Metabolic disorders in cattle

- Acknowledgment

We would like to acknowledge the committee of the National Egyptian Guidelines for Veterinary Medical Interventions, Egyptian Health Council for adapting this guideline.

Executive Chief of the Egyptian Health Council: Prof. Mohamed Mustafa Lotief.

Head of the Committee: Prof. Ahmed M Byomi

The rapporteur of the Committee: Prof. Mohamed Mohamedy Ghanem.

Scientific Group Members: Prof. Nabil Yassien, Prof. Ashraf Aldesoky Shamaa, Prof. Amany Abbas, Prof. Dalia Mansour, Dr Essam Sobhy Dr Mohamed Elsharkawy, Prof. Dr Gamal A. Sosa., Dr Naglaa Radwan, Dr Hend El Sheikh

Editor/Author: Prof. Mohamed Ghanem

- Introduction

Metabolic disorders in cattle represent a significant challenge to global livestock production, animal health, and farm profitability. These disorders commonly arise when nutrient intake does not match physiological demands, particularly during the transition period (three weeks pre‑ and post‑calving). They impair metabolic homeostasis, reduce productivity, and increase susceptibility to secondary diseases.

These disorders typically arise from nutritional imbalances, hormonal irregularities, or genetic predispositions. They are called “production diseases “because of its relation to high milk production in cattle.

- Classifications of metabolic diseases

- Definition of milk fever

Milk fever (parturient paresis) is a metabolic disease of dairy cattle characterized by low blood calcium levels (hypocalcemia) occurring around parturition, usually within 24–72 hours after calving, due to the sudden demand for calcium for colostrum and milk production.

It mainly affects high-producing multiparous dairy cows, especially Jersey and Holstein breeds.

- Etiology of milk fever

Milk fever occurs when calcium homeostasis mechanisms fail to respond quickly to the sudden calcium drain into milk.

Main causes:

1.    Sudden calcium demand at parturition

2.    Reduced calcium mobilization from bone

3.    Insufficient intestinal calcium absorption

4.    Improper dry cow nutrition

Predisposing factors:

• High milk production
• Older cows (3rd lactation and above)
• High calcium diet during dry period
• Low magnesium levels
• Metabolic alkalosis
• Lack of exercise
• Obesity
• Breed susceptibility (Jersey > Holstein)

- Pathogenesis of milk fever

At calving:

• Large amounts of calcium are removed in colostrum
• Blood calcium drops rapidly

Normally the body responds through:

• Increased Parathyroid hormone (PTH) → mobilizes calcium from bone
• Increased Vitamin D activation → increases gut absorption of calcium
• Increased renal calcium reabsorption

In milk fever:

• Tissue response to PTH is delayed
• Bone mobilization is slow
• Intestinal absorption is insufficient

Result:
Serum calcium drops below 5–7 mg/dl (normal 8-10 mg/dl)

Calcium is activator of acetylcholine which is essential mediator at the neuromuscular junction enhancing muscular contractility, therefore decreased Ca level causes:

• Neuromuscular dysfunction
• Muscle weakness
• Paresis
• Reduced smooth muscle contraction

- Clinical Signs of milk fever

Milk fever occurs in three stages:

Stage 1 (Early stage) – Excitement stage

Duration: short (often missed). clinical signs include:

• Restlessness
• Hypersensitivity
• Muscle tremors
• Ear twitching
• Mild weakness

Stage 2 (Sternal recumbency stage)

Is the most commonly observed stage. Clinical Signs:

• Sternal recumbency
• Depression
• Cold ears and muzzle
• Dilated pupils
• Reduced rumen motility
• Constipation
• Tachycardia (weak pulse)
• Body temperature may be normal or low
• Characteristic S-shaped neck

Figure (1): sternal recumbency in a cow with milk fever.

Stage 3 (Lateral recumbency stage - comatosed)

Severe stage (emergency): signs include:

• Lateral recumbency
• Severe depression
• Coma
• Bloat
• Severe hypothermia (cold ears and extremities)
• Weak heart sounds
• Death if untreated

- Diagnosis of milk fever

Clinical diagnosis:

• History at late pregnancy or recently calved cow
• Recumbency (sternal then lateral)
• Cold extremities
• Good response to calcium therapy (therapeutic diagnosis)

Laboratory diagnosis:

• Low serum calcium
• There may be hypophosphatemia, mild hyperglycemia
• Increased CK due to muscle damage

- Treatment in milk fever

Milk fever is considered as a medical emergency.

Primary treatment:

IV Calcium therapy: Calcium borogluconate - or Cal-D-Mag (25%)

• 500 ml slowly IV
• Given over 10–20 minutes

Response:

• Improvement within minutes
• Eructation
• Urination
• Standing within 1–2 hours
• If no response, repeat ca therapy after 12 hrs.

Additional therapy:

• Subcutaneous calcium (to prevent relapse)
• Oral calcium gels
• Phosphorus supplementation if needed
• Magnesium if hypomagnesemia is suspected

Important precautions for calcium therapy in cattle:

• Give slowly (risk of cardiac arrhythmia)
• Monitor heart during IV infusion
• Stop if arrhythmia occurs

- Prevention of milk fever

1. Low calcium diet before calving

Low Ca diet Stimulates calcium mobilization before parturition by activating parathyroid hormone (less than 50 g Ca/day).

2. Dietary Cation Anion Difference (DCAD diet)

Use anionic salts such as Ammonium chloride, Calcium sulfate, and Magnesium sulfate (to produce pH between 6-6.5). This mild metabolic acidosis improves PTH response.

3. Vitamin D supplementation

Given before calving (use cautiously). 10 millin IU given SC  of IV about 10 days before calving.

4.Magnesium supplementation: Magnesium improves calcium metabolism.

- Complications of milk fever

Milk fever predisposes cattle to the following diseases and problems:

• Dystocia
• Retained placenta
• Ketosis
• Displaced abomasum
• Mastitis
• Metritis

Reason:
Smooth muscle weakness and immune suppression.

- Differential Diagnosis for milk fever

- Prognosis of milk fever

Good prognosis if:

• Treated early
• Cow treated within 6–12 hrs

Poor prognosis if:

• Stage 3 (comatose)
• Delayed treatment
• Muscle damage occurs
• Secondary complications

Recovery rate:
85–95% if treated early

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