Metabolism: The process of converting food to energy within cells for vital processes and synthesizing new organic material.
Disruption: Metabolic diseases disrupt normal metabolism.
Affect the cell's ability to perform critical biochemical reactions involving the processing or transport of proteins, carbohydrates, or lipids.
Causes:
Deficiencies or excesses of nutrients altering healthy state.
Enzyme deficiencies necessary for specific chemical reactions.
Abnormal chemical reactions making metabolic processes difficult.
Organ diseases in liver, pancreas, or endocrine glands.
Common in production animals (e.g., livestock).
Example: Dairy cows lacking calcium, magnesium, or energy reserves to meet metabolic needs.
Can be caused by:
Specific nutrient deficiencies, excesses, imbalances, or metabolic disturbances.
Effects include alterations in:
Energy metabolism, immune function, cognitive function, bone formation, muscle function, and fetal growth and development (if pregnant animals have deficiencies).
Often easily cured by adjusting dietary constituents.
Definition: A common disease of dairy cows in early lactation, arising from negative energy balance leading to adipose mobilization and high glucose demand for milk synthesis.
If feed intake is insufficient to meet energy demand, there is not enough ruminal production of propionic acid (main precursor of glucose), leading to hypoglycemia.
Metabolic Processes:
Mobilization of free fatty acids and glycerol from fat stores, which are oxidized to form Acetyl-CoA.
Excess Acetyl-CoA converted into ketone bodies: acetoacetate and β-hydroxybutyrate (BHP), and some acetone.
Ketone bodies accumulate, excreted in milk and urine.
Signs include:
Anorexia, decreased milk production, weight loss, firm dry feces, occasional neurological signs (nervous ketosis).
Can be subclinical or unrecognized.
Diagnosis:
Measurement of BHB, elevated in blood, urine, and milk of fresh cows.
Various on-site tests exist for measuring ketones in urine, milk, and blood.
Early Detection: Leads to quicker recovery and improved milk.
Standard Treatment:
Oral administration of propylene glycol, provides precursors for glucose production.
Additional therapy may include bolus glucose treatment and vitamin B12 for hypoglycemic cases.
Most common metabolic disorder in pregnant small ruminants (sheep, goats) during late gestation.
Caused by inadequate nutrition (low energy) and decreased rumen capacity due to fetal growth, especially with multiple fetuses.
Signs include partial anorexia and hypoglycemic encephalopathy, alongside elevated BHB in blood/urine.
Treatment:
Oral propylene glycol/corn syrup for quick energy.
Caused by insufficient calcium around calving.
Serum calcium levels drop, leading to:
Hyperexcitability of the nervous system, reduced muscle contraction strength, tetany, partial paralysis.
Stages:
Stage I: Loss of appetite, excitability, hypersensitivity, weakness.
Stage II: Lasts 1-12 hours, dullness, incoordination, trembling muscles, constipation.
Stage III: Inability to stand, loss of consciousness, nearly inaudible heart sounds.
Treatment focuses on restoring calcium levels quickly to avoid complications.
Recommended: IV injection of calcium gluconate.
Occurrence: In cows and ewes, especially when grazing lush, rapidly growing pastures with low magnesium levels due to high protein and potassium.
Clinical signs: Excitability, blindness, hypersensitivity, muscle tremors, urination, staggering, convulsions, coma, death.
Preventative: Daily oral Mg supplements, often combined with palatable agents (molasses, etc.).
Affects wild or domestic ruminants, mainly dairy/feedlot cattle and sometimes sheep.
Due to ingestion of excessive fermentable, carbohydrate-rich feeds (corn, wheat, barley).
Acidosis Occurs: When rumen pH drops below 5.5, causing atony, depressed appetite/production, disturbed rumen flora, severe cases leading to shock/death.
Prevention: Reduce fermentable carbohydrate intake per meal.
Essential for epithelial maintenance, visual purple function, kidney function, bone development.
Deficiency: Causes skin disorders and night blindness.
Required for calcium absorption and bone health.
Deficiency: Causes rickets and osteomalacia, particularly in young growing animals.
Important antioxidant protecting cellular membranes.
Deficiency: Causes liver necrosis, specific species disorders (e.g., exudative diathesis, muscular dystrophy).
Critical for prothrombin production, affects clotting time.
Deficiency: Can result in hemorrhages, impaired bone mineralization.
Includes complex B vitamins (B1, B2, B3, etc.).
Deficiencies relate to metabolism and may cause skin issues, anorexia, and impaired blood cell production.
Deficiency leads to black tongue in dogs and can cause pellagra in humans (dermatitis, dementia, diarrhea).
Grazing animals can manufacture it, whereas poultry/swine rely on diet.
Deficiency impacts growth and leads to lesions in nervous system and skin.
Important for tissue growth, immune regulation.
Deficiency: Can cause scurvy and joint issues.
Ruminants need cobalt for B12 synthesis; deficiency leads to ill-thrift and anemia.
Result of calcium/phosphorus imbalance, often due to poor husbandry or vitamin D deficiency.
Symptoms include bowed legs, arched spine, rubber jaw, and fractures.
Associated with vitamin E and/or selenium deficiency, leading to muscle degeneration.
Symptoms: Skeletal muscle pallor, necrosis of muscle fibers.
Result of zinc deficiency/inadequate absorption.
Symptoms: Skin lesions, lethargy, anemia, and delayed growth.
Excessive adipose tissue, defined as >20% above ideal body weight.
Causes: Energy intake exceeding expenditure.
Common health issues: Chronic inflammation, cardiopulmonary issues, diabetes, and decreased life expectancy.
Risk factors include lack of exercise, breed predisposition, age, neutering, etc.