Symptoms and Prevention and Treatment Methods of Pregnancy Toxemia in Dairy Cows

Dairy cows are yellow cattle of the dairy breed, an excellent breed developed through highly intensive selective breeding. In China, dairy cows are mainly Holstein-Friesian cows. This breed was first introduced in 1980 by the cattle and sheep breeding base of the Shandong Provincial Animal Husbandry Bureau. This breed has strong adaptability, a wide distribution range, high milk production, and tolerance to coarse feed. The Holstein-Friesian cow is also called the Chinese Holstein. The Chinese Holstein has a history of more than one hundred years, and its breeding process is very complex. In short, it was developed through long-term selective breeding from advanced-generation crossbreeds of purebred Dutch cattle and local cows. Disease prevention is very important in dairy farming, so what should be done when a dairy cow develops pregnancy toxemia?

What is pregnancy toxemia in dairy cows?

Pregnancy toxemia in dairy cows is a nutritional metabolic disease caused by energy metabolism disorders, characterized clinically by complete loss of appetite, weakness, a tendency to lie down, increased heart rate, coma, severe ketonemia, and a high mortality rate.

Causes of pregnancy toxemia in dairy cows

Unreasonable feeding and management, such as a single feed variety, too much concentrate, lack of roughage, and insufficient exercise, can cause cows to become overweight in late pregnancy. Mixed-group housing, with the diet not adjusted according to different physiological stages, can cause digestive, metabolic, and reproductive dysfunction in cows during the dry period due to excessive energy. Feeding high-energy feed in late lactation or the dry period, such as feeding too much grain or corn silage; or stopping milking too early before calving; or prolonging the dry period too long; or supplying too much feed in early pregnancy, causes excessive energy intake, leading to excessive obesity in cows in late pregnancy, and the disease is likely to occur under stress conditions such as calving, lactation, sudden climate changes, or a sharp drop in feed intake. In addition, cows carrying twins or with oversized fetuses, dairy cows with high milk production, and deficiencies of certain proteins or calcium in the diet can all lead to the occurrence of this disease.

Symptoms of pregnancy toxemia in dairy cows

The dairy cow is abnormally obese, with complete loss of appetite within a few days after calving, decreased milk production, and inability to stand up, showing severe ketosis symptoms, and measures to treat ketosis are also ineffective. The affected cow gradually becomes weaker and usually lies down and dies after 7 to 10 days. Some affected cows have neurological symptoms, staring for long periods, raising the head, muscle tremors in the head and neck, and finally coma, with increased heart rate, and most affected cows die. Throughout the course of the disease, body temperature, pulse, and respiration are normal. If fatty liver occurs 2 months before calving, the affected cow often refuses food for 10 to 14 days, is listless, lies down in a sternal position, has rapid breathing, a cracked muzzle, increased nasal secretions, and clear watery nasal discharge; in the later stage, it passes foul-smelling yellow thin feces, becomes comatose, and dies in a quiet state. The mortality rate of this disease is high, and the course lasts 10 to 14 days. According to its symptoms, it can be divided into acute and subacute types:

Acute type The acute type develops with calving. There is complete loss of appetite, little or no milk, cyanosis and yellow staining of visible mucous membranes, body temperature rising to 39.5°C to 40°C, a stiff gait, dull gaze, and weak response to the outside world. It is accompanied by diarrhea, with yellow foul-smelling thin feces, no response to drugs, and death or inability to stand within 2 to 3 days.

Subacute type The subacute type mostly develops 3 days after calving, mainly manifesting as ketosis. The affected cow has reduced or complete loss of appetite, a sudden drop in milk production, little and dry feces, urine with a ketone odor, and a positive ketone body reaction, accompanied by mastitis, retained placenta, uterine atony, and a large amount of brown foul-smelling lochia accumulated in the birth canal. Drug treatment is ineffective, and the cow lies down, groans, and grinds its teeth.

Diagnosis of pregnancy toxemia in dairy cows

Based on the characteristics of abnormal obesity, sudden refusal to eat after calving, and lying down, this disease should be suspected. Bovine obesity syndrome must be differentiated from left displacement of the abomasum occurring after calving. Left displacement of the abomasum can be identified by combining auscultation with percussion, producing a steel pipe sound; feeding a high-concentrate diet and an excessively obese body condition help distinguish this disease from conditions such as parturient paresis and downer cow syndrome.

Treatment of pregnancy toxemia in dairy cows

The treatment effect will not be satisfactory, and most affected cows with complete refusal to eat will die; for those that can still maintain appetite, supportive therapy still offers hope of cure. The purpose of drug treatment is to inhibit fat breakdown, reduce the accumulation of fatty acids in the liver, accelerate fat utilization, and prevent concurrent ketosis. Its principles are detoxification, liver protection, and glucose supplementation. The following treatment methods can be selected: 50% glucose solution 500 ml to 1000 ml, intravenous injection.

50% dextran 1500 ml for the first intravenous injection, then changed to 500 ml, 2 to 3 times per day.

Nicotinic acid 12 g to 15 g, administered orally at one time, for 3 to 5 consecutive days. Its effects are anti-lipolytic action and inhibition of ketone production.

Cobalt chloride or cobalt sulfate 100 g per day, administered orally.

Propylene glycol 170 g to 342 g, administered orally twice a day for 10 consecutive days. The effect is better if 500 ml of 50% dextran is injected intravenously before feeding. Choline chloride 50 g, administered orally at one time, twice a day.

To prevent secondary infection, broad-spectrum antibiotics may be used. Chlortetracycline or tetracycline 2 million to 2.5 million international units, administered by intravenous injection at one time, and administered orally twice a day.

Prevention of pregnancy toxemia in dairy cows

Strengthen feeding and management Keep the feed stable and avoid sudden changes. Dry cows should have the amount of concentrate limited and the amount of hay increased. Each cow should be fed 3 kg to 4 kg of mixed feed per day, 15 kg of silage, and hay free-choice.

Manage by groups. According to different physiological stages, adjust the nutritional ratio at any time, and feed dry cows and lactating cows separately.

Ensure that dry cows have 1 hour to 1.5 hours of exercise time each day.

Strengthen health examinations Establish a monitoring system to detect affected cows early. Starting one week before calving, measure urine ketones and pH every other day, and treat affected cows immediately when found.

Regularly supplement sugar and calcium. For older, high-yielding cows with poor appetite and a history of ketosis, inject 500 ml each of 20% glucose solution and 20% calcium gluconate intravenously one week before calving, for a total of 1 to 3 supplements.

Prevent and treat postpartum ketosis Nicotinic acid 4 g to 8 g (amount per cow per time, the same below), added to the feed starting 7 days before calving, once a day.

Propylene glycol 200 ml or sodium propionate 125 to 250 g, fed starting 8 days before calving, once a day, for 15 to 30 consecutive days.

Timely breeding Do not miss cows in estrus, improve the conception rate, and prevent excessive obesity in dairy cows caused by an overly long dry period.