Pregnancy toxemia in dairy cows is usually susceptible to disease in the three days before and after production and has a high incidence. It is one of the metabolic, digestive and reproductive diseases that dairy cows are very susceptible to infection, resulting in a significant reduction in economic benefits, and has a greater impact on dairy farming. Therefore, it is of great significance to study the pathogenesis and treatment of pregnant toxemia in dairy cattle.
1. Epidemic characteristics
Pregnancy toxemia of dairy cows is easy to occur in some dairy farms and areas, that is, it is a regional epidemic, and the diseased cows are usually single and sporadic. Sometimes in a period, it can be found that there are successive occurrences of postpartum dairy cows. Dairy cows with different parity can suffer from the disease. Among them, the incidence of 1-6 fetuses is about 78.9%, and that of 6-10 fetuses is about 21%.
That is to say, low parity dairy cows and young dairy cows are more susceptible to the disease. The disease can occur in all seasons of the year. The incidence of the disease is about 55% from December to May of the next year, and about 45% from June to November. That is, the winter and spring seasons are relatively easy to occur. Dairy cows usually begin to suffer from the disease after childbirth. The incidence of the disease is about 82% in the first to seventh day after childbirth, and about 18% on the seventh day after childbirth.
The incidence of the disease is the highest on the second day after childbirth, reaching 16%. Milk production of dairy cows is less than 5000kg. No disease occurs after delivery; milk production is 5000-6000kg, the incidence is about 29%; milk production is 6000-7000kg, the incidence is about 26%; milk production is more than 7000kg, the incidence is about 45%. That is, the higher the yield of dairy cows, the more prone to the disease. Also, cows fed more concentrate during the dairy period are more susceptible to disease.
2. Clinical and anatomical changes
The diseased cattle maintained normal breathing, heartbeat and body temperature for most of the time, but showed loss of appetite, and gradually stopped feeding, rumination also stopped, physical weakness gradually, eventually they could only lie on the ground, at the same time, their weight rapidly decreased, and their skin elasticity was poor. Diseased cattle usually excrete hard feces, and abdominal pain and diarrhea symptoms can occur in severe cases. Some diseased cattle will show some neurological symptoms, such as head and neck raising, gaze and muscle tremor, and eventually in a coma, and the heart beats too fast. Individual diseased cattle can also appear urine ketone phenomenon, that is, urine emits rotten apple flavor, and the taste is obvious.
The dead cattle were dissected and found that the liver was yellow-white, markedly enlarged, and the texture was oily and brittle; the myocardial fat degenerated; the renal tubular epithelium deposited fat, the adrenal gland swelled and yellow; the abomasum and the anterior gastric mucosa fell off and ulcerated, and the intestinal tract was congested and bleeding.
The physical characteristics of cows, such as mental state, excreta odor, color, and consistency, were examined to diagnose whether female cows suffered from gestational toxemia. When it is difficult to make a definite diagnosis, auxiliary diagnosis can be adopted, that is, some auxiliary measures can be taken to help make a definite diagnosis. Commonly used auxiliary diagnostic methods are cow excrement detection and silver nitrate detection, but these auxiliary methods need to be equipped with relevant equipment and reagents.
Protect liver and detoxify, increase blood sugar content: Supplement sugar-raising substances or hypertonic glucose to diseased cattle. It can inject 500-1000 mL 50% glucose injection into diseased cattle intravenously; inject 50% dextran injection into cattle intravenously for the first time, and then inject 500 mL each time, 2-3 times a day; inject 500-1000 ml.25% xylitol injection intravenously twice a day, which has the effect of increasing sugar and lowering ketone; take 117-117-ketone orally. 342g propylene glycol or 114-228g sodium propionate was used twice a day, and 500 mL 50% dextran injection was given intravenously before taking the medicine. The curative effect was better.
Promoting fat oxidation and taking anti-lipid preparations: oral administration of 50-60 950% choline chloride powder to diseased cattle or subcutaneous injection of 250 ml 0% choline chloride injection can promote fatty acid oxidation and lipoprotein synthesis, which has obvious anti-lipid effect; intravenous injection of 10% solution made of 200-300 mg calcium pantothenate, continuous use of 3. Days; 200-250 ml. Compound vitamin B, used twice a day, can stimulate appetite and enhance rumen function; administration of 12-15g nicotinic acid for 3-5 days can inhibit fat decomposition and ketone formation; oral administration of cobalt sulfate or cobalt chloride, 100g per day.
Symptomatic treatment: Avoid secondary infection in the treatment process of diseased cattle, but also can use broad-spectrum antibiotics. Intravenous injection of 500-1000mL5% sodium bicarbonate in diseased cattle can avoid acidosis. If jaundice occurs in diseased cattle, the water solution containing 300-500 g magnesium sulfate can be administered for 3 consecutive days.