INTRODUCTION

Among domestic farm animals, the metabolic diseases achieve their greatest importance in dairy cows and pregnant ewes. In the other species, these diseases occur only sporadically. High producing dairy cows are always on the verge of abnormal homeostasis due to the continuous breeding and feeding for high milk yield which is often the cause of the common occurrence of metabolic diseases in them. Peri-parturient Period in Cattle and Sheep As milk production in dairy cows increases and as herds become larger, the incidence of metabolic disease increases. In dairy cows, the incidence of metabolic diseases is highest in the period commencing at calving and extending until the peak of lactation is reached. During early lactation, there is a rapid rate of exchange of water, sodium, calcium, magnesium, chlorides and phosphates which leads to a sudden variation in their excretion or secretion in the milk or by other routes, or a sudden variation in their intake because of changes in ingestion, digestion or absorption that affects the metabolic stability of the cow. In addition, if the continued nutritional demands of pregnancy are exacerbated by an inadequate diet in the dry period, the incidence of metabolic disease will increase. The effect of pregnancy is particularly important in ewes, especially those carrying more than one lamb. Transition Period in Dairy Cows Monitoring the nutrition requirements of a cow 3 weeks prior to and 3 weeks post parturition is crucial in managing metabolic diseases. The primary challenge faced by cows is a sudden and marked increase of nutrient requirements for milk production and fetal growth, at a time when dry matter intake and thus nutrient supply, lags far behind. Dry matter intake typically declines during the final week before parturition. This decline and changes in endocrine profiles contribute to the precipitation of metabolic diseases. The transition period is also complicated by a multifactorial immunosuppression whose cause is not yet well understood. This further affects the health of the animal. These diseases are therefore also called as Production Diseases which happen due to the continued desire of humans to derive more and more from these farm animals. Breed Susceptibility Between groups of cows, variations in susceptibility appear to depend on either genetic or management factors. Jersey cows are more susceptible to parturient paresis than cows of other breeds and Guernseys seem to be more susceptible to ketosis. Even within breeds, considerable variation is evident in susceptibility between families.

Management Practices The management practices of most importance are housing and nutrition. In cattle that are housed during the winter and in poor pasture areas, ketosis is prevalent. Metabolic diseases are complex and the incidence is high, where farmers follow a practice of having the cows calve in late winter when feed is poor and the practice of depending entirely on pasture for feed. Metabolic diseases are not infectious diseases but sometimes can be introduced due to an underlying infectious disease. Hence it is important to maintain a hygienic environment. Occurrence and Incidence Largely because of variations in climate, the occurrence of metabolic disease varies from season to season and from year to year. In the same manner, variations in the types of disease occur. Further, the incidence of metabolic disease and the incidence of the different syndromes will vary from region to region, depending on factors like rainfall and quality of pasture. Metabolic Profile Tests Changes in the concentration of one or more metabolites in the blood explain the clinical signs and have a diagnostic significance. MPTs are an effective way of monitoring the nutritional status of a herd of cows in order to predict if an animal is likely to suffer from a metabolic disease and also to take corrective measures to prevent the same. Please refer to the article Metabolic Profile Tests: Application in Dairy Farm Management, attached.

PARTURIENT PARESIS (MILK FEVER)

It is a disease of cattle, sheep and goats occurring around the time of parturition caused due to hypocalcaemia and characterized by general muscular weakness, recumbency, circulatory collapse, depression of consciousness and ultimately shock and death. Etiology :

Depression of levels of ionized Calcium in tissue fluids (total plasma Calcium < 1.9 mmol/L). In susceptible cattle, the extent of fall in Calcium levels during pregnancy leads to parturient paresis. The animals body cannot adapt to a sudden fall in levels of Calcium within a short time span. Calcium is drawn by the fetus for growth and also by the mammary glands for their development. Activation of the Parathyroid gland to bring about osteoclastic activity to maintain blood Calcium levels cannot take place immediately as it requires a few days. The period between the switching over from Calcitonin to Parathormone predisposes cattle to this disease.

Physiological Role of Calcium in the Body :

1.

Calcium has a membrane stabilizing effect on peripheral nerves. Therefore, deficiency maybe characterized by hyperaesthesia and mild tetany, seen during early parturient paresis. Calcium is required for the release of Acetyl Choline at the membrane function. Deficiency of Calcium leads to paralysis, since transmission of nerve impulses to the muscle fibers is compromised. Calcium is directly required for the contraction of muscles.

2.

3.

During the dry period, calcium requirements are minimal at about 10-12 g/day. At parturition, the cow must mobilize about 30 g or more of calcium into the calcium pool per day. Hypocalcaemia occurs in spite of apparently adequate function of the Parathyroid and Vitamin D endocrine system. Most cows are able to cope with the sudden demand by increasing intestinal and bone resorption of Calcium but about 5-20% of adult cows are unable to maintain plasma

calcium and consequently develop severe hypocalcaemia (total plasma calcium, 1.0 - 1.4 mmol/L) or clinical milk fever which requires treatment. Epidemiology : The disease occurs most commonly in high-producing adult lactating Dairy Cattle. Lactating beef cows are affected but less commonly. Age : Mature cows, 5 10 years of age are most commonly affected. Disease is common in cows in the 3rd to 7th lactation. Breed : Jersey cows are commonly affected. Individual Variation : incidence of milk fever is positively associated with the level of milk production. Time of Occurrence : Disease can occur during 3 stages of lactation. It may occur during the last few days of pregnancy, most commonly during parturition and rarely several weeks before calving. Most cases occur during the first 48 hours after calving. The danger period can extend up to 10 days post-partum. Stressors : Starvation for 48 hours may also depress serum Calcium levels. Milking Goats mainly within 4 to 6 years of age are affected. Disease can occur before and after kidding. Sporadic cases may occur in Sheep and Pigs. Pathogenesis : Before the onset of milk production, there is not much demand for Calcium. But at the onset of lactation or during pregnancy, the demand increases suddenly. A profound hormonal effect is required to regulate increase or decrease in Calcium. This effect cannot take place immediately as it takes a few days, prior to which hypocalcaemia may set in.

During dry period, mobilization of Calcium from bones and intestines is not required but during lactation there is a sudden demand for Calcium. There is a sudden loss of Calcium in milk (10L of colostrum requires 23g of Calcium which is 9 times the amount present in the plasma calcium pool of a cow. Hypocalcaemia sets in which triggers Calcium homeostasis mechanism.

1, 25 Dihydroxy cholecalciferol (active form of Vitamin D) is stimulated and metabolized into the system. It takes 24 hours for Calcium to be transported from the intestines into the circulation. Therefore, physiologically, the animal is hypocalcaemic for 24 hours. Stimulation of PTH also requires 48 hours of stimulation.

Reasons for failure of Calcium homeostasis :

1.

Deficiency of hormone receptors

2.

Defective metabolic pathway: process of mobilization of Calcium may not get activated or stimulated even though hormones and receptors are normal. This may happen when the cow is maintained on a high Calcium diet just prior to parturition.

3. 4.

Calcium absorption decreases with age. If the pH of blood is high, as in the case of cows fed with diets high in Potassium and Sodium, the action of PTH on the bones is very poor. Pre-partum diets high in phosphorus (>80 g P/day) also increases the incidence of milk fever and the severity of hypocalcaemia. High dietary levels of phosphorus increase the serum level of phosphorus which is inhibitory to the renal enzymes that catalyze production of 1,25 Dihydroxy cholecalciferol, which when decreased reduce the intestinal calcium absorption mechanisms pre-partum.

5.

Clinical Findings : Stage 1 : Brief Stage of Excitability

Animal is slightly excited and hypersensitive and there may be slight tetany. Tremors of muscles of head and limbs. Slight hypocalcaemia, reluctance to move or eat, rumination is suspended. Grinding of teeth. Rectal temperature not significant. Animal may fall due to stiffness of limbs. Hind limbs do not fold and they protrude outwards.

Stage 2 : Stage of Sternal Recumbency

Animals consciousness in depressed. Animal lies down on its sternum and is drowsy. Lateral kink in the neck or head (head turned towards the flank). Tetany disappears due to the flaccid situation. Dry muzzle, cold extremities. Subnormal temperature. Dilated pupils pupillary light reflex absent. Loss of tonicity of body muscles, including gastrointestinal muscles. Reduction in gastrointestinal motility. Constipation and ruminal stasis Tachycardia Weak pulse, low CVP and blood pressure Post expiratory grunt may be heard. Normal respiratory rate.

In small animals :

Increase in body temperature.

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Hyper excitability. Seizures (Eclampsia). Stage 3 : Stage of Lateral Recumbency

Animal is in comatose. Limbs are stretched out, flaccid and atonic. Cow cannot sit up. Depression of body temperature. Circulatory collapse. Heart sounds are totally inaudible and pulse is impalpable. There is an increase in heart rate to compensate for the failing circulatory mechanism. Bloat is present. Raising the jugular vein is impossible. Loss of muscular tonicity may lead to uterine prolapse. Profound hypocalcaemia.

Complications of Milk Fever : Downer cow syndrome Dystocia and reproductive disease
1. 2. 3. 4. 5.

Retention of placenta Metritis Mastitis Abomasal displacement Ketosis

Clinical Pathology :
1.

Total serum Calcium levels reduced to as low as 2 mg/dL. Reduction is not proportional to the severity of clinical signs exhibited. Normal Calcium levels : 8 to 10.5 mg/dL. Ionized Calcium levels are better indicators but are difficult to measure. Serum Magnesium levels are usually elevated from 1.2 3.5 mg/dL to 4 -5 mg/dL. Serum inorganic Phosphorus levels are depressed.

2. 3. 4.

Necropsy Findings : No changes grossly or histo-pathologically.

Diagnosis :
1. 2. 3. 4.

Clinical signs determine stage 1, 2 or 3. History of recent calving. Response to treatment with intravenous administration of Calcium. Clinical pathology can support diagnosis.

In ewes, the disease may be present in the period preceding lambing. Differential Diagnosis :
1. 2.

Hypomagnesaemic tetany / Lactation tetany. Toxaemia due to coliform mastitis and peritonitis (TRP) causing rupture of the vagina or uterus during parturition. Maternal obstetrical paralysis due to prolonged dystocia during which excess traction is administered leading to damaged nerves resulting in paralysis and recumbency. Downer cow syndrome. Physical injuries like dislocation of the hip, fracture of the pelvic bones or rupture of the gastrocnemius muscle. Ephemeral fever.

3.

4. 5. 6.

Treatment :

Immediate treatment must be taken up. Treatment in stage 1 is ideal, before the cow becomes recumbent. Cows with low temperature and lateral recumbency may not have a favourable prognosis in spite of treatment. Prolonged recumbency leads to ischaemic necrosis and permanent damage to muscles (Downer cow). 400 to 800 ml ( 100 to 200 g) intravenous injection of 25% Calcium borogluconate in Cattle. 15 to 20 g in Goats. Alternatives : 8.3% Calcium borogluconate Calverol : 25 % solution

In early stages when recumbency has not yet set in, half the dose can be administered subcutaneously and the other half can be administered intravenously to avoid cardiac problems and prevent relapse. Pattern of Response to Treatment :
1. 2. 3. 4. 5.

Animal starts belching. Muscle tremors of the flank, which may extend to the whole body. Improvement in pulse. Sweating of the muzzle. Animal slowly stands up, urinates and defecates.
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6.

Faeces are coated with mucus and sometimes have spots of blood.

Precautions :
1.

Calcium is cardiotoxic and therefore must be administered slowly with utmost care and continuous monitoring of the heart. If severe arrhythmia is found, Atropine is administered intravenously. Rapid injection of Calcium may lead to a heart block. 100 to 400 mL of 10% Magnesium sulphate is administered rapidly to counter the cardiotoxic effect of Calcium. Mifex (Calcium, Magnesium and 25% Dextrose) can be administered.

2. 3. 4.

Failure of response to treatment may happen due to incorrect diagnosis. Relapse of the disease is possible. Control :
1. 2. 3. 4. 5.

Diets high in Calcium or Calcium supplements should not be administered very close to parturition. Low Calcium should be fed prior to calving. Palatable diet should be provided to prevent ruminal and intestinal stasis. Feed provided must be reduced in proportion to reduction in milk yield. Calcium gels can be administered orally at the rate of 100 to 150 g daily according to a schedule of 24 hours, and 1 to 2 hours before and then 10 to 14 hours after calving. Vitamin D3 can be administered to enhance Calcium absorption. Acidic diet :

6. 7.

Diets low in Potassium and Sodium should be fed during late pregnancy and early post-partum period. Corn silage and Alpha alpha silage are appropriate sources. Making use of Dietary Anionic and Cationic Differences (DCAD) to prevent parturient paresis : Add more anions (Cl-, SO42-, PO42-) to the diet to counter the effect of cations (Na+, K+, Ca2+ ) and reduce the blood pH.

Sulphates and chlorides of Magnesium, Calcium and Ammonium can be added to the diet. This not only controls milk fever but also increases the milk yield. pH of the urine can be estimated as an indication of the blood pH. A urine pH of 6 to 6.5 for H.Fs and 5.8 to 6.8 for Jerseys is said to be beneficial for prevention of milk fever. Ammonium chloride and Ammonium sulphate are commonly used at the rate of 100 g per cow per day in pre-partum diets, 21 days prior to parturition. This does not require feeding of a low Calcium diet. They are inexpensive, safe and convenient.

KETOSIS OF RUMINANTS
It is a disease of cattle and sheep caused by impaired metabolism of carbohydrates and volatile fatty acids, characterized by ketonuria, ketonemia, hypoglycemia and low levels of hepatic glycogen. It is also known as Acetonemia of Cattle or Pregnancy Toxaemia of Sheep. Etiology : The disease commonly occurs in high yielding cows during the post-partum period that develop negative energy balance. Most high yielding dairy cows are subclinically ketotic post-partum do not require any treatment but some cows may be affected by clinical ketosis if there is additional nutritional or metabolic insult during the post-partum period. As productivity of the cows increases, there is an increased susceptibility to ketosis since a lot of energy is needed for milk production. Milk production sometimes goes beyond the capacity of the animal with respect to energy derived from feed. Physiology of Carbohydrate Metabolism : Carbohydrates or their precursors are ingested and get converted to Acetic acid, Butyric acid and Propionic acid. Acetic and Butyric acids are Ketogenic fatty acids whereas Propionic acid is a Glycogenic fatty acids. Propionic acid is utilized in the TCA cycle to generate Oxaloacetic acid, Glucose and Lactose. In the presence of Oxaloacetate, Ketogenic fatty acids are utilized for production of energy and provided the Glucose metabolism is normal, the excess is condensed to fat. However, in the absence of Oxaloacetate, Ketone bodies, namely, Aceto acetic acid and - hydroxy butyric acid are formed. This fragile mechanism can be intruded by small changes in the diet or small increase in the diet. Since ruminants are dependent upon Volatile Fatty Acids for their energy requirement, they are predisposed to ketosis. Epidemiology : Animals more prone to ketosis : 1. 2. 3. High producing dairy cows and housed cows. Cattle fed on pasture and rations with inadequate calories. Cattle under conditions of specific nutrition deficiency.

4. Cattle suffering from a primary disease, as a complication of which ketosis develops.

Pathophysiology : The demand for Glucose during gestation is very high. It increases by 30% during late gestation and by 75% during early lactation. A cow weighing 500 Kg requires approximately 50 g of Glucose every hour. Only 10% of this requirement is met directly through the diet and the rest must be derived from Volatile Fatty Acids in the liver, bacterial proteins and small amounts amino acids that escape denaturation in the rumen. Lactating cows require large quantities of Propionate. Lack of adequate amounts of Propionate results in insufficient Oxaloacetate leading to slowing down of the TCA cycle. Thus the utilization of Acetyl CoA is affected and hence, Ketone bodies are produced. In the absence of Glucose, the body attempts to derive energy via gluconeogenesis. Fat deposits and triglycerides are mobilized and hydrolysed. This produces Free Fatty Acids (FFAs) and Non Esterified Fatty Acids (NEFAs). NEFAs may be converted in the liver to triglycerides. FFAs and NEFAs can also enter the TCA cycle through Acetyl CoA. In the absence of Oxaloacetate, they are oxidised to Aceto-acetyl CoA, leading to the formation of Ketone bodies. Pathogenesis : Types of Ketosis : 1. Primary Ketosis : It is also known as Production Ketosis and occurs in herds that are well fed and well looked after and have an excess body condition. These cows have a high lactation potential. 2. Secondary Ketosis : It occurs due to decrease in appetite as a result of other underlying diseases (such as Abomasal Displacement, Metritis, Mastitis and TRP), some of which commonly occur soon after parturition. 3. Alimentary Ketosis : It occurs due to excess amount of butyrate in the silage leading to decreased palatability and in turn decreased feeding which ultimately results in Ketosis. 4. Starvation Ketosis : It occurs in cattle with poor body condition and in cattle that are fed with poor quality ration. Ketosis results from the deficiency of protein, energy and Propionate in the diet.

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5. Ketosis Due to Specific Nutritional Deficiency : Deficiency of Cobalt, Phosphorous, Cyanocobalamine required for entry of Propionate into the TCA cycle can result in Ketosis. Ketosis occurs most commonly in the first month of lactation, around 28 to 30 days after calving. It is less common during the 2nd month of lactation and occurs rarely in late gestation. Prevalence is low during the first calving and at its peak during the fourth calving.

In Ewes, Ketosis is known as Pregnancy Toxaemia and is common during the last month of pregnancy. It is more common in Ewes carrying more than one lamb or a large foetus. Nervous signs are caused due to production of Isopropyl alcohol which is a breakdown product of Aceto-acetic acid in the rumen. Hypoglycaemia itself can produce nervous signs. Clinical Findings : Two major forms of disease can be identified : 1. Wasting Form : It is the most common type of ketosis observed. There is a moderate decrease in appetite and milk yield over 2 - 4 days. The animal may eat grain and silage but not hay. Depressed appetite. Rapid loss of body weight. Loss of subcutaneous fat and cutaneous elasticity. (Referred to as Woody). Faeces are firm and dry. Animal is depressed and reluctant to move. Mild abdominal pain may be present. Normal temperature, pulse rate and heart rate. Ketotic odour emanates from the breath. Milk may emanate a fruity odour. Very low mortality. Sometimes spontaneous recovery occurs within a month but the peak milk yield is never regained. 25% of milk yield and SNF content can be affected. Nervous signs like staggering gait and partial blindness may rarely be observed.

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2.

Nervous Form : Signs develop very suddenly. Animal becomes subdued. Aggression or ferocity does not develop and the animal goes into a state of delirium. Crossing of legs while walking. Head pressing. Walking in circles. Aimless movement and wandering. Decreased appetite. Vigorous licking of self and inanimate objects. Chewing movements, hyperaesthesia, bellowing on being pinched. Tremors, tetany and staggering gait.

These signs last for 1 to 2 hours and recur every 8 to 12 hours. The animal may injure itself. Sub clinical Bovine Ketosis : Clinical signs are not easily recognizable. Ketonuria. Drop in milk yield and SNF content. Malodour of milk. Decreased fertility. No typical clinical signs.

Ovine Ketosis : It is comparable to the nervous form of Bovine ketosis. Ewe isolates itself from the flock and is very cautious while placing feet. Reluctance to move. Blindness results in the animals walking into objects or bushes and falling or hurting themselves. Grinding of teeth. Scanty, dry faeces. Muscle tremors, twitching of lips, champing of jaws and salivation. Cog wheel type of clonic contraction of cervical muscles, lateral deviation of the head and circling. Sheep may become recumbent and suffer from convulsions in 3 to 4 days. They remain in a state of depression for further 3 to 4. Foetal death occurs and there is a transient recovery Ewe. If the foetus is not aborted, toxemia sets in and there is a relapse of the condition. Dystocia may be seen in affected cows. Recovery is possible if a Caesarean section is performed at an early stage.
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Clinical Pathology : 1. 2. 3. Ketonuria and Ketonemia. Free Fatty Acids are detected in the plasma. Hypoglycaemia : 20 to 40 mg/dL in cattle and sheep (Normal : 50 mg/dL).

4. Ketone bodies : 10 to 100 mg/dL. 5. Ketone bodies in milk : 40 mg/dL (Normal : 3 mg/dL). Necropsy Findings : Fatty changes of the liver and secondary changes in the anterior pituitary gland and adrenal cortex. the rectum) Diagnosis : 1. 2. 3. History of recent calving. Pregnancy in Ewes. Hypoglycaemia. Lambs dead, decomposition has set in. Ewes Fatty degeneration of liver , twin lambs in the uterus, evidence of constipation (hard faeces in

4. Ketonemia and Ketonuria : Rotheras Test. Differential Diagnosis : Wasting Form of Ketosis 1. 2. 3. Traumatic Reticulitis (TRP) : does not necessarily coincide with recent calving. Drop in milk production and anorexia is more pronounced than in ketosis. Increased WBC count due to infection and no hypoglycaemia seen. Vagus Indigestion : it can lead to secondary ketosis. Abdominal distention and moderate bloat is present. Simple Indigestion : Ruminal stasis. Other clinical signs seen in ketosis are absent. detected. Sudden drop in milk yield and decrease in abdominal size. 5. Cystitis and pyelonephritis. 6. Diabetes mellitus. Nervous Form of Ketosis 1. 2. 3. Rabies : Rapid progression, ascending paralysis, mania, bellowing and death. Lactation Tetany : Acute or Peracute signs similar to rabies. Lead Poisoning

4. Abomasal Displacement : Occurs at calving. Large quantity of pasty faeces is voided. Abomasal sounds can be

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Pregnancy Toxaemia : 1. 2. 3. Parturient Paresis : seen during late pregnancy or at parturition. Course of the disease is short (12 t0 24 hours) unlike Pregnancy Toxaemia (6 to 7 days). Response to Calcium is very good. Listeriosis : Abortions, isolation of organisms. Rabies : paralysis, mania and frenzy.

4. Coenurus cerebralis . 5. Cerebral abscess. 6. Otitis Media.

Treatment : 1. 2. 3. Intravenous injection of 100 to 500 mL of 50% Dextrose. Subcutaneous injection is not recommended since they produce discomfort. A solution of 25% Dextrose and 25% Fructose can be used. To prevent relapse and overcome repeated injections after the first injection, oral Propylene Glycol or Glycerine at the rate of 225 g, twice a day for two days, followed by 110 g, twice a day for the next two days is recommended (They are converted to Glucose without utilizing Oxaloacetate.) . 4. Glucose may not be utilized well unless administered with Insulin. Alternatively, 1. 2. 3. Slow intravenous infusion of 20 L of 2.5% Glucose saline over a period of 24 hours. Glucocorticoids can be administered. Dexamethasone : 40 mg. They breakdown muscle proteins and make glucose available for utilization. Low doses of long acting Insulin : Potassium Zinc Insulin at the rate of 200 IU subcutaneously, every 48 hours. This supports fatty acid metabolism and increases glucose uptake by tissues. 4. Lipophilic agents like Choline at the rate of 25 to 50 g P.O. and Cysteamine at the rate of 750 mg intravenously every 2 or 3 days. These are phospholipid precursors essential for synthesis of VLDL. 5. Administration of Vitamin B12 to overcome Cobalt deficiency and aid in entry of Propionate into the TCA cycle. 6. 30 g of Chloral hydrate on the first day followed by 7 g twice a day, daily. It increases the breakdown of starch in the rumen and stimulates Glucose production. Control : 1. 2. Cows should never be starved or overfed at calving. An adequate calorie intake must be maintained. Ground maize can be included in the diet. It contains -polymerase glucose which is not fermented in the rumen and is directly absorbed from the intestines.
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3.

Adequate Cobalt, Phosphorous and Iodine must be supplemented in the diet.

4. 350 mL of Propylene Glycol can be administered daily for 10 days after calving. 5. Sodium propionate at the rate of 110 g daily for 6 weeks, commencing at calving can be administered as a prophylactic measure.

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hypomagnesaemic tetany
(Grass tetany, Grass staggers, Lactation tetany, Wheat Pasture poisoning)

Hypomagnesaemic tetany is a complex metabolic disturbance characterized by hypomagnesaemia (plasma tMg <1.5 mg/dL) and a reduction in the concentration of tMg in the CSF (<1.0 mg/dL), which lead to hyperexcitability, muscular spasms, convulsions, respiratory distress, collapse, and death. Adult lactating animals are most susceptible because of the loss of Magnesium in milk. Hypomagnesaemic tetany occurs mainly when animals are grazed on lush grass pastures or green cereal crops but can occur in lactating beef cows fed silage indoors. It is rare in non lactating cattle but has occurred when undernourished cattle were introduced to green cereal crops. Etiology : The disorder occurs after a decrease in plasma Mg concentration when absorption of dietary Mg is unable to meet the requirements for maintenance (3 mg/kg body wt) and lactation (120 mg/kg milk). This can arise after a reduction in food intake during inclement weather, transport, or when cows graze short-grass dominant pastures containing <0.2% Mg on a dry-matter basis. Low herbage availability (<1,000 kg dry matter/hectare) results in live weight losses during lactation, and plasma Mg decreases because insufficient Mg is obtained from body tissues mobilized during loss of live weight to support lactation. Magnesium, a divalent cation, is an intracellular electrolyte essential for enzymatic activity. No hormones are responsible for regulation of Magnesium levels in the body. Change or decrease in the dietary Magnesium content leads to a steep fall in Mg 2+ concentration in the blood, resulting in Hypomagnesaemic tetany. Ruminants are at a great risk of Hypomagnesaemia. Mg2+ is lost in faeces and milk. Mg2+ homeostasis is maintained by the kidneys.

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Mg absorption from the rumen may be reduced when potassium and nitrogen intakes are high and sodium and phosphorus intakes are low. Soils that are naturally high in potassium and those fertilized with potash and nitrogen are high-risk areas for hypomagnesemic tetany. The more complex mineral interactions are likely to be involved in herds in which hypomagnesemic tetany occurs in first- and second-calving cows as well as in older cows.

Cows often do not develop signs of hypomagnesaemic tetany until blood calcium concentrations are <0.8 mg/dL (0.35 mmol/L), which commonly occurs in cattle grazing green cereal crops. The hypocalcaemia arises from either a reduction in calcium intake or absorption, or both.

Lush grass pastures and green cereal crops may predispose cattle to metabolic alkalosis (urine pH >8.5) with a reduced available pool of ionized calcium and magnesium, thereby increasing the risk of hypocalcaemia and hypomagnesaemia.

Urine Mg concentrations are a useful guide to Mg status and are undetectable in cows with hypomagnesaemia.

Epidemiology : 1. 2. 3. It is common in cattle turned out to lush, green pastures after winter housing. Pastures heavily top dressed with fertilizers rich in sodium and potassium. Cattle in first two months of lactation and between 4 to 7 years of age are at a higher risk.

4. H.F. cows are more susceptible when compared to Jerseys. 5. Young cereal crops (wheat/oats) may predispose cattle to Grass tetany. Therefore this disease is also known as Wheat Cereal Pasture Poisoning. 6. Seasonal incidence in spring, summer and autumn due to young, rapidly growing pasture (Jowar and Ragi). 7. High potassium and nitrogen and low levels of sodium and carbohydrates in the pasture predispose cattle to hypomagnesaemic tetany. Pathogenesis : Mg is responsible for release of Acetyl Choline at synapses of neurons, maintaining sensitivity of motor end plates, & threshold of muscle membranes and activation of Choline Esterase enzyme system. Hypocalcaemia and hypomagnesaemia can cause expression of symptoms. Normal serum Mg levels : 1.7 3 mg/dL. Clinical Signs : 1. Acute Lactation Tetany : Animals allowed to graze on lush green pasture suddenly stop grazing. Unusual alertness and discomfort.
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 Twitching of the muscles of the face and ears. Hyperaesthesia, bellowing, galloping, running, hypersensitivity. Staggering gait : animals fall down. Tetany of limbs followed by convulsions lasting about a minute. During convulsions, opisthotonos lasts for a minute. Nystagmus, champing of jaws , frothing of the mouth and pricking of the ears. Retraction of eyelids. Once the animal recovers, convulsions may relapse. Body temperature : 104o to 107o F. High pulse and respiratory rate. Animal may die if not treated within 1 to 5 hours. Very high mortality rate. Response to treatment is good if it is taken up early. 2. Sub acute Lactation Tetany : Develops gradually over a period of 3 to 4 days. Wildness of facial expression. Inappetence. Exaggerated limb movements due to hypocalcaemia resulting in malfunction of Acetyl Choline Esterase enzyme. Cows throw their heads about. Frequent urination and defaecation. Drop in milk yield. Any sudden movement or noise may lead to precipitation of clinical signs and convulsions. Recumbency leading to death. Spontaneous recovery without treatment is possible. Chronic Lactation Tetany : Decrease in blood Calcium levels. No prominent clinical signs. Dullness, ill thrift, decrease in appetite. Drop in milk yield. Sub acute form may lead to the chronic form. 1. Serum and Urinary concentration can be measured.
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3.

Clinical Pathology :

2. 3.

Serum samples from other animals in case of death of an animal. Mg2+ concentrations in the CSF (Normal levels : 1.25 mg/dL).

Necropsy Findings : Extravasation of blood into the subcutaneous and pericardium, endocardium, pleura, peritoneum and intestinal mucosa. Magnesium levels in the Aqueous humor can be estimated upto 48 hours after death, provided the environmental temperature is less than 230C. Differential Diagnosis : 1. 2. 3. Rabies. Acute Lead Poisoning. Nervous form of Ketosis.

4. Bovine Spongiform Encephalopathy. 5. Hypocalcaemia and Staggers in Sheep. Treatment : Treatment must be taken up as early as possible since recovery rates are very high if treated early. 1. 2. 3. Chloral hydrate can be administered intravenously to mange convulsions. Combined treatment of Calcium and Magnesium : Solution of 25% Calcium Gluconate and 5% Magnesium Hypophosphite at the rate of 500 mL in cattle and 50 mL for sheep can be administered intravenously. Magnesium containing solutions can be administered subcutaneously to prevent relapse. A combination of Magnesium adipate and 5% Calcium gluconate at the rate of 500 mL. Magnesium salts alone at the rate of 200 to 300 mL of 20% Magnesium Sulphate, slow intravenous injection. (Must be administered with caution since MgSO4 if given fast may lead to cardiac arrest and respiratory distress due to medullary failure. In such a case, treatment must be stopped and Calcium must be administered intravenously.) Control : 1. 2. 3. Shift animals from a high risk pastures to low risk pastures during season. 60 g and 7 g of Magnesium Oxide can be added to feed for cattle and Sheep respectively, every day. Magnesium Phosphate at the rate of 53 g / Kg.
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Magnesium Lactate can be used in place of Magnesium Sulphate. 15 % solution of Magnesium Gluconate may be used.

4. Magnesium Bullets that settle in the rumen and release 1 g per day can be administered. 5. Top dressing of pasture with Manganese limestone at the rate of 5600 Kg/ Hectare. 6. Magnesium Chloride hexahydrate at the rate of 450 g / 100 L of water.

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Post parturient haemoglobinuria

This is a sporadic condition that commonly affects only individual high-yielding dairy cows at the onset of lactation and is characterized by the development of per acute intravascular haemolysis and anemia with a potentially fatal outcome. It occurs due to Phosphorous deficiency. Cattle fed with rations low in Phosphorous, Selenium or Copper may develop this disease. Feeding of cruciferous plants may also precipitate this disease. Epidemiology : Adult cows often suffer with this condition 2 to 4 weeks after calving. High producing dairy cows between the 3rd to 6th lactation are commonly affected. The disease is not common in beef cattle. Soils deficient in Phosphorous and pastures grown on these soils lead to occurrence of this disease. Drought conditions. Ingestion of cold water in large quantities may precipitate episodes of Haemoglobinuria. Feeding turnips and beetroots may cause haemoglobinuria.

Pathogenesis : When milk production increases, there is draining of Phosphorous from the system. Along with this, if the dietary intake of Phosphorous is less, the glycolytic pathway in RBCs is affected. There is decreased glucose uptake and hence decreased ATP synthesis in RBCs. Low energy metabolism results in altered RBC structure and function. Diapedesis can be affected and RBC membranes become very fragile leading to haemolysis , which ultimately results in haemoglobinaemia and haemoglobinuria. These are irreversible changes and the life span of RBCs is decreased. Clinical Signs : 1. 2. 3. Haemoglobinuria occurs once haemoglobinaemia crosses threshold levels in the blood. Weakness, anorexia, depression in milk yield. Loss or destruction of RBCs exhibited in the form of pallor of oral and conjunctival mucous membranes.

4. Weak jugular pulse. Body temperature may rise up to 103.5oF. 5. Dry and firm faeces. 6. Dyspnoea and tachycardia due to anaemia. 7. Jaundice. 8. Disease extends up to 3 to 5 days.

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9. Recumbency in later stages. 10. Gangrene or sloughing off of the tip of the tail and digits. 11. Spontaneous recovery in 3 weeks. 12. Pica is normally found. Clinical Pathology : 1. 2. 3. Low levels of Phosphorous in blood on a herd basis. In severely affected animals Phosphorous levels may be as low as 0.4 to 1.5 mg/dL of blood. Decreased RBC count.

4. Heinz Bodies may be present in RBCs. 5. Urine may be red, brown or black coloured. 6. No RBCs are found in the urine. Necropsy Findings : Dilute blood. and Icteric mucous membranes. Liver : fatty infiltration and swollen. Urinary bladder contains discoloured urine.

Treatment : 1. 2. Severely anaemic animals may require blood transfusion at the rate of 10 mL/Kg body weight. Intravenous administration of Sodium Acid Phosphate at the rate of 60 g in 300 mL of distilled water. A similar dose can be administered subcutaneously followed by 3 subcutaneous administrations at 12 hour intervals after which a similar dose is administered orally. 3. Tonophosphon inections : 10 to 28 mL intramuscularly. 4. Haematinics and Imferon injections can be administered. 5. Secondary Ketosis may have to be addressed if present. Control : Adequate Calcium and Phosphorous supplements Copper Sulphate in copper deficient areas should be supplemented.

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Downer cow syndrome

It is a condition which occurs in cattle usually following parturient paresis. It is characterized by prolonged recumbency, even after 2 successive treatments with Calcium. Even though blood Calcium levels return to normal after treatment with Calcium, the animal cannot stand up due to setting in of ischaemic necrosis of muscles. Etiology : 1. 2. 3. Milk fever leading to ischaemic necrosis of muscles of pelvic limbs and injuries to the tissues around the hip joint and obturator muscles. Injuries resulting in spread eagling of limbs. This usually happens when the animal is housed on a slippery floor after or immediately before parturition. Dysctocia due to an oversized calf calls for manipulation of all tissues around the pelvis and leads to inflammation of the tissues. Hence the animal cannot get up. 4. Spread eagling or dystocia may be complicated by milk fever. Epidemiology : 1. 2. 3. Downer Cow Syndrome occurs commonly within 2 or 3 days after calving in high producing dairy cows immediately following milk fever. Prolonged recumbency due to milk fever because of delay in treatment is a major risk factor. Traumatic events to the pelvis, sciatic and obturator nerves during parturition associated with electrolyte imbalances (especially Potassium). 4. Serum Phosphorous levels also decline along with Calcium levels in milk fever. Hypomagnesaemia which accompanies hypocalcaemia may also be present. 5. Hypokalaemia itself which occurs because of prolonged recumbency which increases cell membrane permeability. Pathogenesis : Prolonged recumbency before treatment may lead to further delay in treatment. This results in pressure damage to muscles and subsequent inability of the animal to stand up after treatment. Prolonged recumbency leads to varying degrees of ischaemic necrosis of capillaries of major vessels of hind limb muscles (semitendinosus and muscles caudal to the stifle) which leads to tissue anoxia, cell damage, inflammation and swelling of the muscles. The swelling further increases pressure on the muscles and does not allow the muscles to expand since expansion is contained by the fascia surrounding the muscles. This condition is known as Pressure Induced Compartmental Syndrome. In this condition, the Sciatic nerve may also get involved.

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These events may also happen due to traumatic events post parturition. Other complication which can occur during recumbency are acute mastitis, decubitus ulcers, traumatic injuries to limbs.

Clinical Signs : Animals make an attempt to stand but may not be able to, post being affected by milk fever. 30% of the animals treated for milk fever may not be able to stand even after 24 hours. Such animals are called Downer Cows. Food intake may reduce but the animal is bright and alert. The animal may not go completely off feed and water. Body temperature is normal and heart rate may either be elevated or normal. Some cows may have tachycardia and arrhythmia and hence Calcium if not administered carefully may lead to death. Defaecation and urination are normal and depend on the quantity of feed intake. Proteinuria is present indicating muscle damage. Those animals which attempt to stand are able to lift their hind quarters or pelvic area 20 to 30 cm above the ground and then fall back again. Crawling and creeping : the condition is therefore known as Creepers and the animal is said to have a Frog leg Attitude. If such cows are lifted and made to stand on a non-slippery floor, they might be able to stand with assistance from hip slings. Those animals which do not make an attempt to stand cannot stand even with support. Limbs are stiff, painful and numb and cannot bear weight. Heperflexion of the fetlock joint is an indication of Pudendal nerve damage. Hind limbs are stretched towards the elbows in front. Ischaemic necrosis of medial thigh muscles, dislocation of the hip joint with or without rupture of Ligamentum Teres. Some cows are hyperaesthetic with all four legs sticking out and in lateral recumbency. They may be unable to eat or drink. These cows are known as Non alert Downers and are said to have undergone brain damage.

Decubitus ulcers in a recumbent cow

Spread-eagled legs

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Secondary Complications : 1. 2. 3. Coli form mastitis Decubitus ulcers especially at the hock and elbow joints. Trauma of tuber coxae.

4. Death may occur in 48 to 72 hours in case of myocarditis. 40 to 50% cows can stand in 4 days or less if nursed and treated properly. Beyond 7 days the prognosis is poor. Rarely, some animals may stand after 14 days. Clinical Pathology : 1. 2. Calcium, Phosphorous, Glucose and Magnesium levels in the blood may be in the normal range. The haematological parameters may be similar to that of a recently calved normal cow. Creatine Phosphokinase and Aspartate Transaminase levels in the serum may increase 18 to 24 hours after onset of recumbency and remain elevated for the next few days. Continued C.P.K. elevation indicates continued muscle damage. 3. Proteinuria : turbid and brown coloured urine due to Myoglobinuria indicating muscle damage. serious condition with poor prognosis. Necropsy Findings : 1. 2. 3. Traumatic lesions of the hind limbs. Decubitus ulcers. Haemorrhage and degeneration of medial thigh muscles. 4. Serum Creatinine levels higher than 130 mmol/L and Serum Urea levels greater than 25 mmol/L indicating a

4. Haemorrhages around the hip joint. 5. Ischaemic necrosis of large muscles like Gracilis, Pectineus and Adductor muscles (medial thigh muscles). 6. Eosinophilic infiltration of necrotic thigh muscles. 7. Heart is dilated and flabby. Focal myocarditis. Treatment : 1. 2. Magnesium salts, Phosphorous, Corticosteroids, Vitamin E and Selenium supplements. Large quantities of parenteral electrolyte solutions containing Potassium, Calcium, Magnesium and Phosphorous. Once necrosis sets in and muscles lose their normal physiology and texture, treatment may not succeed. 3. The animal must be provided with soft and comfortable bedding. Animal must be rolled from side to side several times a day to minimalize ischaemic necrosis.
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4. Lifting devices can be applied to the tuber coxae or the whole animal. Hip slings or body slings can be used for this purpose. 5. Cows can be made to sit in a tub / water flotation tank filled with hot water (100 to 102 oF). Cows in lateral recumbency will roll into sterna recumbency and gradually attempt to stand. However, Cows with ruptured tendons, fractures, luxated coxofemoral joints, septic polyarthritis, and other physical injuries of the musculoskeletal system are not good candidates for flotation. The most suitable case for flotation would appear to be the downer cow as a sequel to milk fever. 6. If all the above fail, animal must be euthanized.

Body sling
Control : The early detection and treatment of milk fever will reduce the incidence and severity of downer cow syndrome. Under ideal conditions, cows should be treated during the first stage of milk fever before they become recumbent. Once recumbent, cows should be treated as soon as possible and not delayed for more than 1 hour. Cows with milk fever should be well bedded with liberal quantities of straw, or moved to a soft-ground surface. Recumbent cows should be coaxed and assisted to stand if possible after treatment for milk fever. If they are unable to stand, they should be rolled from one side to the other every few hours if possible. Dairy cows should be placed in a comfortable well-bedded box stall prior to calving and should be left in that box stall until at least 48 h after partition in the event that milk fever develops.

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Paralytic myoglobinuria (azoturia)

It is a disease of horses also known as Monday Morning Sickness, Equine Exertional Rhabdomyolysis, or Tying Up, characterized by Myoglobinuria and muscular disease.

Muscle stiffness in a horse affected by azoturia

Etiology : 1. When horses are rested, large amounts of glycogen get stored in the muscles and when the animal is later exercised suddenly, glycogen is rapidly metabolized to Lactic acid. Since the rate of production of Lactic acid is greater than its clearance from the circulation, Lactic acid accumulates in the muscles . This causes coagulation and release of Myoglobin manifested as Myoglobinaemia and finally Myoglobinura. 2. 3. The overfeeding of non-structural carbohydrates (grain and pellets, for example). Poor conditioning or fitness, sudden increase of workload.

4. Electrolyte or mineral imbalances, especially seen with potassium. 5. A deficiency in selenium or vitamin E 6. Imbalance of hormones, including the reproductive hormones in nervous fillies and mares and thyroid hormones in horses with hypothyroidism 7. Wet, cold, or windy weather conditions.

Epidemiology : 1. 2. 3. Race horses fed heavily on grains are at a risk. Horses with a history of inactivity for 2 or more days before onset of disease. Wet, cold or windy weather conditions.

Pathogenesis : Excess lactic acid accumulation in the muscles leads to coagulative necrosis of the muscle fibers leading to a hard and painful swelling of the large muscles. Gluteal muscles are most commonly affected due to their high glycogen content. The swelling causes pressure on the sciatic nerve.
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It leads to neuropathic degeneration of other muscles supplied by the sciatic nerve, such as the Rectus femoris and Vastus muscles. Urine is dark brown in colour due to Myoglobinuria. Prolonged recumbency can lead to decubitus ulcers which may later lead to septicaemia and death. Myocardial degeneration leading to death. Acute renal failure due to Myoglobin which can damage the glomerulus and renal tubules (Pigment nephrosis).

Clinical Signs : 1. Signs involving the loco motor system develop 15 minutes to 1 hour after exercise. Even mild exercise can precipitate this condition. There is swelling of muscles, immobility, reluctance to move and profuse sweating. Sometimes all four limbs or only the hind limbs may be affected. 2. 3. The animal can completely recover in a few hours to days if sufficient rest is provided. Further exercise may lead to recumbency. Initially, animals have a Dog sitting posture and may later become laterally recumbent. 4. Animal becomes very restless and makes repeated attempts to get up (to and fro struggling). 5. Rapid respiration, pulse is small and hard. 6. Rise in body temperature up to 105oF. 7. Dark brownish to red coloured urine. 8. Normal appetite and water intake. Non recumbent animals have a better prognosis. Clinical Pathology : 1. 2. Myoglobin and Protein casts are present in the urine. Increased specific gravity. Increased serum C.P.K. levels.

Necropsy Findings : Gross and microscopic changes of muscles, especially Gluteus and Quadriceps group of muscles. Grossly, waxy cooked appearance of the entire surface of the muscles is evident.

Diagnosis : 1. 2. 3. History of exercise after rest. Discolouration of urine. Reluctance to move due to pain.

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Treatment : 1. 2. 3. Further exercise must be avoided and the animal must be provided rest. Hoists should be kept standing, hoists may be used if required. Chloral hydrate at the rate of 5 mg/50 Kg as a solution can be administered orally through a stomach tube in order to sedate and calm down the animal and also to bring about analgesia. Sedation prevents the animal from struggling and hurting itself in the process. 4. Corticosteroids such as Prednisone or Prednisolone at the rate of 100 to 300 mg/day intramuscularly to bring down the inflammation. Dexamethasone can be administered intravenously. 5. Thiamine hydrochloride at the rate of 0.5 g can be administered intramuscularly. 6. Antihistamines can be administered. 7. Vitamin E supplements must be included. 8. Large volumes of intravenous fluids containing electrolytes must be administered to maintain the urine output. 9. Sodium bicarbonate can be administered intravenously or orally to keep the urine alkaline and neutralize the lactic acid accumulated in the muscles. It prevents precipitation of Myoglobin in the renal tubules. Control : 1. 2. Avoid sudden strenuous exercise after rest. Exercise rested horses very lightly initially and gradually increase the duration and intensity of exercise.

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