Bovine Malnutrition Study Guide

Overview and Clinical Importance

Malnutrition in cattle represents a multisystemic disorder arising when dietary intake fails to meet requirements for energy, protein, minerals, or vitamins. This condition is particularly important in beef cattle during late gestation, early lactation, and periods of environmental stress. Malnutrition predisposes animals to secondary conditions including pregnancy toxemia, hepatic lipidosis, infectious diseases, and reproductive failure. Understanding the pathophysiology, clinical signs, diagnosis, and management of bovine malnutrition is essential for NAVLE success.

Pathophysiology of Bovine Malnutrition

Energy Balance and Metabolism

Cattle require energy for maintenance, growth, reproduction, and lactation. When dietary energy intake is insufficient, animals enter a negative energy balance (NEB). During NEB, the body mobilizes fat reserves through lipolysis, releasing non-esterified fatty acids (NEFAs) into circulation. If NEFAs exceed the liver's capacity for beta-oxidation and export as very-low-density lipoproteins (VLDLs), hepatic lipidosis develops.

Late gestation represents a critical period because fetal energy demands increase dramatically while rumen capacity decreases. At day 130 of gestation, net energy maintenance (NEm) requirement for pregnancy is approximately 0.33 Mcal/day; by day 250, this increases to 3.33 Mcal/day. Protein requirements similarly increase from 9.1 g available protein/day at day 130 to 95.2 g/day at day 250.

Body Condition Scoring (BCS)

Body condition scoring is a subjective assessment of fat reserves using a 1 to 9 scale for beef cattle or a 1 to 5 scale for dairy cattle. Key anatomical areas for evaluation include: backbone (spinous and transverse processes), ribs, hooks (tuber coxae), pins (tuber ischii), tailhead, and brisket.

Beef Cattle Body Condition Score Descriptions

Protein-Energy Malnutrition (PEM)

Clinical Signs

Protein-energy malnutrition typically occurs during the last trimester in spring-calving beef herds. Clinical signs at the herd level include: recumbent but mentally alert cows, deceased cows, poor body condition (BCS less than 3), udders with low milk production, and weak or small calves.

Individual animal signs: Decreased appetite, reduced rumination, decreased fecal output, progressive weakness, ataxia, and recumbency. In severe cases, animals may develop depression progressing to coma. Muscle wasting is evident, particularly in the hindquarters.

Diagnosis

1. Body Condition Scoring: Assess representative sample of herd. BCS less than 4 suggests energy deficiency.

2. Serum NEFA: Non-esterified fatty acids greater than 0.4-0.7 mmol/L (varies by lab) indicate negative energy balance. Sample 12-20 animals for herd assessment. Elevated NEFAs precede clinical disease.

3. Blood Urea Nitrogen (BUN): If 25% or more of sampled animals have BUN less than 6 mg/dL, protein deficiency is likely.

4. Beta-hydroxybutyrate (BHB): Elevated BHB (greater than 1.2 mmol/L) indicates ketosis secondary to NEB.

5. Feed Analysis: Laboratory analysis of forage for TDN (less than 55% is inadequate), crude protein (less than 7-8% is deficient), and NDF content.

Pregnancy Toxemia (Bovine Ketosis)

Pregnancy toxemia occurs when energy demands of late gestation exceed dietary intake, leading to excessive fat mobilization, ketosis, and hepatic lipidosis. It is more common in beef cattle than dairy cattle due to management differences.

Risk Factors

• Twin or large single fetus pregnancy
• Poor body condition (BCS less than 4) OR overconditioned (BCS greater than 7)
• Low quality forage (high fiber, low energy/protein)
• Cold, snowy weather increasing energy requirements
• Concurrent disease reducing appetite (lameness, dental disease)

Clinical Signs and Pathological Findings

Clinical signs: Loss of body condition over 1-2 weeks, decreased appetite and rumination, reduced fecal output, marked depression, weakness, ataxia, recumbency. Terminal signs include opisthotonos, seizures, and coma.

Postmortem findings: Lack of subcutaneous fat, serous atrophy of omental, perirenal, and pericardial fat, hepatic lipidosis (enlarged, yellow, friable liver), muscle atrophy especially in pelvis, large fetus/multiple fetuses.

Treatment

Memory Aid - PREG TOX: P = Pregnancy (late gestation), R = Recumbent cow, E = Energy deficit, G = Glucose needed, T = Twin pregnancy risk, O = Overconditioned OR thin, X = eXtreme fat mobilization leading to hepatic lipidosis.

Mineral Deficiencies

Cattle require 7 macrominerals (Ca, P, Mg, K, Na, Cl, S) and at least 10 microminerals. The most clinically significant trace mineral deficiencies are copper, selenium, and zinc. Mineral interactions are important: excess molybdenum, sulfur, or iron can cause secondary copper deficiency.

Key Trace Mineral Deficiencies

White Muscle Disease (Nutritional Myodegeneration)

White muscle disease (WMD) is caused by selenium and/or vitamin E deficiency. Both nutrients have antioxidant functions protecting cell membranes from oxidative damage. Young, rapidly growing calves are most susceptible.

Clinical Presentations

Cardiac form (Congenital): Acute death or sudden collapse, usually within 2-3 days of birth. Respiratory distress, tachycardia. Postmortem: white chalky plaques in myocardium, especially left ventricle.

Skeletal form (Delayed): Stiff gait, arched back, difficulty rising, muscle weakness. Often triggered by sudden exercise. Calves remain alert with normal appetite initially. Affects muscles of shoulder, back, and thighs.

Diagnosis

Serum Creatine Kinase (CK): Markedly elevated (several thousand-fold increase) indicating myodegeneration.

Blood Selenium: Less than 0.05 ppm is deficient. Normal greater than 0.1 ppm.

Glutathione Peroxidase (GSH-Px): Less than 20-30 U/mg Hb indicates selenium deficiency. Reflects status 4-6 weeks prior.

Plasma Vitamin E: Less than 1.1-2 ppm indicates deficiency.

Treatment and Prevention

Vitamin Deficiencies

Vitamin A Deficiency

Vitamin A (retinol) is derived from dietary beta-carotene found in green plants. Cattle cannot synthesize vitamin A de novo. Liver stores can sustain cattle for 2-4 months on deficient diets. Young animals have lower stores and develop deficiency faster.

Risk situations: Drought (dormant/brown forages), winter feeding on stored forages, high-grain diets (milo, barley replacing corn), prolonged storage of feeds (beta-carotene degrades approximately 10% per month).

Clinical signs: Night blindness (early sign - cattle stumble over obstacles at dusk), rough hair coat, dull eyes, reduced feed intake, diarrhea, excessive lacrimation, stiff gait, edema of legs/brisket, papilledema and permanent blindness (if untreated), reduced fertility, abortions, stillbirths, weak calves.

Diagnosis: Serum vitamin A: less than 20 mcg/dL in calves (normal 25-35 mcg/dL), less than 40 mcg/dL in adults (normal 40-50 mcg/dL).

Treatment: Injectable vitamin A: 1.5 million IU for adult cows, 500,000 IU for newborn calves. Dietary requirement: 30,000-50,000 IU/head/day for adult cows.

Thiamine (Vitamin B1) Deficiency - Polioencephalomalacia (PEM)

Polioencephalomalacia (PEM) is cerebrocortical necrosis resulting from thiamine deficiency or sulfur toxicosis. Thiamine is normally synthesized by rumen microbes but can be destroyed by thiaminases or depleted by excess sulfur.

Causes of PEM

• Thiaminase-producing bacteria: Proliferate with high-concentrate, low-fiber diets
• Thiaminase in plants: Bracken fern, kochia
• Excess dietary sulfur: Greater than 0.4% of DM. Sources include DDGS, water, molasses, beet pulp
• Amprolium toxicity: Thiamine antagonist

Clinical Signs

Acute neurological disease: stargazing, head pressing, cortical blindness (absent menace with present PLR), dorsomedial strabismus, ataxia, opisthotonus, seizures, recumbency with paddling, death. Most common in young feedlot cattle (6-12 months) on high-concentrate diets.

Diagnosis and Treatment

Diagnosis: Clinical signs, response to thiamine, postmortem autofluorescence of cortex under UV light (375 nm).

Treatment: Thiamine 10-20 mg/kg SC or IM twice daily, then daily for several days. Improvement should occur within hours if thiamine-responsive. For sulfur-induced PEM, thiamine may help but response is poor; remove sulfur source.

Adjunctive therapy: Dexamethasone 0.1-0.2 mg/kg IV/IM or Mannitol 1-1.5 g/kg IV for cerebral edema. Diazepam 0.5-1.5 mg/kg IV for seizures.

Summary: Key Nutritional Deficiencies at a Glance