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Parturient hypocalcaemia (milk fever) in dairy cows--a review.

Introduction

Milk fever is an important production disease occurring most commonly in adult cows within 4872 hours after parturition, which is characterized clinically by hypocalcaemia, general muscular weakness, circulatory collapse and depression of consciousness. Milk fever caused by draining a greater amount of calcium from blood to ensure rapid synthesis of milk in udder, affects dairy animals usually within one or two days after calving.

The onset of lactation places such a large demand on calcium homeostatic mechanisms of body that most cows develop some degree of hypocalcemia at calving. Initiation of lactation places one of the greatest stresses on Calcium homeostasis and is associated with hypocalcemic parturient paresis among high producing dairy cows (Horst and Reinhardt, 1983). Most cows adapt to this Calcium stress by rapidly increasing intestinal absorption and bone Calcium resorption, activities regulated by parathyroid hormone and 1-25 dihydroxy Vitamin D (Goff et al., 1991). These cows often develop hypocalcaemia or abnormally low levels of calcium in blood.

Causes

There are several predisposing factors that influence the occurrence of milk fever:

1. Breed: Several investigators (Erb and Martin, 1978; Kusumanti et al., 1993) have been suggested that Jersey and to lesser extent, Swedish Red and White and Norwegian Red breeds have a higher incidence of milk fever as opposed to Holstein cows. The exact reasons for this increased susceptibility are unclear. Goff et al. (1995) have suggested that intestine of Jersey cows possesses 15% fewer receptors for 1,25 [(OH).sub.2][D.sub.3] than intestine of Holstein cows. Lower receptors would result in a loss of target tissue sensitivity to 1,25 [(OH).sub.2][D.sub.3]. At parturition, plasma 1,25 [(OH).sub.2][D.sub.3] is elevated as the cow becomes hypocalcemic. Normally, the elevated 1,25 [(OH).sub.2][D.sub.3] would result in enhanced bone Calcium resorption and intestinal Calcium absorption. However, with a reduced number of 1,25 [(OH).sub.2][D.sub.3] receptors, the activation of genomic events by 1,25 [(OH).sub.2][D.sub.3] is less efficient, resulting in increased susceptibility to milk fever. This would indicate a genetic predilection for this disease and is probably related to relatively high production level for a small breed.

2. Age: The risk of a cow developing milk fever increases with age. As dairy cows become older, the incidence of milk fever increases. It is rare for milk fever to occur at first calving and relatively uncommon at second. Incidence increases dramatically in third and greater lactations (Curtis et al.,1984). Aging also results in a decline in the ability to mobilize Calcium from bone stores and a decline in the active transport of Calcium in the intestine, as well as impaired production of 1,25 [(OH).sub.2][D.sub.3]. Collectively, these impairments result in an inability to respond to acute Calcium stress (Horst et al., 1978). More importantly, the bones of heifers are still growing. Growing bones have large numbers of osteoclasts present, which can respond to parathyroid hormone more readily than the bones of mature cows. Lower number of active osteoblasts in older cows means fewer cells to respond to PTH and mobilize bone Calcium. Horst et al. (1990) demonstrated that intestinal receptors for 1,25 [(OH).sub.2][D.sub.3] decline as age advances. In addition, Johnson et al. (1995) showed that the C 24-hydroxylase, an enyme that inactivates 1,25 [(OH).sub.2][D.sub.3], increases dramatically in the older cow.

3. Nutrition: Metabolic alkalosis predisposes cows to milk fever and sub-clinical hypocalcaemia. Metabolic alkalosis blunts the response of the cow to parathyroid hormone (PTH) (Goff et al., 1991). In-vitro studies suggest the conformation of the PTH receptor is altered during metabolic alkalosis rendering tissues less sensitive to PTH. Lack of PTH responsiveness by bone tissue prevents effective utilization of bone canaliculi fluid Calcium, sometimes referred to as osteocytic osteolysis, and prevents activation of osteoclastic bone resorption. Metabolic alkalosis is largely the result of a diet that supplies more cations (K, Na, Ca, and Mg) than anions (chloride (Cl), sulfate (S[O.sub.4]), and phosphate (P[O.sub.4]) to the blood. Manipulation of dietary Calcium and Phosphorous is known to have dramatic effects on the incidence of milk fever (Jorgensen 1974). Studies have shown that feeding low Calcium diets (Kichura et al.,1982) or adjusting the ratio of dietary Calcium to P to 2:1 (wt/wt) lowered the incidence of milk fever (Gardner and Park, 1972). Jorgensen (1974) suggested that total amount of dietary Calcium was more important than the dietary ratio of Calcium to Phosphorous. He suggested that the incidence of milk fever could be reduced by supplying [less than or equal to] 100 g of Calcium/d.

In Vitamin D deficiency, reduction in production of 1,25 [(OH).sub.2][D.sub.3], resulting increase the risk for milk fever. Horst et al. (1994) have determined the plasma 1,25 [(OH).sub.2][D.sub.3] concentration below 5ng/ ml are indicating of Vitamin D deficiency. Normal cows have plasma 25 [(OH).sub.2][D.sub.3] concentrations between 20 and 50ng/ml. Dietary factors can greatly influence the incidence of milk fever in dairy cows. Feeding a low calcium diet prepartum stimulates parathyroid hormone secretion and 1-25 dihydroxy-Vitamin D production prior to parturition, activating calcium transport mechanism in bone and intestine that would be needed to adapt to lactational Calcium demand (Takagi and Block, 1991). Cows fed diets that are relatively high in potassium or sodium are in a relative state of metabolic alkalosis, which increases likelihood to develop milk fever. A second cause of hypocalcemia is hypomagnesemia. Low blood magnesium can reduce PTH secretion from the parathyroid glands and also can alter responsiveness of tissues to PTH. High dietary potassium reduces ruminal magnesium absorption in addition to causing metabolic alkalosis.

4. Parity: Incidence of subclinical hypocalcemia (<8.0 mg plasma Calcium/dl) typically rises with increasing parity, affecting 25% of heifers and almost half of cows of second and greater parity (Reinhardt et al., 2011). It is thought that heifers especially are less susceptible because they have greater bone depletion/repletion activity and are more able to mobilize bone Calcium from their Calcium reserves than are later parity cows (van Mosel et al., 1993). Additionally, later parity cows produce more colostrum and milk making demand for Calcium greater. History of milk fever seems to be a large determinant of whether or not a cow develops hypocalcemia and milk fever at subsequent parturitions. This is presumably due to a decreased ability of these particular cows to respond immediately to biological signals and increase Vitamin D receptor (VDR) numbers in a timely manner (Goff et al., 1995).

Mechanism

Initiation of lactation places one of the greatest stresses on Calcium homeostasis and is associated with hypocalcemic parturient paresis among high producing dairy cows (Horst and Reinhardt, 1983). On the day of parturition, dairy cows commonly produce ten liter or more colostrum containing 23 g or more of Calcium that is six times as much as extra cellular pool contains (Goff et al., 1987). In order to prevent blood calcium from decreasing, the cow must replace calcium lost to milk by withdrawing calcium from bone or by increasing efficient absorption of dietary calcium. Plasma Calcium concentration is under control of parathyroid hormone, calcitonin and metabolites of Vitamin D (Goff et al., 1995).

Most cows in first and second lactations adapt to this Calcium stress by rapidly increasing intestinal absorption and bone Calcium resorption, activities regulated by parathyroid hormone and 1-25 dihydroxy-Vitamin D (Goff et al., 1991). PTH increases renal reabsorption of calcium from the glomerular filtrate. If the perturbation in blood calcium is small (less than 1g Calcium/day), blood calcium returns to normal and PTH secretion returns to baseline levels. If the calcium drain from the extracellular pool is large, continued PTH secretion stimulates resorption of calcium stored in bone. This calcium comes from both dissolved calcium in solution within bones as well as from calcium released by osteoclastic activity on organic bone collagen matrix. Parathyroid hormone, acts only poorly on bone or kidney tissues when blood pH is high (Goff and Horst, 1997). Blood pH of cattle is often alkaline because forage potassium is often excessively high. Oestrogens also inhibit calcium mobilization and as oestrogen levels rise at parturition this will have a negative effect on the adaptation process to maintain calcium levels.

Calcium is absorbed across the intestine and forestomachs by both Vitamin D dependent and Vitamin D independent means. Vitamin D independent absorption of calcium is primarily by passive diffusion. Vitamin D dependent absorption is by active transport; it occurs when dietary calcium is low or when calcium demand is very high. The activity of renal enzyme responsible for converting 25-hydroxy Vitamin D to the steroid hormone 1,25-dihydroxy Vitamin D (1,25 [(OH).sub.2]D is stimulated by and tightly regulated by PTH (Goff, 2006). The most important function of 1,25 [(OH).sub.2]D is its ability to stimulate active transport of dietary calcium across intestinal epithelium. In later lactations, because of decline in ability to mobilize calcium from bone stores and a decline in the active transport of calcium in intestine, as well as impaired production of 1,25 [(OH).sub.2][D.sub.3] results in inability to respond to acute Calcium stress and milk fever develops. (Horst et al., 1978). Calcium homeostatic mechanism is influenced by mainly 3 factors-

a) excessive loss of Calcium++ in colostrums beyond capacity of absorption from intestine,

b) impairment of absorption of Calcium++ from intestine at parturition and

c) mobilization of Calcium++ from storage in skeleton may not be sufficiently rapid to maintain normal serum level (Sharma et al., 2006).

Signs: Clinical signs of milk fever around calving may for convenience, be divided into three stages. Clinical signs usually occurs within 72 hours of parturition.

First stage: Stage I milk fever is early signs without recumbency. It may go unnoticed because its signs are subtle and transient. Affected cattle may appear excitable, nervous or weak. Some may shift their weight frequently and shuffle their hind feet (Oetzel, 2011). Stiffness of hind legs, rapid heart rate, rectal temperature is usually normal or above normal (>39[degrees]C).

Second stage or Stage of sternal recumbency: Sternal recumbency comprising down on chest and drowsiness, Characteristic 'S' shaped posture, sitting with lateral kink in neck or head turned to lateral flank. Depression, fine muscle tremors, rapid heart rate with decreased intensity of heart sounds, cold extremities, decreased rectal temperature (35.6-37.8C), decreased gastro-intestinal activity, pupils dilated and unresponsive to light.

Third stage or Stage of lateral recumbency Lateral recumbency, comprising of almost comatose condition, progressing to loss of consciousness, severe bloat, flaccid muscles, profound gastrointestinal atony, rapid heart rate, impalpable pulse and almost inaudible heart sounds. They will die within few hours without treatment (Oetzel, 2011).

Large multi-site study shows that hypocalcemia around calving is most strongly associated with reduced milk yield (Chapinal et al., 2012) and increased risk for displaced abomasum (Chapinal et al., 2011). Rajala-Schultz et al. (1999) found that milk fever alone caused a milk loss of between 1.1 and 2.9 kg/d during the first 4-6 weeks following parturition. It can also reduce the productive life of the cow by as much as 3.4 years.

Milk fever is also a common cause of dystocia and hence stillborn calves. Hypocalcaemia or low blood calcium also impairs abomasum contraction leading to more metabolic disorders. Hypocalcaemia cause secretion of cortisol which impairs the immune system of fresh cow (Wang et al., 1991). Cows developing milk fever have higher plasma cortisol concentrations than do non-milk fever cows (Goff et al., 1989). Muscle tone decreases in most body systems, particularly in the cardiovascular, reproductive and digestive systems and possibly in mammary system. Blood flow to extremities is reduced, causing characteristic cold ears of cow suffering from milk fever. Milk fever cows also exhibit a greater decline in feed intake after calving than non-milk fever cows (Goff and Horst, 1997), exacerbating the negative energy balance commonly observed in early lactation. In addition, hypocalcaemia prevents secretion of insulin (Littledike et al., 1970), preventing tissue uptake of glucose which would exacerbate lipid mobilization at calving, increasing the risk of ketosis.

Treatment

Treatment is usually initiated based on clinical signs only. Treatment is directed toward restoring the serum calcium level to normal as soon as possible to avoid muscular and nervous damage and recumbency. This would minimize the associated problems of hypocalcaemia.

Oral Calcium supplementation

Oral calcium supplementation is the best approach for hypocalcaemic cows that are still standing, such as cows in Stage 1 hypocalcaemia or who have undetected subclinical hypocalcaemia (Oetzel, 2011). A cow absorbs an effective amount of calcium into her bloodstream within about 30 minutes of supplementation. Blood calcium concentrations are supported for only about 4-6 hours afterwards for most forms of oral calcium supplementation (Goff and Horst, 1993). Intravenous (IV) calcium is not recommended for treating cows that are still standing (Oetzel, 2011).

The source of calcium in an oral supplement and its physical form greatly influence calcium absorption and blood calcium responses. A series of experiments has shown that calcium chloride has the greatest ability to support blood calcium concentrations (Goff and Horst, 1993). This can be explained by its high calcium bioavailability and its ability to invoke an acidic response which causes mobilization of calcium stores. Providing a typical amount of elemental calcium chloride (e.g., 50 grams of elemental calcium) in a small oral dose (e.g. 250 ml water) provided the best absorption. The risk of aspiration is great when thin liquids are given orally and calcium chloride is very caustic to upper respiratory tissues. Calcium propionate is more slowly absorbed (presumably because it is not acidogenic) and must be given at higher doses of elemental calcium (usually 75 to 125 grams). Calcium propionate has the property of being glucogenic as well as providing supplemental calcium. Calcium carbonate in water did not increase blood calcium concentrations at all (Goff and Horst, 1993). This may be explained by its poorer bioavailability and by alkalogenic response it can invoke.

Strategies for giving oral calcium supplements around calving should include at least two doses one at calving and a second dose the next day. The expected blood calcium concentrations occurs between 12 and 24 hours after calving (Goff, 1999; Sampson et al., 2009). Giving only one oral calcium supplement around calving time leaves the cow without support when her blood calcium concentrations are naturally the lowest. It was very difficult to predict when at cow was in fact about 12 hours from expected calving and many cows calved without receiving this dose (Oetzel, 1996). The dose at calving is not practically challenging to administer, and providing a dose sometime the day after calving will provide critical support.

Intravenous(I/V) Calcium treatment

Stage II and Stage III cases of milk fever should be treated immediately with slow I/V administration of 500 ml of a 23% calcium gluconate solution. This provides 10.8 grams of elemental calcium, which is more than sufficient to correct cow's entire deficit of calcium (about 4-6 grams). A general rule for dosing is 1 g calcium/45 kg body wt. Giving larger doses of calcium in I/V treatment has no benefit (Doze et al., 2008). Treatment with I/V calcium should be given as soon as possible, as recumbency can quickly cause severe musculoskeletal damage. The thumb rule is when the animal is showing signs of peripheral vascular failure, hypothermia and cold extremities; calcium borogluconate should be administered intravenously. To reduce the risk for relapse, recumbent cows that respond favorably to I/V treatment need additional oral calcium supplementation once they are alert and able to swallow, followed by a second oral supplement about 12 hours later (Oetzel, 2011). Heart rate should be closely monitored for toxic effects while giving I/V calcium. Calcium borogluconate containing products with or without added magnesium and phosphorus are mostly used in the India, usually 400 ml of 40% calcium borogluconate. For cattle, 400-800 ml of 25% solution is the usual dose.

The response to properly administered calcium therapy is quite characteristic. Approximately 85% of cases will respond to one treatment, in many cases cows recumbent from milk fever will rise within 10 minutes of treatment and others will get up 2-4 hours later. The cow's symptoms will appear to reverse themselves as they had previously progressed. The laterally recumbent cow will sit up to sternal position, and then it will often begin to have tremors over its body. As all body functions affected by hypocalcaemia begin to reverse, the affected animal may urinate, belch, and then begin the wobbly effort to rise. Cows generally rise within one hour. Repeated treatment may be necessary in 12 hours if cow is still unable to rise.

Use of Negative DCAB Diets

Acid base balance, as affected by acidogenic diets alters calcium metabolism (Wang and Beede, 1992) via resorption (Goff et al., 1991), intestinal calcium absorption (Block, 1994) and renal handling of calcium (Jackson et al., 2000). The cation-anion difference of diet is commonly described in terms of mEq/kg of just sodium, potassium, chloride and sulfate as follows: Dietary Cation-Anion Difference (DCAD)= (mEq [Na.sup.+] + mEq [K.sup.+]) - (mEq [Cl.sup.-] + mEq [S-.sub.2]) (Horst et al., 1997).

A negative DCAB diet (1) may increase the intestinal absorption of calcium by reducing pH in GIT, causing an increase in more soluble forms of calcium (ionized form) present, (2) may cause an alteration in acid base balance of animal, resulting in an increase of calcium availability from exchangeable calcium pool and (3) may cause the reduction in the calcium absorption by interference created by the presence of excess of cation mineral elements such as aluminum and magnesium (Tucker et al., 1991). This idea is supported by the work of Block (1984), who reported that feeding a diet low in DCAB during dry period completely prevented parturient paresis.

Anionic diets prepartum may enhance milk production and health in subsequent lactation, simply because hypocalcemia is decreased and animal does not have secondary problems associated with milk fever (Oetzel, 1991). Commonly used anion sources are calcium chloride, ammonium chloride, magnesium sulfate, ammonium sulfate and calcium sulfate.

Subcutaneous Calcium treatment

Subcutaneous calcium can be used to support blood calcium concentrations around calving, but has substantial limitations (Goff, 1999). Absorption of calcium from subcutaneous administration requires adequate peripheral perfusion. It may be ineffective in cows that are severely hypocalcemic or dehydrated. Subcutaneous calcium injections are irritating and can cause tissue necrosis; administration should be limited to no more than 75 ml of a 23% calcium gluconate solution (about 1.5g elemental calcium) per site. Calcium solutions that also contain glucose should not be given subcutaneously. Glucose is very poorly absorbed when given by this route. Abscessation and tissue sloughing may result when glucose is given subcutaneously.

The kinetics of subcutaneously administered calcium indicate that it is well-absorbed initially, but that blood concentrations fall back to baseline values in about 6 hours (Goff, 1999). Thus, repeat doses would be necessary to equal the sustained blood calcium support that is possible with oral calcium boluses.

Prevention

The traditional method of preventing milk fever in fresh dairy cows is to restrict dietary intake of calcium during prepartum period. However feeding low-calcium diets prior to parturition to stimulate intestinal absorption and enhance skeletal reabsorption is not as effective as once thought. If extremely low calcium diets (<20 grams of daily calcium) are fed before parturition and high-calcium diets are fed after parturition, the incidence of milk fever can be drastically reduced (Green et al., 1981).

DCAD (dietary cation-anion difference) diets are the new method of prevention. They involve decreasing the blood pH of cows in late prepartum and early post-partum periods by providing an excess of anions over cations. This is believed to enhance calcium absorption from intestine and reabsorption from bone. Cations have a positive charge like sodium (Na), potassium (K), calcium (Ca) and magnesium (Mg). Cations in diet promotes more alkaline (higher blood pH) metabolic state which has been associated with an increased incidence of milk fever. Anions have a negative charge such as chloride (Cl), sulfur (S) and phosphorus (P). It has been discovered that milk fever can be effectively treated and/or prevented by feeding dairy cows during the close up period (14 to 21 days pre-calving) a diet containing substantial amounts of negative ions (i.e. anionic salts) (Markandeya et al., 2009). Dietary Acidification. Dietary acidity or alkalinity is more important in controlling milk fever than calcium intake. The use of diets low in dietary cation-anion difference (DCAD) to prevent milk fever has been extensively studied and reviewed (DeGaris and Lean, 2008). A large meta-analysis demonstrated that reducing pre-fresh DCAD by 300 meq/kg of diet dry matter (a typical approach) reduced the odds for clinical milk fever 5.1-fold, reduced urinary pH from 8.1 to 7.0 and reduced dry matter intake by 11.3% (Charbonneau et al., 2006). Despite the expected decrease in pre-fresh dry matter intake, post-fresh intakes are improved when low DCAD diets are fed (Joyce et al., 1997).

Dietary Magnesium also plays an important role in maintaining calcium homeostasis around calving (DeGaris and Lean, 2008). A large meta-analysis found that increasing dietary magnesium greatly reduced the odds for clinical milk fever (Lean et al., 2006). Magnesium is known to participate in calcium homeostasis via release of parathyroid hormone and the synthesis of the active form of Vitamin D (1,25 dihydroxy-cholecalciferol). Total intakes of about 40-50 grams of dietary Mg (about 0.30-0.45% of diet dry matter, depending on total dry matter intake) have been suggested (DeGaris and Lean, 2008), although this is complicated because of the interactions between other dietary factors (DCAD, dietary calcium, and dietary phosphorus).

Conclusions

Parturient hypocalcaemia (Milk fever) occurs in cows within 48-72 hours after parturition. The lowered blood calcium in milk fever is due to the failure of the blood 'calcium regulatory mechanism to mobilize calcium from the tissue reserves rapidly enough to equal the withdrawal of calcium from the blood into the udder secretions. Any preventive measure must be aimed at eliminating the precipitous fall in blood calcium at parturition. Affected animal shows clinical symptoms when the serum calcium falls below 6.5 mg per dL. Jersey cows have a higher incidence of milk fever as compared to Holstein cows. Incidence of milk fever increases in third and greater lactations. Metabolic alkalosis predisposes milk fever. Milk fever is a metabolic disorder which can be prevented by adopting appropriate nutritional practices such as low calcium and low DCAB diets pre-partum and supplementing calcium rich diets and negative DCAB diets post partum.

References

Block, E. (1984). Manipulating dietary anions and cations for prepartum cows to reduce incidence of milk fever. J. Dairy Sci. 67: 2939-46.

Block, E. (1994). Manipulation of dietary cation-anion difference on nutritionally related production diseases, productivity, and metabolic responses of dairy cows. J. Dairy Sci. 77: 1437-42.

Chapinal, N., M. Carson, T. F. Duffield, M. Capel, S. Godden, M. Overton, J. E. Santos, and S. J. LeBlanc. (2011). The association of serum metabolites with clinical disease during the transition period. J. Dairy Sci. 94:4897-4903.

Chapinal, N., M. E. Carson, S. J. LeBlanc, K. E. Leslie, S. Godden, M. Capel, J. E. Santos, M. W. Overton, and T. F. Duffield. (2012). The association of serum metabolites in the transition period with milk production and early-lactation reproductive performance. J. Dairy Sci. 95:1301-09.

Charbonneau, E., D. Pellerin, and G. R. Oetzel. (2006). Impact of lowering dietary cation-anion difference in nonlactating dairy cows: A meta-analysis. J. Dairy Sci. 89:537-48.

Curtis, C.R., H. N. Erb, C. J. Sniffen, and R. D. Smith. (1984). Epidemiology of parturient paresis: predisposing factors with emphasis on dry cow feeding and management. J. Dairy Sci. 67:817.

DeGaris, P.J. and I.J. Lean. (2008). Milk fever in dairy cows: a review of pathophysiology and control principles. Vet. J. 176: 58-69.

Doze, J.G., R. Donders, and J. H. van der Kolk. (2008). Effects of intravenous administration of two volumes of calcium solution on plasma ionized calcium concentration and recovery from naturally occurring hypocalcemia in lactating dairy cows. Am. J. Vet. Res. 69:1346-50.

Erb, H.N. and Martin, S.W. (1978). Age, breed and seasonal patterns in the occurrence of ten dairy cow diseases: a case control study. Can. J. Comp. Med. 42: 1.

Gardner, R. W., and R. L. Park. (1972). Effects of prepartum energy intake and calcium to phosphorus ratios on lactation response and parturient paresis. J. Dairy Sci. 56:385.

Goff, J. P., and R. L. Horst. (1993). Oral administration of calcium salts for treatment of hypocalcemia in cattle. J. Dairy Sci. 76:101-08.

Goff, J. P. (1999). Treatment of calcium, phosphorus, and magnesium balance disorders. Vet. Clin. North Am. Food Anim. Pract. 15: 619-39.

Goff, J.P., R.L. Horst and T.A. Reinhardt. (1987). The patho-physiology and prevention of milk fever. Vet. Med. 82: 943-50.

Goff, J. P., R. L. Horst, F. J. Mueller, J. K. Miller, G. A. Kiess and H. H. Dowlen. (1991). Addition of chloride to pre-partal diets high in cations increases 1,25-dihydroxyvitamin D response to hypo-calcemia preventing milk fever. J. Dairy Sci. 74: 3863-70.

Goff, J.P. (2006). Major advances in our understanding of nutritional influences on bovine health. J. Dairy Sci., 89: 1292-01.

Goff, J.P., Kehrli, Jr. M.E. and Horst, R.L. (1989). Periparturient hypocalcemia in cows: prevention using intramuscular parathyroid hormone. J. Dairy Sci. 72: 1182.

Goff, J.P. and Horst, R.L. (1997). Physiological changes at parturition and their relationship to metabolic disorders. J. Dairy Sci. 80: 1260-68.

Goff, J. P., T. A. Reinhardt, D. B. Beitz, and R. L. Horst. (1995). Breed affects tissue vitamin D receptor concentration in periparturient dairy cows: a milk fever risk factor. J. Dairy Sci. 78:184. (Abstr.)

Green, H. B., R. L. Horst, D. C. Beitz, and E. T. Littledike. (1981). Vitamin D metabolites in plasma of cows fed a prepar-tum low-calcium diet for prevention of parturient hypocalce-mia. J. Dairy Sci. 64: 217.

Horst, R. L., J. P. Goff, and T. A. Reinhardt. (1994). Calcium and vitamin D metabolism in the dairy cow. J. Dairy Sci. 77: 1936.

Horst, R.L. and T.A. Reinhardt, (1983). Vitamin D metabolism in ruminants and its relevance to the pre-parturient cow. J. Dairy Sci. 66: 661-69.

Hibbs, J. W. (1950). Milk fever (parturient paresis) in dairy cows: a review. J. Dairy Sci. 33:758.

Horst, R. L., H. F. DeLuca, and N. A. Jorgensen. (1978). The effect of age on calcium absorption and accumulation of 1,25-dihydroxy Vitamin D3 in intestinal mucosa of rats. Metab. Bone Dis. Rel. Res. 1: 29.

Horst, R. L., J. P. Goff, and T. A. Reinhardt. (1990). Advancing age results in reduction of intestinal and bone 1,25-dihydroxy Vitamin D receptor. Endocrinology 126:1053.

Horst, R.L., J.P. Goff, and T.A. Reinhardt. (1997). Strategies for preventing milk fever in dairy cattle. J. Dairy Sci. 80:1269-80.

Jackson, J.A., V. Akay, S.T. Franklin and D.K. Aaron. (2000). The effect of cation-anion requirement on feed intake, body weight gain and blood gasses and mineral concentrations of dairy calves. J. Dairy Sci. 84: 197-205.

Jorgensen, N. A. (1974). Combating milk fever. J. Dairy Sci. 57: 933.

Johnson, J. A., M. J. Beckman, A. Pansini-Porta, S. Christakos, M. E. Bruns, D. C. Beitz, R. L. Horst, and T. A. Reinhardt. (1995). Age and gender effects on 1,25-dihy-droxyvitamin D3-regulated gene expression. Exp. Gerontol. 30: 631.

Joyce, P. W., W. K. Sanchez, and J. P. Goff. (1997). Effect of anionic salts in prepartum diets based on alfalfa. J. Dairy Sci. 80:2866-75.

Kichura, T. S., R. L. Horst, D. C. Beitz, and E. T. Littledike. (1982). Relationships between prepartal dietary calcium and phosphorus, vitamin D metabolism, and parturient paresis in dairy cows. J. Nutr. 112:480.

Kusumanti, E., Agger, J. F. and Jensen, K. (1993). Association between incidence risk of milk fever and lactation number, breed and season. Acta. Vet. Scand. S89: 141.

Lean, I. J., P. J. DeGaris, D. M. McNeil, and E. Block. (2006). Hypocalcemia in dairy cows: meta-analysis and dietary cation anion difference theory revisited. J. Dairy Sci. 89:669-84.

Littledike, E. T., S. C. Whipp, D. A. Witzel, and A. L. Baetz. (1970). Insulin, corticoids and parturient paresis. Academic Press, New York.

Markandeya, N.M., Patil, A.D. and Bharkad, G.P. (2009). Intas Polivet 10: 13-19.

Oetzel, G. R. (2011). Non-infectious diseases: Milk fever. in Encyclopedia of Dairy Sciences. Vol.2. F. J. W. Fuquay, P.F, McSweeney, P.L.H., ed. Academic Press, San Diego.

Oetzel GR. (1991). Meta-analysis of nutritional risk factors for milk fever in dairy cattle. J Dairy Sci 74: 3900-12.

Oetzel, G. R. (1996). Effect of calcium chloride gel treatment in dairy cows on incidence of periparturient diseases. J. Am. Vet. Med. Assoc. 209:958-61.

Rajala-Schultz, P.J., Grohn, Y.T. and McColloch, C.E., (1999). Effects of milk fever, ketosis, and lameness on milk yields in dairy cows. J. Dairy Sci. 82: 288-94.

Reinhardt, T.A., J.D. Lippolis, B.J. McCluskey, J.P. Goff, and R.L. Horst. (2011). Prevalence of subclinical hypocalcemia in dairy herds. Vet. J. 188:122-24.

Sampson, J. D., J. N. Spain, C. Jones, and L. Carstensen. (2009). Effects of calcium chloride and calcium sulfate in an oral bolus given as a supplement to postpartum dairy cows. Vet. Ther. 10:131-39.

Sharma, Neelesh, Gupta, S.K., Soodan, J.S. and Singh, R. (2006). Important production diseases of dairy animals-A review. Dairy Planner 2: 6-8.

Takagi, H. and E. Block. (1991). Effects of reducing dietary cation anion balances on response to experimentally induced hypocalcemia in sheep. J. Dairy Sci., 74: 4215-4224.

Tucker, W. B., J. A. Jackson, D. M. Hopkins and J.F. Hogue. (1991). Influence of dietary sodium bicarbonate on the potassium metabolism of growing dairy calves. J. Dairy Sci. 74: 2296-06.

van Mosel, M., A. T. van't Klooster, F. van Mosel, and J. van der Kuilen. (1993). Effects of reducing dietary [(Na+ + K+) - (Cl- + S04=)] on the rate of calcium mobilisation by dairy cows at parturition. Res. Vet. Sci. 54: 1-9.

Wang, C. and D. K. Beede. (1992). Effects of ammonium chloride and sulfate on acid-base status and calcium metabolism of dry Jersey cows. J. Dairy Sci. 75: 820-30.

Wang, C., Beede, D.K., Donovan, G.A., Archbald, L.F., DeLorenzo, M.A. and Sanchez, W.K. (1991). Effects of dietary negative cation-anion difference and high calcium content prepartum on calcium metabolism, health, lactational and reproductive performance of Holstein cows. J. Dairy Sci. 74: 275.

P. Kavitha (1), B. Sreedevi (2), J.V. Ramana (3) and D. Srinivasa Rao (4)

Department of Instructional Livestock Farm Complex College of Veterinary Science Sri Venkateswara Veterinary University (SVVU) Tirupati-517502 (Andhra Pradesh)

(1.) Assistant Professor

(2.) Professor and Head, Department of Veterinary Microbiology

(3.) Professor and Head, Department of Animal Nutrition and Corresponding author. E-mail: jvenkataramana@rediffmail.com

(4.) Professor and Head
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Author:Kavitha, P.; Sreedevi, B.; Ramana, J.V.; Rao, D. Srinivasa
Publication:Intas Polivet
Article Type:Report
Geographic Code:9INDI
Date:Jul 1, 2014
Words:5208
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