METABOLIC AND DEFICIENCY DISEASES IN DAIRY CATTLE :ADVANCES IN DIAGNOSIS AND THERAPEUTIC APROACH

METABOLIC AND DEFICIENCY DISEASES IN DAIRY CATTLE :ADVANCES IN DIAGNOSIS AND THERAPEUTIC APROACH

Dr. Archana Jain, Professor & Head

Department of Veterinary Physiology and Biochemistry

College of Veterinary Science & A. H., NDVSU, Mhow (MP)453446

 

Introduction

Metabolism is defined as all physical, chemical, and metabolic processes occurring in a living cell related to absorbance, breakdown or synthesis of necessary organic substances in the body. Metabolic processes are associated with the release of a variety of metabolites that are either used as building blocks or degraded and excreted from the body as waste. During metabolism the organisms extract energy from nutrients for normal functioning of the body. Therefore, metabolism includes all metabolic processes that make life and normal of the organism possible. Dysfunction of any of the metabolic processes is associated with malfunctioning of different systems of the body. Disturbance of one or multiple metabolic processes, related to regulation of a certain metabolite in the body fluids, is known as metabolic disease or disorder or production diseases. The term metabolic or metabolic disorder has been used to indicate the deficiency or excesses of one or more nutrients. This may indicate a group of diseases characterized by disturbance of one or more plasma metabolites such as ketone bodies, calcium, minerals, vitamins or nonesterified fatty acids. A production disease is a concept developed by Jack Payne and his team at Compton Research Institute during 1970s to indicate the breakdown of animals’ capacity to meet the demands of high production couple with unsuitable feeding during modern husbandry. The term production disease is focused more on High producers.

Metabolic disorders of cattle are a group of diseases related to the fact that they are associated with the disturbance of one or more blood metabolites that affect dairy cows immediately after parturition/ sick cows. There are several metabolic disorders identified in dairy cows during the first month after parturition and the most frequent ones are the following: (1) subacute and acute ruminal acidosis, (2) laminitis, (3) ketosis, (4) fatty liver, (5) left displaced abomasum (LDA), (6) milk fever, and (7) bloat. For example, ketosis is associated with enhanced ketone bodies (i.e. beta-hydroxybutyric acid – BHBA) in the blood; fatty liver is associated with enhanced nonesterified fatty acids (NEFA) and their accumulation in the liver; acidosis is associated with increased production of organic acids/ hydrogen ions (e.g. acetic, propionic, and butyric acids) in the rumen and low rumen pH; and milk fever is associated with decreased blood calcium. The most interesting observation with regards to the occurrence of metabolic disorders is that they are highly associated with each other. For example, cows affected by milk fever are more prone to mastitis, retained placenta, metritis, LDA, dystocia, udder edema, and ketosis; cows affected by acidosis are more prone to laminitis, LDA, milk fever, mastitis, and fatty liver. One speculation is that there might be a common etiological factor that initiates the cascade of metabolic disorders. Therefore, scientists are searching to identify such a common causal agent of metabolic disorders; however, no such agent has been identified so far. One of the cause may be feeding high-grain diets which gives initial stimulus for disturbing the multiple metabolic processes appearing as interrelated metabolic disorders.

Main Metabolic Disorders of Dairy Cattle 

1. Ruminal Acidosis: Symptoms: Subacute and acute rumen acidosis (i.e. SARA and ARA) are very prevalent disorders of dairy herds. Two groups of cows at special risk for acidosis are early lactation cows and cows with high intake of grain in their diets. Acute acidosis is characterized by specific symptoms, can be treated directly; however, symptoms of subclinical acidosis are not very well defined. Which may be due to either poor forage quality or poor bunk management, because subclinical acidosis inflicts major economic losses to dairy herds? The most typical clinical manifestation of subclinical acidosis is reduced or inconsistent feed intake. Other associated signs include decreased milk production, lowered fat content in the milk, poor body condition score, high culling rate, diarrhea, and laminitis. Subclinical acidosis occurs very often even in well managed and in high producing dairy herds.

Acute acidosis results in very sick cows: physiological functions may be significantly impaired and death may occur. Acute acidosis is characterized by a significant decrease in ruminal pH (≤ 5.0), enhanced concentrations of volatile fatty acids (VFA) and lactate in the rumen as well as a large decrease in the number of protozoa and bacteria. Acidosis is most prevalent following intake of large amounts of grain or other rapidly fermented carbohydrates. Excessive intake of readily fermented starch often occurs immediately after calving when cows are first being adapted to a high-grain diet. For optimum ruminal fermentation and fiber digestion, ruminal pH should range between 6.0 and 6.4. Under normal conditions, bacteria in the rumen ferment the starch contained in cereal grains into weak organic acids such as VFA and lactic acid. VFA are readily absorbed by papillae on the rumen wall, then enter in the bloodstream and used for energy and milk production. However, under acidic conditions VFA accumulate in the rumen and contribute to acidosis. This may increased the acidity in blood stream

Treatment

It is important to treat the sick cow as soon as possible and the treatment depends on the severity of the clinical symptoms. If cows show mild signs of acidosis such as diarrhea, they should be fed a diet with smaller proportion of grain or increased amount of roughage. Cows with more severe signs such as severe diarrhea, off feed, and in a depressed state should be removed from the grain diet and fed roughage only. Cows should be given orally about 120 g of sodium bicarbonate and an electrolyte replacer dissolved in four to five liters of water. This treatment should be repeated three times per day if possible and the cows need to be encouraged to walk around.

Prevention

There are two commonly used management practices for prevention of ruminal acidosis: (1) increasing the proportion of roughage in the diet, and (2) decreasing the intake of starch (i.e. cereal grains such as corn, wheat, or barley). The reason for increasing the amount of roughage, in the form of hay or forages, is that it lowers the frequency of eating as well as the size of a meal. In addition, by increasing the proportion of roughage in the diet the time of chewing and the amount of saliva produced will be increased. Moreover, feeding roughage has two other beneficial effects: (1) the size of grain particles entering the rumen decrease and thereby increases its rate of fermentation, and (2) the time of mastication increases and thereby the amount of buffers from saliva which neutralizes and dilutes ruminal acids. Feeding direct-fed microbials or probiotics that utilize glucose or lactate prevents their accumulation and the lowering of rumen pH.

 

2. Laminitis: Symptoms: Laminitis is an inflammatory, non-infectious condition of the foot. Feeding diets rich in highly fermentable carbohydrates that induce an acidotic state has been identified as one of the key factors in pathogenesis of laminitis. Digestive disorders such as acidosis, changes in the gastrointestinal bacterial flora, and translocation of endotoxin into the bloodstream predisposes cows to laminitis. Gram negative- related infectious diseases such as mastitis, metritis, and foot rot also contribute indirectly to the etiology of the disease by providing large sources of endotoxin. Several environmental factors including hard surfaces, poor bedding, body weight, feet and leg structure and lack of or excessive exercise. Laminitis may be developed due to: (1) transferring of endotoxin from gastrointestinal tract into the systemic circulation and damage of blood vessels, (2) lowering of the availability of nutrients and oxygen to the foot tissue, (3) breakdown and degeneration of the foot tissue, and (4) separation of bone and soft tissue with bleeding and bruises signs and development of inflammation (i.e. laminitis). There are three main forms of laminitis recognized as acute, sub acute, and chronic laminitis. During acute laminitis, although the cow is systemically ill and inflammation of the corium is evident, very few clinical signs are observed. However, local sign such as pain, swelling of the foot tissue and temperatures slightly greater than normal above. Sub acute laminitis is less apparent form of the disease with signs like softer horn, yellow coloration of the sole and bleeding stains in the solar area. Chronic laminitis is associated with the growth pattern of the keratinized horn is disrupted and the shape of the digit is altered into a more elongated, flattened, and broadened one. Moreover, grooves and ridges on the dorsal wall become more prominent, giving a rippled appearance to the foot. Other important signs include ulcerations on the solar area, double soles with yellowish coloration, destruction of the small blood vessels, separation between the dermal and epidermal junction, and finally internal foot destruction. If the disease process has progressed to this irreversible point no medication can return the foot to its original normal structure.

 

3. Parturient paresis: parturient paresis, also called milk fever, in cattle, a disorder characterized by abnormally low levels of calcium in the bloodespecially in high milk producers. It is an acute to per acute, non-febrile, flaccid paralysis of mature dairy cows that occurs most commonly at or soon after parturition. It is manifest by hypersensitivity and excitability, generalized paresis, and circulatory collapse. It occurs within three days after calving, at a time when the cow’s production of milk has create severe strain on calcium stores. The early signs include loss of appetite and depression or restlessness, followed by muscle weakness and spasms of the hind legs. In acutecases generalized paresis and apparent coma occur, followed by circulatory collapse and death. The death rate in untreated animals may run as high as 90 percent. Fever is not a sign in this disorder.

Diagnosis: Animals show signs of hypersensitivity and excitability. Cows may be mildly ataxic, have fine tremors over the flanks, display ear twitching and head bobbing, may appear restless, shuffling their rear feet and bellowing. If calcium therapy is not instituted, cows are unable to stand but can maintain sternal recumbency. They are obtunded, anorectic, have a dry muzzle, subnormal body temperature, and cold extremities. Auscultation reveals tachycardia and decreased intensity of heart sounds. Peripheral pulses are weak. Smooth muscle paralysis leads to GI stasis, which can manifest as bloat, failure to defecate, and loss of anal sphincter tone. An inability to urinate may manifest as a distended bladder on rectal examination. Cows often tuck their heads into their flanks, or if the head is extended, an S-shaped curve to the neck may be noted. Cows lose consciousness progressively to the point of coma. Differential diagnoses include toxic mastitis, toxic metritis, other systemic toxic conditions, traumatic injury (eg, stifle injury, coxofemoral luxation, fractured pelvis, spinal compression), calving paralysis syndrome, aspiration pneumonia, may also occur concurrently with parturient paresis or as complications.

Treatment:  Mainly IV injection of a calcium gluconate salt, although SC and IP routes are also used. A general rule for dosing is 1 g calcium/45 kg (100 lb) body wt. Most solutions are available in single-dose, 500-mL bottles that contain 8–11 g of calcium. In heavily lactating cows, a second bottle given SC may provide a prolonged release of calcium into the circulation Many solutions contain phosphorus and magnesium in addition to calcium. Magnesium may protect against myocardial irritation caused by the administration of calcium. Magnesium is also necessary for appropriate parathyroid hormone (PTH) secretion and activity in response to hypocalcemia. Most products available to veterinarians contain phosphite salts as the source of phosphorus.

 

4. Transport Tetany : Transport tetany occurs after the stress of prolonged transport, typically in cows and ewes in late pregnancy, although it is also seen in lambs transported to feedlots and in cattle and sheep transported to slaughter. Crowded, hot, poorly ventilated transport vehicles (railroad cars or trailers) with minimal or no access to feed or water appear to predispose animals to the condition; however, prolonged travel by foot is also a risk factor. The disease is characterized by recumbency, GI stasis, and coma, and is generally fatal. Although cows in late gestation are most commonly affected, the disease is also seen in cows that have recently calved, as well as in bulls, and dry cows. Risk factors include heavy feeding before shipment, deprivation of feed and water for >24 hr during transit, and unrestricted access to water and exercise immediately after arrival. Exposure to hot environmental conditions is also associated with an increased incidence. Hypomagnesemia may be a precipitating factor in cattle and a contributing factor in sheep. Early clinical signs include restlessness and excitement, trismus, and grinding of teeth. A staggering gait may be seen, and later, if recumbent, cattle often demonstrate paddling of the hindlegs. Rumen hypomotility and GI stasis are seen, and animals become completely anorectic. Tachycardia and rapid, labored respiration may develop. Abortion may be a complication. Cattle that do not recover gradually become more obtunded to the point of coma and die within 3–4 days. Moderate hypocalcemia and hypophosphatemia may be seen in cattle.

Some animals respond to treatment with combinations of parenteral calcium, magnesium, and glucose. IV injections of calcium borogluconate (25% solution at 400–800 mL/cow or 100 mL/ewe) or calcium borogluconate with magnesium sulfate (5% solution, same volumes) can be administered slowly. A dose of 50 mL/day can be given SC to affected lambs in feedlots. Repeated injections may be warranted, but failure to respond is common (50%) and most likely due to concurrent muscle necrosis. Additional treatment considerations include IV administration of large volumes of polyionic fluids such as lactated Ringer’s solution. Animals should be offered good quality feeds (eg, alfalfa hay), fresh water, and soft bedding with good footing underneath. Sedation may be necessary if animals are hyperexcitable or convulsing.

5. Potassium Metabolism: Potassium homeostasis is mainly determined by the balance between absorption of potassium from the GI tract and subsequent excretion by the kidneys (all animals) and saliva (in adult ruminants). Transport of potassium is passive in the small intestine and active in the colon under the influence of aldosterone. The most important hormone affecting renal and salivary potassium excretion is aldosterone, which is released from the zona glomerulosa of the adrenal gland in response to hyperkalemia and other factors. One of aldosterone’s primary actions is to enhance the secretion of potassium ions in the distal renal tubules and collecting ducts.

At least 95% of whole body potassium is intracellular, with skeletal muscle containing 60%–75% of the intracellular potassium. Marked changes in serum or plasma potassium concentrations alter the resting membrane potential of cells, because the potassium gradient generated by Na⁺/K⁺-ATPase is the main cause for the negative electric potential across cell membranes. Therefore, hypokalemia or hyperkalemia alters the resting membrane potential, resulting in clinically important changes in cellular and organ function.

Hypokalemia can occur in any animal receiving large volumes of IV fluid or having a marked and sustained reduction in feed intake. Clinical signs in most animals with mild to moderate hypokalemia are mild and nonspecific. Severe hypokalemia is associated with ventroflexion of the head or recumbency due to generalized muscle weakness and cardiac arrhythmias, including both atrial and ventricular premature complexes that may lead to more complex cardiac arrhythmias. Prolonged and profound hypokalemia can result in a myopathy difficult to treat. Cats can be affected by a feline hypokalemic polymyopathy, and Burmese cats have an autosomal recessive disorder that leads to hypokalemic myopathy.

Hyperkalemia usually results from inadequate urinary excretion of ingested potassium and is common in monogastric animals with urinary tract obstruction and bladder rupture. Hyperkalemia in horses and ruminants can also result from exertional rhabdomyolysis, because skeletal muscle contains a large percentage of whole body potassium. Severe hyperkalemia is associated with generalized muscle weakness, depression, and cardiac conduction disturbances that may lead to lethal cardiac arrhythmias. Pseudohyperkalemia in serum can occur in animals with thrombocytosis as a result of the excessive release of intracellular potassium stores from platelets during clotting. Pseudohyperkalemia in serum and plasma occurs when extensive hemolysis is present because of the high potassium concentration in RBCs in most species, although some species have genetic differences in their erythrocytic potassium concentration.

 

6. Fatigue and exercise: Muscular fatigue during exercise is the decline in the ability of a muscle to generate force of contraction, resulting in the inability of the animal to continue to perform at the same level of intensity. Alterations in cardiovascular parameters, serum electrolytes, and muscle tissue may be observed if physiologic compensatory mechanisms are exhausted. Treatment involves rest, rehydration, restoration of normal serum electrolyte concentrations, and cooling strategies.  Fatigue may occur during both aerobic and anaerobic exercise and at submaximal effort.

Factors affect the onset of fatigue:

• ambient environmental temperature
• hydration status and serum electrolyte concentrations
• external motivators
• the animal’s desire to work

As muscular effort increases, glycogen depletion, intracellular acidosis, and accumulation of metabolic byproducts will contribute to the onset of fatigue. Fatigue during exercise can also be the result of pathologic conditions, including diseases that affect oxygen uptake, energy metabolism, or neuromuscular function. This discussion focuses on muscular fatigue in healthy animals.

Pathophysiology of Fatigue: Fatigue is considered a normal consequence of exercise of prolonged duration or high intensity, and it is regarded as an intrinsic safety mechanism. Without the onset of fatigue, or if fatigue is delayed, structural damage to the myocytes and supportive tissues may occur. There are two types of fatigue: peripheral and central.

Peripheral fatigue is fatigue secondary to altered muscle function. The primary cause is failure of ATP to resynthesize, with accumulation of ADP and inorganic phosphate ions. Studies of muscle metabolism after exercise to identify peripheral fatigue have relied mainly on muscle biopsies and direct measurement of muscle glycogen, creatine phosphate, ATP, ADP, inosine monophosphate, inorganic phosphate, glycolytic intermediary products, pH, and other metabolites. Other studies have investigated the expression of mRNA in muscle tissue to monitor adaptations in gene expression of proteins that regulate oxygen-dependent metabolism, glucose metabolism, and fatty acid utilization.

Indirect serum biomarkers associated with peripheral fatigue:

• lactate
• ammonia
• hypoxanthine and xanthine
• markers of oxidative damage (thiobarbituric acid reactive substances, glutathione, and glutathione peroxidase)
• inflammatory mediators (IL-1, TNF-α)
• lymphocytes

Central fatigue is defined as an alteration in the signals arising from the CNS, directly decreasing performance by modifying the frequency of the action potential in the motor neurons. Central fatigue may occur secondary to pain, dyspnea, perceptions of exertion, hypoglycemia, hyperthermia, ammonia accumulation, increases in serotonin, altered amino acid metabolism, and changes in extracellular ions.

Central fatigue is associated with:

• decreased motivation
• lethargy
• loss of muscle coordination

However, the cause of central fatigue is multi-factorial, and the response to these stimuli is highly variable. For example, some horses can continue endurance exercise at speed despite severe hyperthermia, dehydration, and plasma electrolyte disturbances.

 

Nutritional deficiency diseases: Deficiency diseases which occur due to vitamins, minerals deficiency. These include, but are not limited to, Protein Energy malnutrition, Vitamin deficiencies, and mineral deficiencies.

1. Energy and Protein Deficiency: Animals require energy and proteins for different body functions. Energy is required for maintenance (to maintain the body, respiration and digestion), production (growth, milk and workforce) and reproduction (pregnancy). An animal derives energy from dietary carbohydrates. Proteins are required for formation of body tissue. Proteins can be derived from feed and are formed by intestinal flora. Adequate supply of both energy and protein is essential for the general health of any animal. The requirement of both energy and protein by any animal depends on the bodyweight of the animal and the degree of production expected from the animal. Prolonged deficiency of both proteins and energy would result in loss of condition and in ability to be productive.
   Malnutrition caused by lack of energy and proteins may occur all over the world but is more prevalent in the tropics. Prolonged malnutrition leads to death. Animal feeds vary in their levels of energy and proteins. Straws such as rice straw and wheat straw are poor sources of both proteins and energy whereas concentrates like dairy meal may be rich in both.  In the tropics, good quality pastures may provide adequate protein and energy for maintenance and production. However in situations of drought or overgrazing, animals are liable to receive inadequate energy or proteins from pastures.

Deficiency of energy is the most common nutrient deficiency which limits the performance of grazing animals. Feed may be inadequate due to overgrazing, drought, poor quality or digestibility or expense. Sometime forage may contain an excess of water, limiting energy intake.

Energy and Protein deficiencies: 

• Retarded growth in young animals, reduced appetite, lower feed intake, and a delay in the onset of puberty.
• A short lactation period in animals and decline in milk production.
• Marked loss of bodyweight, especially during late pregnancy and early lactation.
• Prolonged periods of anoestrus, lasting several months, which have marked effect on the reproductive performance of a breeding herd.
• Calves and lambs may be born weak and undersized, prolonged time to reach maturity, Lack of muscle development.

Prevention – Control – Treatment

Treatment and prevention of malnutrition is beyond the reach of most farmers. Diseases that worsen the effects of malnutrition can be alleviated by appropriate treatment e.g. deworming. Severely malnourished animals usually do not survive even when food again become available, so if a drought is expected or feed sources otherwise too few, it is wisest to sell/slaughter the weaker animals before the condition goes down too much. Malnourished animals should not be forced to be productive e.g. by putting them to work. This will only worsen the condition.

2. Vitamin Deficiency: In ruminant diseases, only fat soluble vitamins A, D, E and K have real importance.

Vitamin A: This is available in most green plants, and if the animals graze on well managed pastures and forage, deficiencies will not occur. However, cattle fed on poor quality roughage, such as poor quality hay and straw, require supplementation.

Clinical Signs: Decreased appetite leading to reduced growth, impaired night vision, increased still births in pregnant animals due to affected reproductive function, especially in cases where dry cows are offered poor diets, fainting fits in calves: the calf collapses as if in a deep sleep then gets up and walks away quite normally, in latter stages of deficiency, bone growth is affected and this may cause pressure on nerves to the eye, which may lead to total blindness.

Diganosis :
This can be done by investigating the history of animals and their diets, and by analysis of blood and liver samples in a laboratory.

 

Vitamin D: There is little vitamin D in plants. Animals obtain most of it from the sun. Vitamin D is necessary for the absorption of calcium and phosphorous from the intestines and the deposition of the minerals in bone as well as in the maintenance of normal blood levels. Vitamin D deficiency in young calves is likely to occur when they are housed in dim lights and offered poor quality diets.

Clinical Signs: Reduced Growth Rates, legs may be bent and there is abnormal swelling, with stiffness and lameness occurring in a number of animals, the teeth may be out of line and the jaw bone deformed.

Treatment: Treatment is by injecting vitamin D and by correcting the ration, including oral supplementation with vitamin D.

 

Vitamin K: This is available in plenty in leafy forages. Primary deficiency does not occur. Deficiency can be induced by dicoumarol poisoning such as warfarin rat poison and mouldy clover hay, which inhibit the action of vitamin K. Vitamin K is involved in blood-clotting mechanisms.

Clinical Signs: Failure of blood clotting, including excessive bleeding from cuts, appearance of large red hemorrhagic areas in the membranes of the mouth, eyes and nose, abdominal pain and lameness.

Treatment and Prevention

• Identify and remove the source of poison.
• Give Vitamin K by mouth or through injection.

 

B Vitamins: This group of vitamins is formed by micro-organisms in the rumen and any excess is absorbed by the cow. They are also present in sufficient quantities in milk and therefore primary dietary deficiency is never seen.

Vitamin C: This is produced in tissues of all farm livestock (cattle, sheep and goats) and dietary supply is unnecessary.

 

3. Mineral Imbalance: Minerals are essential for all animals and influence the efficiency of livestock production. Five percent of the bodyweight of an animal consists of minerals.

Causes of Mineral Imbalance

Farming practices can determine the presence or absence of specific mineral nutrients in animal feed. Heavy applications of nitrogen fertilizer can reduce the copper, cobalt, molybdenum, and manganese content of the pasture. Lime may reduce plant copper, cobalt, zinc and manganese levels but increase the molybdenum content. Cattle sometimes deteriorate in spite of an abundant feed supply. Mineral imbalances (deficiencies or excesses) in soils and pastures may be responsible for low production and reproductive problems among grazing animals in the tropics. Mineral deficiencies in grazing animals are associated with specific regions and are directly related to soil characteristics. Plants grown on tropical soils have been shown to be highly deficient in a number of major and trace minerals needed by grazing animals. Thus, it is necessary to provide these elements as dietary supplements to promote efficient and profitable livestock production in warm climatic regions. In tropical regions marked leaching and weathering of soils under conditions of heavy rainfall and high temperatures make the deficient in plant minerals. Increasing crop yields remove minerals from the soil at a faster rate so deficiencies are frequently found on the most progressive farms.
Even though a diet may contain adequate amounts of nutrients, but certain other factors may decrease the absorption of these nutrients, thus reducing the value of the dietary supply. Excess phosphate reduces calcium absorption. Excess calcium reduces the absorption of iodine. Many other examples exist of antagonisms between elements.

Signs of Mineral Imbalance

• Wasting diseases, loss of appetite or depraved appetite
• Loss of hair, de-pigmented hair and skin disorders.
• Non-infectious abortion.
• Diarrhea, tetany, bone abnormalities
• Low fertility.

Mineral Requirements

Around 15 mineral elements have been identified which are nutritionally essential for ruminants. These are 7 major minerals – Calcium, Phosphorus, Potassium, Sodium, Magesium and Sulphur and 8 trace minerals – Cobolt, Copper, Iodine, Iron, Manganese, Molybdenum, Selenium and Zinc. Mineral requirements depend on the level of productivity. The zinc requirements for spermatogenesis and testicular development in male sheep are higher than for growth. Manganese requirements are lower for growth than for fertility in sheep. Improved management practices that lead to improved milk production and growth rates for ruminants will necessitate more attention to mineral nutrition. Levels of mineral deficiencies that are small under low levels of production become more severe with increased levels of production, and previously unsuspected nutritional deficiency signs usually occur as production levels increase. Specific mineral imbalances are associated with specific soil types. Important differences in mineral metabolism are the result of breed and adaptation. It is not unusual for cattle introduced into an area to show deficiency signs while the indigenous breeds which are slow-growing and late-maturing do not exhibit the deficiencies to the same degree. The cattle which are new to the region and have not adapted may sweat profusely and lose saliva and mucous from the mouth, thus losing significant quantities of minerals, particularly in the arid tropics. Since tropical plant foods contain fewer minerals during the dry season, it is assumed that grazing livestock would most likely suffer mineral inadequacies during this time. However it has been found that mineral deficiencies are more common during the wet season. During the wet season livestock gain weight rapidly and there is thus a greatly increased requirement for these elements by the grazing animal. During the dry season, inadequate protein and energy results in animals losing weight which lowers mineral requirements.
Mineral Deficiencies and Toxicities

The mineral elements most likely to be lacking under tropical conditions are Calcium, Phosphorus, Sodium, Copper, Cobalt, Iodine, Selenium and Zinc. In some regions, under specific conditions, Magnesium, Potassium, Iron and Manganese may be deficient and excesses of Fluorine, Molybdenum and Selenium and extremely detrimental.

Diagnosis of Mineral Deficiencies and Imbalance

Mineral nutrition disorders range from severe mineral deficiencies or toxicities characterized by well-marked clinical signs and obvious signs of disease to mild and temporary conditions difficult to diagnose and expressed as a vague ill health or unsatisfactory growth and production. The mild conditions assume great importance because they occur over large areas and affect a large number of animals in addition to the fact that they can be confused with the effects of energy and/or protein deficiencies and various types of parasite infestation.  Clinical signs of mineral deficiencies, pathological and biochemical examinations, along with mineral analyses of soil, water, plant and animal tissues and fluids have all been used, with varying degrees of success to establish mineral deficiencies and excesses, but the most reliable method of confirming mineral deficiencies is in the response from specific mineral supplementation.

• Blood mineral data must always be viewed with caution. Bone and liver tissue are much more reliable.
• Common salt, because it tastes good, is a valuable ‘carrier’ for other minerals. Mineral supplements should be available ‘free choice’ and offered in rain-proof boxes. Consumption is often 10% less when provided in block versus loose form.
• Properly formulated supplements are of benefit to livestock only if they are available at all times in a fresh, dry form and presented in suitably constructed feeder boxes, accessible by all members of the herd or flock.
• A complete mineral mixture must contain a Fluorine-Phosphate source, Calcium, Cobalt, Copper, Iodine, Manganese, and Zinc, Selenium, Magnesium, Potassium, Sulphur, Iron or additional elements can be incorporated into a mineral supplement as new information suggests a need.
• Information printed on the tag attached to the bag of mineral supplement is sometimes incorrect or expressed in a way that makes it difficult for the farmer to know what is being purchased and if it is adequate for the purpose intended. Seek expert advice in case of doubt.

Calcium and Phosphorus

In cattle the most common mineral deficiency is lack of Phosphorus. In most livestock grazing areas of tropical countries, soils and plants are low in Phosphorus. These elements have a vital function in almost all tissues in the body and must be available to livestock in the proper quantities and ratio.

• 99% of the Calcium and 80% of the Phosphorus in the entire body are found in the bones and teeth. Calcium is essential for skeletal formation, normal blood clotting, neuromuscular excitability, enzyme activation and permeability of membranes.
• Phosphorus is essential for proper functioning of rumen micro-organisms, especially those which digest plant cellulose, utilization of energy from feeds, buffering of blood and other fluids, many enzyme systems and protein metabolism

Requirement: Dietary Calcium: Phosphorus ration between 1:1 and 2:1 is assumed to be ideal for growth and bone formation as this is approximately the ratio of the two minerals in bone. If there are excessive amounts of Calcium and Phosphorus in the diet, the availability of certain trace elements may be decreased.
Symptoms: Deficiency signs of borderline Calcium and Phosphorus deficiencies are not easily distinguishable from other deficiencies. An inadequate intake of Calcium may cause:

• Weakened bones, Slow growth, Low milk production, Convulsions in severe deficiencies.

Signs of Phosphorus deficiency are not easily recognized except in severe cases, when the following can be seen:

• Fragile bones, General weakness, Emaciation, Stiffness.
• Reduced milk production, and Chewing of wood, rocks, bones and other objects (Note that abnormal chewing of objects may also occur with other dietary deficiencies).

Severe Phosphorus deficiency results in sub-normal growth and reproduction and a depraved appetite or “pica”, as illustrated by bone chewing, which may lead to botulism. Cattle suffering extreme Phosphorus shortage may go for two to three years without producing a calf, or even coming into heat. In Phosphorus deficient areas, if a calf is produced, cows may not come into regular heat until the body phosphorus levels are restored. Due to limitations of serum Calcium and Phosphorus as an indicator of status, an analysis of the ration and bone composition and breaking strength are the best ways of assessing a deficiency of Calcium and Phosphorus.
Prevention and Control

• Calcium and Phosphorus deficiencies can be prevented or overcome by direct treatment of the animals through supplementation, in the diet or water supply, or indirectly by appropriate fertilizer treatment of the soils on which the pasture to be consumed are grown.
• In intensively farmed areas Phosphate applications designed primarily to increase pasture yields also increase Phosphorus concentrations.
• The easiest and cheapest procedure is to provide a phosphatic mineral supplement in troughs or boxes protected from the rain. Good sources of mineral Phosphate are Dicalcium Phosphate or Superphosphate.

Magnesium: Magnesium is abundant in most common feedstuffs. It is widely distributed among plant and animal tissues with some 70% of body Magnesium present in the skeleton. Magnesium is important for neuromuscular activity.

Requirement: The dietary Magnesium requirements of livestock depend on the species and breed, age, and rate of growth or production. The general requirements for maintenance are 3 mg/kg bodyweight for maintenance and 120 mg/kg milk.

Symptoms:

Hypo-magnesium Tetany: Violent convulsive episodes caused by a reduction in the concentration of Magnesium in the cerebro-spinal fluid, leading to hyper excitability, muscular spasms, convulsions, respiratory distress, collapse and death. The disorder occurs after a decrease in plasma Magnesium concentration or the absorption of dietary Magnesium is unable to meet the requirements for maintenance. The condition is not common in the tropics; it’s a disease of colder climates, associated with cold, wet, windy weather, little sunshine and no access to shelter or to supplementary feed. Failure to eat during bad weather may be a factor and cold weather stress may increase urinary excretion of Magnesium. The condition is also associated with lush pastures heavily fertilized with potash and nitrogen which interfere with the absorption of dietary Magnesium.
In the most acute form, affected cows, which may appear to be grazing normally, suddenly throw up their heads, bellow, gallop in a blind frenzy, fall and exhibit severe convulsions. Death may occur within half an hour. Animals may be found dead but an indication that the animal has had convulsions before death may be deduced from the marks on the ground.

Treatment: Slow intravenous in jection of Magnesium salts or a combination or a solution containing both Magnesium and Calcium is generally effective, but treatment must be given quickly to prevent death.

Prevention and Control: Magnesium fertilizers, such as calcined magnesite, can significantly increase pasture concentrations.

• Foliar dusting of pastures at regular intervals is another method of delivering Magnesium to pastures.
• Daily oral supplements of 60g for cattle or 10g for sheep may be given during the danger period.
• For calves and cows being fed concentrates, provision of 50g Magnesium Oxide in 300-400g of concentrate mixture is adequate. Incorporating it into mineral mixes, drenches, molasses-based free choice supplements or sprinkling the mineral onto feed such as grains, chopped roots or silage, are satisfactory means of supplementation.

Potassium: Potassium is essential for life and is required for a variety of body functions. Excitement and stress tends to increase urinary loss of Potassium and diseases with fever or diarrhea further increase Potassium loss.
Symptoms: Potassium deficiency results in non-specific signs such as:

• Slow growth, Lowered feed efficiency, Reduced feed and water intake.
• Muscular weakness, Nervous disorders, Stiffness and emaciation.

Prevention and Control:
Young plants generally contain adequate amounts of Potassium but during an extend dry season deficiencies may occur. Supplemental Potassium salts may be added when grazing dry range pastures and when urea is substituted for plant proteins.

Sodium and Chlorine (Salt): Sodium and Chlorine are essential for proper water metabolism, nutrient uptake and transmission of nerve impulses.
Requirement: The need for Sodium and Chlorine by livestock has been demonstrated for thousands of years by a natural craving for common salt. Sodium is the critical nutrient in salt. Giving livestock salt in the diet at a level of 0.5% is adequate for all farm species.

Symptoms: The entail sign of Sodium and Chlorine deficiency is a craving for salt. Deficient animals lick wood, soil and sweat from other animals and drinking water. A prolonged deficiency causes loss of appetite, decreased growth, unhealthy appearance, reduced milk production and loss of weight. Livestock deprived of salt may be so anxious to get it that they may injure themselves in attempting to reach salt.

Sodium deficiency is most likely to occur during lactation, due to secretion of Sodium in milk, rapidly growing animals, large losses of water and Sodium occur in sweat and where pastures are low in Sodium in tropical or hot semi-arid conditions or grazing pasture heavily fertilized with Potassium, which depresses plant Sodium levels.

Even after prolonged severe deficiency salt levels secreted in milk remains high. Thus, lactating animals suffer most from lack of salt in the diet.

Prevention: Tropical plant feeds normally do not contain sufficient quantities of Sodium to meet the requirement of grazing livestock throughout the year. This inadequacy is easily overcome by providing salt mixes, usually containing added Iodine and Cobalt. Most animals can tolerate large quantities of dietary salt when an adequate supply of water is available. However when animals are deprived of salt for a period of time, re-introduce it slowly and with care. Sudden re-introduction can result in severe diarrhoea and in some cases,, violent nervous symptoms due to swelling of the brain.

Cobalt – Cobalt is required by micro-organisms in the animal’s stomach in order to make Vitamin B12. Vitamin B12 is necessary for proper energy utilization.

Causes: Primary Cobalt deficiency occurs on soils which are deficient in Cobalt. Land which is extremely deficient in cobalt is unsuitable for raising ruminants and where it is somewhat deficient low growth and production may make rearing sheep and cattle unprofitable. A wasting disease of ruminants, known locally as ‘Nakuruitis’ because it occurs near the township of Nakuru, is caused by cobalt deficiency. Cattle in poor conditions, dosed with cobalt pellets over a seven month period, gained almost 200 lb more than those that were not given cobalt. The deficiency occurs only in grazing animals and primary cobalt deficiency occurs only where soils are deficient in cobalt. Heavy liming may reduce the amount of cobalt in the soil. Most severe deficiencies occur when animals graze on lush pastures because they have lower cobalt content than more slowly growing plants.

Symptoms of Deficiency: Animals on Cobalt deficient pastures gradually lose appetite, and failure of growth or loss of weight is followed by extreme loss of appetite, rapid muscular wasting, depraved appetite, severe anemia and death. If the deficiency is mild or marginal the above signs may not occur and only the young most susceptible animals may exhibit signs of weakness, indistinguishable from those caused by parasitism or low feed intake. Mild forms of Cobalt deficiency in grazing ruminants are difficult to diagnose as the only signs may be a state of weakness and no anemia. As a result the only sure way of establishing that a Cobalt deficiency is present is by observing and measuring the response to the oral administration of Cobalt or Vitamin B12 injections in terms of increased appetite and weight gain.

Treatment: Affected animals respond to oral dosing with Cobalt or intramuscular injections of Vitamin B12.

Prevention and Control: This is best done by top-dressing affected pastures with Cobalt salts. At the same time cobalt should be included in the supplemented mineral mixture at a rate of 0.1 mg Cobalt daily for sheep and 0.3 to 1.0 mg Cobalt daily for cattle. In extensive range grazing the use of heavy Cobalt pellets of Cobalt Oxide is the preferred method. The pellet is in the form of a bolus – 5g for sheep and 20g for cattle – which, when given by mouth, lodges in the reticulum and gives off Cobalt in very small but adequate amounts.

Copper and Molybdenum: Copper is essential for haemoglobin production, functioning of enzyme systems, component of various body pigments, in central nervous system, bone metabolism and heart function. Copper is interrelated with other dietary factors including Molybdenum, Sulphur, Zinc, protein Iron and other trace elements. These interactions are important to understand and recognize when considering dietary Copper requirements. An excess of Molybdenum in the diet will interfere with the uptake of Copper. Selenium has the effect of increasing the uptake of Copper in sheep.

Requirement: Copper requirements of ruminant animals are powerfully influenced by interactions with other dietary components, especially Molybdenum and Sulphur. Ideal conditions are those in which all the dietary factors affecting Copper absorption and utilization in the animal are at optimal levels.

Deficiency: With the exception of Phosphorus, deficiency of Copper is the most severe mineral deficiency to grazing livestock in the tropics. Deficiencies in ruminants occur mainly under grazing conditions. Most deficiencies are ‘conditioned’ deficiencies i.e. normal amounts of Copper are inadequate due to higher than normal amounts of other elements such as Molybdenum and Sulphur and other factors which block the utilization of Copper by the body.
Clinical signs: Scours, Pale mucous membranes, Rough and bleached hair, Slow growth and loss of body weight Bones may break easily and affected cattle may move like a pacing horse rather than like normal cattle. Copper-deficient cattle may die suddenly when exerted. PM lesions may reveal small lesions on the heart. Determination of the amount of Copper in the diet or the pasture has limited diagnostic value but with other elements like Molybdenum and Sulphur is determined along with copper.

Prevention and Control: Under range conditions, deficiency can be prevented by the provision of Copper containing supplements, by dosing or drenching the animals at intervals with Copper compounds, or by injection of organic complexes of Copper. Subcutaneous or intramuscular injection of some safe and slowly absorbed forms of Copper is a satisfactory means of treating animals in Copper deficient areas where the Molybdenum contents of the pasture are moderate. The application of Copper containing fertilizers can be an effective means of raising the Copper content of pasture to levels adequate for grazing livestock and increasing pasture yields. 5-7 kg/hectare of Copper Sulphate is usually sufficient for three or four years.

Iodine: A deficiency of iodine causes goitre, but now declined due to the widespread use of iodised salt.

Iron and Manganese: Iron deficiency rarely occurs in adult livestock and supplementation with Iron and Manganese is much less important than for other trace minerals. Most tropical soils are acid, resulting in animal plant feeds having levels generally in excess of requirements. In addition, soil consumption will provide substantial quantities of these minerals to grazing livestock diets, particularly Iron.
Selenium: Symptoms due to Selenium deficiency are uncommon in the tropics. Nutritional muscular dystrophy or white muscle disease affects young, rapidly growing calves, lambs and foals, born from dams which have been fed on diets low in Selenium and Vitamin E for long periods, usually during the winter months and in temperate regions. When such animals are turned out after winter housing or they begin unaccustomed exercise, they may collapse, be unable to walk, or die suddenly. One condition that affects animals even in the tropics is retained afterbirth in mature dairy cows, which may be caused by Selenium/Vitamin E deficiency.

Zinc: Zinc deficiency causes a chronic, dry, scaly, cracked skin, non-inflammatory in nature and although well recognized in Europe is uncommon in the tropics.

Toxic Elements:

Fluorine: In limited amounts Flourine strengthens teeth and bones but excessive amounts it causes damage. Chronic fluorosis is generally seen under these conditions:

1. Continuous consumption of high Fluorine mineral supplements.
   2. Drinking water high in Fluorine and Grazing on contaminated feeds close to industrial plants which emit toxic levels of fumes and dust.
   Normally plant feeds are not involved in Fluorosis as they have a limited capacity to absorb this element. Toxicity of Fluorine in livestock depends on the amount and duration of ingestion, age of the animal, nutrition, stress factors and individual animal differences.
   If animals are young the teeth may become modified in shape, size and color.

• The incisors may become pitted, and the molars may show cavities due to facture or wear.
• The jaw and long bones develop exostosis and joints may become thickened causing the animal to become stiff and lame.

Prevention:

• Determine the Fluorine content of water and of supplemental phosphates, which may contain unacceptably high levels of the element.
• Observation of animals to detect early signs of fluorosis.
• If water levels are high, you can use filters or add fresh slaked lime to the water.
• Watering young stock on fluorine free supplies of water and permitting only adults to drink dangerous supplies and rotating between safe and dangerous water every three months may make it possible to utilize otherwise unsuitable land.

Conclusion:

Advances in technology will allow for real-time measurement and automatic monitoring of metabolic health, provides an immediate feedback and information on effectiveness of herd-level feeding and management strategies. The ability to directly measure or estimate energy, protein, biologically important minerals and vitamins will improve ability to detect these metabolic diseases with minimal disruption to farm and cow routines. Integration of these forthcoming discoveries with epidemiological evidence for herd-level strategies to optimize cow health will enhance knowledge and ability to improve the metabolic health of dairy cattle throughout the peri-parturient period and lead not only to better detection of opportunities but also to better and more specific and actionable cow- and herd-level recommendations.

https://www.pashudhanpraharee.com/reproductive-disorders-of-dairy-cattle-practices-to-improve-conception-rate/