ewe to voluntarily reduce food intake, due to a reduction in ruminal capacity secondary to the increased presence of intraabdominal fat, and the enlarged gravid uterus (Photo 1). Paradoxically, the change of sheep from good pastures to a stabling regimen, with nutritional supplements of improved quality, can trigger the disorder as a result of temporary loss of appetite among the animals.

Figure 4: Appearance of the livestock. Loss of wool in sheep and birth of weak animals.

2.- Stress factors which induce an increased energy expenditure and/or a decrease in food consumption. Among these factors, mention should be made of bad weather conditions (humid heat, windy or very rainy conditions) without adequate protection for the animals, or situations in which such conditions prevent the sheep from going out to pasture — thereby requiring the introduction of dietary changes (Photo 2). Prolonged transport, competition for food, or large excursions over poor quality pastures are additional and important sources of stress (Bonino et al., 1987; Ford, 1988; Radostits et al., 1994).

3.- Factors inherent to the animals, such as individual susceptibility, poor dentition, parasitosis, liver pathology with possible alterations in carbohydrate transformation capacity, or other diseases which reduce ingestion capacity or increase metabolism (Bonino et al., 1987; Radostits et al., 1994).

Once the energy imbalance has become established, the host systems attempt to maintain sufficient blood glucose levels to satisfy the needs of the more vital tissues (neurons) and of the fetus. This is done by means of liver gluconeogenesis from propionate (at least 50% propionic acid) derived from carbohydrate digestion, amino acids (20-30%), and from lactate and glycerol (digestive production or glucose recycling) — adapting gluconeogenesis performance to the body glucose requirements. When the availability of propionate proves insufficient, gluconeogenesis makes use of body reserves in the form of fat (Figure 1) and proteins (Figure 2) via the secretion of glucocorticoids and the release of ACTH — thereby generating large amounts of acetyl-coenzyme A (acetyl-CoA)(Bonino et al., 1987; Brus, 1989).

Photo 2. Adverse climatic conditions may induce gestational toxemia in pregnant ewes. Photograph facilitated by Juan José Ramos.

Thus, the biochemical explanation for gestational toxemia centers on deficient performance of the tricarboxylic acid cycle as a result of inadequate supplies of oxalacetate derived from glucose or certain gluconeogenic substances (propionate, glycerol, various amino acids). As a result of this situation and the lack of oxalacetate, acetyl-CoA, which derives from fat or acetate, does not incorporate to the tricarboxylic acid cycle. Instead, acetyl-CoA follows an alternative metabolic pathway culminating in the production of acetoacetate and the rest of ketone bodies (Figure 3)(Bonino et al., 1987; Ford, 1988; Brus, 1989; Radostits et al., 1994). An additional factor to be considered is the increase in glucocorticoid output (cortisol) on the part of the adrenal glands in response to stress, with the purpose of again elevating glycemia. The blood glucose levels fail to normalize, however, due to the continuous demand originating from the fetal tissues; hyperketonemia therefore persists as a result.

Figure 1. Fat follows a series of metabolic pathways which may be schematically represented as follows:

 

Figure 2. Protein metabolism.

 

Figure 3. The metabolism of volatile acids (the main energy source in ruminants) is as follows:

In the event of energy deficiency, the body makes use of its fatty tissue reserves, thereby leading to important lipolysis (Figure 1), which in turn increases the presence of circulating free fatty acids (FFA) that reach the liver where they may follow two metabolic pathways:

a) Triglyceride (TG) synthesis

b) Oxidation and formation of acetyl-CoA

Acetyl-CoA can in turn incorporate to another two pathways:

1.- Oxidation in the Krebs cycle to produce energy with the release of carbon dioxide and water.

2.- The formation of ketone bodies.

Ketone bodies can be used by the muscles as an energy source, or they may be eliminated in urine (physiological ketonemia and ketonuria). If the Krebs cycle is blocked for some reason, or the production of oxalacetate is impeded, short chain fatty acids accumulate in blood (since oxalacetate is necessary for their oxidation) and generate ketone bodies in much larger amounts from the abundant acetyl-CoA produced (i.e., the b2 metabolic route is followed).

Photo 3. Sheep presenting gestational toxemia. Photograph facilitated by Juan José Ramos.

If in addition fatty tissue depletion is increased by the lack of carbohydrates or as a result of excessive consumption, ketone body formation is facilitated. Since these ketone bodies cannot be adequately oxidized or eliminated, they tend to accumulate in the bloodstream and produce ketosis. Ketone bodies not only induce metabolic acidosis but also exert toxic action upon the nervous system; this situation and the lack of glucose can in turn lead to irreversible brain damage (Hay and Baird, 1991).

On the other hand, the abundant free fatty acids reaching the liver induce fatty infiltration, since triglyceride export from the liver — which should take place in the form of low-density lipoproteins (LDL) — is clearly diminished.

SYMPTOMS

The manifestations of gestational toxemia usually appear in the 2-3 weeks before birthing. The process has a duration of about seven days, though only the final stages are observed in affected animals. The clinical signs develop gradually, beginning with extreme depression. The affected sheep appear apathetic, clumsy and depressed, and tend to separate from the rest of the herd and remain immobile (Photo 3). In the subsequent 24-48 hours the depression increases and the animal fails to respond to stimuli, with the loss of auditory and ocular reflexes (threat reflexes are abolished, though the pupils are normal) and proprioception. The base of body support tends to increase, and walking becomes difficult (stumbling into objects and resting the head against objects standing in the way). Under these conditions the animals clearly do not feed or drink, and suffer constipation with dry and hard feces. Likewise, a loss of abdominal wall muscle tone is observed, and the fetuses can be easily detected on both sides of the abdomen (Bonio et al., 1987; Ford, 1988; Hay and Baird, 1991; Radostits et al., 1994; Andrews, 1997).

After 2-3 days, the sheep are seen to positioned in sternal decubitus and are unable to get up. Generally, in 90% of cases, death results within one week from the onset of symptoms (Ford, 1983; Prieto, 1994; Radostits et al., 1994). The irreversible phase of gestational toxemia is a consequence of hypoglycemic encephalopathy with neuronal metabolic depression — thus again confirming the importance of hypoglycemia as a key factor in the disorder. Also ketonemia can exert additional effects, since acetoacetic acid is toxic and can reduce brain oxygen consumption (Bonio et al., 1987; Ford, 1988; Radostits et al., 1994). The ketone body increments and subsequent metabolic acidosis induce compensatory dyspnea, which is worsened in the presence of decubitus-associated pneumonia (Prieto, 1994).

A classical sign in such situations is the smell of acetone in the exhaled air and urine, since acetone is eliminated via both routes and is relatively volatile — unlike acetoacetate or ß-hydroxybutyrate (Craplet and Thibier, 1984; Bonio et al., 1987).

In some cases one or more of the fetuses die, followed by recovery of the ewe provided the disease is not too advanced and the toxemia induced by fetal decomposition does not cause prompt relapse. Recovery tends to occur if the ewe gives birth spontaneously or if the fetuses are extracted by cesarean section in the early stages of the disease. Nevertheless, miscarriage as a result of the toxemia is not frequent, despite dexamethasone injection.

In principle, the disorder does not involve fever, unless secondary complications occur with respiratory processes, or fetal death and decomposition results (Bonio et al., 1987; Prieto, 1994).

Photo 4. Liver showing fatty degeneration. Photograph facilitated by Luis Miguel Ferrer.

LESIONS

The liver presents fatty infiltration followed by hepatic degeneration (Photo 4). The organ appears enlarged, pale and friable, with intense steatosis. The color ranges from pale pink to brilliant orange-yellow, and in some cases floats on water. The adrenal glands also appear enlarged and friable, with cortical hemorrhage and a pale medullary zone. In most cases the renal lesions are not particularly defined, though the cortex appears pale and glomerular degeneration can be seen. No cerebral lesions have been described (Craplet, 1984; Bonino et al., 1987; Ford, 1988; Hay and Bird, 1991).

DIAGNOSIS

The process is easily diagnosed, combining the information obtained from the assessment of herd management and the clinical examination of the affected animals (Bonino et al., 1987; Koening and Contreras, 1984; Hay and Baird, 1991).

The anamnesis should take into account the fact that the sheep are in the later stages of pregnancy, with an assessment of the likely number of fetuses involved. The existence of stress factors must also be considered, including handling of the animals, weather conditions, feeding, and the sanitary status of the herd.

The clinical examination should evaluate the existence of neurological and muscular manifestations, and the necropsy may reveal the existence of hepatomegalia with fatty infiltration-degeneration of the liver, with the presence of two or more well developed fetuses in the uterus.

On the other hand, the diagnosis can be confirmed by the biochemical results. Hypoglycemia is not a constant finding, since temporary normal or even elevated blood glucose levels can be recorded as a consequence of endogenous corticoid release or as a result of fetal death. Ketone body elevations are of interest from the diagnostic point of view when the concentrations exceed 30 mg/dl in blood. Levels in excess of 3.0 mmol/l of ß-hydroxybutyrate in blood are not intrinsically diagnostic of toxemia, though they offer useful clues for evaluating the energy intake of the herd. The diagnosis can be confirmed when concentrations of over 5.0 mmol/l are recorded. In many cases hypocalcemia and hypomagnesemia are observed, with an increase in serum liver enzymes (AST, dehydrogenase, etc.).

In any case, urine diagnostic strips are advisable to obtain a semiquantitative estimation of ketone body presence — this being a very useful approach for securing field evidence.

The differential diagnosis must be established mainly with hypocalcemia, hypomagnesemia, listeriosis, coenurosis, and enterotoxemia (Skerritt, 1991; Buxton and Donachie, 1991; Low and Donachie, 1991; Sykes and Russel, 1991; Scott and Woodman, 1993; Scott, 1995).

In any case, it is essential to establish an early diagnosis. In this sense, it has been shown that treatment applied to sheep with only mild clinical manifestations affords a 90% healing rate, with a percentage mortality of only 6.9%. In contrast, only 55% of animals with severe clinical conditions fully recover, and the associated mortality reaches 33% (Buswell et al., 1986).

PROGNOSIS

It is difficult to establish a prognosis in these situations. It is advisable to determine whether the fetuses are alive (via ultrasound or auscultation). The prognosis is poorer when the fetuses are dead, the sheep appear weakened, or when the diagnosis is established and treatment provided in later stages of the process (Buswell et al., 1986; Hay and Baird, 1991).

TREATMENT

In general terms, the response to treatment is irregular, and in many cases poor. Success depends on the early detection of the problem and a prompt normalization of the appetite and ingestion of the affected animal.

Many treatment modalities have been proposed by different authors, and although all coincide in the essential aspects, some variations have been suggested, with distinct results. In general terms, the following areas should be dealt with:

1.- Reduction of liver glycogen expenditure, administering glucose and glucoplastic substances:

A liter of isotonic glucose solution should be administered via the intravenous route, fractionated into three daily doses (Bonio et al., 1987; Ford, 1988; Radostits et al., 1994).

Other authors have reported good results administering a solution containing glucose (approximately 40%) and other electrolytes, dissolved in various liters of water (4-5 liters) — with administration through an oral tube, twice a day (Sargison et al., 1994).

With the administration of a concentrated oral rehydration solution (160 ml every 4-8 hours) composed of glucose (44.6 g), sodium chloride (8.55 g), glycine (6.17 g), dihydrogen potassium phosphate (4.084 g), potassium citrate (0.12 g) and citric acid (0.25 g) to sheep with gestational toxemia, full recovery was achieved in 68% of the animals (Buswell et al., 1986). The mortality rate was 23%, and significantly lower than that recorded in the absence of treatment (90%) (Ford, 1983).

Scott and Woodman (1993) applied the following treatment, with variable results: 24 mg of dexamethasone-21-isonicotinate via the intramuscular route, in combination with a concentrated oral electrolyte solution (160 ml) in 5 liters of water through a gastric tube, twice a day.

The possibility has also been evaluated of administering glucose solution after inducing the sealing of esophageal passage with an intravenous dose of lysine-vasopressin (0.08 IU/kg). The introduction of glucose directly into the abomasum induces a rapid increase in glycemia (López-Mendez et al., 2001).

As regards glucoplastic substances, the following can be administered: sodium propionate (50 g twice a day), propylene glycol (100 g twice a day), molasses (250g/day), or sodium lactate (100 g twice a day).

The combined administration of glucose via the parenteral route and propylene glycol per os is a valid option for treating gestational toxemia in sheep (Andrews, 1982).

2.- Combating metabolic acidosis by administering bicarbonated solution or Ringer lactate (Koening and Contreras, 1984; Bonino et al., 1987).

3.- Facilitating liver elimination of triglycerides by administering lipotropic substances: choline chloride, acetyl-methionine, vitamin B12, etc. (Bonino et al., 1987).

4.- Normalization of appetite, digestion and ruminal processes by providing appealing foodstuff, bitter elements (tartrates) and choleretic and digestive substances (clanobutin). Treatment with this latter agent at the end of pregnancy induces a rise in glycemia and a reduction in ketone body levels. Combined administration with hyperglycemia-inducing products is advised (González, 1992).

5.- Interruption of pregnancy. Extraction of the fetus or fetuses via cesarean section reduces the energy expenditure and allows the ewe to recover for subsequent pregnancy episodes. However, even when this is attempted in the early stages of the process, the results are sometimes disappointing. This is all the more so when the measure is applied in late-stage gestational toxemia.

The use of glucocorticoids has not afforded good results. High and long-acting doses are required, and their administration to animals which already present high cortisol levels increases uremia as a result of the increased protein catabolism (Koening and Contreras, 1984; Radostits et al., 1994).

Extended insulin treatment can be useful in advanced processes. The oral dosing of 12.5 g of sodium propionate, 12.5 g of calcium lactate and 7.5 g of potassium chloride dissolved in 250 ml of water twice a day, together with the subcutaneous injection of 0.4 IU/kg/day of extended insulin, increased the percentage survival to 86.7% - versus 62.7% when using glucose precursors and oral electrolytes, or 53.6% with infusions of glucose and fructose (Henze et al., 1998). In this context, insulin contributes to overcome the antagonistic effect of cortisol upon endogenous insulin and on glucose metabolism (Bonino et al., 1987; Prieto, 1994).

In the experimental setting, the subcutaneous administration of bovine somatotropin (0.15 mg/kg live weight)(Andrews et al., 1996; Andrews and Wilkinson, 1998) has yielded highly variable results. It is used as a complement to therapy with 100 ml of dextrose (50%)(i.v.) and 60 ml of propylene glycol (via the oral route)(Andrews et al., 1996); 50 ml of calcium borogluconate (40%)(i.v.), 100 ml of dextrose (50%)(i.v.) and 60 ml of propylene glycol (via the oral route)(Andrews and Wilkinson, 1998); or 160 ml of a solution of dextrose and electrolytes 3 times/day (via the oral route)(Scott et al., 1998). In some studies these measures seem to improve the efficacy of glucose and ketone body utilization at cellular level, with a reduction in ewe and neonate mortality.

PROPHYLAXIS

The best approach for avoiding development of the process is to feed the ewes correctly in the later stages of pregnancy (months 4 and 5). It is essential to ensure early control of the sheep in this period, with the prompt detection and correction of any possible deviations. The ideal situation is to divide the animals into three batches according to their body status (fat, normal and thin), in order to implement an adequate nutritional regimen (Hay and Baird, 1991).

The introduction of feeding during gestation should be gradual, and the increases in the amounts of concentrate should be sufficient for the growth needs of the fetuses. The appetite of the ewes decreases in the last 2-3 weeks due to the reduced available space within the abdomen — a situation that must be taken into account (Ford, 1988; Koening and Contreras, 1984; Radostits et al., 1994).

The fodder rations should contain energetic and highly digestible elements (oats, corn, molasses), an adequate amount of digestible protein that does not degrade within the rumen (10%), a vitamin-mineral supplement, and easy access to fresh and clean water.

If some case of gestational toxemia is detected within the herd, simple carbohydrate supplements should be provided for the rest of the animals in advanced-stage pregnancy, ensuring that all have easy access to the food (González and Rejas, 1995).

Moderate physical exercise (in protected confinements) and parasitosis control, as well as the avoidance of stress-generating situations are also good prophylactic measures.

BIBLIOGRAFIA

    Andrews, A.H.; Effects of glucose and propylene glycol on pregnancy toxaemia in ewes. Veterinary Record 110: 84-87 (1982).

    Andrews, A. Pregnancy toxaemia in the ewe. In Practice: 306-312 (1997).

    Andrews, A.H.; Wilkinson, J. Recombinant bovine somatotropin and propylene glycol following glucose injection in treating pregnancy toxaemia. Large Animal Practice: 31-33 (1998).

    Andrews, A.H.; Holland-Hoewes, V.E. Wilkinson, J.I.D. Naturally occurring pregnancy toxaemia in the ewe and treatment with recombinant bovine somatotropin. Small Ruminant Research 23: 191-197 (1996).

    Bonino Morlán, J.; Sienra, R.; Sorondo, M.L. Toxemia de la gestación. En: Enfermedades de los lanares. Vol 2. J. Bonino Morlán (ed.) Hemisferio Sur, Montevideo, pp. 239-265 (1987).

    Brus, M.L. Ketogenesis and ketosis. En: Clinical biochemistry of domestic animals. J.J. Kaneko (ed.) 4ª ed. Academic Press, San Diego, pp. 86-105 (1989).

    Buswell, J.F.; Haddy, J.P.; Bywater, R.J. Treatment of pregnancy toxaemia in sheep using a concentrated oral rehydration solution. Veterinary Record 118: 208-209 (1986).

    Buxton, D.; Donachie, W. Clostridial diseases. En: Diseases of sheep. W.B. Martin and I.D. Aitken (ed). 2nd ed. Blackwell Scientific Publications, Oxford, pp. 104-114 (1991).

    Cantley, C.E.L.; Ford, C.M.; Heath, M.F. Serum fructosamine in ovine pregnancy toxaemia: a possible prognostic index. Veterinary Record 128: 525-526 (1991).

    Craplet, C.; Thibier, M. Pathologie de la gestation. En: Le mouton. 4ª ed. Vigot, París, pp. 405-409 (1984).

    Ford, E.J.H. Pregnancy toxaemia. En: Diseases of sheep. W.B. Martin (ed.) 1st ed. Blackwell Scientific Publications, Oxford, pp. 147-151 (1983).

    Ford, E.J.H. Toxemia de la gestación. En: Enfermedades de las ovejas. W.B. Martin (ed.). Acribia, Zaragoza, pp. 159-164 (1988).

    González Montaña, J.R. Dismetabolismos energéticos en ovejas de alta producción profilaxis y tratamiento. Tesis Doctoral. Universidad de León (1992).

    González, J.R.; Rejas, L.J. Toxemia de la gestación. Medicina Veterinaria 12 (9): 513-522 (1995).

    Hay, L.A.; Baird, G.D. Pregnancy toxaemia. En: Diseases of sheep. W.B. Martin and I.D. Aitken (ed). 2nd ed. Blackwell Scientific Publications, Oxford, pp: 254-257. (1991).

    Henze, P.; Bickhardt, K.; Fuhrmann, H.; Sallmann, H.P. Spontaneous pregnancy toxaemia (ketosis) in sheep and the role of insulin. J. Vet. Med. A 45: 255-266 (1998).

    Koenig, M.V.; Contreras, P.A. Alteraciones del metabolismo energético en rumiantes y sus principales manifestaciones clínicas. Aarch. Med. Vet. 16 (1): 7-13 (1984).

    López Mendez; S.; Alonso Díez, A.J.; Prieto Montañés, F.; González Montaña, J.R. Toxemia de la gestación ovina: tratamiento con glucosa por vía oral. Datos preliminares. XXVI Jornadas Científicas y V Internacionales de la Sociedad Española de Ovinotecnia y Caprinotecnia. Sevilla, 20-22 de Septiembre de 2001.

    Low, J.C.; Donachie, W. Listeriosis. En: Diseases of sheep. W.B. Martin and I.D. Aitken (ed). 2nd ed. Blackwell Scientific Publications, Oxford, pp. 174-178 (1991).

    Prieto, F. Toxemia de la gestación. En: OVIS. Tratado de patología y producción ovina. López Sebastián A. (ed.). Madrid (1994).

    Radostits, O.M.; Blood, D.C.; Gay, C.C. Ketosis of ruminants (acetonemia of cattle, pregnancy toxemia of sheep). En: Veterinary medicine. 8ª ed. Baillière Tindall, Londres, pp. 1343-1354 (1994).

    Sargison, N.D.; Scott, P.R.; Penny, C.D.; Pirie, R.S.; Kelly, J.M. Plasma enzymes and metabolites as potential prognostic indices of ovine pregnancy toxaemia-a preliminary study. British Veterinary Journal 150: 271-276 (1994).

    Scott, P. Differential diagnosis of common metabolic disorders of sheep. In Practice: 266-269 (1995).

    Scott, P.R.; Sargison, N.D.; Penny, C.D. Evaluation of recombinant bovine somatotropin in the treatment of ovine pregnancy toxaemia. The Veterinary Journal 155: 197-199 (1998).

    Skerritt, G.C. Coenurosis. En: Diseases of sheep. W.B. Martin and I.D. Aitken (ed). 2nd ed. Blackwell Scientific Publications, Oxford, pp. 188-194 (1991).

    Sykes, A.R.; Russel, A.J.F. Deficiencies of macro-elements in mineral metabolism. En: Diseases of sheep. W.B. Martin and I.D. Aitken (ed). 2nd ed. Blackwell Scientific Publications, Oxford, pp. 225-238 (1991).

    Van Saun, R.J. Pregnancy toxemia in a flock of sheep. JAVMA 217 (10): 1536-1539 (2000).

 

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