Hypocalcaemia In Dairy Cattle :Economic Impact

Periparturient hypocalcemia is a common metabolic disorder in dairy cows that leads to an increased risk of detrimental health and production outcomes and in severe cases can be life threatening. Physiologically, serum calcium concentration in the adult cow is maintained above 2.0 mmol/L (Martin-Tereso and Martens, 2014). Due to the start of colostrum production and consequently increasing calcium demand, the nadir of serum calcium concentration occurs 12 to 24 h after parturition (Kimura et al., 2006; Goff, 2008). For example, a cow producing 10 L of colostrum, it loses about 23 g of Ca in a single milking. This amount is about nine times as much Ca as is present in the entire plasma Ca pool of the cow. Calcium lost from the plasma pool must be replaced by increasing intestinal Ca absorption, or increasing bone Ca resorption, or both. As a consequence of this sudden Ca requirement, nearly all cows experience some degree of hypocalcemia during the 1st d after calving as the intestine and bone adapt to the Ca demands of lactation. In some cows, the mammary drain of Ca causes extracellular and plasma Ca concentrations to decline to levels that disrupt neuromuscular function, resulting in the clinical syndrome of milk fever.

A disease of cattle, sheep and goats occurring around the time of parturition and caused by hypocalcemia and characterized by weakness, recumbency and ultimately shock and death.

Etiology

Hypocalcemia just before or after parturition: A depression of the levels of ionized calcium in tissue fluids is the basic biochemical defect in milk fever. A transient period of subclinical hypocalcemia (total plasma calcium <1.9 mmol/L) occurs at the onset of lactation caused by an imbalance between calcium output in the colostrums and influx of calcium to the extracellular pool from intestine and bone. The onset of lactation results in a sudden large demand on the calcium homeostasis.

A cow producing 10 kg of colostrum (2.3 g of Ca/kg) will lose 23 g of calcium in a single milking. This is about nine times as much calcium as that present in the entire plasma calcium pool of the cow.

Calcium lost from the plasma pool must be replaced by increasing intestinal absorption and bone resorption of calcium.

During the dry period, calcium requirements are minimal at about 10-12 g/d. At parturition, the cow must mobilize about 30 g or more of calcium into the calcium pool per day.

Hypocalcemia occurs in spite of apparently adequate function of the parathyroid and vitamin D endocrine system and most cows adapt within 48 h after calving by increases in plasma concentrations of parathyroid hormone and 1,25- (OH)2D vitamin at the onset of the hypocalcemia and mobilize calcium by increasing intestinal absorption and bone resorption.

Epidemiology:

Mature dairy cows are most commonly affected in the 5-10-year age group, although rare cases have been observed at the first and second calvings.

The hypocalcemia at calving is also age related and most marked in cows at their 3rd to 7th parturition; it is infrequent at the first parturition.

Most cases occur within the first 48 h after calving and the danger period extends up to about the 10th postpartum day. Occasional cases occur 6-8 weeks after parturition (mid-lactation).

Hypocalcemic episodes lasting 1-2 days may occur two or three times with a periodicity of about 9 days. These cows are referred to as ‘calcium cyclers’.

Calcium homeostasis: Three factors affect calcium homeostasis and variations in one or more of them may be important in causing the disease in any individual:

1. Excessive loss of calcium in the colostrum beyond the capacity of absorption from the intestines and mobilization from the bones to replace.
2. Impairment of absorption of calcium from the intestine at parturition.
3. Mobilization of calcium from storage in the skeleton may not be sufficiently rapid to maintain normal serum levels.

Body condition score (BCS): A high BCS increases the risk of milk fever.

Dietary and environmental risk Factors: Dietary calcium. Feeding more than100 g of calcium daily during the dry periodis associated with an increased incidenceof milk fever.

Dietary phosphorus: Prepartum diets high in phosphorus (>80 g P/d) also increases the incidence of milk fever and the severity of hypocalcemia.

Dietary cation-anion difference (DCAD): The anion-cation dietary difference exerts a strong, linear effect on the incidence of milk fever. The dietary cation-anion balance in the prepartum diet may be more important than the level of dietary calcium as a risk factor for milk fever.

Prepartum diets high in cations such as sodium and potassium are associated with an increased incidence of milk fever, while diets high in anions, especially chloride and sulfur are associated with a decrease in the incidence of the disease.

Alkaline diets containing an excessive concentration of sodium and potassium can result in an increased incidence of the disease. Most forages such as legumes and grasses are high in potassium and are alkaline.

Effects of milk fever and subclinical hypocalcemia

• Economic loss
• Milk fever relapses.
• Downer cow complications
• Dystocia and reproductive disease
• Retained placenta
• Metritis.
• Milk production
• Mastitis
• Displacement of abomasums
• Ketosis

PATHOGENESIS

Hypocalcemia

Plasma calcium concentration is normally maintained between 2.1 and 2.6 mmol/L (8.5 -10.4 mg/dL). Almost all dairy cows will experience subclinical hypocalcemia, <1.8 mmol/L (7.5 mg/dL) within 24 h after calving.

In some cows, the hypocalcemia is more severe, <1.25 mmol/L (5 mg/dL) causing neuromuscular dysfunction resulting in clinical milk fever. Without treatment, levels may continue to decline to about 0.5 mmol/L (2 mg/dL) which is usually incompatible with life.

CLINICAL FINDINGS

Three stages of milk fever in cattle are commonly recognized and described.

Stage 1

• In the first stage, the cow is still standing. This is also the brief stage of excitement and tetany with hypersensitivity and muscle tremor of the head and limbs.
• The animal is disinclined to move and does not eat. There may be a slight shaking of the head, protrusion of the tongue and grinding of the teeth. The rectal temperature is usually normal to slightly above normal.
• Stiffness of the hindlegs is apparent, the animal is ataxic and falls easily and, on going down, the hindlegs are stuck out stiffly.
• Prodromal Stage: It is characterized by anorexia, agalactia, rumen stasis, scant feces and a normal temperature, heart rate and respirations.
• There are no obvious signs of excitement and hypersensitivity characteristic of the first stage. Affected cows may remain in this prodromal stage for several hours; they are perplexing diagnostically and respond quickly to calcium therapy. Cows with this form of hypocalcemia may be the ‘calcium cyclers’ described earlier.

Stage 2

• The second stage is prolonged sternal recumbency. Consciousness is usually depressed; the cow has a drowsy appearance in sternal recumbency, usually with a lateral kink in the neck or the head turned into the flank.
• When approached, some of these cows will open their mouths, extend their head and neck and protrude their tongues, which may be an expression of apprehension and fear in an animal unable to stand.
• There is a marked decrease in the absolute intensity of the heart sounds and an increase in rate (about 80 bpm). The arterial pulse is weak and the venous pressure is also low, making it difficult to raise the jugular veins.
• The respirations are not markedly affected, although a mild forced expiratory grunt or groan is sometimes audible. The eyes are usually dry and staring. The pupillary light reflex is incomplete or absent and the diameter of the pupil varies from normal to maximum dilatation.

Stage 3

• The third stage is lateral recumbency. The cow is almost comatose and although the limbs may be stuck out there is complete flaccidity on passive movement and the cow cannot assume sternal recumbency on its own. In general, the depression of temperature and the cardiovascular system are more marked.
• The heart sounds are almost inaudible and the rate increased up to 120 bpm; the pulse is almost impalpable and it may be impossible to raise the jugular veins.
• Bloat is usual because of lateral recumbency. Without treatment, a few animals remain unchanged for several hours but most become progressively worse during a period of several hours and dye quietly from shock in a state of complete collapse.

Concurrent hypomagnesemia: Mild to moderate tetany and hyperesthesia persisting beyond the first stage suggests a concurrent hypomagnesemia.

There is excitement and fibrillary twitching of the eyelids and tetanic convulsions are readily precipitated by sound or touch. Trismus may be present. The heart and respiratory rates are increased and the heart sounds are much louder than normal.

Without treatment death occurs during a convulsion.

Concurrent hypophosphatemia: With a concurrent hypophosphatemia, the clinical findings are typical of milk fever which responds to calcium therapy in all respects except that the cow is unable to stand after treatment.

CLINICAL PATHOLOGY

Total serum calcium levels are reduced to below 8 mg/dL (2.0 mmollL), usually to below 5 mg (1.2 mmol/L) and sometimes to as low as 2 mg (0.5 mmol/L). The reduction is usually, but not always, proportional to the severity of the clinical syndrome.

Serum magnesium levels are usually moderately elevated to 4-5 mg/dL (1.65-2.06 mmol/L) but in some areas low levels may be encountered, especially in cows at pasture.

Serum inorganic phosphorus levels are usually depressed to 1.5-3.0 mg/dL (0.4S-0.97 mmoI/L).

Blood glucose levels are usually normal, although they may be depressed if ketosis occurs concurrently.

Serum muscle enzymes: Prolonged recumbency results in ischemic muscle necrosis and increases in the serum muscle enzymes creatine phosphokinase (CPK) and aspartate aminotransferase (AST) or SGOT.

Hemogram

Changes in the leukocyte count include an eosinopenia, a neutrophilia, and a lymphopenia suggestive of adrenal cortical hyperactivity, but similar changes occur at calving in cows which do not develop parturient paresis.

NECROPSY FINDINGS

There are no gross or histological changes unless concurrent disease is present.

Differential diagnosis

Metabolic and nutritional disease

• Hypophosphatemia
• Hypomagnesemia
• Downer cow syndrome
• Fat cow syndrome
• Carbohydrate engorgement.

Toxemias

• Peracute coliform mastitis
• Aspiration pneumonia
• Acute diffuse peritonitis.

Injuries to pelvis and pelvic limbs

• Maternal obstetrical paralysis
• Dislocation of coxofemoral joint.

Diagnostic confirmation

Hypocalcemia and response to treatment with calcium borogluconate.

TREATMENT

Every effort should be made to treat affected cows as soon as possible after clinical signs are obvious. Treatment during the first stage of the disease, before the cow is recumbent, is the ideal situation.

Standard treatment

• Most cows with milk fever can be treated successfully with 8-10 g of calcium (calcium borogluconate is 8.3% calcium).
• For cattle, 400-800 mL of a 25 % solution is the usual dose.  As an initial dose a large cow (540-590 kg) requires 800-1000 mL of a 25% solution and a small cow (320-360 kg) 400-500 mL.

TYPICAL RESPONSE TO CALCIUM BOROGLUCONATE

Cows with milk fever exhibit a typical pattern of response to calcium borogluconate, if the response is favorable, including:

• Belching
• Muscle tremor, particularly of the flanks and often extending to the whole body
• Slowing and improvement in the amplitude and pressures of the pulse
• Increase in the intensity of the heart sounds
• Sweating of the muzzle
• Defecation

Unfavorable response to calcium borogluconate

An unfavorable response is characterized by a marked increase in heart rate in cows affected with toxemia and acute heart block in apparently normal animals especially with overdosage, with too rapid injection and in cases in which treatment has been unduly prolonged.

Udder insufflation

Insufflation of the udder with air was an alternative treatment for cows which continued to relapse following repeated calcium injections.

With the availability and effectiveness of orally administered calcium gels, udder insufflation cannot be recommended.

General management practices

The following management practices are suggested:

• Avoid over-fattening by either reducing the energy concentration of the ration or restricting the intake during the prepartum period. This also appears to stimulate appetite, thus keeping cows on feed.
• Avoid stresses at the time of parturition.
• Provide a clean well-bedded box stall with conditions conducive to cow comfort and allow the animal to exercise.
• Make frequent observations of cows prone to milk fever from 48 h before to 48 h after parturition for evidence of milk fever and immediate treatment will reduce the incidence of the downer cow syndrome associated with milk fever.
• At calving the cow should receive an oral dose of a calcium salt in a gel, as set out later, followed by a diet with a high calcium content (over 1 % of dry matter). The critical day is the day of calving and a sharp increase in calcium intake on this day can significantly reduce the occurrence of milk fever.
• If hypomagnesemia is a likely concomitant, the diet should be supplemented with 60 g magnesium oxide daily.

CONTROL

Various methods for the control of milk fever in ruminants, especially dairy cows, are available. They include

1. Dietary management during the transition period before and after calving
2. Administration of calcium gels orally at the time of parturition
3. Administration of vitamin D and its metabolites and analogs immediately before parturition to enhance the mobilization of calcium.

Economic consequences of milk fever

Economically, milk fever is important diseases that can reduce dairy cow’s productive life by 3.4 years as well affect

reproductive performance. Mostly in untreated cases of milk fever, 60-70% cows die (McDowel et al., 2002). Economic losses due to clinical cases of milk fever are substantial and include losses from deaths (~8% of affected cows), premature culling (~12% of affected cows), treatment costs and decreased milk production in the subsequent lactation (Khan et al., 2015). In addition, each episode of clinical milk fever increases the risk for other parturient diseases such as retained placenta, ketosis, displaced abomasums and environmental mastitis (Oetzel, et al., 2011). More recently it has been reported subclinical hypocalcaemia exacerbate the level of immuno-suppression experienced by peri-parturient dairy cattle (Kimura et al., 2006).

Milk fever, dystocia and uterine prolapse

It has been recognized that subclinical hypocalcaemia reduce the ability of the transition cow to effect smooth and skeletal muscle contraction (Kimura et al., 2006). Loss of uterine muscle tone due to hypocalcemia in cows suffering from hypocalcaemia is a major cause of uterine prolapse. Cows with milk fever are developing dystocia six times more than that of normal cows. This is because of a reduced ability of smooth and skeletal muscle contraction causes for cow’s long period in labour, which predisposes to dystocia (Tadesse et al., 2015).

Milk fever and fertility

From many study it was reported that cows with clinical hypocalcaemia had a greater diameter of the gravid uterine horn and nongravid uterine horn between 15 and 45 days post-partum (indicative of slower uterine involution) and a significantly reduced likelihood of having a corpus luteum (indicative of ovulation since parturition) than normal cows. These results in reduced fertility in dairy cows due to its effect on uterine muscle function, slower uterine involution and reduced blood flow to the ovaries. There are also indirect effects of milk fever on fertility, which is mediated through dystocia, endometritis and ROP (Mulligan et al., 2006).

Milk fever and mastitis

Both milk fever and subclinical hypocalcaemia cause an increase in the normal cortisol response at parturition. Cortisol is believed to be an important component of the suppressed immunity experienced by periparturient dairy cattle. Cows that have suffered from clinical hypocalcaemia are 8 times more likely to develop mastitis than normal cows. This phenomenon is mainly due to a reduction in smooth muscle function at the teat sphincter and hence an easy routine for infection after milking and an exacerbated suppression of immunity in milk fever cows when compared with normal cows.

Milk fever and GIT function

There is a reduction in the motility of rumen and abomasum in clinically hypocalcaemic cows. This reduction in ruminal and abomasal motility will likely cause a reduction in feed intake (Whiteford et al., 2006). Furthermore, Goff (2003) has indicated that low plasma Ca concentration around calving will result in reduced motility and strength of abomasal contractions and hence abomasal atony and distension of the abomasum. Therefore, milk fever has been implicated as a predisposing factor for many other transition cow disorders.

Retained placenta

Several studies indicated that increased risk for the occurrence of retained placenta following milk fever, with milk fever cows being up to three times more likely to experience retained placenta than normal cows (Houe et al., 2001).The direct effect of milk fever on the occurrence of retained placenta (excluding any interaction for the effect of milk fever on dystocia) has been reported to double the odds of retained placenta occurring (Mulligan et al., 2006). Furthermore there is also a large indirect effect of milk fever on retained placenta, as milk fever is a risk factor for dystocia and dystocia is a risk factor for retained placenta. Melendez et al., (2004) have reported a significantly lower plasma Ca concentration in cows with retained foetal membranes in comparison to cows with normal placental expulsion. The point should also be made that, in this case, the hypocalcaemia experienced by cows with retained foetal membranes was subclinical not clinical. There is, therefore, a clear link between milk fever and the occurrence of retained placenta.

Endometritis

The link between milk fever and periparturient immuno-suppression, provide a strong basis for the suggested association between milk fever and endometritis (Kimura et al., 2006). In support of this, White ford and Sheldon (2005) observed a significantly higher incidence rate of endometritis in UK cows that suffered clinical hypocalcaemia in comparison to normocalcaemic cows. Metabolic diseases are of great economic impact; it usually affects the animals about to reach their maximum potential production. Dietary deficiencies as a result of poor ration formulation is the most probable cause of metabolic disorder. Milk fever is a common metabolic disturbance in dairy cows resulting from hypocalcaemia that occurs in older, third to sixth lactation, high producing dairy cows that are near calving or have recently calved. It is mainly characterized by progressive muscle weakness and depression that progresses into coma if not treated promptly. Hypocalcaemic cows will begin trembling and will no longer be able to stand. Subsequently the cow becomes recumbent, first in the sternal position and then laterally. Parturient paresis is favorable to early treatment with intravenous calcium supplementation. Economically, it reduces milk yield and fertility. Hypocalcaemic cow are more sensitive to various reproductive disorder like ROP, endometritis and mastitis. Dietary calcium levels must be low in the weeks leading up to calving. Management practices like body condition score management and shortening the dry period are also critical for the prevention of the disease.

 

HYPOCALCAEMIA IN DAIRY ANIMALS

Compiled  & Shared by- Team, LITD (Livestock Institute of Training & Development)

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