Diagnosis and treatment of mildewed rice straw poisoning in dairy cows

Is mildewed rice straw poisoning in cows harmful?

Posted on  December 3, 2019, Edited by Eleanor, Category  
Diagnosis and treatment of mildewed rice straw poisoning in dairy cows
Diagnosis and treatment of mildewed rice straw poisoning in dairy cows

1. Incidence

The disease was first discovered in the rice-producing areas of Pakistan in 1939. Subsequently, in New Zealand, the United States, etc., the rotten hoof caused by the fungus infection of the fescue was found. Similar diseases have been reported in Australia, Italy, India, and Japan. According to reports, the disease occurred in the southwestern part of Shaanxi Province before 1949. In the 1960s, the disease was popular in southwestern China, south China, and central China.

The disease is mainly caused by numerous moldy straws eaten by animals. Under natural conditions, the disease has obvious seasonal and regional occurrence, mainly in cattle farming, which occurs frequently in the main rice-producing areas of southern provinces of China, in mid-October. It started to happen. In November and December, it reached its peak and stopped in March and April of the next year. It mainly occurs during the feeding of dry straw, and the rain is continuous due to the harvesting season, which causes the straw to mold. It has been thought that cows only develop under test conditions, but this is not the case.

According to reports, in April 1987, a dairy farm in a county of Central China had a disease in which the swelling of the front limbs or hind limbs was the main symptom, and the disease was diagnosed as mildew straw poisoning. In March 2008, dairy cows in a village in Hebei were fed mildew. A swollen leg disease occurred after straw, and it was diagnosed as mildew straw poisoning.

2. Poisoning mechanism

Butenolide is absorbed into the blood by the body, and its main toxic effect is to cause peripheral blood circulation disorder in animals. Toxins act on peripheral blood vessels, causing spastic contraction of local blood vessels and damaging vascular endothelial cells, resulting in vascular thickening, stenosis, slow blood flow and thrombosis, and then vasculitis. Due to local blood circulation disorders, local tissue breaks, edema, hemorrhage, and necrosis.

Because the function of the skin barrier is destroyed, a secondary bacterial infection will aggravate the condition. In severe cases, the lower part of the bulbar joint will be corrupted or fall off. Low ambient temperature is an important contributing factor to the occurrence of bovine mildew and straw poisoning. Low temperature is conducive to the production of butyrolactone by Fusarium, which can constrict the distal end blood vessels and slow the blood circulation, which further strengthens the role of toxins and promotes the occurrence of diseases.

The content of malondialdehyde (MDA), a lipid peroxidation product, increased and the content of non-protein thiol decreased after oral administration of butyrolactone 193mg/kg. In vitro, butyrolactone could also induce lipid peroxidation, and the content of MDA in liver homogenate increased significantly with the increase of dose, showing a significant dose-effect relationship. The content of the total sulfhydryl group and non-protein sulfhydryl group decreased significantly with the increase of dose, and the dose was negatively correlated with the effect, indicating that the peroxidation of butyrolactone had a certain effect on the occurrence of disease.

The structure of butyrolactone is N-acetamide, which can change hemoglobin into methemoglobin. In vitro experiments have proved that 12 mg/kg butyrolactone can change hemoglobin into methemoglobin, which can destroy the normal function of hemoglobin. It has been found that butyrolactone can cause the dissolution of the human erythrocyte. Butenolactone reduced the endogenous fluorescence of erythrocyte membrane proteins, showing a significant dose-effect relationship, indicating that the changes of erythrocyte membrane structure led to fluorescence quenching, further indicating that erythrocyte lysis is related to the destruction of the cell membrane, which is the result of the oxidative effect of Butenolactone on the body.

3. Clinical symptoms

The disease mainly occurs in house cattle in cattle companies. The acute type had toxic symptoms in 12 days, and the chronic type had symptoms in about 15 days. The diseased cow limps, feet and legs are swollen, festering, even the hoof box falls off; the gait is stiff, the hind limbs are more obvious: the swelling spread upward, the skin of the swollen part changes from slightly hot to cool, painless, the surface exudes yellow-white or yellow-red liquid; and then, the skin of the diseased cow's swollen part ULDs and necroses, causing the hoof shell to fall off.

4. Differential diagnosis

(1) Trypanosomiasis: The diseased cattle have the symptoms of festering, festering, and abscission of tail joints, which are easily confused with the disease. But the animals with trypanosomiasis also have intermittent fever, severe anemia, progressive emaciation, and symptoms of hypogastric edema. Blood tests showed trypanosomes, horses can also be infected, and the disease mostly did not change body temperature, blood can not detect trypanosomes.

(2) Necrobacteriosis: Similar to this disease, some diseased cows have necrosis, decay and limping symptoms. Necrobacteriosis mainly occurs in calves, animals with fever, anorexia, purulent rhinorrhea, ulcers on the gum, tongue and buccal mucosa in the mouth, and round necrotic foci in the liver and lungs. Necrobacterium necrosis can be isolated from the foci. Most of the sick animals had no temperature change, only the nasal mucosa and the extremities had rotten spots, but the focus could not isolate Necrobacterium necrosis, and the diet was normal.

(3) Ergot poisoning: gangrene at the limb, ear and tail tips of chronic poisoning cattle is easily confused with this disease. However, ergot poisoning animals also show symptoms of dyspepsia, abdominal pain, constipation symptoms, vomit and diarrhea.

5. Treatment

(1)Western medicine therapy.
Method 1: Penicillin 4 million IU, streptomycin 5 million IU and injection water 40 mL. This is a dose of intramuscular injection twice a day for 5 days.
METHODS 2: Prednisone acetate 250 mg was injected intramuscularly once every other week.
Method 3: Dexamethasone injection 40 mg, 10% calcium gluconate injection 300 mL, 10% glucose injection 2000 mL, once the intravenous injection.

(2) Chinese medicine therapy.
Prescription 1: Eggplant pole 1000g, hot pepper pole 1000g, pepper 30g, scallion 1000g, boiled water hot compress on swollen hoof leg, twice a day. Prescription 2: Camphor powder 50g, pepper powder 30g, Vaseline 500g, heated to make an ointment, the affected part after rubbing the hole. Prescription 3: Yinqiao Jiedu Powder plus or minus Honeysuckle 9g, Forsythia 45g, Achyranthes Bidentata 45g, Yinchuan 60g, Dandelion 60g, Tufuling 30g, Wood board 25g, Gentiana 30g, Scutellaria Baicalensis 30g, Zhihu 30g, Shenqu 30g, Chen Pei 30g, Mutong, Jingmustard 15g, Fangfeng 18g, Liquor 12g, Decoction once a day, three doses continuously.

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