Pregnancy Toxemia in Cows

Pregnancy toxemia is more common in beef cattle than in dairy cattle, primarily because of differences in dietary management and typical timing of late gestation. Individual cows of any breed can be affected by pregnancy toxemia; however, herd problems are most common in beef cattle, which frequently are managed so that late pregnancy coincides with the poorest availability of feed due to the season. Pregnancy toxemia is precipitated by large or multiple fetuses, feed low in energy or protein or high in poorly digestible fiber, and health conditions that increase energy demand or decrease ability to take in nourishment (eg, lameness, oral diseases). Cold, snowy weather may contribute by increasing the animal’s energy requirement and by covering available forage.

Although the mechanism is unknown, clinical disease develops in some cows with negative energy or carbohydrate balance. Proposed contributors to clinical disease include glucose deficiency with intermittent hypoglycemia, ketone body accumulation with metabolic acidosis or appetite suppression, and death of the fetus with secondary infection and toxemia.

The gravid uterus and fetoplacental unit are major consumers of maternal oxygen, glucose, and amino acids to support metabolism and growth. Glucose accounts for approximately 50%–60% of fetal-placental energy substrates, with amino acids accounting for an additional 30%–40%. In periods of maternal undernutrition and hypoglycemia, the fetus also becomes hypoglycemic and subsequently utilizes amino acids preferentially for energy metabolism. The dam supplies amino acids regardless of dietary adequacy by mobilizing body stores. Amino acids serve this purpose because they are actively transported across the placenta, in contrast to insulin-independent facilitated diffusion of glucose.

Maternal adaptations in late gestation direct glucose away from maternal tissues via reduced secretion of insulin and decreased tissue insulin insensitivity. Low insulin concentration allows for greater adipose tissue mobilization, providing nonesterified fatty acids (NEFA) for use as a maternal energy substrate, because fatty acids do not cross the placenta. Excessive mobilization of adipose tissue can lead to excess ketone body production and fatty infiltration of hepatocytes.

Both thin and well-conditioned cows can be affected by pregnancy toxemia; often, however, the first clinical sign is loss of body condition over 1–2 weeks. Decreased appetite, rumination, fecal production, and nose-licking are general clinical signs of illness. Affected cows become markedly depressed, weak, ataxic, and recumbent. Opisthotonos, seizures, or coma may occur terminally.

Postmortem lesions include a lack of subcutaneous adipose tissue and serous atrophy of omental fat. Serous atrophy of perirenal and pericardial fat depots indicates more severe and prolonged energy deficiency. Hepatic lipidosis in conjunction with large or multiple fetuses is common, as is evidence of muscle pressure necrosis and toxemia. Muscles of the pelvis may show obvious atrophy, although all muscles will show some loss of tissue mass.

History and clinical signs in a cow in late gestation with marginal feed quality support a presumptive diagnosis of pregnancy toxemia. Ketonuria is present from the early stage of disease and is the most specific finding; even mild ketonuria should not occur in healthy pregnant cows until a few days before calving. Inexpensive glucometers are available to test blood concentrations of beta-hydroxybutyrate (BHB) and glucose. Hypoglycemia is also common; however, cows with seizures or signs of excitement may have hyperglycemia.

Other clinical chemistry findings may include low BUN concentration (< 3.57 mmol/L), hypoproteinemia (< 50 g/L), hypoalbuminemia (< 22 g/L), hypocholesterolemia (< 1.8 mmol/L), and hypokalemia (< 4 mmol/L); all reflective of low nutrient intake. Secondary hypocalcemia, hypophosphatemia, or both may also be present. Increased blood BHB (>1.5 mmol/L) and NEFA (>0.6 mmol/L) concentrations reflect the negative energy balance and ketogenesis; however, NEFA concentrations depend on available adipose tissue for mobilization. With more advanced disease, there may be variable increases in serum activities of muscle or liver enzymes, as well as clinicopathologic evidence of infection, metabolic acidosis, internal organ dysfunction or failure, and circulatory collapse.

Successful treatment of pregnancy toxemia requires early identification of the disease. There are few differential diagnoses, and pregnancy toxemia must be considered a factor in any disease affecting cows in late gestation. Cattle that have lost weight but are still eating may be managed by feeding high quality forage and concentrate or propylene glycol (0.5–1 g/kg/day for up to 5 days). Anorectic cattle must be treated aggressively, because a decrease in energy intake causes the disease to progress rapidly. Transfaunation with rumenal fluid from a healthy animal can stimulate rumen microbial populations, and a slurry of alfalfa pellets, beet pulp, and soybean meal can be offered to provide microbial resources. Propylene glycol can be force-fed, or dextrose administered intravenously (0.5 g/kg at least once a day).

Cattle with dehydration, organ dysfunction, or metabolic acidosis should be treated with large volumes (20–60 L/day, PO or IV) of electrolyte fluids; if intravenous fluid administration is practical, continuous dextrose infusion (5%) is recommended. Protamine zinc insulin (200 U, SC, every 48 hours) may be given after dextrose administration to suppress ketogenesis. However, insulin is not approved for use in cattle in the US. Recumbent cattle may benefit from good nursing care but rarely respond to treatment. To decrease the energy drain in any cow with pregnancy toxemia, induction of parturition or removal of the fetus by cesarean should be considered.

At the herd level, pregnancy toxemia can be prevented by adequate attention to the nutrition and health care of cows in late gestation. Body condition score should be >3.0 (1–5 scale) or >5 (1–9 scale) for dairy and beef cattle, respectively, as they enter the final trimester of pregnancy. Body condition is best managed before this period. For cows with lower body condition scores, additional concentrates should be provided.

Feed analysis, primarily of the forage, should be undertaken to assess quality and intake concerns. Neutral detergent fiber limits intake, and protein inadequacy limits fiber digestion. The National Academy of Science, Engineering and Medicine (NASEM, 2016) suggests an NDF intake capacity of 1% of body weight for beef cattle, though this may be lower (0.8%) for late pregnant cows. Rumen degradable protein should be sufficient (9–10% of dry matter) to ensure microbial fiber digestibility (NASEM, 2016). A minimum of 1 kg crude protein intake should be delivered by the diet, though calculations of metabolizable protein intake is more precise.1

A minimum of 1 kg crude protein intake should be delivered by the diet, although calculation of metabolizable protein intake is more precise. Use of ionophores to facilitate ruminal propionate generation leading to greater glucose availability is recommended. Pregnant beef cattle can consume 180 mg of monensin per day. Pregnant dairy cows can consume between 115 and 410 mg of monensin per day. Feeding of monensin sodium is not approved in all countries. For individual cows, recognition of the precarious state of energy and carbohydrate balance during late gestation dictates careful monitoring of energy intake, attitude, and fat mobilization, especially during times of illness or other stress.