How should be diagnosed and treated by aflatoxin poisoning?

Aflatoxin is a kind of hepatotoxic substance. After poisoning, liver damage was the main one, accompanied by vascular permeability damage and central nervous system damage. The clinical characteristics were jaundice, hemorrhage, edema and neurological symptoms. Acute poisoning is more common in calves, chronic poisoning is more common in adult cattle. Aflatoxin poisoning disease can be preliminarily diagnosed according to clinical manifestations and pathological changes. This disease is mainly to prevent, there is no specific treatment, the following mainly introduces specific treatment methods.

1. Clinical symptoms of aflatoxin poisoning Calves are more sensitive to aflatoxin than adult cattle, which can be expressed as acute poisoning, while adult cattle have stronger resistance to toxins, which are mostly chronic.① Acute poisoning: mostly seen in calves, mainly manifested as depression, loss of appetite, arched back, convulsions, circular movement, unstable standing, easy to fall; ear tremor, dry nose mirror, mouth foam, molars; submandibular edema; conjunctivitis, corneal turbidity, yellow staining of mucous membranes, allergic reaction to light, blindness on one or both sides; diarrhea, abdominal pain, tenesmus, blood clots and mucus mixed in feces, anal prolapse, collapse. Death occurs within 48 hours and mortality is high.② Chronic poisoning: Calves show loss of appetite, slow growth and development, malnutrition, coarse hair, reverse standing, more dull, dry nose, emaciation. Panic, aimless wandering, diarrhea; adult cattle show depression, reduced feed intake, molars, jaundice, decreased milk production, forestomach atony, rumen distension, intermittent diarrhea, low mortality. 2. Pathological acute cases of aflatoxin poisoning include microcytic anemia, neutrophil especially lobulated leukocytosis, increased blood bilirubin, decreased erythrocyte hematocrit and prolonged coagulation time. Conjugated bilirubin was 39.2 mg/L and total bilirubin increased to 117.6 mg/L [2]. AST, γ-glutamyl transferase and alkaline phosphatase activity increased, while plasma carotene and vitamin A decreased significantly. Isocitrate dehydrogenase activity approached normal, but serum lactate dehydrogenase activity decreased. Blood urea nitrogen, albumin and total protein levels decreased. 3. Diagnosis of aflatoxin poisoning For the diagnosis of this disease, veterinary personnel should start with medical history investigation, and examine feed samples fed on site, combined with clinical manifestations, such as jaundice, hemorrhage, edema, digestive disorders and neurological symptoms; pathological changes, such as hepatocyte degeneration, necrosis, hyperplasia, liver cancer, etc., can be initially diagnosed. To make a definite diagnosis, it is necessary to isolate and culture the toxic mold and determine the aflatoxin content in the suspicious feed. If necessary, biological identification methods can also be carried out, that is, toxicity tests. The operation method of visual screening method is as follows: take suspicious feed samples, such as a small amount of corn, peanuts, etc., put them in plates in batches, spread them into a thin layer, and put them under ultraviolet lamp with wavelength of 365nm for fluorescence observation. If the feed contains aflatoxin G1 and G2, yellow-green fluorescence can be seen from corn and peanut particles; if the feed contains aflatoxin B 1 and B 2, blue-purple fluorescence can be seen. When no fluorescence is seen, repeat the operation and place it under ultraviolet lamp again. If no fluorescence is seen, it can be judged as negative sample. It should be noted that yellow-green and blue-purple fluorescence is observed under ultraviolet light, which must be distinguished from the fluorescence presented by other impurities, otherwise it is easy to lead to false positives of the sample. There are biological methods, immunological methods and chemical methods for aflatoxin determination. The commonly used methods are silica gel thin-layer chromatography or microcolumn chromatography. In recent years, aflatoxin detection methods, such as immunochemical assay, enzyme-linked immunoassay, gold-labeled test paper, affinity microsphere rapid detection technology, have been established and applied continuously. Generally, aflatoxin content in cattle diet exceeds 100μg/g, milk exceeds 0.5μg/g, it can be diagnosed as poisoning. 4. Treatment of aflatoxin poisoning There is currently no specific treatment for this disease. When aflatoxin poisoning has been suspected, the entire dairy farm must immediately stop feeding the existing feed and feed a feed rich in energy substances, such as green feed and high protein feed, and no or less high fat feed. Organize manpower to carefully observe the herd, find other sick cattle in time and separate them out for early treatment. Mildly ill cattle usually recover within a short period of time with intensive care. However, for cattle with severe poisoning disease, salt laxatives should be administered in time to facilitate detoxification. In addition, it is necessary to apply some liver-protecting, detoxifying and hemostatic drugs, such as 500~1000mL of 20% calcium gluconate injection, or 25%~30% glucose injection plus vitamin C preparation for intravenous injection at one time. For heart failure disease cattle, can be subcutaneous injection or intramuscular injection of sodium camphor sulfonate (cardiac stimulant). In order to control or avoid secondary infection, antibiotics should be used as appropriate, such as penicillin, streptomycin, etc., but sulfonamides cannot be applied. Intramuscular injection of oxytetracycline has a certain effect, 10mg per kilogram of body weight, 1~2 times a day, for 5 days. Alkaline activated carbon can also be taken orally to promote intestinal excretion of aflatoxin. Activated carbon diluted with phosphate buffer solution with pH value of 7 can be taken orally in large quantities; lipid alcohol compound 2mg/kg·w, once/day, intramuscular injection for 5 days. Cysteine or methionine 200mg/kg·w, intraperitoneal injection once, or sodium thiosulfate 50 mg/kg·w, intraperitoneal injection once.