Milk Fever in Cows

Milk fever in cows is also known as Parturient paresis or Hypocalcaemia. It is a metabolic disease of adult females that occurs most commonly around the time of parturition and is characterised by hypocalcaemia, severe muscle weakness, sternal recumbency, and lateral recumbency.

Etiology

The principle cause of milk fever is a depression in the levels of ionised calcium in the extracellular space, including plasma, which may be due to:

1. Excessive loss of calcium in the colostrums and milk. The colostrums is rich in calcium.
2. Decreased absorption of calcium from the intestine at the time of parturition
   • Reduced feed intake at parturition
   • Ruminal atony / indigestion
   • Deficiency of Vit. D
   • Improper calcium-phosphorus ratio in the diet
   • Diseases of the intestine
3. Slow mobilisation of calcium from the bone
   • Parathormone deficiency
   • High calcium level in the blood
   • Excessive calcium intake during the dry period depresses the activity of PTH

Epidemiology

• Milk Fever in cows is sporadic disease.
• The cows and buffaloes are most affected. Sometimes ewes, does, sows, mares and bitches are affected.
• Jersey cows are more susceptible than Holstein–Friesian cows.
• Most common in 5-10 years age group.
• It is a diseases of females.
• Most cases occur during calving period.
• It occurs in cows with their 3rd to 7th calving.
• Disease occurs at 3 main stages in the lactation cycle:
  • Most Prepartum cases occur in last few days of pregnancy
  • Some cases occur few hours before calving or at the time of parturition
  • Majority of cases (80%) occur within the first 48 hours after calving
• Cold climate, long distance transport, forced exercise, sudden deprivation of feed and grazing on oxalate rich plants are predisposing factors for milk fever in animals.
• High milk yielding animals are mostly affected.

Dietary and Environmental Risk Factors:

• Dietary Calcium: Feeding more than 100 g of calcium daily during the dry period is associated with an increased incidence of milk fever.
• Dietary Potassium: High potassium concentrations (>2% of the ingested dry matter) in the ration fed to cows in their last weeks of gestation can considerably increase the incidence of periparturient hypocalcemia.
• Dietary Magnesium: Magnesium deficiency during late gestation is a major risk factor for periparturient hypocalcaemia, and hypomagnesaemia is considered to be the most common cause of milk fever occurring in mid lactating dairy cows.
• Dietary Phosphorus: Prepartum diets high in phosphorus (P > 80 g P/d) greatly increase the incidence of milk fever and the severity of hypocalcaemia.
• Dietary Cation–Anion Difference: Prepartum diets high in cations such as potassium are associated with an increased incidence of milk fever, whereas diets high in anions, especially chloride and sulfur, result in a decrease in the incidence of the disease.

Pathogenesis

• Due to failure of calcium homeostasis.
• Due to Concurrent hypomagnesemia: The two mechanisms through which Mg deficiency may predispose to hypocalcemia-
  • An impaired release of PTH in response to hypocalcemia
  • Decreased tissue sensitivity to PTH in hypomagnesemia states. hypomagnesemia can therefore predispose to clinical or subclinical milk fever by blunting the main counter-regulatory mechanism of hypocalcemia.
• Due to Concurrent Hypophosphatemia: Low serum Pi concentrations are commonly observed in milk-fever cows, but also in healthy dairy cows, around parturition. Although the clinical relevance of hypophosphatemia in recumbent cattle remains uncertain.

Clinical Signs

The sign develops in 3 stages-

1. First stage or stage of excitement:

• Excitement
• Tetany
• Hypersensitiveness
• Muscle tremors
• Ataxia
• Cow is still standing
• Disinclined to move and often has a decreased or no feed intake
• Agalactia, rumen stasis, and scant feces
• Heart rate and respirations may be within normal limits or slightly elevated

2. Second stage or stage of sternal recumbency:

• Animal is unable to stand and rests on sternum with head turned towards shoulder or flank
• Drowsiness
• Cold skin and extremities, dry muzzle
• Dilatation of pupil with absence of papillary light reflex
• Relaxation of anus with loss of anal reflex
• Heart sounds muffled, tachycardia
• Suspended defecation and urination
• Low venous pressure

3. Third stage or stage of lateral recumbency:

• Animal is unable to stand or sit and remains in lying down condition
• Markedly subnormal body temperature
• Extremely cold skin with inaudible heart sounds
• Bloat
• Impossible to raise the veins

Diagnosis

• History of parturition and high milk yield.
• Based on symptoms like sterna or lateral recumbency with subnormal body temperature.
• Based on clinical pathology (serum calcium levels, serum magnesium level, serum inorganic phosphorus level, blood glucose level, serum muscle enzyme activity and hemogram).

Serum Calcium Levels:

Levels of ionized Ca in the venous whole blood of cows are as follows:

• Normal: 1.06 to 1.26 mmol/L (4.3 to 5.1 mg/dL);
• Slight hypocalcemia: 1.05 to 0.80 mmol/L (4.2 to 3.2 mg/dL)
• Moderate: 0.79 to 0.50 mmol/L (3.2 to 2.0 mg/dL)
• Severe hypocalcemia: less than 0.50 mmol/L (<2.0 mg/dL).

Total serum calcium levels are reduced below normal in all cows at calving, whether they have milk fever or not, but not in ewes.

Serum Magnesium Levels:

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

Serum inorganic phosphorus (Pi):

Serum inorganic phosphorus (Pi) levels are usually depressed to 0.48 to 0.97 mmol/L (1.5 to 3.0 mg/dL).

Blood Glucose Levels:

Blood glucose levels are usually normal, although they may be depressed if ketosis occurs concurrently. Higher-than-normal blood glucose levels are likely to occur in cases of long duration and are presumable because Ca is required for the release of insulin from the pancreas.

Serum Muscle Enzyme Activity:

Prolonged recumbency results in ischemic muscle trauma and necrosis and increases in the serum muscle enzyme activity of creatine kinase (CK) and aspartate aminotransferase (AST).

Hemogram:

Eosinopenia, neutrophilia, Lymphopenia ,high plasma cortisol levels and increased PCV seen in hemogram of milk fever affected case.

Differential Diagnosis

• Other metabolic diseases (Hypomagnesemia, Hypophosphatemia and Severe hypokalemia, Ketosis).
• Diseases associated with toxemia and shock (Acute or peracute coliform mastitis, Aspiration pneumonia, Acute diffuse peritonitis, Carbohydrate engorgement (grain overload), Toxemic septic metritis).
• Injuries to the pelvis and pelvic limbs.
• Degenerative myopathy.
• Downer-cow syndrome.

Treatment

• Calcium gluconate (equivalent to 8 to 12 g Ca/cow IV or SC as single dose)
• Calcium borogluconate (equivalent to 8 to 12 g Ca/cow IV or SC as single dose)
• Calcium chloride (equivalent to 8 to 12 g Ca/cow IV as single dose)
• Calcium chloride (equivalent to 50 g Ca/cow) PO q12 for 48h
• Calcium propionate (equivalent to 50 g Ca/cow) PO q12 for 48h

Typical Response to Calcium Therapy:

Cows with milk fiver exhibit a typical pattern of response to calcium borogluconate, including:

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

The feces are firm fecal ball with a firm crust and covered with mucus. Urination does not follow until the cow stands. Many cows will eat and drink within minutes following successful treatment.

Unfavorable response to calcium borogluconate therapy:

Marked increase in heart rate in cows affected with toxemia and acute heart block. Some degree of arrhythmia occurs in most cases but if gross arrhythmia or a sudden increase in heart rate, the injection should be stopped temporarily or continued with great caution. ECG changes in hypercalcemia shows increased ventricular activity and reduced atrial activity. Atropine is capable of abolishing the resulting arrhythmia.

Prevention and Control

• Reduce dietary calcium intake 2 to 3 weeks before calving to < 20 g Ca/cow/day
• Reduce dietary potassium content as much as possible in late gestation (in any case, below 2% in feed dry matter)
• Provide adequate dietary magnesium in late gestation ( 0.4% of feed dry matter)
• Anionic salts mixed into feed to obtain a dietary cation–anion difference of −100 to −150 mEq/kg of feed dry matter for at least 2 weeks before calving
• Zeolite A (250 to 500 g/cow/day) PO q24h for at least 2 weeks before calving
• Supplement diet in late gestation with vitamin D
• Vitamin D3 (10 million IU/cow IM as single dose 3 to 7 days before expected calving
• Vitamin D2 (10 to 20 million IU/cow PO for at least 7 days before expected calving)
• Calcium chloride (equivalent to 50 g Ca/cow PO q12h for 48 hours from the time of parturition)
• Calcium propionate (equivalent to 50 g Ca/ cow PO q12h for 48 hours from the time of parturition)
• Partial milking during the first days of lactation
• Udder insufflations in the first days of lactation
• Provide good shelter and protect from clod stress
• Avoid stress of transportation during advance pregnancy
• Give exercise to maintain normal G.I function and also to stimulate bone metabolism
• Maintain appetite at calving
• Provide ammonium chloride to the pregnant animals along with grains @25g orally over last few weeks of pregnancy and increase to 100gm/day at calving