Pregnancy Toxemia in Cows

Core Definition & Characteristics

Nature of Disease: A metabolic disease or ketosis occurring in late gestation when maternal glucose homeostasis is disrupted.
Primary Cause: Nutrition is inadequate to meet the high energy demands of the developing fetus and gravid uterus.
Primary Targets: Predominantly occurs in beef cows because their last trimester often coincides with seasonal poor feed availability.

Etiology & Risk Factors:

Dietary Factors: Poor-quality diets low in energy or protein, or high in poorly digestible fiber.
Fetal Demands: Large or multiple fetuses significantly increase energy requirements.
Environmental Stress: Cold, snowy weather which increases energy needs and covers available forage.
Concurrent Health Issues: Conditions that decrease the ability to eat, such as lameness or oral diseases.

Pathophysiology:

Substrate Consumption: The gravid uterus consumes 50%–60% of maternal glucose and 30%–40% of amino acids.
Maternal Adaptation Failure: Reduced insulin secretion and sensitivity are meant to direct glucose to the fetus; however, when severe, this leads to excessive adipose tissue mobilization.
Metabolic Consequences:
- Increased nonesterified fatty acids (NEFA) for maternal energy.
- Excessive ketone body production leading to metabolic acidosis.
- Hepatic Lipidosis: Fatty infiltration of the liver due to massive fat mobilization.

Clinical Findings:

Early Signs: Rapid loss of body condition over 1–2 weeks and decreased appetite.
General Signs: Depression, decreased rumination, reduced fecal production, and nose-licking.
Advanced/Terminal Signs: Weakness, ataxia, recumbency, seizures, and coma.
Postmortem Lesions: Lack of subcutaneous fat, serous atrophy of internal fat depots (omental, perirenal, pericardial), and liver damage (hepatic lipidosis).

Diagnosis:

Clinical Indicators: History of late gestation and marginal feed quality.
Ketonuria: The earliest and most specific finding; even mild ketonuria is abnormal in healthy pregnant cows.
Blood Chemistry:
- Hypoglycemia: Low blood glucose (though hyperglycemia may occur with seizures).
- Energy Markers: Increased beta-hydroxybutyrate (BHB >1.5 mmol/L) and NEFA (>0.6 mmol/L).
- Nutritional Markers: Low BUN, hypoproteinemia, hypoalbuminemia, and hypokalemia.

Treatment Protocols:

Early Intervention (Still Eating): High-quality forage/concentrate and oral propylene glycol (0.5–1 g/kg/day).
Aggressive Therapy (Anorectic):
- Transfaunation: Rumen fluid from a healthy animal to restore microbial populations.
- Nutritional Slurry: Force-feeding a mix of alfalfa pellets, beet pulp, and soybean meal.
- IV Dextrose: Bolus (0.5 g/kg) or continuous 5% infusion for hospitalized cases.
- Insulin: Protamine zinc insulin may be used to suppress ketogenesis.
Termination of Pregnancy: Induction of parturition or C-section to remove the metabolic drain of the fetus.

Prevention Strategies:

Body Condition Management: Target a BCS of >5 (1–9 scale) for beef cattle as they enter the final trimester.
Nutritional Analysis: Feed analysis to ensure adequate protein (9%–10% of dry matter) and fiber digestibility.
Ionophores: Daily administration of monensin to facilitate ruminal propionate generation and increase glucose availability.

Stress Monitoring: Careful observation during weather events or periods of illness.

Pregnancy Toxemia in Cows

Core Definition & Characteristics

Nature of Disease: A metabolic disease or ketosis occurring in late gestation when maternal glucose homeostasis is disrupted.

Primary Cause: Nutrition is inadequate to meet the high energy demands of the developing fetus and gravid uterus.

Primary Targets: Predominantly occurs in beef cows because their last trimester often coincides with seasonal poor feed availability.

Etiology & Risk Factors:

Dietary Factors: Poor-quality diets low in energy or protein, or high in poorly digestible fiber.

Fetal Demands: Large or multiple fetuses significantly increase energy requirements.

Environmental Stress: Cold, snowy weather which increases energy needs and covers available forage.

Concurrent Health Issues: Conditions that decrease the ability to eat, such as lameness or oral diseases.

Pathophysiology:

Substrate Consumption: The gravid uterus consumes 50%–60% of maternal glucose and 30%–40% of amino acids.

Maternal Adaptation Failure: Reduced insulin secretion and sensitivity are meant to direct glucose to the fetus; however, when severe, this leads to excessive adipose tissue mobilization.

Metabolic Consequences:

Increased nonesterified fatty acids (NEFA) for maternal energy.

Excessive ketone body production leading to metabolic acidosis.

Hepatic Lipidosis: Fatty infiltration of the liver due to massive fat mobilization.

Clinical Findings:

Early Signs: Rapid loss of body condition over 1–2 weeks and decreased appetite.

General Signs: Depression, decreased rumination, reduced fecal production, and nose-licking.

Advanced/Terminal Signs: Weakness, ataxia, recumbency, seizures, and coma.

Postmortem Lesions: Lack of subcutaneous fat, serous atrophy of internal fat depots (omental, perirenal, pericardial), and liver damage (hepatic lipidosis).

Diagnosis:

Clinical Indicators: History of late gestation and marginal feed quality.

Ketonuria: The earliest and most specific finding; even mild ketonuria is abnormal in healthy pregnant cows.

Blood Chemistry:

Hypoglycemia: Low blood glucose (though hyperglycemia may occur with seizures).

Energy Markers: Increased beta-hydroxybutyrate (BHB >1.5 mmol/L) and NEFA (>0.6 mmol/L).

Nutritional Markers: Low BUN, hypoproteinemia, hypoalbuminemia, and hypokalemia.

Treatment Protocols:

Early Intervention (Still Eating): High-quality forage/concentrate and oral propylene glycol (0.5–1 g/kg/day).

Aggressive Therapy (Anorectic):

Transfaunation: Rumen fluid from a healthy animal to restore microbial populations.

Nutritional Slurry: Force-feeding a mix of alfalfa pellets, beet pulp, and soybean meal.

IV Dextrose: Bolus (0.5 g/kg) or continuous 5% infusion for hospitalized cases.

Insulin: Protamine zinc insulin may be used to suppress ketogenesis.

Termination of Pregnancy: Induction of parturition or C-section to remove the metabolic drain of the fetus.

Prevention Strategies:

Body Condition Management: Target a BCS of >5 (1–9 scale) for beef cattle as they enter the final trimester.

Nutritional Analysis: Feed analysis to ensure adequate protein (9%–10% of dry matter) and fiber digestibility.

Ionophores: Daily administration of monensin to facilitate ruminal propionate generation and increase glucose availability.

Stress Monitoring: Careful observation during weather events or periods of illness.