Aflatoxin is a very toxic poison and also contains carcinogenic substances. Among the many toxins, it is the most toxic and can easily cause aflatoxin poisoning. Some foods may become mildewed due to improper storage, and all moldy foods may contain aflatoxin. We should pay special attention to this when feeding cats.
Mold is easy to grow on grains, oils and their products and nuts, such as peanuts and cotton seeds, etc., walnuts, almonds, hazelnuts, dairy products, dried salted fish, sea rice, dried peppers, dried radish strips, etc. Among them, peanuts and their products have the highest content of aflatoxin. After the food is contaminated by aflatoxin, at a suitable temperature (about 37℃) and humidity (relative humidity is 80% to 85%), aflatoxin quickly reproduces and produces toxins, called aflatoxin. Animal experiments have proved that aflatoxin is a severe liver cancer-causing toxin. Experiments have proved that aflatoxin is a fungimycin produced by flavonoids. It is one of the strongest chemical carcinogens found at present. It mainly damages liver function and has strong carcinogenic, teratogenic, and mutagenic effects. It can cause liver cancer and can also induce bone cancer, kidney cancer, rectal cancer, breast cancer, ovarian cancer, etc. Aflatoxin has relatively stable chemical properties and can only be destroyed at high temperatures above 280℃. It is insensitive to heat and cannot completely remove its aflatoxin at 100℃/20 hours.
1. Pathogenic process:
Initially, AFB1 rapidly accumulates and binds to hepatocyte DNA and protein conjugation, disrupting intracellular metabolism, cell renewal, protein synthesis and fat secretion. GSH depletion in hepatocytes leads to oxidative damage to the cell membrane and loss of intracellular enzymes (including GSH-S-transferases). Cells around the hepatic vein are affected first, because this site produces the most CYP450s. Eventually, the toxin causes cell lysis and necrosis and the liver cell parenchyma collapses. Structural destruction inhibits blood outflow in the sinusoidal space of the liver, causing intrahepatic portal hypertension, and increased production of disse lacunar ultrafiltrate (lymph). Increased hepatic lymphogenesis causes it to leak from the liver envelope into the abdominal cavity. Acute portal hypertension is accompanied by impaired synthesis of coagulation factors, causing oozing bleeding and bleeding of intestinal red blood cells (RBC). Intestinal bleeding provokes the occurrence of hepatoencephalosis, which is consistent with the semi-coma state of cats with end-stage aflatoxin poisoning. Some cats may experience multiple acquired portal system short circuits, which confirms the occurrence of portal hypertension.
2. Clinical symptoms:
Poor mental health, decreased appetite, normal body temperature, different degrees of yellowness of the mucosa can be seen. As the condition develops, the spirit becomes more depressed and the appetite is dysfunctional. Severe dogs vomit with blood and have yellow abdominal skin, body temperature drops below 38 degrees, feces appear in the color of coal tar, bloody stool, dark yellow urine, and neurological symptoms such as convulsions before death.
III. Clinical pathology:
Clinical pathology abnormalities are mainly reflected in the following aspects:
(1) Coagulation disorders: activated part of the thrombin kinase time (aPTT), prothrombin time (PT), reduced fibrinogen concentration, reduced plasma antithrombin activity, C protein and FVII:C - 96%, and diffuse intravascular coagulation (secondary to procoagulant and anticoagulant factor depletion).
(2) Electrolyte disorder: reflects dehydration, vomiting, diarrhea, abnormal fluid retention or disordered distribution.
(3) Hypoalbuminemia.
(4) Hepatic enzyme activity varies slightly to significantly: ALT increased, 83%; AST increased, 79%; ALP increased, 66%; GGT increased, 44%.
(5) Hyperbilirubinemia.
(6) Hypocholesterolemia (71%).
Ultrasound examination may show hyperechoic or hypoechoic liver nodules, thickening of gallbladder walls and hyperplasia, enlarged mesenteric lymph nodes, and some abdominal exudates without echo. The liver surface configuration may be abnormal. Some cats have stomach relaxation and use of gastrointestinal exercise promoters is ineffective. The blood cell and histological examination of the cats with dead were consistent with fine needle aspiration of liver, and both showed diffuse hepatocyte lipid vacuolation, and hepatocyte degeneration and mild inflammatory cell infiltration may also occur.
IV. Diagnosis:
Usually, it is necessary to test the aflatoxin content in food to confirm the diagnosis. In terms of clinical pathology, the reduction of plasma C protein, antithrombin activity and serum cholesterol concentrations are the most sensitive biochemical detection indicators for cats with less obvious symptoms, and the sensitivity of liver enzyme activity is slightly worse.
V. Treatment:
The cat is subject to supportive treatment. After the initial diagnosis of cats, thiol donors (such as N-acetylcysteine, adenosine methionine) were used for 2 months. When vomiting occurs, antiemetics and gastrointestinal mucosa protective agents are given. In the presence of coagulation disorder, frozen plasma is infused. In addition, vitamin K1, vitamin E (≤10IU/kg/d), etc. must be given.
In order to prevent the production of aflatoxin, it is necessary to keep the temperature low, ventilated, dry, and avoid direct sunlight when storing grain, oil and other foods. Do not use plastic bags to store food, and do not stock up on food as much as possible. Pay attention to the shelf life of the food and eat it during the shelf life as much as possible. In daily life, you can use tea tree oil, olive oil and other vegetable oils that are not prone to aflatoxin. In addition, do not eat moldy, wrinkled, or discolored foods. Moldy Chinese medicine contains a lot of aflatoxin and should not be taken again.