08:50,11,May,2008 | (2106/0/0) | Original

aflatoxin poisoning symptoms


About the main cause of aflatoxin poisoning, liver cell degeneration, necrosis and hemorrhage. On clinical diagnosis with systemic bleeding, digestive function disorders, ascites, is characterized by neurological symptoms. Aflatoxins are mainly produced by Aspergillus flavus and parasitic toxic metabolites. Aflatoxin was not a single substance, but a class of compounds very similar structure. Aspergillus flavus and parasites such as widespread in nature, the main contamination of corn, peanuts, beans, wheat, straw. Aflatoxin is mainly distributed in the liver, liver microsomes via mixed function oxidase catalyzed hydroxylation occurs, demethylation and epoxidation. Effects of aflatoxin DNA, RNA synthesis and degradation, protein and fat synthesis and metabolism, mitochondrial metabolism and lysosomal structure and function. Aflatoxin is also carcinogenic, mutagenic and teratogenic nature. Clinical symptoms of acute type occurs in 2 to 4 months old piglets, pigs depression, anorexia, weight loss. Visible mucous membranes pale, post-stained. Normal appetite and a high incidence of able-bodied pig. Elevated or normal body temperature, mental depressed; stool dry and hard spherical surface coating of mucus and blood. Unsteady gait, and intermittent convulsions, opisthotonus, the skin surface purpura. The late onset of neurological symptoms. Disease characterized by the eat less, weak, pale conjunctiva, jaundice, fecal dry. Occurs when severe intermittent seizures. Pathological changes of the main lesions were anemia and bleeding. Body mucosa, serosa, skin and muscle bleeding; kidney, diffuse gastric bleeding, mucosal bleeding, edema, enlargement of the liver, spleen bleeding. Acute cases were acute toxic hepatitis, chronic liver patients seen and interstitial tissue cells. Diagnosis and clinical differential diagnosis with a history of performance (jaundice, bleeding, edema, digestive disorders and neurological symptoms) and pathological changes (liver cell degeneration, necrosis), etc., can be the initial diagnosis. Diagnosis of isolated fungi needs to be done, and the determination of aflatoxin. Prevention Expelling liver detoxification. 1 capillaris prescription rhubarb 20g 20g 20g Gardenia Usage: water to cook to the residue to cool, add glucose 30-60g, vitamin C 0.1-0.5g mixed, one fed. Description: its replacement feed, environmental disinfection. 2 15g licorice prescription wind bean 500g white sugar 60g 30g Usage: before the shamisen Tong Jian juice, add sugar, mix a fed.
aflatoxin poisoning symptoms

For more information see aflatoxin poisoning symptoms of aflatoxin poisoning map
Overview of aflatoxin poisoning (Aflatoxicosis) are zoonotic diseases. Disease to liver damage, systemic bleeding, ascites, digestive dysfunction, and neurological symptoms such as features. Countries in the world of aflatoxin production, distribution an
d toxicity aspects of a comprehensive, systematic and in-depth research, published research papers, reviews, and monographs and other literature, more than 3 000. China's Jiangsu, Guangxi, Guizhou, Hubei, Heilongjiang, Tianjin, Beijing and many other provinces also have reports of the disease, livestock and poultry.
(A) cause
The pathogen is aflatoxin, although literature data indicate that the bacteria can produce aflatoxin, including Aspergillus flavus, Aspergillus parasitic, slip Aspergillus niger, which are more than 20 species. However, recent research confirms many of the researchers, only the parasitic Aspergillus flavus and aflatoxin production. Moreover, not all A. flavus strains produce aflatoxins. Early records, Aspergillus flavus isolated from nature, only 10% of the strains producing aflatoxin. However, recent research shows that the proportion of strains producing toxin, a clear upward trend.
Now determined the structure of aflatoxins are B1, B2, B2α, B3, D1, G1, G2, G2α, M1, M2, Pl, Q1, R0 and other 18 kinds, and have been chemically synthesized. Where B1, B2, G1 and G2 are 4 basic aflatoxins, other types are derived from these 4. Their chemical structure is very similar, and both contain a double furan ring and a naphthalene-oxa-o-one (also known as coumarin). Aflatoxin B1 crystal is very stable, high temperature (200 ℃), ultraviolet radiation, do not make the damage. Heated to 268 ~ 269 ℃, began to decompose. 5% sodium hypochlorite, can completely destroy aflatoxin. In Cl2, NH3, H202 and S02 in aflatoxin B1 have been destroyed.
The distribution of aflatoxin wide range, any aflatoxin contamination of the fungus can produce food, forage, are likely to exist aflatoxin. Found even in the absence of fungi, fungal mycelium and spores of the food and agricultural products, but also found aflatoxin. Poisoning is due to extensive grazing of livestock and poultry those containing large amounts of aflatoxin and agricultural forage and disease. Due to gender, age and nutritional status, etc., the sensitivity is different. The sensitivity order: duck child> Fire chicks> chicks> Japanese quail; pig> calf> Pigs> adult cattle> sheep . and poultry are the most sensitive, especially Youqin.
According to the census at home and abroad, to peanuts, corn, soybeans, cotton seed and other crops and their by-products, the most susceptible Aspergillus flavus, aflatoxin content with more. Countries and relevant United Nations organizations have developed a food, feed, the maximum allowable amount of aflatoxin standards.
(B) the toxicity
Large amount of experimental data show that aflatoxin is not only animals and plants, microbes and people have very toxic, but also poultry, a variety of animal and human cancer has obvious ability. Aflatoxin B1 is found in most chemical carcinogens, B1 can cause mutations and lead to deformities.
Large number of experimental results show that aflatoxin can inhibit participation labeled precursors into deoxyribonucleic acid (DNA), ribonucleic acid (RNA) and protein synthesis. Particularly marked inhibition of precursor incorporation induced enzyme protein. Carcinogenic effects of aflatoxins and other toxic effects in this molecular mechanism.
Further studies scholars confirmed aflatoxin inhibition of nucleic acid synthesis, possibly by direct effect on aflatoxin induced DNA synthesis enzymes, or due to aflatoxin and the combination of DNA, changing the DNA template.
Electron microscopy studies confirmed that the granting of aflatoxin observed after the initial 30min of cell changes that occur in the nucleolus, including the redistribution of its contents. Followed from changes in the cytoplasm, a reduction in ribosomal ribosome disassembly, the proliferation of endoplasmic reticulum, glycogen loss and degradation of mitochondria.
Aflatoxin B1 in animals there are two major metabolic pathways: first, hydroxylation, generating a single hydroxyl derivatives M1, commonly found in milk, urine, faeces and liver; the second is the role of demethylation to produce phenol ring derivatives of P1, mainly in the urine. In addition, epoxidation occurred in part to generate 2,3 - epoxide, further combined with glutathione to produce glutathione conjugates.
Clinical symptoms in poultry in young ducks and turkeys on the most sensitive to aflatoxin, poisoning, to take on more acute after. Most patients ducklings appetite loss, unsteady gait, ataxia, cervical muscle spasm, to present the opisthotonus symptoms and death. Turkey 2 to 4 weeks of age more than the incidence of death, 8-week-old turkeys for more than a certain degree of resistance to aflatoxin. After the onset of a small turkey, the performance of lethargy, loss of appetite, weight loss, drooping wings, hair loss, diarrhea, cervical muscle spasm and opisthotonos. Disease symptoms of chicken and duck are basically similar to young and small turkey, but lightly stained or pale comb, diarrhea, and more dilute manure mixed with blood. Adult chicken mostly chronic poisoning symptoms, mainly characterized by cachexia, to reduce Salmonella and other pathogenic microorganisms in the resistance, fatty liver syndrome caused by the hens, egg production and hatching rate decreased.
Blood test, serum protein components are sick is lower than normal, showing severe hypoproteinemia; significantly reduced red blood cell count, WBC count increased, coagulation time. Grass Valley, one of acute cases of transaminase, citrulline transferase and prothrombin activity increases; sub-acute and chronic type of case, isocitrate dehydrogenase and alkaline phosphatase activity also significantly increased
Dead poultry in the pathological changes characteristic of liver damage. Acute type of liver enlargement, diffuse hemorrhage and necrosis. Subacute and chronic type of hepatic cell proliferation, fibrosis and stiffening of the liver volume reduced. Course in 1 year or more, can be found in the liver cell tumors, hepatocellular carcinoma or cholangiocarcinoma.
First, to investigate the history of differential diagnosis, feed quality and mold inspection situation, feed and poultry feeding incidence of suspected positive correlation, do not eat this batch of poultry feed, not the incidence of suspicious, non-infectious disease of poultry but also performance. Then, with symptoms of clinical diagnosis, blood tests and pathological changes in other materials, to undertake a comprehensive analysis of excluding infectious diseases and the possibility of nutritional and metabolic diseases, and in line with fungal toxins poisoning the basic characteristics of the disease, you can make a preliminary diagnosis. To achieve the exact diagnosis, tests must be carried out following procedures.
1. Suspected pathogenic fungi feed Isolation and identification. Czapek culture with hypertonic 24 ~ 30 ℃ temperature on incubation, observe the colony growth rate, colony color, surface, and exudate, texture and smell of the colony, recorded after the culture with the microscope examination of live training, and to stop the checks to the dominant bacteria identified, or parasitic Aspergillus flavus.
2. Determination of aflatoxin suspect feed.
(1) Suspicious feed intuitive method: prediction method can be used as aflatoxin. Take representative samples of suspicious feed (such as corn, peanuts) 2 ~ 3kg, Sheng plate batches, the share into a thin layer, directly on the 365nm wavelength ultraviolet light green fluorescence; if there is aflatoxin G1 samples , G2, G family of toxins can be seen with the feed particles issued bright yellow-green fluorescence; Should a family of toxins with aflatoxin B, you can see the blue-violet fluorescence. If you do not see the fluorescent particles can be broken up after the observation.
(2) Chemical analysis: first suspected aflatoxin extraction and purification, and then use the thin-layer chromatography with known standards of aflatoxin contrast, measured to confirm the nature and amount of aflatoxin (Refer to Food Hygiene Law of the PRC and other relevant information).
3. Biological assay
(1) duckling method: This is the world's statutory common method. Optional 1-day-old ducklings, will test samples dissolved in propylene glycol or water, ducklings fed through a gastric tube to feed 4 to 5 days. Ducklings fed the control of the amount of aflatoxin B1 from 0 to 16
1 incidence
A small amount of chicken in large chicken cough, shakes phenomenon, accompanied by individual Swollen face, runny nose fluid, that drug treatment of chronic respiratory disease by 3 days is not valid. Subsequent reduction of feed intake, egg fade, white, yellow-green loose stools appear individually, which they suspected bird flu, plus antiviral drugs, but after a few days still valid. Chicken feed intake and decreased egg production rate decreased gradually, egg quality deterioration, there white eggs, sand shell eggs, broken egg, in late March to 50% reduction in feed intake, egg production dropped to 30%, and of death, ranging from 5 to 8 a day, I stand with the laboratory to diagnosis and treatment.
2 necropsy lesions
Inspection of chicken are weight loss, dehydration, nasal mucosa congestion, within the mucus. Individual serious chicken ascites, hepatomegaly, hardened, yellow and white necrotic spots. Most of all chicken necropsy showed pericarditis, peritonitis, perihepatitis, balloon inflammation. Pericardial thickening, pericardial yellow liquid inside, heart, heart crown heavy bleeding spots on the chest wall is also a large number of blood spots; peritoneum, thickened air bags, coated with a layer of the liver, abdominal cavity has broken most of the abdominal cavity filled with yolk; the intestinal mucosa of severe bleeding; liver enlargement, hardening, bleeding spots, some with yellow-white necrotic spots; spleen enlargement, bleeding spots; the pancreas with bleeding spots; kidney swelling, discoloration, bleeding spots.
3 Diagnosis and treatment
According to the incidence and pathological changes, diagnosed as aflatoxin poisoning, the following treatment.
3.1 remove the residual feed trough, and 0.05% copper sulfate solution with cleaning trough, replacement feed.
3.2 in the feed by adding nystatin tablets, according to one kilogram feed 2 for 5 days.
3.3 U.S. drinking water can be added to the net, by 250 kg / bottle for 5 days.
3.4 coop spray disinfection with 0.05% copper sulfate, 1 day, 3 days.
3 days using the above measures, death to stop, 5 days after the disease under control, feed intake increased egg production rate of recovery after a half months to 88%.
4 Analysis
4.1 As long rainy autumn of 2003, resulting in the widespread occurrence of a large area of corn mildew, which is leading a major factor in aflatoxin poisoning.
4.2
Aflatoxin poisoning occurred for another reason: as a result of aflatoxin poisoning, chicken feed intake decreased, eating is not a net slot, and breeder chickens in the pathogenesis of the day, add the feed to the feed tank, do not eat chicken End, plus the period of temperature and humidity, then led to further moldy feed in the trough, so that the extent of poisoning increased.
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