Truong Minh Hieu, Tran Duy Thanh, Pham Trang Thanh Nguyen,
Nguyen Khanh Thuan, Nguyen Phuc Khanh, Nguyen Thanh Lam*
1. Introduction
Milk fever (parturient paresis, postparturient hypocalcemia, eclampsia) is one of the most common mineral-related metabolic conditions affecting dairy cows at parturition, a disorder that occurs immediately after or close to calving, especially in high producing dairy cows and most commonly in high-productive cows from three years and older (Goff, 2008). The disease is characterized by a rapid decline in plasma calcium (Ca) concentrations in the blood resulting from the relatively expeditious loss of Ca to the formation of colostrum (hypocalcaemia). Milk fever is a common disease in dairy cows but also occurs in beef, cattle, causing significant economic losses to the livestock industry in general and dairy farming in particular. A mild degree of hypocalcaemia develops in the majority of cows during the peripartum period and has been linked to calving problems, retained placenta, uterine prolapse, metritis, mastitis, ruminal stasis, depression of the immune system and generally reduced reproductive performance, resulting in reduction of productive life by 3.4 years and/or death if left untreated (Khan et al., 2015). In a small proportion of animals, hypocalcaemia becomes severe and results in paresis, recumbency and, occasionally, death (Bhanugopan MS et al,. 2014).
2. History of disease
Eberhardt (1793) have pointed out that milk fever was first mentioned in the literature in Germany. Price refers to milk fever in 1806 in his book "The New Useful Farrier and Complete Cow Leech". According to Hutyra and Marek (1926), the time that the disease became known corresponding with the period when it became customary to feed cows more generously with the object of increasing milk production. As intensive feeding and selection for higher milk production increased, the number of milk fever cases also increased until by the middle of the 19th century, numerous publications on the subject by veterinarians were appearing in the literature from nearly all civilized countries Skellet an English veterinarian, gave a good clinical description of the disease in 1807, and it was particularly discussed by Jorg in 1808.
3. Aetiology
Blood Ca is kept under tight homeostatic control via parathyroid hormone (PTH), 1,25-dihydroxy cholecalciferol (calcitriol) and calcitonin. A cow yielding 40 liters of milk daily suddenly requires an extra dietary intake of 80 g of Ca per day over that needed during late pregnancy. To maintain the normal concentration of Ca in the blood there must be increased absorption of Ca from the gut and/or mobilization from the skeleton. These processes take 2-3 days to become fully active and, if they fail, hypocalcaemia results.
There are a number of factors that affect the speed and extent of the response to PTH and 1,25-dihydroxy cholecalciferol. Older cows respond more slowly and are thus more prone to milk fever. Low magnesium status may interfere with release of PTH, the ability of PTH to act on its target tissues and hydroxylation of vitamin D, in the liver.
Low dietary Ca levels during the dry period stimulate PTH secretion and therefore mobilization of Ca from bone and absorption from the gut. The acid - base status of the animal affects Ca metabolism whereby metabolic alkalosis predisposes cows to milk fever (see Prevention). Nutritional factors, including depressed dry matter (DM) intakes in cows at calving and digestive upsets (e.g. diarrhea), will reduce Ca absorption from the gut. Channel Island breeds (especially Jerseys) are more susceptible to milk fever than Holstein Friesians (Phillip R. Scott et al., 2011).
4. Risk factors for milk fever
Milk fever in cattle is a metabolic disease that occurs around calving. More precisely, three to four days before calving the levels of Ca and inorganic phosphorus in the blood serum drop. The drop in Ca is a consequence of the start of milk production, when the demand of Ca for milk production exceed the body’s ability to mobilize Ca reserves. Cows with milk fever, however, experience a greater drop in these minerals than cows without the disease. Cows with serum Ca lower than 7,5 mg/dL are considered hypocalcemic (Figure 1). Moreover, the delay in the operation of Ca homeostatic mechanisms is vital in causing milk fever. Ca homeostasis is affected by three factors and variations in one or more of them are instrumental in causing the disease in any individual. These are excessive loss of Ca in the colostrums beyond the capacity of absorption from the intestines and mobilization from the bones to replace, impairment of absorption of Ca from the intestine at parturition and insufficiency of mobilization of Ca from storage in the skeleton, which could arise because of parathyroid insufficiency since the gland is relatively quiescent due to the decreased Ca and phosphorus metabolism of the dry period (Mulligan F et al., 2006). In addition, Ca is eliminated from the cow to endogenous fecal Ca++, clearance in glomerular filtration, placental Ca++ transport to the fetus, bone deposition, and Ca++ secretion in the mammary gland (El-Samad H et al., 2002). When approximately 50 % of the circulating blood Ca++ is lost, a hypocalcemic event, which is known as milk fever, is likely to occur. Thus hypocalcemia occurs as the dairy animal’s complex mechanisms for maintaining Ca homeostasis fail during a sudden and severe Ca outflow (Oetzel G R, 2011).
4.1. Hormonal changes as start of lactation
At the moment that the cow is adapting hormone-wise to lactation, there is a big difference between the supply of Ca and the demand for the fetus and colostrum/milk. In a single milking, a cow can lose about 23 g of Ca, which is 9 to 10 times more than the Ca supply. This gap must be filled by either increasing the absorption from the gut or bones or decreasing the outflow of Ca other than to milk. It is important to note that milk fever is a production disease, meaning that as milk production increases the prevalence and severity of milk fever generally increases as well (Resco, 2021).
Other hormonal changes around calving have also shown to be an antecedent of milk fever. Increased estrogen and glucocorticoids may reduce serum Ca. Furthermore, increased estrogen is known to reduce appetite. Also, stress from calving may prompt the release of a number of hormones that reduce blood Ca.
4.2. Milk production
A high milk production is a risk factor for parturient paresis (Bendixen et al., 1987). Since every liter of milk requires a certain amount of Ca, a larger production leads to a greater Ca loss, increasing the risk of milk fever. A high production equals an increased risk of cows suffering from milk fever (Chiwome et al., 2017).
4.3. Dry cow feed: Ca to phosphorus ration
We find another reason for the occurrence of milk fever in the dry cow feed. Dry cow feed high in Ca (over 100 to 125 g/kg) has proven to inactivate the parathyroid gland. However, around calving, the need for Ca is extremely high. In consequence, an inactive gland suffers to adequately supply Ca to the blood, leaving the cow with a Ca deficiency.
As for phosphorus, it is shown that rations high in phosphorus interfere with the metabolism of vitamin D, especially with the conversion of 25-hydroxycholecalciferol to 1,25- dihydroxycholecalciferol. Another feed-related cause of milk fever can be a reduced intake of feed around parturition, again with older cows showing a greater reduction of intake in the last four days before calving.
4.4. Previous cases of milk fever
It has been reported that cows that have suffered from milk fever in previous lactations are at greater risk of developing milk fever in the current lactation. In a review article, Erb and Grohn (1988) found a 2 to 5 times higher chance of a cow developing milk fever if she had already undergone illness in a previous lactation. Roche and Berry (2006) found that the odds of parturient paresis were 2.2 times higher in cows that had previously suffered from milk fever. Saborio-Montero et al. (2017) similarly found that previous milk fever increased the risk of this disease in the next lactation. These cows were seen to be 2.35 times more likely to develop parturient paresis.
4.5. Breed
Although reasons are unclear it is known that certain breeds are more susceptible to milk fever than others (Resco, 2021). For instance, cross breed cows are more susceptible to milk fever than local breeds. This could be attributed to high milk yield and low ability to maintain Ca homeostasis in cross breed cows compared with local breeds. It was shown that Jerseys had lower numbers of intestinal receptors for 1,25-dihydroxy cholecalciferol than same-aged Holsteins. Lower receptors would result in a loss of target tissue responsiveness and sensitivity to 1,25-dihydroxy cholecalciferol.
4.6. Age
How much the levels of Ca and inorganic phosphorus in the blood serum drop, is highly dependable on the cow itself, with older cows showing a bigger drop since they absorb less dietary Ca and may have less exchangeable bone Ca. The risk of a cow developing milk fever will increase with age. From the third lactation, onwards, dairy cows produce more milk, resulting in a higher Ca demand. In addition to increased milk production, ageing also results in a diminished ability to mobilize Ca from bone stores and a decline in the active transport of Ca in the intestine, as well as impaired production of 1,25-dihydroxy cholecalciferol. The skeletal bones of heifers are still in a growth phase and therefore have a large number of osteoclasts present, which can respond to PTH more readily than the bones of mature cows (NRC, 2001). Increased age also causes a decrease in the number of 1,25-dihydroxy cholecalciferol receptors (Rezac D J et al., 2010). The hypocalcaemia at calving is age related and most marked in cows from third to seventh parturition; it is infrequent at the first parturition. This is because while some degree of hypocalcaemia occurs during the first few days of lactation, they are able to adapt rapidly to the high demands of Ca for lactation. With increasing age, this adaptation process is decreased and results in moderate to severe hypocalcaemia in most adult cows. The adaptation mechanism is directly related to the efficiency of intestinal absorption of Ca, which decreases with increasing age. Most cases occur in animals older than five years of age. This is as a result of increasing milk production with age and decreasing efficiency of dietary Ca absorption and bone resorption (Tadesse E et al., 2015). In other word, as dairy cows become older, the prevalence of milk fever increases (Resco, 2021).
5. Pathophysiology
Changes in Ca metabolism induced by lactation are more significant than parturition of itself to the pathogenesis of parturient paresis, as the loss of blood Ca to milk may exceed 50 g per day. Before calving, the approximate daily requirement for Ca is only 30 g, comprising 15 g in faecal and urinary loss and 15 g to fetal growth. This demands for Ca may only be satisfied by increasing absorption from the rumen or intestines, and increasing mobilisation from tissue, especially bone reserves of Ca, as circulating blood Ca reserves are limited. Most cows have some degree of hypocalcaemia at calving.
Blood Ca is maintained within a narrow range (2.0–2.5 mmol/L). Cows can only afford to lose approximately 50% of circulating blood Ca reserves before a hypocalcaemia crisis is precipitated. Physiological controls over Ca homeostasis include calcitonin, secretion of which is stimulated in response to elevated blood Ca concentrations. PTH is released from the parathyroid glands in response to lowered blood Ca. The final hydroxylation of 25-hydroxycholecalciferol (25-hydroxy D3) to 1,25-dihydroxy cholecalciferol in the kidney is regulated by PTH. PTH increases mobilisation of Ca from bone. The active metabolite of vitamin D, acts to increase intestinal absorption of Ca and resorption from bone. Vitamin D is provided by the photochemical conversion of 7-dehydrocholesterol to cholecalciferol (vitamin D3) and is provided by ingestion of vitamin D2 in plants. There are many vitamin D3 metabolites present in blood, but the major circulating form is 25-hydroxy D3, which follows hydroxylation in the liver of vitamin D3 from the diet or skin.
Ensuring adequate magnesium (Mg) supplementation is vital for the prevention of milk fever Mg plays a very important role in Ca metabolism (Figure 2), for example it is a key intermediate in the resorption of Ca from bone by parathyroid hormone. In a recent review, increasing Mg supplementation was found to have the greatest influence amongst dietary strategies for the prevention of milk fever et al., 2006). Therefore, dietary Mg concentration for pregnant dairy cattle should be in the region of 0.4% of DM (Mulligan et al,. 2006).
Dietary levels of Ca influence the absorption of Ca from the intestine, under the control of 1,25(OH)2D3, and the mobilisation of Ca from bone. As dietary Ca concentration increases, total dietary intake of Ca also increases resulting in a decrease in the efficiency of intestinal absorption and a decrease in Ca mobilisation from bone.
The normal periparturient cow responds to decreased plasma Ca concentrations by increasing PTH and subsequently, 1,25(OH)2D3 concentrations. The result is increased intestinal absorption of Ca, increased resorption of Ca from bone and increased renal tubular reabsorption of Ca. The cow is, however, limited in its capacity to respond to increased metabolic demands by the rate at which increased absorption may occur from the intestine and the rate at which Ca may be mobilised from the bones. Availability of dietary Ca to the intestine gradually changes even if more dietary Ca is supplied due to the buffering action of the rumen which acts as a reservoir for Ca. The capacity for cows to absorb Ca through the rumen is uncertain. In vivo and in vitro absorption across the rumen can occur, but at present the quantitative importance of this is to be determined.
The cow depends on a constant supply of dietary Ca and may be placed at risk by gut hypomotility and stasis that are associated with hypocalcaemia. Huber et al. (1981) found in artificially induced hypocalcaemia that rumen contractions ceased well before the onset of signs of clinical hypocalcaemia. Such stasis may be an important factor in the development of hypocalcaemia because even temporary alimentary stasis can induce acute hypocalcaemia through reduced intestinal absorption of Ca.
While 99% of body Ca reserves are in bone, mobilisation of Ca from bone sources has been shown to have variable onset. Ca mobilisation from bone is less rapid in older cows and in cows fed on pre-calving diets that are high in Ca or probably on alkalogenic salts. Cows are more dependent on gut absorption than bone resorption to maintain Ca homeostasis. It has been suggested that hormonal insufficiencies or lack of response of PTH or 1,25(OH)2D3 may be important in the pathogenesis of hypocalcaemia. Diets that are deficient in Ca before calving have been associated with higher plasma levels of 1,25(OH)2D3. In contrast, cows on pre-calving diets which are high in Ca are associated with high plasma concentrations of vitamin D metabolites which could have an antagonistic action on 1,25(OH)2D3. 24,25-Dihydroxycholecalciferol increases the incidence of parturient paresis and this metabolite was elevated in paretic cows.
Cows with clinical milk fever have PTH and 1,25(OH)2D3 in higher concentrations than normal cows. Various forms of vitamin D3 have been used in pharmacological doses before calving to prevent milk fever in cows with varying results. The two metabolites most investigated are 1-alpha-hydroxylcholecalciferol and 1,25(OH)2D3. The vitamin D metabolites have a hypercalcaemic effect that is mediated through increased intestinal absorption of Ca and possibly increased bone resorption. The major difficulty associated with using the vitamin D metabolites remains the accurate prediction of calving date, as treatment is generally most effective between 1 and 4 days prior to calving. Low Ca concentrations in the pre- and post-calving diet also can adversely impact on the success of vitamin D3 supplementation. Another concern with the vitamin D3 metabolites is the risk of toxicity resulting in persistent hypercalcaemia and metastatic calcification of body tissues (Peter J. DeGaris and Ian J. Lean, 2008).
6. Clinical signs
Milk fever usually attacks good milking cows within a few days of an easy labour and seldom before the third or fourth parturition. In many cases of milk fever do not externalize the clinical signs in animals (Goff, 2004). Hypocalcaemia can be clinical or subclinical based on whether an animal may or may not show clinical signs. Clinical milk fever (hypocalcaemia) is the most severe hypocalcaemia results in a cow that is unable to rise (from lying to stand position). In 24 to 48 hours after calving the cow becomes excited and restless, strikes at the abdomen with the hind feet, whisks the tail, lows, grinds the teeth, staggers, falls, makes ineffectual attempts to rise, and eventually lies comatose, stretched on her side with the head extended or inclined towards the shoulder. The eyes are dull, injected and insensitive; general sensation, voluntary motion and the power of swallowing are lost. Secretion of milk fails, digestion is suspended, fermentation of the contents of the paunch sets in, with tympany, constipation and retention of urine. The pulse becomes feeble or imperceptible. Respiration is slow, sometimes stertorous or groaning, and the temperature is low or subnormal. If not treated the animal dies in two or three days from prolonged coma or heart failure. According to Oetzel (2011), animals that are supplemented with minerals prior to calving have reduced risk of milk fever and the hypocalcaemia percentage of cows is reduced to about 15 to 25%. He also stated that based on the degree of hypocalcaemia and time of occurrence the clinical sign of milk fever in dairy cattle around calving can be divided into three stages.
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.
Stage II (Sternal Recumbency): Cows in stage II milk fever are down but not flat out on their side. They exhibit moderate to severe depression, partial paralysis, and typically lie with their head turned into their flank. The clinical signs of stage II milk fever can last from 1 to 12 hours. This is frequently seen with lateral kink or S-shape neck curvature in which the cow tends to lie with her head tucked into her flank. Her temperature is subnormal, her muzzle dry, coldness of skin and extremities. The heart rate will be rapid exceeding 100 beats per minute, gastrointestinal atony predisposes to constipation and mild bloating; In addition the animal exhibits incoordination when walking (Tadesse E et al., 2015).
Stage III (Lateral Recumbency): hypocalcemic cows are flat out on their side completely paralyzed, typically bloated, and are severely depressed (to the point of coma). They will die within a few hours without treatment. Generally this stage is characterized by inability to stand and a progressive loss of consciousness leading to coma. There is a marked fall in temperature and heart sounds become nearly inaudible and the heart rate increases to 120 beats per minute or more. Cows will not survive for more than a few hours without treatment in this stage (Radostits M et al., 2007).
7. Diagnosis and difference diagnosis
7.1. Diagnosis
Diagnosis is based on the cow's history, clinical signs and response to intravenous Ca borogluconate solution within minutes. Clinical signs occur when serum Ca levels fall to <1.5 mmol/l (normal 2.2-2.6 mmol/l) and are often as low as 0.4 mmol/l in cattle with advanced disease.
Hypophosphataemia (<1.0 mmol/I; normal range 1.4-2.5 mmol/I) is frequently observed in blood collected from cows with milk fever. Treatment with Ca borogluconate solution alone will restore normal phosphorus levels in almost all cases.
Blood Mg levels normally increase at calving, samples pue most cases of milk fever have a slight hypermagnesaemia >1.25 mmol/l (Phillip R. Scott et al., 2011).
7.2. Difference diagnosis
Acute toxic mastitis; physical injury/nerve paralysis; uterine rupture; haemorrhage caused by dystocia; acidosis/grain overload.
8. Management
The majority of cases seen by veterinarians will have already been given Ca borogluconate by subcutaneous injection and not responded, usually because of poor absorption due to impaired peripheral blood circulation (absorption from subcutaneous sites takes up to 3-4 hours or may not occur at all). After careful clinical examination, 400 ml of 40% Ca borogluconate solution (containing 12 g Ca), warmed to body temperature, should be administered by slow intravenous injection (over 5-10 minutes) into the jugular vein using a 14 gauge needle and flutter valve with the bottle held 30-40 cm above the infusion site. Some veterinary surgeons also administer Mg and/or phosphorus at the same time, but this is unnecessary in most cases. Toward the end of the intravenous infusion, the cow will typically eructate several times and defaecate, passing firm faeces. The cow should be propped in sternal recumbency and it will frequently make attempts to stand 5-10 minutes after intravenous infusion. There is no advantage to be gained by forcing the cow to stand. Some veterinary surgeons also administer 400 ml of 40% Ca borogluconate subcutaneously in an attempt to prevent recurrence, which can occur in approximately 25% of cases. However, it is important not to overtreat. Dairy cows should not be milked for 24 hours and the calf removed after feeding colostrum (Phillip R. Scott et al., 2011).
LIST OF PRODUCTS TO PROVIDE CANXI AND MAGNE IN CASE OF MILK FEVER FOR CATTLE
*Click on the name of product to have more specific information
| No. | Product name | Indication | Image |
| 1 | Canxi- Magne | Prevention and treatment of acute calcium AND magnesium deficiency. | |
| 2. | Chlorphemin | Effective solution for allergy treatment. Supportive treatment of Rhabdomyolysis, lanata Poisoning, milk fever, Mastitic, hoof inflammatory. |
|
| 3 | Vimeral | Mineral and amino acid for animals. |
9. Prevention
Farmers, veterinarians, nutritionists and other farm advisors often focus on outcomes, such as milk yield and fertility, in the absence of reviewing 'up-stream' factors such as management practices, nutritional regimes and health status of the herd. The occurrence of milk fever or subclinical hypocalcaemia is related to increased incidence rates of several other transition cow disorders. For example, it has been reported that milk fever cows are up to eight times more likely to develop mastitis in the following lactation, are three times more likely to develop dystocia and two to four times more likely to develop displaced abomasum. Therefore, it is of utmost importance that both milk fever and subclinical hypocalcaemia are prevented.
It is still quite common to find farms that have absolutely no control strategy in place for milk fever prevention. Many of these farms may escape for a good deal of time and then one important factor, such as an increase in grass availability or silage quality, will increase BCS (body condition score) at calving and result in a milk fever problem. It is the authors' view that good milk fever preventative strategies are essential on all farms. This paper discusses the consequences of milk fever and subclinical hypocalcaemia (Figure 7) (Mulligan et al,. 2006).
Farmers, veterinarians, nutritionists and other farm advisors often focus on outcomes, such as milk yield and fertility, in the absence of reviewing 'up-stream' factors such as management practices, nutritional regimes and health status of the herd. The occurrence of milk fever or subclinical hypocalcaemia is related to increased incidence rates of several other transition cow disorders. For example, it has been reported that milk fever cows are up to eight times more likely to develop mastitis in the following lactation, are three times more likely to develop dystocia and two to four times more likely to develop displaced abomasum. Therefore, it is of utmost importance that both milk fever and subclinical hypocalcaema are prevented. It is still quite common to find farms that have absolutely no control strategy in place for milk fever prevention. Many of these farms may escape for a good deal of time and then one important factor, such as an increase in grass availability or silage quality, will increase BCS (body condition score) at calving and result in a milk fever problem. It is the authors' view that good milk fever preventative strategies are essential on all farms. This paper discusses the consequences of milk fever and subclinical hypocalcaemia (Figure I)Farmers, veterinarians, nutritionists and other farm advisors often
focus on outcomes, such as milk yield and fertility, in the absence of reviewing ‘up-stream’ factors such as management practices, nutritional regimes and health status of the herd. The occurrence of milk fever or subclinical hypocalcaemia is related to increased incidence rates of several other transition cow disorders. For example, it has been reported that milk fever cows are up to eight times more likely to develop mastitis in the following lactation, are three times more likely to develop dystocia and two to four times more likely to develop displaced abomasum. Therefore, it is of utmost importance that both milk fever and subclinical hypocalcaemia are prevented. It is still quite common to find farms that have absolutely no control strategy in place for milk fever prevention. Many of these farms may escape for a good deal of time and then one important factor, such as an increase in grass availability or silage quality, will increase BCS (body condition score) at calving and result in a milk fever problem. It is the authors’ view that good milk fever preventative strategies are essential on all farms. This paper discusses the consequences of milk fever and subclinical hypocalcaemia (Figure 1 Farmers, veterinarians, nutritionists and other farm advisors often focus on outcomes, such as milk yield and fertility, in the absence of reviewing ‘up-stream’ factors such as management practices, nutritional regimes and health status of the herd. The occurrence of milk fever or subclinical hypocalcaemia is related to increased incidence rates of several other transition cow disorders. For example, it has been reported that milk fever cows are up to eight times more likely to develop mastitis in the following lactation, are three times more likely to develop dystocia and two to four times more likely to develop displaced abomasum. Therefore, it is of utmost importance that both milk fever and subclinical hypocalcaemia are prevented. It is still quite common to find farms that have absolutely no control strategy in place for milk fever prevention. Many of these farms may escape for a good deal of time and then one important factor, such as an increase in grass availability or silage quality, will increase BCS (body condition score) at calving and result in a milk fever problem. It is the authors’ view that good milk fever preventative strategies are essential on all farms. This paper discusses the consequences of milk fever and subclinical hypocalcaemia (Figure 1 Farmers, veterinarians, nutritionists and other farm advisors often focus on outcomes, such as milk yield and fertility, in the absence of reviewing ‘up-stream’ factors such as management practices, nutritional regimes and health status of the herd. The occurrence of milk fever or subclinical hypocalcaemia is related to increasedincidence rates of several other transition cow disorders. For example, it has been reported that milk fever cows are up to eight times more likely to develop mastitis in the following lactation, are three times more likely to develop dystocia and two to four times more likely to develop displaced abomasum. Therefore, it is of utmost importance that both milk fever and subclinical hypocalcaemia are prevented. It is still quite common to find farms that have absolutely no control strategy in place for milk fever prevention. Many of these farms may escape for a good deal of time and then one important factor, such as an increase in grass availability or silage quality, will increase BCS (body condition score) at calving and result in a milk fever problem. It is the authors’ view that good milk fever preventative strategies are essential on all farms. This paper discusses the consequences of milk fever and subclinical hypocalcaemia (Figure 1 Farmers, veterinarians, nutritionists and other farm advisors often focus on outcomes, such as milk yield and fertility, in the absence of reviewing ‘up-stream’ factors such as management practices, nutritional regimes and health status of the herd. The occurrence of milk fever or subclinical hypocalcaemia is related to increased incidence rates of several other transition cow disorders. For example, it has been reported that milk fever cows are up to eight times more likely to develop mastitis in the following lactation, are three times more likely to develop dystocia and two to four times more likely to develop displaced abomasum. Therefore, it is of utmost importance that both milk fever and subclinical hypocalcaemia are prevented. It is still quite common to find farms that have absolutely no control strategy in place for milk fever prevention. Many of these farms may escape for a good deal of time and then one important factor, such as an increase in grass availability or silage quality, will increase BCS (body condition score) at calving and result in a milk fever problem. It is the authors’ view that good milk fever preventative strategies are essential on all farms. This paper discusses the consequences of milk fever and subclinical hypocalcaemia (Figure 1) and outlines some veterinarians, nutritionists and other farm advisors often focus on outcomes, such as milk yield and fertility, in the absence of reviewing ‘up-stream’ factors such as management practices, nutritional regimes and health status of the herd. The occurrence of milk fever or subclinical hypocalcaemia is related to increased incidence rates of several other transition cow disorders. For example, it has been reported that milk fever cows are up to eight times more likely to develop mastitis in the following lactation, are three times more likely to develop dystocia and two to four times more likely to develop displaced abomasum. Therefore, it is of utmost importance that both milk fever and subclinical hypocalcaemia are prevented.
Over fatness in dry cows should be avoided : the aim should be calve cows at body condition scores of 2.5-3.0 out of 5. The primary cause of milk fever problems is usually the mineral content of the transition dry cow diet fed during the last two weeks of pregnancy either a high Ca content or a high dietary cation - anion balance (DCAB). Manipulation of the dry cow diet is the most cost - effective method of controlling the incidence of hypocalcaemia. There are two very different approaches available:
i) The amount of Ca in the transition dry cow diet (583) should be limited to less than 50 g/head/day (ideally less than 30 g/day) to maintain PTH activity. Magnesium levels in the diet should be above 40 g/day. This can prove very difficult to achieve in grass-based forage systems due to the relatively high levels of Ca in grass. The use of Ca- binding agents such as zeolite may help reduce Ca absorption .
ii) Manipulation of the DCAB, which by lowering blood pH allows PTH to act on its receptor and releases cations (mainly Ca) from bone. Sodium, potassium, sulphate and chloride ions exert the strongest effects on acid- base balance, and are referred to as the strong ions.
DCAB = (Na+ and K+) minus (Cl- and S--)
The aim of a 'full DCAB' system is to reduce the overall DCAB of the diet to between -100 and -150 mEq/kg DM by increasing sulphate and chloride ions and/or reducing sodium and potassium cations, thus inducing mild metabolic acidosis. Grass silage has a DCAB of +300 to +400 mEq/kg DM, and grass has an even higher positive DCAB (mainly due to the high sodium and potassium levels). Anionic salts commonly used to reduce DCAB include magnesium chloride, ammonium chloride and Ca chloride.
The majority of dairy farmers utilize a partial DCAB approach, which manipulates the forages fed in the transition dry cow diet to favour the DCAB balance (e.g. minimizevuse of grass and grass silage and increase use of maize silage , wholecrop and straw in the diet , which have lower DCAB values), as well as adding magnesium chloride or other anionic salt preparations such as Biochlor to the diet. Under such situations, the DCAB of the diet will be around 0 to +50 mEq/kg DM. Given the high forage content of the transition dry cow diet and faced with a high incidence of milk fever cases on a farm, changing the forage fed to the dry cows may assist in milk fever control (i.c. reduce grass intakes , increase levels of maize silage and wholecrop with lower DCAB values). Low dietary magnesium may be a factor and provision of magnesium chloride will also lower the DCAB of the diet. An alternative method of milk fever control (practised widely in Scandinavia) involves giving high levels of Ca by mouth at calving. Cows known to be at risk of milk fever can be given Ca at/just before calving using drenches (150 g Ca chloride daily), gels and Ca boluses. Administration of 250 mg vitamin D, (cholecalciferol) or alfacalcidol (1a-hydroxycholecalciferol) can be carried out prior to calving, but this necessitates accurate prediction of calving date. Measures to prevent excessive Ca withdrawal after Ca include no pre-calving milking, removal of the calf at birth (remember to give colostrum) and no milking out for 3-4 days after calving (Phillip R. Scott et al., 2011).
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