Fatty Liver Disease of Cattle

Nature of Disease: A metabolic disorder of highly productive dairy cows resulting from excessive negative energy balance (NEB) at the onset of lactation.

Key Pathological Feature: Excessive deposition of triglycerides (TAG) within hepatocytes (liver cells).

Clinical Impact: Associated with pronounced ketosis, depressed feed intake, decreased productivity, and, in severe cases, liver failure and death.

Timing: Primarily a postpartum disorder, though it often begins developing before and during parturition.

Etiology & Pathogenesis

The Mobilization Trigger: Insufficient dietary energy leads to the mobilization of body fat reserves, releasing nonesterified fatty acids (NEFAs) into the blood.
Hepatic Uptake: The liver retains approximately 15%–20% of circulating NEFAs.
Processing Failure:
- NEFAs in the liver are either oxidized (producing ATP or ketones) or esterified into TAG.
- In ruminants, the export of TAG as lipoproteins (VLDL) occurs at a very slow rate.
- Result: When NEFA uptake exceeds the liver's capacity to oxidize or export them, triglycerides accumulate in the liver cells.
Hormonal Influence: Low insulin and glucose concentrations favor fat mobilization and fatty liver development.

Risk Factors:

Conditioning: Overconditioned (obese) cows (BCS ≥4) are at the highest risk because they experience more pronounced feed intake depression around calving.
Management Stressors: Crowding, sudden ration changes, limited feed bunk space, heat stress, and unpalatable feeds.
Concurrent Diseases: Metritis, mastitis, abomasal displacement, hypocalcemia, or lameness (which decreases eating time).
Animal Factors: Older, highly productive cows are more susceptible.

Clinical Findings:

Spectrum of Severity: Ranges from mild ketosis to liver coma.
General Signs: There are no pathognomonic (unique) signs; common indicators include depression in feed intake, decreased milk production, and ketosis.
Metabolic Consequences:
- Reduced gluconeogenesis (leading to hypoglycemia).
- Reduced ureagenesis (leading to hyperammonemia).
- Altered endocrine profiles and impaired immune function.
Thresholds: Mild signs appear at TAG contents of ~100 g/kg liver wet weight; liver coma occurs at values ≥300 g/kg.

Diagnosis:

Indirect Assessment (Common Practice): Assessing the severity and duration of NEB through clinical signs and blood/urine metabolites.
Direct Diagnostic Tools:
- Liver Biopsy: The gold standard and most reliable method to determine severity.
- Copper Sulfate Flotation: A rapid field test to estimate total lipid content from biopsy samples.
- Microscopic Evaluation: Estimating the percentage of cell volume occupied by fat.

Biochemical Markers:

- 1. High NEFA: (>600 mcM/L) and high beta-hydroxybutyrate (BHB) concentrations.
  2. Low Glucose and Cholesterol: Reflecting impaired liver function and anorexia.
  3. Liver Enzymes: Increased activity of AST, SDH, and GLDH indicates liver cell damage.

Prevention Strategies

Dry Period Management: Focus on optimizing cow well-being and maintaining an ideal BCS of 3–3.5.
Dietary Stability: Avoid rapid diet changes and ensure access to palatable feeds.
Prophylactic Treatments (for at-risk cows): 1) Propylene Glycol: Oral drench (300–600 mL/day) during the final week prepartum, 2) Monensin: An ionophore antibiotic that modulates rumen fermentation to increase propionate synthesis, 3) Glycerol: A palatable alternative to propylene glycol.

Treatment Protocols

Mild Cases: Oral administration of gluconeogenic substances like propylene glycol (250–300 g twice daily) or sodium propionate.
Moderate to Severe Cases:
- IV Dextrose: Bolus of 500 mL of 50% solution to trigger an insulin response and interrupt fat mobilization.
- Continuous Dextrose Infusion: Reserved for clinical settings to maintain normoglycemia.
Controversial Adjuncts:
- Glucocorticoids (Dexamethasone): Debated due to potential lipolytic effects, though they may improve feed intake.
- Lipotropic Agents: IV choline, methionine, or Vitamin B12 are sometimes used to aid TAG export, though their effectiveness in ruminants is not definitively proven.

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Fatty Liver Disease of Cattle

Nature of Disease: A metabolic disorder of highly productive dairy cows resulting from excessive negative energy balance (NEB) at the onset of lactation.

Key Pathological Feature: Excessive deposition of triglycerides (TAG) within hepatocytes (liver cells).

Clinical Impact: Associated with pronounced ketosis, depressed feed intake, decreased productivity, and, in severe cases, liver failure and death.

Timing: Primarily a postpartum disorder, though it often begins developing before and during parturition.

Etiology & Pathogenesis

The Mobilization Trigger: Insufficient dietary energy leads to the mobilization of body fat reserves, releasing nonesterified fatty acids (NEFAs) into the blood.

Hepatic Uptake: The liver retains approximately 15%–20% of circulating NEFAs.

Processing Failure:

NEFAs in the liver are either oxidized (producing ATP or ketones) or esterified into TAG.

In ruminants, the export of TAG as lipoproteins (VLDL) occurs at a very slow rate.

Result: When NEFA uptake exceeds the liver's capacity to oxidize or export them, triglycerides accumulate in the liver cells.

Hormonal Influence: Low insulin and glucose concentrations favor fat mobilization and fatty liver development.

Risk Factors:

Conditioning: Overconditioned (obese) cows (BCS ≥4) are at the highest risk because they experience more pronounced feed intake depression around calving.

Management Stressors: Crowding, sudden ration changes, limited feed bunk space, heat stress, and unpalatable feeds.

Concurrent Diseases: Metritis, mastitis, abomasal displacement, hypocalcemia, or lameness (which decreases eating time).

Animal Factors: Older, highly productive cows are more susceptible.

Clinical Findings:

Spectrum of Severity: Ranges from mild ketosis to liver coma.

General Signs: There are no pathognomonic (unique) signs; common indicators include depression in feed intake, decreased milk production, and ketosis.

Metabolic Consequences:

Reduced gluconeogenesis (leading to hypoglycemia).

Reduced ureagenesis (leading to hyperammonemia).

Altered endocrine profiles and impaired immune function.

Thresholds: Mild signs appear at TAG contents of ~100 g/kg liver wet weight; liver coma occurs at values ≥300 g/kg.

Diagnosis:

Indirect Assessment (Common Practice): Assessing the severity and duration of NEB through clinical signs and blood/urine metabolites.

Direct Diagnostic Tools:

Liver Biopsy: The gold standard and most reliable method to determine severity.

Copper Sulfate Flotation: A rapid field test to estimate total lipid content from biopsy samples.

Microscopic Evaluation: Estimating the percentage of cell volume occupied by fat.

Biochemical Markers:

High NEFA: (>600 mcM/L) and high beta-hydroxybutyrate (BHB) concentrations.

Low Glucose and Cholesterol: Reflecting impaired liver function and anorexia.

Liver Enzymes: Increased activity of AST, SDH, and GLDH indicates liver cell damage.

Prevention Strategies

Dry Period Management: Focus on optimizing cow well-being and maintaining an ideal BCS of 3–3.5.

Dietary Stability: Avoid rapid diet changes and ensure access to palatable feeds.

Prophylactic Treatments (for at-risk cows): 1) Propylene Glycol: Oral drench (300–600 mL/day) during the final week prepartum, 2) Monensin: An ionophore antibiotic that modulates rumen fermentation to increase propionate synthesis, 3) Glycerol: A palatable alternative to propylene glycol.

Treatment Protocols

Mild Cases: Oral administration of gluconeogenic substances like propylene glycol (250–300 g twice daily) or sodium propionate.

Moderate to Severe Cases:

IV Dextrose: Bolus of 500 mL of 50% solution to trigger an insulin response and interrupt fat mobilization.

Continuous Dextrose Infusion: Reserved for clinical settings to maintain normoglycemia.

Controversial Adjuncts:

Glucocorticoids (Dexamethasone): Debated due to potential lipolytic effects, though they may improve feed intake.

Lipotropic Agents: IV choline, methionine, or Vitamin B12 are sometimes used to aid TAG export, though their effectiveness in ruminants is not definitively proven.