What should I do if the cat is poisoned by aflatoxin? What are the first aid methods? Aflatoxin is a very toxic poison and also contains carcinogenic substances. Among them, it is the most toxic and can easily cause aflatoxin poisoning. Some foods will become moldy due to improper storage, and any moldy food may contain aflatoxin. We should pay special attention to this in the usual feeding and feeding of cats.

Mold easily grows on grains, oils and their products and nuts, such as peanuts, cottonseeds, etc., walnuts, almonds, hazelnuts in dried fruits , dairy products, dry and salted fish, dried sea rice, dried peppers, dried radish strips, etc. Among them, peanuts and their products have the highest content of aflatoxin.

After food is contaminated with aflatoxin, under suitable temperature (about 37°C) and humidity (relative humidity of 80% to 85%), Aspergillus flavus It reproduces quickly to produce a toxin called aflatoxin. Animal experiments have shown that aflatoxin is a severe hepatocarcinogenic toxin. Experiments have shown that aflatoxin is a fungus produced by Flavobacterium, and it is one of the strongest chemical carcinogens found so far. It mainly damages liver function and has strong carcinogenic, teratogenic and mutagenic effects. Cause liver cancer, can also induce bone cancer, kidney cancer, rectal cancer, breast cancer, ovarian cancer and so on. Aflatoxin has relatively stable chemical properties and can only be destroyed at high temperatures above 280°C. It is not sensitive to heat, and aflatoxin cannot be completely removed at 100°C/20 hours.

First, the pathogenic process:

Initially, AFB1 Rapid accumulation binds to hepatocyte DNA and protein conjugation, disrupting intracellular metabolism, cell turnover, protein synthesis and fat excretion. GSH depletion in hepatocytes results in oxidative damage to the cell membrane and loss of intracellular enzymes, including GSH-S-transferase. Cells around the hepatic vein are affected first, as this site has the most epoxide-producing CYP450s. Ultimately, the toxin causes cytolytic necrosis and collapse of the hepatocyte parenchyma. Structural disruption inhibits hepatic sinusoidal blood outflow, causing intrahepatic portal hypertension and increased disse lacunar ultrafiltrate (lymph) production. Increased hepatic lymphogenesis results in leakage from the liver capsule into the abdominal cavity. Acute portal hypertension is accompanied by impaired coagulation factor synthesis, resulting in exudative hemorrhage and bleeding of intestinal red blood cells (RBCs). Intestinal hemorrhage contributes to the development of hepatic encephalopathy, which is consistent with the semi-coma state of cats at the end stage of aflatoxin poisoning. Several acquired short circuits of the portal system can be seen in some cats, confirming the presence of portal hypertension.

Second, clinical symptoms:

Poor spirit, Loss of appetite, normal body temperature, and varying degrees of yellowing of the mucous membranes. Severe dogs vomit with blood and yellow staining of the abdominal skin, the body temperature drops below 38 degrees, and the feces are coal tar color, or bloody stools, dark yellow urine, and neurological symptoms such as convulsions before death.

III. Clinicopathology:

Clinicopathology abnormality It is mainly reflected in the following aspects:

(1) Coagulation disorders: activated partial thromboplastin time (aPTT), prothrombin time (PT) prolongation, fibrosis Decreased proprotein concentration, plasma antithrombin activity, protein C, and FVII:C decreased—96%, disseminated intravascular coagulation (secondary to procoagulant and anticoagulant factor depletion).

(2) Electrolyte imbalance: It reflects dehydration, vomiting, diarrhea, abnormal retention or distribution of body fluids.

(3) Hypoalbuminemia.

(4) Liver enzyme activity was mildly to significantly increased: ALT increased, 83%; AST increased, 79%; ALP increased, 66%; GGT increased, 44%.

(5) Hyperbilirubinemia.

(6) Hypocholesterolemia (71%).

Ultrasound may show hyperechoic or hypoechoic liver nodules, gallbladder wall thickening and bile duct hyperplasia, enlarged mesenteric lymph nodes, and some anechoic abdominal cavities exudate. The liver surface configuration may be abnormal. Some cats develop gastric atony that is not effective with gastrointestinal motility enhancers. The hepatic fine needle aspiration cytology and histological examinations of the dead cats were consistent with diffuse hepatic lipid vacuolation, hepatocyte degeneration and mild inflammatory cell infiltration.

Diagnosis:

It is usually necessary to detect Aflatoxin content to confirm the diagnosis. In terms of clinicopathology, decreased plasma protein C, antithrombin activity and serum cholesterol concentration are the most sensitive biochemical indicators for cats with asymptomatic symptoms, while liver enzyme activity is less sensitive.

V. Treatment:

Supportive care for affected cats . Sulfhydryl donors (eg, N-acetylcysteine, adenosylmethionine) were used for 2 months after the cat's initial diagnosis. Administer antiemetics and gastrointestinal mucosal protectants when vomiting occurs. Frozen plasma transfusion in the presence of coagulation disorders. In addition, vitamin K1 and vitamin E (≤10IU/kg/d) should be given.

In order to prevent the production of aflatoxin, it is necessary to keep low temperature, ventilated, dry, and avoid direct sunlight when storing grain, oil and other foods. Avoid hoarding food as much as possible, pay attention to the shelf life of food, and eat it within the shelf life as much as possible. In life, you can use vegetable oils that are not easy to produce aflatoxin, such as tea tree oil and olive oil. In addition, do not eat moldy, wrinkled, discolored food. Moldy Chinese medicine contains a lot of aflatoxin and should not be eaten.