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1.
1. This study was to evaluate the toxic effects of aflatoxin (AF) on growth performance of quail, and to determine the preventive efficacy of MYCOTOX (oxicinol, tymol, micronised yeast). 2. One hundred and eighty 1-d-old quail (Coturnix coturnix japonica) of both sexes were weighed and randomly divided into 4 experimental groups each with 5 replicates of 9 birds. 3. There were 4 dietary treatments: (1) control with 0 mg AF/kg diet and 0% MYCOTOX; (2) 0 mg AF/kg diet and 0.5% MYCOTOX; (3) 2.5 mg AF/kg diet and 0% MYCOTOX; (4) 2.5 mg AF/kg diet plus 0.5% MYCOTOX. The chicks were maintained on these treatments to 3 weeks of age. Quail consumed the diets and water ad libitum. 4. Body weight (BW) gains in groups receiving AF alone were the lowest at all periods. Feed intake was lowest in the group consuming the AF diet. The addition of MYCOTOX to the AF diet did not prevent or reduce the toxic effects of AF on feed intake at any time period. Feeding diets containing MYCOTOX alone did not change feed intake significantly. With the exception of the 1 to 7 d period, feed conversion of chicks fed the AF diet was similar to those of the other experimental groups. 5. Bursa of Fabricius weight decreased, whereas the relative weights of liver, kidney and spleen increased in quail consuming diets containing AF and AF plus MYCOTOX. Liver colour was normal in the control and MYCOTOX alone group, but was lighter in groups fed AF. 6. The results indicated that MYCOTOX was not effective in preventing the deleterious effects of AF.  相似文献   

2.
A biological assay was carried out to evaluate the impact of dietary tryptophan (TRP) in aflatoxin B1‐contaminated diets (AFB1‐D) on performance, blood parameters, immunity, meat quality and microbial populations of intestine in Japanese quails. Six experimental diets were formulated to include two levels of dietary TRP; 2.9 (moderate high: MH‐TRP) and 4.9 g/kg (excess: Ex‐TRP); and three levels of AFB1 (0.0, 2.5, and 5.0 mg/kg). Each experimental diet was fed to the one of the six groups of birds from 7 to 35 days of age in a completely randomized design with 2 × 3 factorial arrangement. Decrease in feed intake, body weight gain and gain:feed in birds fed 5.0 mg/kg AFB1‐D was restored to the control level by 4.9 g TRP/kg of the diet. The hepatic enzymes in blood were elevated in quails fed on AFB1‐D but attenuated by 4.9 g TRP/kg of the diet (Ex‐TRP; p ≤ .01). High serum uric acid in birds challenged with AFB1 significantly decreased by Ex‐TRP (p ≤ .01). The skin thickness to 2,4‐dinitro‐1‐chlorobenzene challenge suppressed by AFB1 but increased by Ex‐TRP diet (p ≤ .02). The AFB1 increased the malondialdehyde in meat, whereas TRP efficiently diminished malondialdehyde production (p ≤ .01). The greatest drip loss and pH in meat were observed in the birds fed 5.0 mg/kg AFB1‐D but Ex‐TRP augmented the adverse effects of AFB1 (p ≤ .01). The Ex‐TRP reduced the total microbial and Escherichia coli counts (p ≤ .01). The adverse effect of AFB1 on ileal Lactic acid bacteria was completely prevented by Ex‐TRP (p ≤ .03). This study showed that tryptophan supplementation could be considered as a powerful nutritional tool to ameliorate the adverse effects of AFB1 in growing quails.  相似文献   

3.
黄曲霉毒素是由黄曲霉和寄生曲霉产生的有毒代谢产物。当犬采食被黄曲霉和寄生曲霉污染的食物,常可发生中毒。  相似文献   

4.
Experimental aflatoxicosis in young swine   总被引:1,自引:0,他引:1  
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5.
Naturally occurring aflatoxicosis is described in goats fed a concentrate mixture containing polkudu meal (defatted residue from grated coconut after juice extraction). Toxigenic strains of Aspergillus flavus were present in the concentrate and aflatoxins were recovered from the liver and urine of affected animals. Hepatic lesions in poisoned goats consisted of bile duct hyperplasia and periportal fibrosis; renal lesions included necrosis of tubular epithelial cells and proteinaceous exudation in the glomerular space. Similar lesions were produced experimentally in goats with aflatoxin and the coconut cultures of A flavus. High doses of aflatoxin B1 produced, in addition, hepatic centrilobular congestion, haemorrhage and periportal fatty change.  相似文献   

6.
Biochemical studies on aflatoxicosis   总被引:7,自引:0,他引:7  
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7.
Progression of aflatoxicosis in growing barrows   总被引:5,自引:0,他引:5  
The progression of aflatoxicosis was evaluated in growing crossbred barrows given 0, 1, 2, 3, or 4 mg of aflatoxin (AF)/kg of feed for 28 days (6 to 10 weeks of age). On day 28, pigs were euthanatized and necropsied, and tissues were removed for histologic examination. Body weight gains were decreased in barrows fed 2 mg of AF/kg after 7 days and in barrows fed 1 mg of AF/Kg after 14 days. By 28 days, all barrows fed AF had decreased body weights and weight gains. Compared with decreased in all barrows fed AF. Neither liver weights nor bone ash values were altered, although liver lipid values were increased in barrows fed AF. Serum aspartate transaminase, gamma-glutamyl transferase, and alkaline phosphatase activities were increased in barrows fed AF, whereas creatine kinase activity was decreased. Aflatoxin diets resulted in decreases in serum concentrations of urea nitrogen, phosphorus, cholesterol, albumin, and total protein. Histologic alterations in liver included interlobular fibrosis, periportal lipidosis, bile duct hyperplasia, and periportal lymphocytic infiltration. Lymphocytes in the thymus were depleted, and numbers of granulocytic cells in the bone marrow were reduced. The frequency and severity of lesions increased with increased doses of AF.  相似文献   

8.
9.
Immunosuppression in broilers under experimental aflatoxicosis   总被引:2,自引:0,他引:2  
The effects of purified aflatoxin B1 on cell mediated immunity in broilers were carried out using 0.3 p.p.m. and 1 p.p.m. dose level. The percentage of acid alpha-naphthyl acetate esterase reacting lymphocytes was significantly (P less than 0.05) decreased in chicks fed 0.3 p.p.m. and 1 p.p.m. level of aflatoxin B1. The albumin and globulin values were also significantly decreased (P less than 0.05) at both dose levels.  相似文献   

10.
SUMMARY Five cases of aflatoxicosis in pigs in southern Queensland are described. One peracute case where aflatoxin concentrations of up to 5000μg aflatoxin B1/kg were demonstrated in stomach contents was presumed to be caused by consumption of mouldy bread. High levels of toxins were also present in the livers. Two cases of acute toxicity were caused by feeding mouldy peanut screenings containing 22000μg aflatoxin B1/kg. One case of subacute and one of chronic toxicity were caused by sorghum grain based rations with lower aflatoxin levels (4640 and 255 μg/kg). Peracute toxicity caused collapse and deaths within several hours, acute toxicity caused deaths within 12 h and with subacute toxicity deaths occured after 3 weeks on a toxic ration. Anorexia and ill thrift affecting only growing animals were seen with chronic toxicity. Extensive centrilobular liver necrosis and haemorrhage occured with peracute toxicity and in cases of acute poisoning there was hepatic centrilobular cellular infiltration, hepatocyte swelling and bile stasis. With subacute toxicity hepatocyte vacuolation together with bile stasis and bile ductule hyperplasia were seen.  相似文献   

11.
12.
During an outbreak of aflatoxicosis in dogs living in Sao Paulo, two cases of disseminated intravascular coagulation were observed in association with the ingestion of an aflatoxin contaminated dog food. The first dog, a four-year-old, male, German shepherd developed haematemesis, melaena, petechial haemorrhages and jaundice progressing to uraemia, encephalopathy and death. The second dog, an 11-month-old, female, basset hound showed jaundice and ascites with no obvious haemor-rhagic signs, except the persistence of bleeding at the sites of venepunctures and petechiae on the oral mucosa. As overall signs deteriorated and evolved to uraemia, the dog was killed. Both had a prolonged whole blood clotting time (120 and 12 minutes), one stage prothrombin time (300 and 24 seconds) and activated partial thromboplastin time (320 and 180 seconds), reduction in the plasma fibrinogen (0–14 g/litre and 0–6 g/litre), thrombocytopenia (150 × 109/litre and 32 × 109/litre) and a positive protamine sulphate test, indicating the presence of fibrin monomers. The occurrence of disseminated intravascular coagulation was confirmed by the observation of multiple areas of infection in kidney and lung and by the presence of fibrin clots inside pulmonary vessels.  相似文献   

13.
Acute aflatoxicosis: a review   总被引:4,自引:0,他引:4  
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14.
The efficacy of melatonin co-administration on aflatoxicosis in chicks was investigated. Ross PM3 breed chicks were divided into groups of 10 and given conventional feed. One of the groups was kept as a control (C), and the others were given 150 ppb aflatoxin (AF1), 300 ppb aflatoxin (AF2), 150 ppb aflatoxin plus 10 mg/kg/bwt melatonin (AF1+M), 300 ppb aflatoxin plus 10 mg/kg/bwt melatonin (AF2+M), 10 mg/kg/bwt melatonin (M), and 1% ethanol (E). After 21 day-treatment period, the chicks were sacrificed, liver and kidney tissues were collected, processed for immuno-histochemical staining, in situ TUNEL method, and biochemical analyses. Vacuolar degeneration, necrosis, bile duct hyperplasia in liver, and mild tubular degeneration in kidney were detected in AF groups. Pathological changes were markedly reduced in AF+M groups, and a microscopic view similar to group C was observed. Increased immunoreactivity against inducible nitric oxide synthase (iNOS) and nitrotyrosine was detected in AF groups compared to weak immunoreactivity in group C. Immunoreactivity in AF+M groups was markedly reduced compared to AF groups and was similar to group C in liver and kidney. Many apoptotic cells were detected in the livers of AF groups, whereas there were no apoptotic cells in AF+M groups. While reduced glutathione (GSH) levels in liver and kidney of AF groups were greatly reduced, malondialdehyde (MDA) levels increased. With melatonin co-administration, the levels of GSH and MDA approached to the values of group C. These results indicated that nitrosative tissue degeneration caused by aflatoxin could be greatly reduced by melatonin supplementation in chicks.  相似文献   

15.
An outbreak of chronic liver disease was investigated in a kennel of dogs. Anorexia, depression, polyuria, polydipsia, icterus and a terminal hemorrhagic diathesis were noted in clinically affected dogs. Thrombocytopenia, hypofibrinogenemia, elevated fibrinogen degradation products and prolonged activated partial thrombosplastin times (PTT) and one-stage prothrombin times (PT) were associated with the hemorrhagic crisis. Aflatoxicosis was confirmed by the presence of significant levels of aflatoxicosis was confirmed by the presence of significant levels of aflatoxin B in the commercial dog food being fed. A subacute hepatitis was found on necropsy. Disseminated intravascular coagulation was suspected as the cause of the hemorrhage in these cases and treatment was instituted.  相似文献   

16.
通过取发病小天鹅(Cygnus columbianus)的组织进行培养、并对黄曲霉毒素(Aflatoixin)进行定性、定量检测以及动物回归试验,确诊为该病是霉菌病所引发的后遗症,随后采用了保肝排毒的方法进行治疗,取得了明显的疗效。结果表明:采用杀菌与排毒相结合的方法是根治霉菌病及其后遗症的一种有效的方法。  相似文献   

17.
18.
Acute experimentally induced aflatoxicosis in the weanling pony   总被引:1,自引:0,他引:1  
Nineteen weanling ponies and 1 adult pony were given a single oral dose of aflatoxin B1 (AFB1). Dosages were: 0, 0.5, 1, 2, 4, 5, 6, and 7.4 mg of AFB1/kg of body weight. Vital signs were monitored, and whole blood and serum collected for analysis of serum enzymes, prothrombin time, blood cell counts, and serum urea nitrogen. Ponies that died were examined for gross lesions, and tissues were collected for histopathologic examination and analysis of AFB1 and AFM1 residues. Two of the 4 ponies given the 2 mg/kg dose and all ponies given the larger dosages died within 76 hours. Clinical signs included increased rectal temperature, faster heart and respiratory rates, abdominal straining, bloody feces, and tetanic convulsions. At necropsy, ponies that died of acute aflatoxicosis showed visceral petechiae and hepatic focal lesions. Histopathologic changes included severe hepatic necrosis, vacuolation, and bile duct hyperplasia. Aflatoxins B1 and M1 were recovered from liver, kidney, skeletal muscle, and gastrointestinal contents. One other pony given the 2 mg/kg dose died 32 days after dosing, and 1 control pony died after 70 days. Continuous elevations in prothrombin time and serum aspartate aminotransferase, alanine aminotransferase, and gamma-glutamyl transpeptidase levels were observed in ponies dosed at 4 mg/kg or more. Significant (P less than 0.05) elevations in these values, which peaked 2 to 3 days after dosing, were seen in ponies given the 2 mg/kg dose. This group also had significant increases over controls in PCV and hemoglobin concentration 5 days after dosing.  相似文献   

19.
In Brazil, mycoplasmas were isolated from the sinuses of Japanese quails (Coturnix coturnix japonica) from two commercial flocks affected with sinusitis. The major respiratory signs and gross lesions are described. Based on serological and biochemical results, the mycoplasmas isolated were identified as Mycoplasma gallisepticum. One of the isolates was pathogenic for chickens.  相似文献   

20.
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